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2 








Each Kugania eloaen 


LANE MEDICAL LIBRARY 


STANFORD UNIVERSITY 
MEDICAL CENTER 


STANFORD, CALIF. 94305 





LANE | IRRARV CTAAIFAMET ven N 


GENERAL PATHOLOGY 


OR 


THE SCIENCE OF THE CAUSES, NATURE AND COURSE 
OF THE PROCESSES OF DISEASE 


BY 
DR. ERNST/ ZIEGLER 


PROFESSOR OF PATHOLOGICAL ANATOMY AND OF GENERAL PATHOLOGY 
IN THE UNIVERSITY OF FREIBURG IN BREISGAU 


TRANSLATED FROM 
THE TENTH REVISED GERMAN EDITION 


(GUSTAV FISCHER, JENA, 1901) 
AND EDITED 


BY 
ALDRED SCOTT WARTHIN, Pu.D.. M.D. 


PROFESSOR OF PATHOLOGY AND DIRECTOR OF THE PATHOLOGICAL LABORATORY IN THE 
UNIVERSITY OF MICHIGAN, ANN ARBOR, MICHIGAN - 


Profuselp Tllustrated 


NEW YORK 
WILLIAM WOOD AND COMPANY 
MDCCCCHI 


CoPYkıiGaT, 1908 
By WILLIAM WOOD AND COMPANY 


RUDOLF VIRCHOW 


IN AUFRICHTIGER VEREHRUNG 
GEWIDMET 


AUTHOR’S PREFACE TO THE TENTH EDITION. 


N the following pages of the tenth edition of my ‘Text-book of Gen- 
I eral Pathology and Pathological Anatomy ” are to be found the re- 
sults of two and twenty years of labor that has been but rarely inter- 
rupted. Sincethe first edition, which appeared in 1881, I have constantly 
endeavored to improve the book both in its contents as well as in its 
form; and I believe that I dare commit myself to the hope that in this 
edition there is offered a work which, within its assigned limits, presents 
the most important achievements of the nineteenth century in the field 
of general pathology and pathological anatomy in such a form as to 
meet the needs of the practising physician as well as of the student, who 
through the study of such would acquire a scientific foundation for prac- 
tical medicine. 

He who to-day looks back upon the results of medical investigation 
during the nineteenth century finds his attention involuntarily fixed 
upon that investigator who for the full half of the century just passed 
has been constantly active, and who through his scientific labors and his 
teaching has pointed the way to the knowledge of morbid processes, their 
nature and their origin; and in part has himself realized, and in part has 
paved the way and made possible the great advance of the past century 
in the domain of general pathology and pathological anatomy. There- 
fore it appears to me fitting in this year, in which the science of medi- 
cine of Germany and of the whole world is preparing to honor the 
eightieth birthday of its great master, Rudolf Virchow, to dedicate to 
him this book as a duty of gratitude. May he thereby learn that also 
those to whom it was not granted to sit as students at his feet have 
striven to build farther upon the foundation laid by him, and have seen 
in him their master, to whom they are attached in gratitude and venera- 
tion. 


In the revision of the new edition I have gone through each chapter 
with great care, and have supplemented, corrected, and extended the 
subject-matter according to the most recent literature and new investiga- 
tions of my own. 

The first three chapters have been completely worked over and 
reshaped, and I hope that by their new form and order the reader will be 


vi AUTHOR’S PREFACE TO THE TENTH EDITION. 


enabled to orient the conditions there considered more easily than was the 
case in former editions. 

In spite of the criticisms directed against certain portions of my 
presentation of inflammation and tumors I have not been led to make 
any changes touching the essential contents of these chapters. The 
attacks directed against these have inclined rather to strengthen my 
standpoint than to weaken it; although I have been induced, by chang- 
ing somewhat the formulation of my views, to meet certain strictures 
which were caused more by the form of presentation than by the content 
itself. 

Czerny’s support of the theory of the parasitic nature of true tumors 
has not changed my view as to their etiology and nature, and if I have 
altered the phrase ‘“ new-formation of tiesue which is not caused by infection” 
to “new-formation of tissue apparently arising independently,” I have done 
so, as is shown by the subsequent text, not because of any doubt in the 
correctness of the former expression, but for the purpose of avoiding 
the criticism that such a definition might have a retarding influence upon 
investigations as to the etiology of tumors. 

I have given especial attention to the revision of the chapters on 
Vegetable and Animal Parasites, and have enriched these with new and, 
I hope, instructive illustrations. It may be argued as to whether it is 
necessary in a text-book on general pathology to go so far into the sepa- 
rate forms of parasitic diseases as I have done; and whether it would not 
be better to be content with what is said in the first and third chapters 
upon Infection and the Resisting Powers of the Organism. For the 
acquiring of an understanding as to what an infection is and how the 
organism in general behaves toward it, the latter would probably suffice ; 
but it appears to me to meet a pressing need that the student, after he 
has learned to recognize the pathological processes of life, should then be 
instructed more closely regarding the properties of the parasites causing 
the different infections, their manner of action upon the different tissues 
and the organism as a whole, and their mode of spreading throughout 
the body. For the elucidation of these conditions of so great importance 
to the physician I have provided this chapter with numerous illustra- 
tions, particularly the sections treating of Streptococcus pyogenes, Staphy- 
lococcus pyogenes aureus, and Tuberculosis, as well as those treating of the 
pathogenic Protozoa. 

The bibliography has been brought up to the end of 1900, and I have 
endeavored in so far as possible to cite those investigations which are 
adapted to facilitate and advance scientific research in the given field. 
Since such collections of the literature as may be easily utilized are want- 
ing, I believe the bibliography given has met a pressing want, and I 
have already had the satisfaction of knowing that this has been recog- 
nized on various sides. 

I cannot neglect to remember with gratitude in this edition the pub- 


AUTHOR'S PREFACE TO THE TENTH EDITION. | Vil 


lisher, Dr. Gustav Fischer. To the excellent form which he has given 

the book in all the editions is owing a large part of its success. His 

friendly and obliging spirit: has made it possible to provide the book 

with such illustrations as are suitable to explain and ‘to amplify that 

which is described in the text. E. ZIEGLER. 
FREIBURG me BREISGAT, April, 1901. 


TRANSLATOR’S PREFACE. 


N the translation of the tenth edition of Ziegler’s ‘‘General Pathology ” 
the endeavor of the translator has been to render the text and spirit 
of the original in a simple and consistent English form, suitable to 

the needs of the medical student and reader. He has refrained from 
alterations of the subject-matter, and has made but few additions, the 
latter being only of such a nature as to adapt certain statements made in 
the text the better totheir Americanenvironment. The dedication of the 
German edition to Virchow has made the book in a certain sense a Vir- 
chow “ Festschrift”; and it seems especially fitting that it should contain 
the bibliography of the most important achievements of the past half- 
century in the domain of pathology and pathological anatomy. The 
bibliography of the earlier editions was omitted in the previous transla- 
tions, but in the present translation the complete bibliography, as given 
by Ziegler, has been included. In addition the editor has inserted some 
of the most important American references, particularly those of the 
last several years. He has not in any measure attempted to makea fully 
representative American bibliography, but has chosen those references 
which he has found of most service in his teaching. It is not necessary 
here to emphasize the teaching value of such a bibliography as given in 
the present volume. In the study of a science in which such great ad- 
vances are almost daily made, and in which the point of view changes 
at a corresponding rate, it seems essential that the student, in addition 
to a thorough grounding in the established principles, should be given 
also a broader view of the development: and solution of pathological 
problems. 
ALDRED SCOTT WARTHIN. 


Ann ARBOR, MicHiGan, September Ist, 1903. 
NoTE.— Because of the difference in the size of the page it has been found necessary 


to reduce slightly some of the illustrations. In such cases the magnification or amplifi- 
cation has been changed to meet the amount of reduction. 


CONTENTS. 


PAGE 
INTRODUCTION . . . . . ; ; . . . . . . it 
CHAPTER 1. 

EXTRINSIC AND INTRINSIC CAUSES OF DISEARE. 

1. Origin of Disease through Extrinsic Causes, . 5 

. Origin of Disease through Deficient Supply of Food and Ox: gen, 

through Fatigue, Heat, and Cold, Changes of Atmospheric 

ure and Electrical Influences, . . . . ds 
2. The Origin of Disease through Mechanical Influences, . . . . 15 
8. The Origin of Disease through Intoxication, . . . 18 

4. The Origin of Disease through Infection or Parasitism. Miasms, and 
Contagions. Vegetable and Animal Parasites, 31 

II. The Intrinsic Causes of Disease. Predisposition, Idiosy ncrasy and Immu- 
nity. Inheritance of Pathological Conditions and Diseases, . . . 4 


CHAPTER II. 


THe SPREAD AND GENERALIZATION OF DISEASE THROUGHOUT THE ORGANISM. 
AUTOINTOXICATIONS AND SECONDARY DISEASER. 


I. Metastasis and Embolism and their Signiticance in the Etiology of Lym- 


phogenous and Hematogenous Diseases, . 66 
II. Secondary Local and General Diseases. Autointoxication. Diseases caused 
through Disturbances or Cessation of Gland-functions, . . . . 05 
III. Fever and Its Significance, . . . ; . 92 
CHAPTER III. 


THE PROTECTIVE AND HEALING FORCES OF THE Human Bony. THE ACQUIRING 
OF IMMUNITY. 
]. The Natural Protective Contrivances, Protective Forces, and Healing Powers 
of the Human Organism, and their Action, 


II. The Acquiring of Immunity against Infection and Intoxication. Protection 
through Inoculation, . . . . . . . . . 


CHAPTER IV. 


DISTURBANCES IN THE CIRCULATION OF THE BLOOD AND OF THE LYMPH. 


I. General Disturbances of the Circulation Dependent upon Changes in the 
Function of the Heart, Changes in the General Vascular Resistance, and 


Changes in the Mass of the Blood, . . . . . . . . 128 

II. Local Hyperemia and Local Anemia, . . . ; . . . . 129 

III. Coagulation, Thrombosis, and Stasis, . . . . . . . . 184 
IV. (Edema, . ; . . . . . . 150 
V. Hemorrhage and the Formation of Infarets, . . . . . ; . 156 


VL Lympborrhagia, . . . . . . ... 0.00.0168 


xii CONTENTS. 


CHAPTER V. 
PAGE 


RETROGRADE DISTURBANCES OF NUTRITION AND INFILTRATIONS OF TISSUES. 


I. General Considerations Concerning the Retrograde Disturbances of Nutrition 
and the Tissue-infiltrations, 


II. Death of the Organism, . . . . . . . . . . 166 
III. Necrosis, . . . . . . . 169 
IV. H poplasia, Agenesia, and Atro opt. . . . . . . . 178 
V. Cloudy Swelling and Hydropic egeneration, . . . . 188 
VI. Lipomatosis, Atrophy of Fat- tissue, and Fatty Degeneration, . . . 190 
VII. The Deposit of Glycogen, . . . . 199 
VIII. Mucous Degeneration, . . . 201 
IX. Formation of Epithelial Colloid and Epithelial Hyaline Coneretions, . . 208 
X. The Pathological Cornification of Epithelium, . ; . . 206 


XI. Amyloid Degeneration and the Amyloid Concretions, . 
XII. Hyaline Degeneration of Connective Tissue, and the Hyaline Products of 
Connective-tissue Cells, . . 
XIII. Petrifaction of the Tissues and the Formation of Coneretions and Calculi, . 220 


XIV. The Pathological Formation of Pigment, ; . . . . . 281 

XV. The Pathological Absence of Pigment, . . . . . . . . 250 

XVI. The Formation of Cysts, . . . . . . . . . . 31 
CHAPTER VI. 


HyPERTROPHY AND REGENERATION. RESULTS OF TRANSPLANTATION. METAPLASIA. 


I. General Considerations Concerning the Processes Known as Hypertrophy and 


Regeneration, and the Accom mpanying Cellular Changes . . 255 
II. The Processes of Hyperplasia and Regeneration in the arious Tissues, . 280 
III. The Results of Transplantation and ‚Implantation o of Tissues and Organs, . 805 
IV. The Metaplasia of Tissues, . . . 810 
CHAPTER VI. 
INFLAMMATION. 
I. The Early Stages of Acute Inflammation, . . . . . . 814 
II. The Termination of Acute Inflammation in Healing, . 341 
III. The Inflammatory New-formation of Tissue, Substitution of Exudates and 
Tissue-necroses by Connective Tissue, . 
IV. Phagocytosis Occurring in the Course of Inflammations, and the Formation 
of Foreign-body Giant-cells, . . . . . . . . . 856 
V. Chronic Inflammations, . . . . . . . . ; . 860 
CHAPTER VII. 
Tumors. 
I. General Considerations, . . . . . . . . . . 866 
II. The Different Forms of Tumors, . 880 
1. Tumors Derived from Connective Tissue or the _ Supporting Frame- 
work, . . . 880 
(a) Fibroma, . . . . . . . . . . . 880 
(d) Myxoma, . . . . . . . . . . . 882 
(ec) Lipoma, . . . . . . . . . . . 884 
(d) Chondroma, . . . . . . . . . . . 886 
(e) Osteoma, . . . . . . . 889 


(f) Hemangioma and Lymphangioma, 2 te . . . . 898 


CONTENTS. xii 


PAGE 
a ) Myoma, . . . . . 404 

) Glioma ‘and Neuroglioma Ganglionare, . . . . . 408 

tf Neuroma and Neurofibroma, . . . . . . . 411 

(k) Sarcoma, . . . . . . . . . . 414 

2. The Epithelial Tumors, . . . . . . . . . . 438 
(a) General Remarks, . . . 483 

- (6) Papillary Epithelioma, Adenoma, ‘and Cystadenoma, . . . 434 

(ec) Carcinoma and Cystocarcinoma, . . . . 449 

8. The Teratoid Tumors and Cysts, . . . . . . . . 478 


CHAPTER IX. 
DisTURBANCES OF DEVELOPMENT AND THE RESULTING MALFORMATIONS. 


I. General Considerations Regarding Disturbances of Development at and the Ori- 


gin of Malformations, . 488 
II. The Different Forms of Malformations in Man, . . . . . . 496 
1. Arrests of Development in a Single Individual, . . 496 


(a) Arrest of the Development of the Entire Embryonal Anlage, . 496 
(5) Defective Closure of the Cerebrospinal Canal und the Accom- 


panying Malformations of the Nervous System, . . . 498 
(c) The Malformations of the Face and Neck, . 508 
(d) Faulty Closure of the Abdominal and Thoracic Cavities and the 
Accompanying Malformations, . . 511 
(e) Malformations of the External Genitalia and Anus, due to Ar- 
° rested Development, . 514 


(f) Malformations of the Extremities, "due to Arrested Development, 516 


2. Abnormal Position of the Internal Organs and of the Extremities, . 520 
8. Malformations, due to Excessive Growth or Multiplication of Organs 
or Body-parts, . . . 522 
4. True and False Hermaphrodism, . . . . . . . . 526 
5. Double Monsters, . . . . . . . 581 
(a) Classification of Double Monsters, . . . . . . 581 
(6) The Chief Forms of Double Monsters, . . . . . 531 
CHAPTER X. 


THE PARASITIC FISSION-FUNGI AND THE DISEASES CAUSED BY THEM. 


I. General Considerations Regarding the Schizomycetes or Fission-fungi, . 540 
1. General Morphology and Biology of the Fission. fungi, 540 
2. General Considerations Concerning the Pathogenic Schizomy cetes and 
their Behavior in the Human Organism, . 
II. The Different Forms of Bacteria and the Infectious Diseases Caused by 


Them, . 559 
1. The Coei or Spherobacteria and the Morbid Processes Caused by 
hem, . . . 
(a) General Considerations Regarding the Cocci, . . . . 559 
(d) Pathogenic Cocci, . . 561 


2. The Bacilliand the Polymorphous Bacteria and the Pathological Proc- 
esses Produced by Them, 
(a) General Co Considerations Regarding Bacilli and the Polymorphous 


(d) The Pathogenic Bacilli and Polymorphous Bacteria, . . 584 

8. The Spirilla and the Diseases Caused by Them, . . . . . 659 

(a) General Remarks upon the Spirilla, . . . . . . 659 

(d) The Pathogenic Spirilla . . . . . . . 660 
CHAPTER XI. 


THE YEASTS AND MOULDS AND THE DISEASES PRODUCED BY THEM, . . . 668 


xiv CONTENTS. 


CHAPTER XII. 
THE ANIMAL PARASITES AND THE DISEA8ES PRODUCED By THEM. 


I. Protozoa, . . . . 
II. Vermes. Worms, . . . . . . . . . . . . 

A. Platyhelminthes. Flat-Worms, . . . . . . . . 700 

1. Trematoda. Sucking-Worms, . . . . . . . 700 

2. Cestoda. Tape-Worms, . . . . . . . . 705 

B. Nemathelminthes. Round-Worms, . . . . . . . 718 

III. Arthropoda, . . . . . . . . . . . . . 731 

1. Ärachnida, . . . . . . . . . . . . 731 

2. Insecta, . . . . . . . . . . . . . 735 


INDEX . .. . . . . . . . . . . . . 739 


LIST OF ILLUSTRATIONS. 


1. Lightning-figures on the shoulder, breast, and arm............-.ceeeeeeeees 14 

2. Multiple emboli in the branches of the pulmonary artery.................... 67 

3. Fat-embolism of the lungs............... See t eee e cece ese en cece ce eeeserece 68 

4. Fat-embolism of the kidney........... ccc cece cece eee cte cece ence eeeeees 69 

5. Thyreoprival cachexia....... wee ee eee cee teeta eee ee tee eee eter nenn nen 85 

6. Myxcedema. ..... ccc cece ccc crc cence esse eee tect eae nn nenn nennen ann . 86 

7. Same case after treatment with thyroid extract............ cc ees ee seen eeees 86 

8. Female cretin....... ccc cc cece cece cece cece ere ee ee ee cee nets n ernennen 87 

9. Temperature chart of a continuous remittent fever....... cece cece eee eeeees 93 
10. Temperature chart of a continued fever with rapid rise and fall.............. 94 
11. Temperature curve of an intermittent fever............... cece cece rec ceces 94 
13. Recent hemorrhagic infarct of the lung....... cece e ee cet ee eee een nun ne 134 
13. Bundles and stellate clusters of fibrin threads or rods................00. u... 186 
14. Red thrombus, ......... ccc cece cc cen nenn c ence eee eens ensure nenn 186 
15. Laminated mixed thrombus rich in cells... 0... .... cc ccc cece eet ece ces ncecers 187 
16. White thrombus poor in cells... 1... ... cece cece cece ec eee eee se ese eenaee 137 
17. Rapid blood-stream. ...... ccc cece etc c eee ee ee eee cee neenneeereeeccees 188 
18. Moderately slow blood-stream........ cece cece cece cece cece cee ernennen nn 188 
19. Greatly retarded blood-stream................ cece cc ceease ene accesses ceeees 188 
20. Thrombus-formation in heart. .......... 0... ccc cece cc ee seers ee ese es esences 148 
21. Thrombosis of femoral vein........... Reece eee eee eee e ee nee nese ees ceces 144 
22. Remains of a thrombus of femoral vein. ............ cece eee s cece ern nnnne 145 
23. Obliteration of pulmonary artery by connective tissue................. 2000 146 
24. Remains of embolic plugs in pulmonary artery.............. cece cece eeeeee 146 
25. Embolism of intestinal artery with purulent arteritis.............2...2eeen.00 147 
26. Stasis from venous hyperemia. ...... 2. cece cece cece cece eee e ee nenne 149 
37. CEdema of muscle... 1... ... cece cece ccc cece eee cece areata nenne nenne 151 
28. Heemorrhage into skin. ...... 0... cece eee cece cece ccc seen n nenne nu ne 156 
29. Peripheral portion of an anemic infarct of kidney..............ccceeeeecene 161 
30. Recent hemorrhagic infarct of lung... ...... 0. cece cece cece cece ce ee eee nrens 162 
31. Necrosis of kidney epithelium. ................ ccc essc reece cere renee ence .. 170 
32. Coagulation-necrosis of mesenteric lymph-gland...............ccccesseeeees 172 
83. Waxy necrosis of striped muscle..........0. ccc ec cece cece cen ceccseceseees 178 
84. Caseation-necrosis of tuberculous focus.......... ccc cece cece cece eseceencs 178 
85. Fibrin-containing tubercle of the lung.............. ccc cece cece cece eee enees 174 
86. Liquefaction-necrosis.......... ccc cece cece cece ee eee ee eee teeter eeesneneees 175 
87. Dry gangrene of the toes....... Come ccc eee e ect e eee ee ee eee seen eaten scenes 176 
88. Skeleton of a female cretin, thirty-one years of age..........cceseecee cence 179 
39. Skeleton of a female dwarf, fifty-eight years of age......... ccc cece cece 179 
40. Head of Helene Becker (microcephalia)...........0cccecceecccceecteseseces 180 
41. Brain of Helene Becker..............cccccccccsecce Lecce cee eee eeeseceeres 180 
42. Hypoplasia and microgyria of left cerebral hemisphere.................0..-- 180 
48. Hypoplasia of uterus............... cece cece eens cece tetera eects ee ssesees 181 
44. Hypoplasia of the small intestine............ cece cc cee cece eens nennen nennen 181 
45. Sections of ovary at different ages...........0. 2c cece cece eer eeencceenareees 182 
46. Juvenile muscular atrophy........... ccc cece cece seer t tec e eee ceeeaneeens 183 
47. Excentric atrophy of lower end of tibia and fibula. ..............0.0. cece eee 184 
48. Senile atrophy of skull-cap............. cc ccs c cece seen vec et ee eeeeneceenees 185 
49. Section through atrophic muscle..............20cccesecces cece eee ee ee eee 185 
5. Senile atrophy of the kidney...............cccccccccccccoccceesstecsnceees 186 
51. Arteriosclerotic contracted kidney..... bocce eee n cree twee reece encesennesees 186 
52. Pressure-atrophy of spinal column..............c0. cc cece ec cec ees eeeeeeces 187 
53. Hemiatrophia facialis..............222oossnoooonnonnnnnnn onen ceeceveceeces 187 
54. Cloudy swelling of liver-cells............. ccc cece cece cece eeecnseccs cee. 188 


. LIST OF ILLUSTRATIONS. 


PAGE 

55. Cloudy swelling of kidney-cells...........eroneneoonssosnennensenennennen . 189 
56. Hydropic degeneration of carcinoma-cells........... 0. cccccecccccenccsscces 100 
57. Hydropic degeneration of muscle-fbres. ..........euesesnenennersonenennen: 190 
58. Transverse section of hydropic muscle................cc0c0 ecceccecceceess 190 
59. Fatty infiltration of liver... ..... ccc cect c ec ere teen eee eeeste teens 191 
60. Lipomatosis of calf-muscles.......... cc. cc cece cece eres ete caret rennen nenn 192 
61. Spinal muscular atrophy With lipomatogis........... ccc cece cscs eee cccrsces 192 
62. Fat-containing liver-cella........... ccc cece cece cee eee c ccc eceseeeeeeenes 194 
63. Fatty degeneration of heart-muscle........ cc ccc ccc cece cence eects eeccceece 194 
64. Marked chronic fatty degeneration of heart............... eee ee cee ecer eens 195 
65. Fatty degeneration of kidney epithelium.......... 0.0... ccc ce ec ccceeeeeces 195 
66. Fatty degeneration, vacuolar degeneration and necrosis of heart-muscle...... 196 
67. Fat-granule Cells... . cc. cee ccc cece ence eect ene eeeecenes eee eeeeceeee 196 
68. Cholesterin plates and margarin MNEE]ES. 0.0... ccc ce cece ec ccet enc nennen 199 
69. Mucoid degeneration of epithelial cells........... 0... ccc cece cece cece eceee 201 
70. Mucoid degeneration of epithelial cells, from a cystadenoma of ovary........ 202 
71. Mucoid degeneration of connective tissue. ........... cece cece ccc ceececeees 202 
72. Colloid degeneration of thyroid... .......... cece cece ce cee reece nencceeserees 208 
78. Secretion of colloid in the thyroid......... cece ec c ccc ccc cece ec ccc eeceees 208 
74. Urinary tubules filled with colloid. .......... 0c. cece cece ence nec enscceeens 204 
75. Colloid concretions. ....... cc ccc cece ccc c ccc ence ence cena cn seeeseereseesens 204 
76. Hypertrophic prostate with concretions. .......... cc cece cece cee earecneees 205 
77. Amyloid spleen. ...... cece ecw c cece cece cree ce tee eee nenne nennen ren en nee 208 
78. Amyloid liver treated with iodine. ............ ec cece ccc cece ce ee ce eeeecs 209 
79. Amyloid degeneration of splenic follicles and splenic pulp...oncceeereeneee. 210 
80. Amyloid liver........ 0. ccc ccc cc ecccesecceee ccc cece eeeeeee cee ee cece 211 
81. Amyloid kidney........ be ccc eee cee eee cece tenet tee e tere nee tne essen nee 212 
82. Corpora amylacea...... 0... cece cece cree cece cee ener e nese este ee secre eeenes 214 
83. Hyaline degeneration of the connective tissue of a colloid goitre............. 216 
84. Hyaline degeneration of connective tissue in a tuberculous bursa............ 216 
85. Hyaline degeneration of blood-vessels.......0.....ccccceccececccecencceees: 217 
86. Hyaline degencration of the connective tissue of the myocardium............ 217 
87. Sclerosis and calcification of a uterine artery...........ccsccccscccccccc nes 220 
88. Calcification of the media of the aorta...........0...ee0ee cece cee eee ecc ees 221 
89. Calcified cerebellar vessels. ...... ccc cece ccc c cece ccc enc ee erence eee es eens 221 
90. Calcification of epithelium of urinary tubules.....................-cescecees 221 
91. Concretions of lime salts.............. cect cece cece eee eee eee eee eessees 222 
92. Section of psammoma of dura mater......... ccc eee cece eee nennen nenne 222 
88. Deposit of urates in Knee-joint.... 0... ccc cece ec ccc ee cece ewe etc eee cree eeace 224 
94. Deposit of needle-shaped crystals of sodium urate................-ccececcces 224 
95. Gouty nodules of hand..........-seeseneneonuuenenernennnensnern onen nunne 225 
96. Faceted stones from gall-bladder............cccce csc cece cece cee ccerseeees 226 
97. Section of cholesterin stone........ eee eee cece ence eee eee reece e teren nnnne 227 
98. Uric-acid infarction of Kidney. .......... cece cece eee cece tect ene ceseece 227 
99. Coral-like urinary calculus................cecee cece cece ence cece sees eeeeees 228 
100. Calculi of sodium urate and ammonium-magnesium phosphate............... 228 
101. Incrusted lead-pencil from bladder. .......... 0. e ec cnc cece eee e cece ces eees 229 
102. Large hairy nevus on back and buttocks......... ccc cc ec cece cece cvceceees 281 
108. Pigmented cells from skin in Addison’s disease. ........ccecseccec cece cence: 232 
104. Cells containing amorphous pigment. Crystals of hematoldin............... 236 
105. Hsemosiderin- and hematoidin-containing cells............... ccc e eee e eevee: 237 
106. Deposit of pigment-cells in a lymph-gland................-s sees eeeeeeeseee 238 
107. Infiltration of liver-rods with hsemosiderin............. cc cece eee cceeeeene 239 
108. Heemachromatosis of the liver.........-eeeessesenenennennenennrenenennnen 240 
109. Hemosiderosis of the bone-marrow... ........ 0. csc cece cece sete nec eencceens 241 
110. Hematogenous hemosiderosis of kidney of pernicious malaria .............. 242 
111. Icterus of liver due to compression of common duCt...........cececececoees 244 
112. Icterus of Kidney. .... 2... cece cence eee econ eee cece eee ceeeseses 246 
118. Deposit of cinnabar in tattoo............0..000s Lenten cece cece eee eesecenes 248 
114 ria Of rabbit’s kidney... .... 0... cece eee ee cee cece etree merece ne nn nee 249 
115. Villen endemica........u-eununenunenenenenenenenennnnen Lecce ec eeeeccees 250 
116. Multiple cysts in epididymis. .......... ccc eee eee cece ence nennen nn nenn 252 
117. Dilatation cyst of PAaNCreas............ cee e eee e eee eect eens e eee eeeeeeeees 252 
118. Hydrops tube. .... 00. ccc ccc cee ccc e eect eee eran ete e een teeeeeeees 253 
119. Elephantiasis femorum neuromatosa ..............- cee t eee cee en nennen nenn 255 


. Elephantiasis cruris Ilymphangiectatica.......«.:.-.seresereonsnenennennnnene 256 


LIST OF ILLUSTRATIONS. xvll 

PAGK 

121. Ichthyosis congenita (microscopical)................606- uuessseeerennne nn 256 
122. Ichthyosis congenita............ eer c en cee eee c eee eee ee nern nennen rue ne 257 
123. Cornu cutaneum from back of hand .......0. cc csc cece cece c cee e cece eceees 257 
124. Cornu cutaneum from aFM.......... cece cece sec es ce nenn Lace ee ree eceee 257 
125. Head of a bearded Woman.......... cece cece ec cece eect cent eee nennen 258 
126. Leontiasis 0888.01... ccc cc cece cece ere e teeter ese ee ens nenne ernennen 258 
127. Hypertrophy of left ventricle. ......... ccc ce ccc cece cece tener nnn ceece 260 
128. Hypertrophy of incisor-tooth of a white rat, due to disuse. .................. 261 
129. Elephantiasis scroti ......... ccc cece ccc cece cree cere cere ence ce nn ne 261 
180. Acromegaly ....... cc ccc cece cece cece cnet eerste ers acesee esse nase nn nee wee 282 
181. Skeleton of hand from case of acromegaly.........-..-.-rsoessenonsnnnuene ~ 268 
132. Cutaneous portion of a laparotomy wound.................ccce cece eeenees 266 
133. Healing of intestinal ulcer...... chee e cece eee c cect ete c teeter eters eeeece 267 
184. Scar of muscle and tendon... ......... cc cece cece cece eee teen cece enveene. 268 
185. Edge of embolic scar. ........ ccc ccc ec ee cee teens cee tees ere senens 269 
136-144. Nuclear changes in cell-division...............00 ccc eee cesses ccens 278-274 
145. Atypical Karyokinetic figures. .......... 0... cece c cece cece cece rec nenne nun ne 275 
146-149. Giant-cells from an osteosarcoma. ......... 2... e eee ete cece nn nenn nn 276 
150. Proliferating adipose tissue........ 0... ccc ccc cc cece eect teen ee ee eseeenees 276 
151-157. Nuclear changes in cell-division....... cece eect cate nee nenececeses 277-278 
158. Regeneration of the epithelium of the bile-ducts ..................cseeesees 281 
1508. Healing blister........ cc ccc cece c cece cet e erect cece ee nenn nun onen onen. 281 
160. Development of blood-vessels. .......... ccc cence ccc c esac cc cccscccceaceeees 284 
161. Two vessels of papillary body, with proliferation of endothelium ........... 285 
162. Proliferating periosteum four days after fracture of bone..................+. 286 
163. Isolated cells from wound-granulation. ..........c ccc cece ccc c cece cece eerere 287 
164. Development of connective tissue from fibroblasts..... ..........ccceeecees 287 
165. Scar from skin, two years Old...... 11. cece cece cece tens ceccescens tees 288 
166. Periosteal formation of cartilage. ......... ccc cec eect cee nce e esas cccceeeere 288 
167. Myelogenous formation of bone from osteoblasts............0--0-sececeecces 289 
168. Formation of osteoid trabecule in the proliferating periosteum.............. 289 
169. Formation of bone upon old bone by deposits of osteoblasts................. 290 
170. Section from a germ-centre of a mesenteric lymph-gland...............0.-:- 298 
171. Regeneration of striped muscle.............. 0. ccee ccc ee eevee cccccsenceces 297 
172. Sclerotic tissue from the posterior columns of spinal cord.................-- 800 
178. Old and newly formed nerve-fibres......... ccc cece cc cccsccccccerccccecess 801 
174. Cross-section of nerve-bundle from median nerve four months after wound... 801 
175. Amputation-neuromAa. ........... cece ec e eee cece ce cece ceeececccescsccen: 802 
176. Skin-transplantation of about four and a half days............ cece cece ee ees 307 
177. Metaplasia of cartilage into reticular tissue............ cece see c nce ecceeees 811 
178. Formation of bone from cartilage in a callus............. Lew ce rece ccc ereeees 812 
179. Formation of bone from connective tissue..........c cece cece cece ernennen 812 
180. Inflamed human mesentery. ..........ccccccccccccccce cesar eerssencseeece 817 
181. Meningitis recens purulenta. .......... ccc ccc cece e cece eee ne tee cecseeeece 822 
182. Hematogenous staphylococcus myositis. .......... cece ccc ccc ence ccsv ences 822 
183. Section through the edge of a blister... 00... .. ccc cece eee n cee enences 823 
184. Parenchymatous hepatitis.......cc.cccccesscccccsc cess csssccesces ne cee 323 
185. Mucous catarrh of a bronchua.....ooeesesooeeoonsuonsennerereennen nenn nn 824 
186. Purulent desquamative catarrh of trachea..........0. 20. c cece cnet cs eccecces 826 
187. Catarrhal secretions of different mucous membranes .............cccceeceees 827 
188. Acute hemorrhagic-fibrinous inflammation of trachea..................00.-. 328 
189. Croupous membrane from trachea. ........ cece ceee cc ec enc eacec cease cceces 828 
190. Section of diphtheritic membrane... ..............c cece eee e eects cccceceees 829 
191. Croupous tracheitis.. 2.0.0... cc cece cee ccc cece teen es eaecenesececes 2200. 380 
192. Traumatic fibrino-purulent peritonitis ............ ccc cece cee ccc ccceccccace 830 
198. Fibrinous pleuritis.... 2.0... ccc cece cece cnet cece ct eersesecceces 330 
194. Fibrino-purulent diplococcus pleuritis ............... cece cee ccvee nen un. 881 
195. Croupous PDECUMONIA, 2.0.0... cee cece cece een ns cece cece cece secceosene 332 
196. Purulent bronchitis, peribronchitis, and peribronchial bronchopneumonia.... 884 
197. Section of a pock pustule....... 0... cece ce ce cece cence teeceeceees 834 
198. Embolic abscess of intestinal wall................ ccc cee ee ceeeces eee eeees 335 
199. Suppuration and necrosis of the mucosa of the intestine in dysentery......... 386 
200. Phlegmon of subcutaneous tissue... ........... cece cc ceccceesenscecsceseces 837 
201. Necrosis of the epithelium of the epiglottis.......... cece cece cee ewereas 388 
202. Bacillary diphtheritis of colon in dysentery............ Lecce eee reece eeeeee 339 
208. Section of uvula in diphtheria... ........... ccc ccc cece ccc c ccc es scence: 839 


xvii LIST OF ILLUSTRATIONS. 


PAGE 
204. Diphtheritic necrosis of a mesenteric lymph-gland................-.-.+2+00- 840 
205. Isolated cells from a wound-granulation ..............ccecceee conccneccees 844 
206. Cross-section of blood-vessel from the deeper layers of the skin.............. 344 
207. Granulation tissue from open wound............... 00.0 cece ec ereeee os „un. 845 
208. Healing of incised wound of skin..........-..22-.-20r cn nern cece cen eeeee 847 
209. Cutaneous portion of a laparotomy scar... 2.1... 22. eee eee eee eee e eee 348 
210. Beginning organization of pericardial exudate...............e-erenoreenencn. 349 
211. Granulation-tissue formation on the pleura in pleuritis...................... 849 
212. Organization of pericardial exudate. ......... 0. cc cece cece cee eee eceeees 350 
213. Intraseptal and intra-alveolar development of connective tissue in the lung... 350 
214. Development of formative tissue in a thrombosed femoral artery............ 351 
215. Edge of fresh hemorrhagic infarct of lung..........--o2creeecnnenennennn. 351 
216. Edge of organizing hemorrhagic infarct of lung..............-...-606% un. 352 
217. Fibroid area in heart-imuscle, ......... 0... ee ee eee ee nen e eee n en 858 
218. Granule-cells in a focus of degeneration of the brain. ............. 2... eee 856 
319. Phagocytes from granulation tissue. ..... 0.0.0.0. cece e ee eee een ceees 857 
220. Collection of pigment-granule celis in a ly mph-gland bce e terete eee cee e eens 857 
221. Dog's hair encapsulated in subcutancous tissue........ Toe e cece e eee eenees 358 
322. Necrosis in lower portion of femur.............. 0... cece ce eee ence eesees 360 | 
223. Changes in lung and pleura in chronic purulent pleuritis.................... 861 
224. Stone-cutter’s lung... 2.0... cece eee eee eee ee eee eee eee tence eens nee 362 
325. Condyloma acuminatum, ......... 0c eee cee cece cee nennen nennen 863 
236. Periostcal hy perostosis of the tibia. ..................508 rn 368 
227. Section through mucosa of atrophic colon. . soceccceccce oe cee eee BOF 
228. Induration and atrophy of kidney tissue in chronic nephritis eee e ccc e ee ccene 864 
229. Hyperplasia of connective tissue and proliferation of bile-ducts in chronic 

. hepatitis. .....eooceceeeeeeeesaeneeneennenne en ween eee seeateeteneuseeees 865 
230. Tissue from mammary cancer with many division- ‘figures eee cece eee eeeeee 367 
2331. Fungoid carcinoma of body of uterus... .......... cece cee eee nennen 868 
233. Papillary adenoma of rectum.............-. 0. eee c ener cere eee teen ee tees 868 
233. Primary carcinoma of gall-bladder............... 2... eee eee eee ence eens 872 
284. Primary carcinoma of Hiver...... 0... ee cece cece e een eee eeeeneee 875 
285. Metastases in periglandular lymph-vesscls of axillary region................ 876 
286. Metastases of carcinoma in portal vein and liver capillaries...............06. 876 
237. Metastatic sarcoma of liver. ..........6. coe ce cece cece ee renee ons nennee 877 
288. Recurrent sarcoma of femur................+.- eee ce ee eee eeeeeeees .. 878 
239. Hard fibroma of ear-lobe.. 2.0.0... ce cece ce cette ee nenn nennen nenn 880 
240. Section of adematous fibroma of uterus. .......... 2... cc cece teen cence 880 
241. Fibroma pericanaliculare mamm®@®..........0. cece cece cee eee nennen 881 
242. Cells from a myxomaof the periosteum... ............ 0. cece ee cee nennen 883 
243. Section of a MYXOSATCOMA, 2.6... cee cece eee t cette nennen nennen ne 883 
244. Lipoma of the shoulder region........... 0... cee cece eee cece ence ence nenn 884 
245. Lipomyxoma of the back .......... ccc cece eee cee cence renee seen enenne 885 
246. Periosteal chondroma of finger-phalanx............2-eceroussoenennennenne ne 886 
247. Section of chondroma of ribS......... 0. ccc ccc eee erence cree ee eeees 886 
248. Chondromyxosarcoma parotidis......... 00 ccc cee ee ee reer e neces 887 
249. Periosteal chondroma of calcaneus............ 00. cece cee cece nenne en 887 
250. Osteochondroma of humeruS,........... cc ccc ect e ee cc ete eee et eesaeeees 888 
251. Ivory-like exostosis of parietal bone... ...... 0... ce eee eee eee nen 889 
252. Exostosis cartilaginen of tibia ............ ccc cece cece eect e cece ee eesaseeees 890 
253. Ivory-like osteoma of parietal bone... oo. cece eee ee eee c eee eeenee 391 
254. Osteoma of dura mater... 0... ccc ee cece eee ete eee eee e en ernennen. 391 
255. Osteochondroma of Humerus. .... 00... cee ec cee eee eee cece nenn nennen 
256. Teleangiectasis of abdominal panniculus................ ccc eeee cece ceenees 898 
257. Dilated capillaries from a teleangiectatic tumor of the brain...............-- 894 
258. Angioma cavernosum cutaneum congenitum,..............0. cece eee nun nn 894 
259. Angioma cavernosum hepatis............... cece cece ee msn nun en een 895 
260. Angioma simplex hypertrophicum...........-. cc esc cee cee tere ee eeee anne 896 
261. Anginma simplex hypertrophicum cutaneum et subcutaneum............... 896 
262. Angioma cavernosum hypertrophicum ........... 6... see e eens cee reeeeeee 897 
263. Angioma arteriale plexiforme ............. 0 cece ccc e cece ee cee ces eeeasees 898 
264. Weeping subepithelial lymphangioma of skin. ............... ccc c eee ec ences 899 
265. Lymphangioma cavernosum subcutaneum.......... ccc ccc c eee c ese eeececes 400 
206. Large hairy pigmented nevus. ............ 2. cc cece cee teen ence none eceees 401 
267. Lymphangioma hypertrophicum..................ecececeecceceesees onen. 401 
268. Lymphangioma hypertrophicum.................. cs ce cec cece eeeres nenn 402 


PAGE 
369. Section through two papille of a fieshy wart.............. ccc ces c ec eenee 402 
270. Myoma of uterus. ...... 00. ccc ccc cece ee cer nenn nennen nenn nen une 404 
271. Angiomyoma subcutaneum dorsi..... 2.2.0... cece cee cece cece een ecerees 405 
272. Cells from rhabdomyomats. ................ ce cece cece ecw eee c eect veces 406 
278. Glioma cerebri....... Cee cee cette cee ee ee ee eee eee eter e ee te eee estes 408 
374. Section of a glioma cerebri............... cee cece eee ee eee crnees enernnne 409 
375. Neuroglioma ganglionare....... uueesneoesneenennene see se nern en een une 410 
376. Amputation neuroma of sciatic nerve. .......... ccc cee eee nsec eceeeeees 412 
277. Nerves from a cirsoid neuroma...... 2.6... cece eee eee cc eect ee eeeeenees 418 
278. Cirsoid neuroma of sacral region... ........ cece cece eee cece cee nenn nenn. 413 
279. Sarcoma of intermuscular septa of cervical muscles...............ceeceecees 416 
280. Lymphosarcoma of nasal mucosa... ..... cee ce ee cence sonne nn en e 416 
281. Large round-celled sarcoma of skin ............. ccc cc cece cece en cee sonen ne 417 
282. Sarcoma of MAMMBA.......... cece eee cece cee eee cee e nes ece sence eeees 417 
283. Spindle-cells from a large spindle-celled sarcoma of cheek.................-. 418 
284. Cells from a myelogenous giant-cell sarcoma. ..........6.. cece eee eee eenes 418 
285. Giant-cell sarcoma of upper Jaw........... cece cece cee c nce eeeveees oe. 419 
286. Endothelioma of pia mater.... . eee eect eee tree erate none nennen nennen 421 
287. Endothelioma durte matris......... 0... cee cece cece nennen en nennen nen 422 
288. Endothelioma of pleura... ........... ccc cece ee cece cece econ ernennen. 422 
389. Endothelioma of mamma......... ccc ccc eect cece ee nenne seen nenn nenne 48 
200. Hemangioendothelioma of kidney... ........... cc cee cee cect cece eee nenn nn 424 
291. Angiosarcoma of thyroid... ..... 2... cece cee cece tence ere ecceseeeeeee . 425 
2392. Angiosarcoma of testicle. ............ cc ce cc eee e cect acne eee nenn rennen nn ne 425 
2393. Chondrofibroma of parotid. ....... ccc ccc cece cee cece eee e cence see nennen 426 
294. Melanotic alveolar sarcoma of skin. .........0. cee cceeceeeeseees La eeneecees 427 
295. Melanotic sarcoma of skin........ 0 6. cece ec ere cere e teen eect eee eeeees 428 
296. Metastasis of a melanotic sarcoma Of SKin........... 000+. sce e cece ec enneee 420 
297. Osteoid sarcoma of the ethmoid bone. ..........0.. cece cece cess eee eecceecee 439 
298. Petrifying large-celled sarcoma of tibia........... 0. cece ee cee ence nen cee 480 
299. Section of a psanımoma of dura mater.......... ccc cee cece enone eeeeeeens 430 
800. Myxoangiosarcoma of parotid............. cece cece eee ete ne eee en nn 431 
801. Papillary epithelioma................ ccs cece eee ace c eee n cect ees ceeseerese 438 
8303. Senile horny wart.......... ccc ce cece cee eee ee nennen ernennen san une 434 
803. Papillary epithelioma of larynx............. cc cece cc ee cee cence nen 435 
304 Papillary epithelioma of bladder.................... euneennereeeernenenen 435 
805. Papillary epithelioma of bladder... ............ 0. cece cece ee eet ere eetees 436 
306. Adenoma tubulare of intestine ............ cece cece e eee eee e ee teeetees 438 
807. Adenoma tubulare of stomach... 2.0... . ccc ccc cee cee ween cece eset ences 438 
808. Adenoma mamme tubulare. ............ ccc cece cece eee eee one none ne 439 
809. Adenoma mamme@ alveolare.......... 0. ccc eee c cent eect eee ete seennes 439 
810. Adenoma renum tubulare papilliferum............... ccc eee cece cence 440 
811. Fibroma intercanaliculare Mamm® ...............0. cece secrete cece nenne 441 
813. Section of cystadenoma ovarli papilliferum. ........... wc. ce cece cee eeee 443 
818. Adenocystoma of bile-ducts........ ccc cece cee cette ete nennen nn 448 
814. Portion of a multilocular adenocystoma of the ovary............... cee eee 448 
815. Section of an adenocystoma of testicle.......... 0... cece cece cece neces 443 
$16. Multilocular adenocystoma of liver...... 20.222000 cece eee c cee ernennen nen 444 
817. Cystoma of kidney.......0. 0. ccc ccc cee cece een eeseter ssn on nennen ne 444 
$18. Adenocystoma ovarii partim simplex partim papilliforum.................... 445 
$19. Portion of an adenocystoma papilliferum ovarii........ ... ...... Bere vee 445 
820. Cystoma papilliferum ovarii............ rauen ce eee eee eee tee ees teeesone 446 
$21. Papillary adenocystoma of OVAary.... 1.2... cece ccc ce eee eee nenne nenne 447 
822. Papillary cystoma of breast..............00..0 cee eee e wesc eee ee rn 448 
823. Section of carcinoma of the lip........ 0... ccc cece cence cece eet eeeeeeaes 454 
$24. Beginning cancer of portio vaginalis uteri.............. Laden eee e ene eeeees 455 
825. Development of adenocarcinoma of colon. ................ 0. ccc ee cee eee ees 456 
826. Developing adenocarcinoma of stomach................. 0. cc ceee wee ee ences 456 
$27. Cystocarcinoma of mamma ........ 6c c eee eect nent eee ee nennen 457 
328. Tubular adenoma of mamma with beginning carcinoma ................... 457 
$29. Carcinoma placentare of uterus........ ........... Lek eect aces eet eeeeeenes 458 
330. Horny carcinoma of tongue. ...........0 cece ee cere ee te cee eneeees 460 
831. Epithelial plug from a cancer of the skin.... ......... 6c cece eee eee eee 460 
382. Adenocarcinoma recti tubulare........ 0. ccc ccc ccc cece cece cece netees 461 
388. Adenocarcinoma fundi uteri...............0 cece cece cee teres rennen nn 461 
334. Carcinoma simplex mamm®@................ ccc cee c eee ccccceeecerencsees 462 


LIST OF ILLUSTRATIONS. xix 


xx LIST OF ILLUSTRATIONS. 

PAGE 
335. Acinous carcinoma Of mammaA.......e-sesesoncnerennesr rennen nenn nenn nenn 4623 
836. Tubular scirrhous cancer of breast.......ee.cescesossenennnnennnnn cece or... 468 
337. Segment of a cancer of breast..........-e:-ssoeneusnnnenenenonennenn nenne 464 
838. Mucoid carcinoma of breast.......... 00. ce cece cet c ent eee seen ccs eenes .. 465 
839. Development of a mucoid cancer in atrophic gastric mucoga.............066. 465 
340. Carcinoma MUCOSUM MAMMB.........- cece rere ce cee cccce unseren nn une 466 
341. Carcinoma with hyaline Crops.......... ccc c cece ee eee c cect ence ees ern nn 466 
842. Enlarged hydropic cancer cells... 21... .. cece cece reece este eee tees eeeeenee 467 
343. Carcinoma myxomatodes............-.eeeeceees Lecce ete e eee nee eceeeenes 467 
344. Adenosarcoma malignum of kidney ..............sccee cee ec eter ee nenn nun 468 
345. Cystocarcinoma papilliferum mamm@............6. 0. sess ee eee e sree enone 469 
346. Cystocarcinoma papilliferum Ovarii................ eee eres eee eee eee eees 470 
347. Papillary cystocarcinoma of MAMMB.............. eee eee ecco sence seesees 470 
348. Colloid carcinoma of thyroid. ........ cc. cece cece reve torcencesccssece 471 
349. Section of enlarged axillary lymph- gland with beginning metastases of carci- 472 

DOMR ..2o2seeneonensaes seen snnn seen ere nennen een ne. nan treten ano 

350. Metastatic cancer-cell in liverapillary...........eossersenncnenennnonennnn 418 
351. Metastatic cancer in liver from primary carcinoma of the pancreas.......... 473 
352. Spina bifida occulta with a myolipoma.......oc-ueorensenenenenen cece erees 474 
353. Adenoma-like snaring-off of portions of mucosa of small intestine............ 476 
854. Adenoma-like remains of Wolffian body in the uterine wall................. 477 
855. Portion of the wall of a dermoid cyst of the ovary...............0..cceeeees 482 
356. Section of a prominence in a multilocular dermoid...................6- eu. 483 
857. Congenital adenocystoma of testicle............ 0. cece eee cee tee eccees ... 484 
358. Teratoma of testicle... 0... ce ccc cece eee eect eee ee nenne nenn nenn 485 
359. Malformation of head due to amniotic adhesion.............cccccsecesevees 489 
$60. Malformation of face due to amniotic adhesion................ cece ceeeees 490 
361. Hand stunted by amniotic adhesion.................eee008 eee cee rece ceves 491 
362. Deformity and stunting of hand due to pressure... ..............cceseees .. 491 
863. Hydatidmole....... -.. cece cece cece cece ce eee teense ee nen un nen rue. 496 
364. Lithopzdion..........- wee c ce eee tee eee e en ernennen euere nenne 0. 497 
865. Craniorachischisis.................. occ e eee eee e eee eect ete nennen anne. 499 
866. Spina bifida sacralis........... 0.0. ccc c cece e ere cece sete eeeseteanae „or... 500 
867. Myelomeningocele sacralis.......... cece ce cece cet ccc e eee e ee eesnteenseees 501 
868. Anencephalia et acrania........ ccc cece ccc cece cence eee e sure eee eeesens 504 
869. Cranioschisis with exencephalus.............. ec cee acces ser cecseees PER 504 
870. Partial agenesia of the cranium... .......... cece cece ccc seen eesceecenes 504 
871. Hydrencephalocele occipitalis............ cc ccc cece ec cence tens ceseeccesees 505 
372. Eincephalomeningocele maSOfrontalis....... cc cece cece cece rece ccs nennen une 505 
373. Synophthalmus or cyclopia. ......-. 6... cece eee eee ween cece crete eeeereees 506 
374. Te ntal section of cranial cavity in synophthalmus microstomus............ 506 
875. Wolf’s Jaws... 0... cece cc cc ee ec cee cee re eee eee eee rene see e essen nennen 509 
376. Agnathia and synotin. .......... cece cece cece creer eee e ec ees nr erenennne 509 
877. Hernia funiculi umbilicalis............. cece eee ce eee cece ener eeeneaes 513 
378. Fissura abdominis et vesice urinaria....... 6... cece nennen une nne 518 
379. Hypospadias... 2.0... . ccc cece ee ee eee A) (| 
880. Epispadias . 0... 0... ccc cc cee ce cece cence ee te eee e nenn ne nenn une ne un... 514 
381. Complete absence of urethra and external genitals. wee cece ete c eee e ene sees 515 
8382. AMCIUS ...... cece ee eee eee eee nennen esse nen ernennen ern nn 517 
383. Micromelus......... ccc cee eee eee tect eee ee eee tenet ene eteeeseseceees 517 
384. SyMpuSapus. ...... ccc cece ce cee cette n eet e ee eeeeeeeeeences wee eeaees 517 
885. SyMpus Cipus...... cece cece ee cee ce ween eee eee e cere eet nenn ns re nen ne 517 
386. Defect of femur and fibula.........oeeeseeueecsronennesnnnennss nen nenne 518 
887. Perodactylism and syndactylism...........0. cee cece ence eee cree ences ereees 518 
388. The same hand illuminated by Roentgen 0 6. ernennen 518 
389. Perochirus........ ccc ccc esc ee ccc cere ee eee nennen nn nn ern ene uno. 618 
390. Skeleton of perochirus. ...... 0.0.0... ccc cece eect e eect e cee eee nennen 518 
391. od 28) 0 | een enn nee nenne sen e sense nr e nn 519 
392. Skeleton Of peropus.... 20... cece eee cee eee mens nennen sen en nenn 519 
893. Polydactylism. ......... 0. cee cece eee cee eee eee ee es ennen nennen ren ne 524 
394. Polydactylism in the new-born skeleton ..........cccccceess coe sceeeceeees 524 
895. Polydactylism and syndactylism of left hand........... ccc cece ee eee e scene 524 
396. Polydactylism and syndactylism of right foot... .........ccecccecceceeeces 524 
897. Hermaphrodismus veruslateralis.............00cccececeecccccccnccceee es 527 
398. External genitalia of a female pseudohermaphrodite ...............0.20e0008 528 
399. Acardiucus acephalus..........0... 0. ccc cee cece cence eter nennen nun nn 533 


LIST OF ILLUSTRATIONS. xxi 


PAGE 
400. Acardiacus pseudoacormus...... cer caves ccc cc enccerecssccvsccsesccecs 082 
401. Fygopagus occ cecceeec ec cees Kaneosensecnecnne ee cccees ron. cevecesccecees OBS 
402. IschiopaguS.......-.....csceveces oer c cca e ccc nennen enu nenne ecesese 583 
408. Dicephalus dibrachius dipus. ........... cece ec ecc cece c cree cecccsccecs oe 534 
404. Diprosopus distomus tetrophthalmus diotus dibrachius................ sono... 534 
405. Craniopagus parietalis. ......-soosccncsonnonesunnennnnnnenunnnenne wee scees 635 
406. Cephalothoracopagus .. 11... cece cece cece nceneecceces cee cccees escececes 0888 
407. Thoracopagus tribrachius tripus......... tec eccenece bec ecccccccceres ee 536 
408. Polymelos.... 2... cesses cccecccccccccscee secesceeecseessccecensccces .. 537 
409. Polymelos.......... “eae ceeeee weet e ccc eet eee nee e cee e cece aces eee esecesees 537 
410. Pygopagus parasiticus........ deem h cence ene c eee e cance nern een essen nun 587 
411. Thoracopagus parasiticus. ........cccccccsccccccccccccucececseseceus wees. 587 
413. Thoracopagus parasiticus. ........ ccc cscs cece cc ecccrecessnevees ev ecceees 538 
418. Epignathus... 0.0... 2.02000 cece cree emcee nenne ernennen cceecesasces 538 
414. Gelatin plate with colonies of bacteria....... 0. cc cece cece eee c ec eecceees . 554 
415. Streptococcus from a purulent peritoneal exudate........:-serreonee coeces 559 
416. Micrococcus-colonies in liver-capillary.........ccesceecseecees cece scereces 559 
417. Cocci grouped in tetrads....... cece cc eee eee ec ees ccnees cece ce se cceees 559 
418. Sarcina ventriculi.... 2. ccc cc ccc cece cece cette ener cece cnenereeesece 559 
419. Streptococcus tracheitis in scarlatina .......... ccc cece cece esc cecesevens .. 562 
420. Streptococcus pyogenes from phlegmon of stomach................ece08 oes 562 
421. Streptococcus erysipelatis in lymph-vessel............cccccccccseccsecccess 562 
422. Section of skin in erysipelas bullosum.............cceccccccccesscccceccees 563 
423. Erysipelas of head in child of one month........ cece e reece rot ee ee nennen 563 
424. Beginning streptococcus phlegmon on BUNK... .. cece cece eee e we ret veecece 564 
425. Streptococcus infection of petrous Done... .......... cece eee eres c ev eeees 565 
426. Metastatic hematogenous streptococcus pneumonia. ...........cceccee scons 566 
437. Parietal endocarditis of left auricle, due to streptococci...............0c000 567 
428. Erythema multiforme caused by streptococci..............cccsecccrsenceees 567 
429. Marked streptococcus infection of kidney..............00. ecw cece een cesees 568 
480. Diplococcus p1.ceuMONi®@..... 0... ccc cece cece eee ee cece cee sceeseeeces u... 570 
481. Diplococeus pneumonia in early stage..........-oeresosenorononce ee eceees 571 
483. Multiple abscesses of skin caused by staphylococci.............0cscceee sees 573 
483. Miliary abscesses of kidney caused by staphylococci...............-ceeecees 574 
434. Metastatic colonies of staphylococci in liver... 0... cece e cee n cece eneons 575 
485. Gonococci in urethral secretion ....... 0... cece cece c ccc c een catccseneneees 577 
436. Urethritis gonorrhoica..... Cece ae teem eee eee eect eens ne bern nenn une 577 
487. Bacillus subtilis in different stages of development.............0cccceseesces 581 
438. Clostridium butyricum.... ......... cece ee cece cece etree eee sen seen nnene 581 
439. Anthrax-bacilli in liver capillaries..............00.00. Lene e cee ec er ereeesees 585 
440. Anthrax-Spores.......... cece ccc ec cece cece ceeceersecs veces ec eeeeeneers 585 
441. Anthrax pustule we cee tee ee eee teen tree tee ernennen one ences ee en nme 586 
442. Portion of anthrax pustule, containing bacilli..... 2.0... cece eee e ee cence 587 
443. Typhoid bacilli from a pure culture........ ccc cece eee cece cee essen tenes 589 
444. Typhoid bacilli with flagella..........ceesoosseeesssennensenenenn en nn nenn 589 
445. Typhus abdominalis. Section of Peyer’s patch...............0.. 20-00 none 591 
446. Bacillus pneumoniae ....... 2. ccc ccc ee cece cence nee te ernennen nenn .... 595 
447. Nail-shaped stab-culture of pneumonia-bacilli in gelatin..................6. 595 
448. Influenza-bacilli from sputum. ...........- ccc cece cece cece nent eens ceenees 597 
449. Diphtheria bacilli from a pure culture. ......... ccc cece ee cet cee etenvees 598 
450. Tetanus bacilli with terminal spores. ........... cece sec e cere ceecececcecene 601 
451. Pest-bacilli... o.oo ccc ccc ce cee ec e nce eee teeta ner ernennt one nenne 605 
452. Tubercle-bacilli ........ coc ccc cece cee eee tect eee ec eeee eee entnce 608 
458. Tissue changes caused by fresh invasion of tubercle-bacilli.................. 609 
454. Giant-cell containing tubercle bacilli ............ cece cece eee ee cece en eee 609 
455. Tubercle from a fungoid granulation tissue of bonc............. cece eee cees 609 
456. Tuberculosis of pleura. ........... cece cee ec cece ete eee eee e ee erent ene 610 
457. Large-celled tubercle with fibrin. .......... ccc cee ccc meee eee r eee e seen eens 610 
458. Caseous necrosis of tuberculous granulation tissue..............c sec eeeeeees 611 
459. Miliary tubercle of omentum............ceesescecscece ene cence ccc eewecens 611 
460. Fibrocaseous tubercle of lung.... 12... cc ccc eee cece cen e cence se eeseeeens 612 
461. Fibrous tubercle in thickened synovial membrane ................ccceeesse: 612 
462. Lupus of skin with atypical proliferation of epithelium................-000. 617 
463. Tuberculous granulation tissuc from the synovial membrane of the knee..... 618 
464. Large solitary tubercle of pia mater cerebelli...............0 ccc eee seco 618 
465. Tuberculous induration of the lung.......... ccc cece cece cece esse eee eeenes 619 


LIST OF ILLUSTRATIONS. 


PAGE 
486. Tuberculous induration of the lung. .....essunenossserenursnnsseenennnn une 619 
487. Encapsulated caseous focus in lung, with induration........ ee 620 
468. Encapsulated caseous focus in LUDg....... cee eee ccc e cence nennen nenne 620 
469. Tuberculous cavity in tibia........ wee cece cece sete ence eect ee eccence on... 631 
470. Tuberculous ulcer of intestine .......22-eocenoneonureenennsnnun sn nen ossceee- 622 
471. Beginning pulmonary tuberculosis without catarth.........s0.cseeece- .... 622 
472. Beginning pulmonary tuberculosis in child of two years............-..00..-. 628 
478. Eruption of tubercles in a lymph-gland........... 1... cece ees ee eens encees 624 
474. Tuberculosis of veins in neighborhood of a tuberculous retroperitoneal gland. 625 
425. Heematogenous miliary tuberculosis of liver. ..............0 2c cee ceeecee ces 626 
476. Tuberculosis of omentum........c. cee cca c ec ee ere cece een ssnece ee ce eee eee 626 
477. Proliferations of pleura in “ pearl-disease ” of cattle..... eee cecees cece cece 628 
478. Initial sclerosis.............-.se008 cee eee cece tee eee nen eeeecens wee cencee 632 
479. Section of sy philitic initial sclerosis. ..... 2.0... 00. ccc cece wee e nec cenees 632 
480. Condyloma latumani........... ce cece cet w ee cence cece cece otc ee ee cenaes 638 
481. Meningoencephalitis syphilitica gummosa...............-...4- eee eee eeeee 634 
482. Gumma hepatis................. 0008 Cece nce e cee e eee eeeeeees wee e ec eeces 635 
483. Syphilitic ulceration of larynx......eeeeeecenerenecnenene erneuern „u... 686 
484. Congenital syphilitic induration ofliver........urerersnnnensneenenenennenn 637 
485. Changes in lung in congenital syphilis............ cece cece tees ee ee eeeees 687 
486. Tissue from a leprous nodule........... FE ace e cence eee eeaneeeecesees 689 
487. Giant-cell containing lepra-bacilli......... 0... 0. cece ce cence a sccceccee. 689 
488. Section of leprous nodule of skiu....... See e ccc e eee ee ee eees cee eeens 00. 640 
489. Leontiasis leprosa.............-6. vee wee eee cece cece see esescees coe ceees 641 
490. Lepra an:esthetica ulcerosa....... bec e cree eeeneercceee ernennen 2... 642 
491. Lepra anesthetica mutilans............... Lee eeeee cece cece cee cece cee cees 643 
492. Glunders of cat’s testicle........ cece e eee cece ees e eens cseesnes ccc ee sc eeee- 645 
498. Section of rhinoscleroma... 2.1... cece eee eee cece rece eens tee wee eeeee ... 648 
494. Hyaline cells and spherules from rhinoscleroma ...........s.cseceevceseeees 648 
495. Actinomyces hominis............ bec e cece teen tenet ents nee nennen en nn nne 650 
496. Actinomycosis of the tongue............. sec eect eee ence eee ence eneee .... 650 
497. Actinomyces druse surrounded by giant-cells and pus-corpuscles ernnencre. CW 
498. Actinomycosis of lUNZ... 2... ccc ccc eee e ee ete nenn uses nnn nennen 651 
499. Frontal section of nose and upper jaw of a cow affected with actinomycosis. . 6852 
500. Spirillum rugula and spirillum undula...............200ecees nnenee ern. 660 
501. Cholera-spirilla... 0.0.0... ce cece ee wee cece e eee eee nennen nennen nee 661 
502. Stab-culture of cholera-spirilla in gelatin ................. cece tees ce wences 661 
503. Stab-culture of the Finkle r-Prior spirillum. ...... 0... cece ewes cecceeens +. 665 
504. Spirochste Obermeieri from the blood of a patient suffering with relapsing fever 666 
505. Portion of tissue and isolated cells from a splenic follicle in case of typhus 
TECUITENS. 0... ce ec cee eee cee eee ner ernennen nn ce cccerancccse OOF 
506. Saccharomyces ellipsoideus............. 62sec cence eee e eens cece eesene ... 669 
507. Fresh favus-mass consisting of hyphae. .............. 0s eee e eens ecceceseee 660 
508. Thrush, from tongue of man dying of typhoid fever........... ese cecccness. 6B 
509. Section through a thrush-covered esophagus of a small child.......... nun. 670 
510. Mucor corymbifer in fructification. ......... ccc cece ccc esc eeeees cesecoese. 678 
511. Hyphe of Aspergillus fumigatus, with conidia-bearers ........ erenncnnnnne. 672 
512. Culture of Tricophyton tonsurans.........0. cece eee ce cee eee e cece eee c ee eeee 677 
513. Amacba coli mitis.. 2... 0... eee cee cee e cece e eee eeeeece ur 680 
514. Amaba dysenteri@... 0... 0. cee cee cee tener nene sen nenne 2... 681 
515. Balantidium coli... 0... 0... cc cece cence ete teen eeteee eee eeeee -... 681 
516. Cercomonas intestinalis... 2.00... eee cece eee nennen ernennen ne „ur. 682 
517. Trichomonas vaginalis.......... 0.0.00. eee cece eee cece ee nnne nennen 6823 
518. Trichomonas intestinalis. ......0. 0.0... ccc cece cee nennen anne nn nenne 68? 
519. Trypanosoma sanguinis MUTIUM ........ eee rennen ce eee nennen 683 
520. Section of a bile-duct filled with coccidia ........222.2 2200 ecnereennnnne un... 686 
521. Coccidia from the bile-ducts of a rabbit'sliver ..........e2eoseennenononancne 686 
§32. Epithelioma contagiosum. ...........0. 0. ee eee eee cnet eee nenn une 687 
528. Parasites of Epithelioma contagiosum. ........... 0. ccc cee eee e cece ees nenn nen 688 
524. Miescher’s sacs from muscle of hog....... 0... cece eee cee wenn ee onen 688 
525. Cycle of development of Coccidium Schubergi...........0. ce ccs cece eee e eens 689 
526. Plasmodium malaria of quartan fever......... Levee eeeene re 698 
527. Plasmodium malarie of vernal tertian fever......... 0. cece cece ee eces o.oo. 683 
528. Plasmodium vivax of autumnal tertian..................... wee e eee eseeeee 694 
529. Anopheles Claviger 2.26.1... 6 ee cece cece eee e cece een e ere ee ee ener enees 695 
580. Odkinete of pernicious malaria in intestinal wall of mosquito................ 695 


LIST OF ILLUSTRATIONS. xxiii 


. PAGE 
581. Odcyst of pernicious malaria, filled with sporozoites.............ceseceseece 696 
532. Cycle of development of Proteosoma..............seeeeees eee eecsser ences 697 
583. Distoma hepaticum.. ......... ccc cece ccc eee nce ere e eee n ns e nennen nee 701 
534. Eggs of Distoma hepaticum. .............. 0. ccc cee cee cence eeeeenes 701 
535. Development of the liver-fluke..............2222csssoeronenononennnsurenne 702 
586. Distoma lanceolatum,........... 0. ce cece cece eee e ene n nennen nenn 702 
537. Distoma spathulatum............ ccc ccc ce cee renner en nenn nennen 708 
538. Distoma Westermanni........... 0... cece ec c cece cece eee e cece en ne nenn 708 
539. Distoma hematobium........ 2... cc eee eee cee erence teed e ewe anes eeees 704 
340. Eggs of Distoma hematobium........... 0... cece eee ce cee er cent eee ceeee 704 
. 541. Head of Tenia solium, ......... ccc ccc ccc cece ee eee n nennen nen une 706 
542. Half-ripe and ripe segments of Tania solium. ............... ccc eee cence cee 706 
513. Two proglottides with uterus. ......... ccc cece cece cee reece rece eseesees 706 
544. Segment of Tenia solium, with mature sexual apparatus ................... 707 
545. Eggs of Trenia solium. . ... 10. cece ccc ccc cece e er cee cece ence reesnces 707 
546. Cysticerus cellulose... 00... cece ccc cece cece eer e eee nennen neuen 707 
547. Cysticerci of Trenia solium........... 0. cece ce cece cee c ene c eee eene cece 708 
548. Portion of a Tania saginata ......... 0.00 sec e cere cee eee eces Lee eeee nonne 709 
549. Head of Tania saginata. ......... ccc ce cece cece eect cence cence ee teees 709 
550. Segment of Tenia saginata...... eee eee ewe center ence ee eee eres tee en en 709 
551. Mature Tenia echinococcus............ Lace e ee cee cece ee tence see seeeees 712 
553. Wall of echinococcus cyst with brood-capsules...... 00... .ccees cece seaees 712 
553. Echinococcus hydatidosus. ............ cece cee cece reece eee enee neeenun nee: 718 
554. Portion of an Echinococcus multilocularis. .......... 0.0... ccc cece cece ence 714 
555. Bothriocephalus latus ........ 0. cc ccc ccc eee cece rete tree eeeeeeveccens 716 
556. Head of Bothriocephalus latus. ............ ccc cee ccc ce cree eee e eset once neees 716 
557. Middle portion of a proglottis of Bothriocephalus latus.................006: 717 
558. Eggs of Bothriocephalus latus.............eesocccneronoesrennunnnennne nen 717 
559. Free embryo of Bothriocephalus latus...............ceeeeeees BE 717 
560. Ascaris lumbricoides............oo--esosossonsnsnnnnrann nennen nenn nenn 719 
561. Egg of Ascaris lumbricoides...........ee-eeeosesonneonnuersensennn nn 4... 719 
562. Oxyuris vermicularis... ........ eee eee e eee cement cece ce neat eee eeeeeees 721 
568. Lege of Oxyuris vermicularis... ........ 0. ccc cee cece wee ence eee ernennen 721 
564. Male of Anchylostoma duodenale................... cee cence cece cece tees 722 
565. Head of Anchylostoma duodenale................ ccc cece eee eee eeeees 722 
566. Eggs of Anchylostoma duodenale.................. ccs cecs ce secscseenenes 722 
567. Anguillula intestinalis... .......... 00. c eee ee cece ee neee a eee eee ceecene 724 
568. Female of Anguillula stercoralis ............. cece eee eee nes nerenenne ne 724 
569. Triocephalus dispar...... Leen cece senenne heen cece tate tee t ee cece ee conseees 726 
570. Egg of Tricocephalus dispar........... ccc cece eer c eee cece et ees ceeenees 726 
571. Sexually mature trichin®......... 0... ccc cee eee eee e tenets eecaes 727 
573. Encapsulated muscle-trichin® ........... cc cece cece cece cece see etncceenes 728 
578. Filaria or Dracunculus medinensis .......... 2... cece cece cect eee teeteees 729 
574. Embryo of Filaria Bancrofti, known as Filaria sanguinis hominis............ 729 
575. Female itch-mite. .... 0... ccc ccc cece tect eee ete eee eee eee tees sun ne 731 
576. Scabies... 0... ccc cece cece eee c ene eetene Lecce cence eee Lee eeeeees 732 
577. Leptus autumnalis................. eee e ce ec tence eect cece crete eeeeeers . 7833 
518. Acarus folliculorum hominis. ........ cc. c ccc cece ccc e emcee cece tent eeeneees 783 
579. Ixodesricinus 2... cece cee cee ce tee eee eee nenne rennen nenn 7 
580. Cephalic end of Pentastoma denticulatum............. ccc cece ec eet eee neers 733 
581. Male of Dermatophagus commuDis............. 0. cc cee cen cece cesar eesnes 734 
582. Male of Dermatocoptes communiß. .eseecoesesenennsenennne seen een essen 734 
583. Female of Pediculus capitis.......... 0... ccc cece cee ete ee eee nennen nen 735 
584. Male of Pediculus pubis............ 00. cece cece cee ce rent ee nennen nn nn 135 
585. Female of Pediculus vestimentorum.............0 0. ccc cece ccc ee eeecsenees 735 
586. Gastrophilus equi... .... cece cece cece eee ee ete ence eens nenne 736 


GENERAL PATHOLOGY. 


INTRODUCTION. 


- General Pathology, the science of disease, has for its especial prov- 
ince the investigation, from all sides, of the processes of disease, the deter- 
mination of their nature and significance, their causes and origin, their 
course and termination. 

The life of an organism reveals itself by means of certain peculiar 
activities which we regard as the manifestations of life. In the case of 
unicellular organisms these manifestations consist chiefly of changes of 
form, movement, and division of cells, the taking-up of food and the 
giving-off of waste products; the last-named processes being visible un- 
der the microscope in the case of formed material, but in the case of 
soluble substances they are revealed by changes in the chemical compo- 
sition of the medium in which the cells complete their existence. In 
multicellular organisms, particularly in the more highly developed 
mammals and in man, these vital functions are much more varied and 
complicated. In the general metabolism of the organism a very great 
variety of tissues and organs takes part: the intestinal tract, the respi- 
ratory apparatus, the blood, and glands of different structure, some 
especial individual function being assigned to each. Reproduction is 
accomplished by means of special organs and apparatus. Motion is 
dependent upon special tissue formations. The perception of external 
influences is made possible through highly developed sense-organs, and 
the entire organism is controlled by a complicated nervous system, the 
functions of which are so individual and many-sided as to render their 
study extremely difficult. The investigation of the normal processes of 
life, which falls to the province of physiology, is accordingly very diffi- 
cult and complicated, and we are yet far from an exact knowledge of all 
the processes of the healthy or normal life. 

The study of disease-processes, as well as of the normal, takes its 
departure from the life-manifestations of the human body, and such indi- 

- viduals are regarded as ill whose functions in part deviate from those recog- 
nized as normal. The science of general pathology, whose exposition 
forms this study, is, accordingly, first of all to be designated as patho- 
logical physiology ; that is, the science which seeks to recognize the 
significance and character of the manifestations of disease. It can, 
however, do justice to this task only when it at the same time deter- 
mines also the anatomical changes which give rise to disturbances of 
function in tissues and organs, the causes which produce them, and their 
mode of origin; that is, the pathological anatomy, the etiology, and 
the pathogenesis of the processes of disease are essential parts of gen- 
eral pathology. . 

Every manifestation of life is dependent upon a material substratum, 

1 


2 INTRODUCTION. 


every form of vital activity presupposes some special condition of this 
substratum, and physiology teaches us that the individual functions of 
tissues and organs are dependent upon the special structure of their in- 
dividual organization. A change of function in this or that direction 
presupposes also a change in the tissue or organ, and experience teaches 
that such changes in reality take place; and, further, that for the same 
a causa efficiens may at times be demonstrated. It isto be noted, however, 
that the tissue-lesion underlying a disturbance of function cannot always 
be discovered, nor is it always possible to ascertain the etiology or patho- 
genesis of the same; but the number of such cases is constantly dimin- 
ishing through the improvement of our methods of investigation, as 
afforded by means of modern microscopical technique, animal experi- 
mentation, and the utilization of chemical research; and this number is 
already reduced to a small percentage of pathological processes. The 
experienced physician is, therefore, enabled from given symptoms of 
disease to diagnosticate certain organic changes; and, further, from the 
same to recognize often the causes of the disease and the manner of its 
origin. 

The symptoms of disease may at one time point to a certain organ 
as the seat of disturbance, or at other times the organism as a whole may 
appear to be involved; we may distinguish accordingly local and gen- 
eral diseases. Not rarely a number of organs may be affected at the 
same time—this may be spoken of as multiple localizations of disease; 
or in other cases the disease may have a localized seat, but runs its course 
with such changes of tissue that a diseased condition of the entire or- 
ganism results. 

The specific grouping of pathological symptoms which repeats itself 
in many cases makes it possible for us to distinguish different forms of 
disease, and occasionally the physician finds it difficult in a given case 
to determine the exact form of the disease. As criteria for the origin of 
different types, the especial causes of the disease, the location of the tis- 
sue-lesion, and the nature of the process are to be considered. There 
results, therefore, a great variety of disease-pictures; and it is not al- 
ways easy, often impossible, to determine either the seat of the disturb- 
ance, the character of the tissue-lesion, or the causes leading to the same. 

The duration of different diseases is very variable, and we may 
therefore distinguish acute, subacute, and chronic processes, the last 
extending through years or even decades. An illness may terminate in 
recovery and cure or with the death of the affected individual. A cure 
is assumed when all symptoms of disease have vanished, but experience 
teaches that the complete restoration of the affected part often takes 
place much later than the disappearance of the symptoms. Not infre- 
quently healing is delayed and the disease becomes latent; that is, ex- 
tensive tissue changes remain, the injurious agent is not. removed from 
the body, though symptoms of the disease are no longer present. For 
example, the symptoms of a tuberculous affection may completely disap- 
pear, though foci containing tubercle bacilli are still present in the body 
from which by chance a further extension of the disease may take place, 
and, accompanying this, new symptoms may arise. 

When in the course of a disease a local loss of tissue is not replaced 
by the process of healing, a defect remains; a defect of large size, on 
the visible external portions of the body, such as the loss of a finger or 
leg, is spoken of as a mutilation. 

If, in the place of a highly organized tissue which has been destroyed, 


INTRODUCTION. 3 


connective tissue of a lower grade is formed, or if an external defect is 
closed by such formation of tissue, there results a scar. When, as the 
result of some disturbance of the normal intra-uterine development, cer- 
tain tissues at birth present pathological alterations, the condition is 
designated as a congenital malformation or anomaly. If the affected 
organs show functional disturbances, the condition may be termed a con- 
genital disease. 

The broad field covered by general pathology necessitates a narrowing of 
its subject-matter ; and it happens conveniently that a part of pathological 
physiology, which may he designated clinical pathology, is best relegated to 
study at the bedside, to special courses and lectures, or to text-books. The 
disturbances of function pertaining to the different organs and systems, 
heart, nervous system, organs of special sense, respiratory tract, urinary 
apparatus, digestive tract, etc., cannot be discussed in this connection. 

A detailed consideration can be undertaken only of those phenomena of 
disease which are consummated in the elementary constituents of the tissues, 
the tissue-cells and the intercellular substance ; and these can be judged and 
properly valued only through an exact study of the anatomical and histological 
changes thereby presented. General pathological anatomy becomes, 
therefore, the indispensable foundation for general pathology ; but it 
leads to a complete knowledge of the processes of disease only when at 
the same time the etiology and pathogenesis of the tissue-lesion are re- 
vealed in a satisfactory manner. 


Literature. 
(General Pathology. ) 


American Text-Book of Pathology, Philadelphia, 1901. 

Aschoff und Gaylord: Cursus der pathologischen Histologie, Wiesbaden, 1900. 

Birch. Hirschfeld: Patholog. Anatomie, 1896-1897; Allgem. Pathologie, Leipzig, 
1892. 

Bollinger: Atlas und Grundriss d. pathol. Anatomie, München, 1896-1897. 

Bouchard: Traité de pathologie générale, Paris, 1895-1900. 

Coats: Manual of Pathology, London, 1895. 

Cohnheim: Vorlesungen über allgemeine Pathologie, Berlin, 1882. 

Cornil et Ranvier: Manuel d’histologie pathologique. Paris, 1881. 

Cruveilhier: Anatomie pathologique (Atlas), Paris, 1842. 

Delafield and Prudden: Pathological Anatomy, New York, 1892. 

Dirck: Atlas und Grundriss d. pathol. Histologie, München, 1900. 

Graupner und Zimmermann: Technik u. Diagnostik am Sektionstisch, Zwickau, 
1898. 

Hallopeau: Traité elementaire de pathologic générale, Paris, 1898. 

ten: Physiolog. Chemie, Wiesbaden, 1896. 

Henle: Handbuch der rationellen Pathologie, Erlangen, 1846-1853. 

Israél: Praktikum der pathologischen Histologie, Berlin, 1893. 

Karg und Schmorl: Atlas der pathologischen Gewebelehre, Leipzig, 1893. 

Ka : Specielle patholog. Anatomie, Berlin, 1896. 

Klebs: Die allgemeine Pathologie, i., Jena, 1886, und ii., 1889. 

Krehl: Pathologische Physiologie, Leipzig, 1898. 

Lancereaux: ité d’anatomie pathologique, i.-iii., Paris, 1877-1889. 

Lazarus-Barlow: A Manual of General Pathology, London, 1899. 

Lukjanow: Grundzüge einer allgemeinen Pathologie der Zelle, Leipzig, 1891; 

rundzüge einer allgemeinen Pathologie des Gefässsystems, Leipzig, 1894; 

Grundzüge einer allgemeinen Pathologie der Verdauung, Leipzig, 1899. 

Neumeister: Physiologische Chemie, Jena, 1897. 

v. Noorden: Pathologie des Stoffwechsels, Berlin, 1893. 

Orth: Lehrbuch der speciellen pathologischen Anatomie, Berlin, 1893-1897. 

Paschutin: Vorlesungen Ober allgemeine Pathologie, St. Petersburg, 1881. 

Perls-Neelsen: Lehrbuch der allgemeinen Pathologie, Stuttgart, 1898. 


4 INTRODUCTION. 


von Recklinghausen: Allgemeine Pathologie des Kreislaufs u. der Ernährung, 
Stuttgart, 1888. 

Bibbert: Pathologische Histologie, Bonn, 1896; Die Lehre von dem Wesen der 
Krankheit in ihrer geschichtlichen Entwickelung, Bonn, 1899. 

Rindfleisch: Die Elemente der Pathologie, Leipzig, 1896. 

Rokitansky: Lehrbuch der pathologischen Anatomie, i.-iii., Wien, 1855-1861. 

Bumpel und Kast: Puthologisch-anatomische Tafeln, Hamburg, 1892-1897. 

Schmaus: Grundriss der pathologischen Anatomie, Wiesbaden, 1899. 

Stricker: Vorlesungen über allgemeine und experimentelle Pathologie, Wien, 1883. 

Thoma: Lehrbuch der patholog. Anatomie, Stuttgart, 1894. 

C. Thommasi-Crudeli: Istituzioni di Anatomia Patologica, Torino, 1882. 

Valenti: Lezioni di Patologia Generale, Roma, 1881-1885. 

Virchow: Handb. d. spec. Pathologie, i.. Erlangen, 1854; Die Cellularpathologie, 
Berlin, 1871. 

Weichselbaum: Grundriss der pathologischen Histologie, Wien, 1892. 

Woodhead: Practical Pathology, London, 1892. 


CHAPTER I. 
The Extrinsic and Intrinsic Causes of Disease. 


1. The Origin of Disease through Extrinsic Causes. 


1. Origin of Disease through Deficient Supply of Food and Oxygen, through 
Fatigue, Heat and Cold, Changes of Atmospheric Pressure, and Electrical 
Influences. 


- §1. From his birth to his death man is constantly exposed to the in- 
fluences of the world surrounding him, many of these external influences 
being favorable to the normal exercise of his functions, while others are 
unfavorable. 

As long as the human organism is able to offset these influences, 
through independent changes of its relations to the external world or 
through adaptation of its functions to external conditions, it will remain 
in health. If his regulating mechanism no longer suffices for successful 
opposition to unfavorable external influences, and if he cannot escape 
these or change his conditions of life, man becomes ill or dies. 

For its preservation the body needs first of all a certain amount of 
food, water, and oxygen; and though it may exist for a short time with- 
out these, an insufficient supply of oxygen, food or water beyond a 
certain limit and after a certain time must of necessity lead to disease 
or death. 

A total deprivation or diminution of the supply of oxygen to the 
tissues may take place at any period of life, either because of a lack of 
oxygen in the surrounding medium, or some obstruction to the entrance 
of the oxygen of the air into the lungs or blood, or inability on the part 
of the blood to take up a sufficient amount of oxygen. The foetus in 
utero may be insufficiently supplied with oxygen as a result of diminished 
supply to the mother, premature separation of the placenta, disease of 
the placenta, or compression of the cord, whereby the interchange of 
gases between the maternal and foetal blood is hindered. After birth an 
insufficient supply of oxygen may be due to hindrances to respiration, 
or the child may be so weak that its respiratory movements are insufl- 
cient to expand the lungs. 

When the supply of oxygen is completely shut off, as may happen 
from the entrance of water or other fluid into the respiratory tract or 
from closure of the air-passages, the affected individual dies in a very 
short time from choking or suffocation. Animals confined in closed 
chambers die as soon as the oxygen of the air reaches two or three per 
cent by volume, the normal volume percentage being 20.8 (Cl. Bernard, 
P. Bert). 

If the supply of oxygen is not wholly shut off, but only greatly 
diminished, as in the case of carbon-monoxide poisoning, in which the 
firm combination of carbon monoxide with the hemoglobin prevents the 
taking up of oxygen by the red blood-cells, death by suffocation may 

5 


6 THE EXTRINSIC CAUSES OF DISEASE. 


take place only after several days. In gradually increasing hindrances 
to the entrance of oxygen and resulting accumulation of carbonic acid 
in the blood, as in cases of narrowing of the lumen of the larynx through 
inflammatory exudates, compression of the trachea from goitre, weaken- 
ing or obstruction of respiration, ete., a condition of breathlessness, 
cyanosis, convulsions, and disturbances of consciousness is produced, 
which is termed asphyxia. 

If the taking up of oxygen is diminished in only a slight degree but 
for a long time, as in the case of a lessened number of red blood-cells 
in oligocythsmia, degenerative processes characterized by increased de- 
struction of albumin and by fatty changes may occur in the tissues and 
organs, and these may lead not only to disease but under certain condi- 
tions to death. 

Total deprivation of food and water leads to a rapid loss of body- 
weight, inasmuch as the fat and albumin continue to be decomposed ; 
death finally ensues. According to Lehmann, Müller, Munk, Senator, 
and Zuntz, the total amount of oxidation in cases of starvation does not 
fall below that of the same individual in the fasting state under the 
same conditions. A marked deconiposition of albumin and loss of water 
take place. Im animals death occurs after the loss of about forty per cent 
of the body-weight, about one-half of the loss being due to the waste of 
muscle. 

The fat disappears most rapidly; even as much as ninety-three per 
cent may be lost. The other organs show diminution of substance in the 
following order: liver, spleen, testicles, muscles, blood, intestines, skin, 
kidneys, and lungs. The heart, nervous system, and bones show the 
least loss of weight; but, according to the researches of Lehmann, Muller, 
Munk, Senator, and Zuntz, destruction of bone-tissue takes place during 
starvation, as is shown by the increase of calcium and phosphoric acid 
in the urine, following ingestion of water. In the blood there is a rapid 
diminution of the leucocytes (Luciani); the red blood-cells, on the other 
hand, may be relatively increased in number. The organs of animals 
dying from starvation show simple atrophy of the tissue-elements, par- 
ticularly of the liver (Lukjanow), hyperemia, scattered hemorrhages, 
degenerations, and inflammatory changes, especially in the intestine, 
liver, kidneys, and nervous system. 

In the case of total deprivation of food and water, death occurs in 
man after from seven to twelve days; bodily exercise hastens the end, 
ingestion of water may delay it markedly, so that some individuals have 
been enabled through the use of water to endure a period of total absti- 
nence from food for thirty days or longer, without dying or suffering 
permanent harm. The consumption of water leads to an increased ex- 
cretion of nitrogen in the urine. 

Life may be maintained for a long time upon insufficient nourish- 
ment, but a wasting of the body takes place which may lead to a condi- 
tion of extreme emaciation, marasmus, or cachexia, and finally to death. 
The same thing happens when the composition of the food is unsuitable 
and only a portion of the necessary food-elements is present in sufficient 
amount, so that the body is starved either in albumin, fat, salts, or 
water. Dogs deprived of all nitrogenous food die in from thirty-one 
to thirty-four days (Magendie). When the food is abundant but poor in 
albumin, there occur after a time (in dogs after six weeks) loss of appe- 
tite and repugnance toward the proffered food, with impairment of diges- 
tion and assimilation (Munk). This is especially the case when the food 


DEPRIVATION OF OXYGEN, FOOD, AND WATER. 7 


is lacking in fat, less so when albumin or the carbohydrates are wanting. 
It is very probable that the lessened absorption ischiefly dueto diminished 
secretion of the digestive juices, this being capable of quantitative de- 
monstration in the case of the bile. The feces are finally nearly desti- 
tute of bile. 

An insufficient supply of iron for a long period gives rise to anemia 
and general disturbances of nutrition. 

If for experimental purposes an animal well supplied with food is to- 
tally deprived of water, there is a rapid loss of body-weight followed 
in from eight to twelve days by death. The pathological changes found 
in the different organs are similar to those resulting from starvation. 
They are caused partly by lack of water and insufficient absorption of 
food, and partly by the retention of harmful products of metabolism. 


Literature. 
(Results of Diminished Supply of Oxygen, Food, and Water.) 


Ahlfeld: Der Uebergang der intrauterinen Athmung zur extrauterinen, Marburg, 

1891. 

Beneke: Grundlinien der Pathologie des Stoffwechsels, Berlin, 1874. 

Bischoff und Voit: Die Gesetze der Ernährung des Fleischfressers, 1860. 

Coen: Bull inanizione acuta. Bull. delle Scienze Med. di Bologna, ser. vii., vol. i., 
190. ° 

Daddi et Treves : Observations sur l'asphyxie lente. A. ital. de biol., xxviii., 1897. 

Dennig: Bedeutung der Wasserzufuhr für den Stoffwechsel. Zeit. f. Ther., i., 1898. 

Dreyfus-Brissac: l’asphyxie non toxique, Paris, 1883. 

Ehrlich: Das Sauerstoffbedürfniss des Organismus, Berlin, 1885. 

Fränkel: Einfluss d. verminderten Sauerstoffzufuhr. Virch. Arch., 67 Bd., 1876. 

Halliburton: Lehrb. der chemischen Physiologie und Pathologie, Heidelberg, 1896. 

Hofmann: Lehrbuch der gerichtl. Medicin, Wien, 1895. 

Hoppe-Sey ler: Stoffwechsel bei Sauerstoffmangel. Festschr. d. Assist. f. Virchow, 

rlin, 1891. 

Krehl: Die Athmung. Pathol. Physiologie, Leipzig, 1898. 

Lehman, Miller, Munk, Senator, und Zuntz: Untersuchung an zwei bungernden 
Menschen. Virch. Arch., 131 Bd., Supplement, 1893. 

Luciani: Das Hungern (übersetzt von O. Fränkel), Leipzig, 1890. 

Lukjanow: Veränd. d. Zellkerne unt. d. Einfl. d. Hungerns. Arch. des Sc. biol., vi. 
und vii., 1897 u. 1898. 

Meltzer and Norris: On the Influence of Fasting upon the Bactericidal Action of 
the Blood. Jour. of Exp. Medicine, 1899. 

Monti: Alterat. del sist. nervoso nell’ inanizione. Arch. ital. de Biol., xxiv., 1895. 

Müller: Stoffwechseluntersuchungen bei Krebskranken. Zeitschr. f. klin. Med., xvi., 
1889. 

Mühlmann: Russische Literatur über die Pathologie des Hungerns (zahlreiche und 
vielseitige Untersuchungen). Centralbl. f. allg. Pathol., x., 1899. 

Munk: Ueber die Folgen einer ausreichenden aber eiweissarmen Nahrung. Virch. 
Arch., 182 Bd., 1898. 

v. Noorden: Pathologie des Stoffwechsels, Berlin, 1893. 

Ottolenghi: Osserv. sperim. sul sangue asfittico. Arch. p. le Sc. Med., xvii., 1893. 

Peri: Alterations du syst. nerv. prod. par l'inanition. Arch. ital. de Biol., xviii., 1892. 

Pernice und Scagliosi: Wirkung d. Wasserentziehung. Virch. Arch., 139 Bd., 1895 
(Lit.). 

Penzoldt u. Fleischer: Einfluss von Respirationsstörungen. Virch. Arch., 87 Bd., 
1882. 

Range: Die Krankheiten der ersten Lebenstage, Stuttgart, 1893. 

Statkewitech: Veränderungen d. Muskeln u. Drüsen b. Hungern. Archiv f. exp. 
Path., 33 Bd., 1894. 


~ 82. An unusual demand upon the functional activity of an organ 
for an extended period of time leads sooner or later to a state of ex- 
haustion, which is, in part, due to the consumption of cell-substance, 


fe THE EXTRINSIC CAUSES OF DISEASE. 


and in part to the formation of toxic products of metabolism, whereby 
the organ is incapacitated for further extended activity. Most often 
the results of overwork are manifested in the museles and nervous 
system in the form of such symptoms as soreness and stiffness of the 
muscles, mental excitement, sleeplessness, heavy feeling in the head, loss 
of appetite, great weakness, unnatural sweating, and sometimes fever. 
Overwork of the heart leading to exhaustion may cause death. This may 
occur either when the heart is for a short time taxed to the extreme limit 
of its power or when for a longer period it works slightly under its 
maximum capacity. If the exhausted tissues are permitted to rest and 
supplied with an abundance of nourishment, the loss of cell-material 
due to the excessive activity will be replaced, the products of metabol- 
isin, Which are hindering the functional activity of the tissue, will be 
removed, and the part restored to its normal condition. 

If atissue is frequently subjected to excessive functional demands, 
and if the periods of rest are too short to admit of its complete restora- 
tion, there will result ultimately a condition of permanent functional in- 
sufficiency, a chronic exhaustion, which may under certain circumstances 
manifest itself in a degeneration or atrophy of the affected organ. For 
example, a muscle through overwork may become atrophic, and a brain 
too constantly stimulated to activity without proper periods of rest may 
finally reach such a state of weakness and exhaustion that it is incapable 
of performing even its normal function. Through rest and properly 
regulated nourishment such a brain may recover; but beyond a certain 
limit of exhaustion the functional insufficiency may become permanent 
and eventually manifest itself in anatomical changes. 

A very severe over-stimulation of the nervous system, even for a 
very short time, may under certain conditions lead to a paralysis of its 
functions, which, in case the heart and respiratory apparatus are af- 
fected, may cause death, but in the majority of cases is of a transitory 
nature. 

Overwork of any organ is more quickly followed by fatigue and 
functional insufficiency in the case of impaired nutrition. Fatigue and 
insufficiency of the heart are most frequently observed when the general 
nutrition is lowered, as in cases of fever, or when there is deficient oxy- 
genation of the blood, as in poorly compensated heart lesions or pulmo- 
nary diseases. 

It is very probable that overwork lowers the resistance of the body 
to various infections. 

When the functional demands upon a muscle or gland are only mod- 
erately increased, and if the nutrition is good and in proportion to the 
increase of labor, the affected tissue becomes hypertrophied, and is 
thereby enabled to perform the increased work permanently. 


Literature. 
(Overexertion and Fatigue.) 


Abelous: Contrib. a l’Ctude ce la fatigue. Arch. de Phys., v., 1893. 

Blake and Larrabee: Observations upon Long-Distance Runners. Boston Med. and 
Surg. Jour., 1908. 

Bouveret: La neurasthenie, Paris, 1891. 

Brauns: Die Neurasthenie, Wiesbaden, 1891. 

Carrieu: De la fatigue ct de son influence pathogénique, Paris, 1878. 

Edinger: Neue Theorie über die Ursachen einiger Nervenkrankheiten, Leipzig, 1894. 


THE EFFECTS OF HIGH TEMPERATURE. 9 


E:b: Die zunehmende Nervosität unserer Zeit, Heidelberg, 1898. 

De Fleury: Pathogénie de l’&puisement nerveux. Rev. de Méd., 1896. 

Guerrini: Action de la fatigue sur les cellules nerveuses. Arch. ital. de Biol.. xxxii., 
1899 


Kraepelin: Zur Teberbürdungsfrage, Jena, 1897 (Lit.). 

v. Krafft-Ebing: Lehrbuch der Psychiatrie, 1893; Gesunde u. kranke Nerven, 1896. 

Krshl u. Romberg: Bedeutung d. Herzmuskels u. d. Herzganglion. f. d. Herzthätig- 
keit. Arch. f. exp. Path., 80 Bd., 1892. 

Leyden: Herzkrankheiten in Folge v. Ueberanstrengung. Zeitschr. f. klin. Med., 
xi., 1886. 

Marfan: Fatigue et surmenage. Path. gen. publ. par Bouchard, i., 1895. 

Mosso: Die Ermüdung, Leipzig, 1893. ' 

Seitz: Ueberanstrengung d. Herzens. D. Arch. f..klin. Med., xi., 1873, u. xiii., 1874 
(Lit.). 

Williams and Arnold: The Effects of Violent and Prolonged Exercise upon the 
Heart. Phil. Med. Jour., 1899. 

Ziehen: Neurasthenie. Eulenburg’s Realencyklop., xvii., 1898 (Lit.). 


- 83. High temperatures may act, either through local destruction o7 
tissue (burning) or through overheating of the entire body. The latter 
eondition is possible only when the body is exposed to an increased tem- 
perature for such a time that it cannot protect itself from overheating 
by increased heat-dispersion. In dry air of from 55-60° C. (131-140° 
F.) the most profuse perspiration is no longer able to protect the body 
permanently from overheating, and in a moist atmosphere the same is 
true at even lower temperatures. ° 

If rabbits are placed in well-ventilated incubators at a temperature 
of 36-10° C. (96.5-104° F.), their body temperature will rise to 39-40° 
C. (102.3-104° F.), the respiration and pulse being at the same time 
‘greatly increased in frequency. A very marked elevation of body tem- 
perature may lead in one to three days to death through paralysis of the 
nervous and muscular systems, the chief symptoms being a marked in- 
crease of both respiration and heart’saction. If the increase of body tem- 
perature is not greater than 2-3° C. (3-5° F.), the animals may, if 
properly nourished, live from ten to thirty days or even longer, but they 
will lose in weight and ultimately die, showing before death a gradually 
increasing diminution of hemoglobin and of red blood-cells. Degenera- 
tive changes, particularly fatty degeneration, occur in the liver, kidneys, 
and heart-muscle. During the experiment there is an increased produc- 
tion of urea. 

If the human body is subjected to high temperatures, it may become 
overheated, and the condition known as heat-stroke may result. The 
pulse-rate is increased, the respiration very rapid and labored, the pupils 
are dilated, and finally death may occur as in the case of the animals 
made the subject of experiment. The occurrence of heat-stroke is 
favored by heavy bodily labor, interference with heat-dispersion through 
impermeable clothing, or by a lack of water in the body. 

The direct action of the rays of the sun upon the head may cause 
cerebral and meningeal irritation, a condition characterized by hy- 
peremia and inflammatory exudations, and known as sun-stroke or 
insolation. 

The local effects of heat upon the skin, burns, are, according to the 
intensity of the heat and the time of its duration, either hyperemia 
(burn of first degree), formation of a blister (second degree), tissue- 
eschar (third degree), or carbonization (fourth degree). The heat pro- 
duces local changes in the tissues, and kills them at a certain height of 
temperature or after a certain time of exposure to its action. 


10 THE EXTRINSIC CAUSES OF DISEASE. 


When a large part of the surface of the body, about one-third, is 
burned, the affected individual usually dies, even though the burn is 
only of a slight degree and eschars are not formed. This phenomenon 
has been explained in various ways. Billroth, Foä, Mendel, and others 
believed the cause of death to lie in a suppression of perspiration and 
the resulting accumulation of toxic substances in the blood; while oth- 
ers, as Sonnenburg and Falk, sought the cause in a reflex lowering of 
‘vascular tone. In the foudroyant cases, according to Sonnenburg, the 
overheating of the blood causes paralysis of the heart. Ponfick, Klebs, 
von Lesser, and others, on the other hand, are of the opinion that the 
fatal issue is due to injury and destruction of the red blood-cells. Sil- 
bermann, Welti, and Salvioli also seek the cause of death in an injury to 
the blood, emphasizing, however, not so much the destruction of the red 
cells as the occurrence of stasis and coagulation of the blood in the 
vessels of different organs, which are interpreted as resulting from the 
changes in the blood. On the other hand, Kijanitzin and Parascandolo 
hold that there is formed in the bodies of burned individuals a poison 
(ptomain) which has an injurious effect upon the nervous system. 

The anatomical findings in fatal cases of superficial burns would in- 
dicate, when death has not resulted very quickly from the severe shock 
to the nervous system and the overheating of the body, that the cause 
of death is to be sought in the changes in the blood and in disturbances 
of the circulation. The blood-changes consist in destruction of the red 
blood-cells, or in such injury to them as to diminish their function and 
to give rise at the same time to a deposit of the products of destruction 
and of hemoglobin in the liver, spleen, and kidneys. The changes are 
further characterized by a tendency on the part of the blood to stasis 
and intravascular coagulation, through which vessels of both the pul- 
monary and the systemic circulation may be obstructed. In this con- 
nection should be mentioned also the fact that both during life and after 
death venous stasis and hemorrhages, as well as arterial anemia, are oc- 
casionally observed, and that local tissue-degenerations and necrosis may 
occur in certain organs, as, for example, in the kidneys, liver, mucosa 
of the stomach and intestine, bones, and soft parts. 

Low temperatures act in the same manner as high ones, in part 
through local injury and death of tissues, in part through refrigeration 
of the entire body. Severe and lasting lowering of temperature causes 
tissue death; after mild chilling there occur, as the result of tissue-de- 
generation, thrombosis, hyperzemia, and exudations which are relatively 
rich in leucocytes. A very short refrigeration at the freezing-point is 
sufficient to produce degenerative changes which are quickly followed by 
regenerative proliferation on the part of the cells remaining uninjured. 
Epithelial thickenings may be produced (Fuerst) by repeated slight re- 
frigerations (as well as by repeated slight increase of temperature). 
The tips of the extremities, nose, and ears are the most easily frozen. 
After repeated chillings of mild degree inflammatory redness and swell- 
ing of the skin, associated with severe itching, often occur (chilblains, 
perniones). 

If the temperature of the entire body be markedly lowered, a condi- 
tion of general paralysis results from the diminished excitability of the 
tissues, the nervous system and heart being especially affected. The 
sensorium becomes dulled, the heart-beat and respiration gradually grow 
weaker, and finally cease entirely. If the body be again warmed, be- 
fore the excitability of the tissues is wholly lost, the power of movement 


THE EFFECTS OF HIGH AND LOW TEMPERATURES. 11 


in the limbs is gradually restored, and after a time consciousness re- 
turns. In man, instances of complete recovery have been observed, even 
after refrigeration of the body to from 24-30° C. (75-86° F.). 

Besides the more severe forms of local or general lowering of the tis- 
sue temperature there may occur, as harmful pathogenic influences, mild 
general or local chillings, the so-called colds, as the result of which dis- 
ease-phenomena may manifest themselves partly at the seat of chilling, 
partly in organs in distant parts of the body. For example, after wide- 
spread refrigeration of the skin there may occur diarrhea, catarrh of the 
respiratory tract, or disease of the kidneys; after local chilling of the 
skin, painful affections of the deep-seated muscles. The exact relation 
between these phenomena and the refrigeration is unknown (the oft-re- 
peated hypothesis that they are due to hyperemia of the internal organs 
caused by the chilling of the body-surface has not been proved), but 
there is no reason on this account to deny the existence of diseases caused 
by cold. Though many diseases formerly attributed to “catching cold ” 
have been shown to be of infectious origin, there yet remain a number 
of diseased conditions for which we know no other etiology than that of 
refrigeration. Conditions of the body in which the skin is hyperemic 
and the perspiratory function active favor the taking of cold. Many in- 
dividuals appear to possess a predisposition on the part of certain tissues 
to the effects of refrigeration; in one person certain muscles, in another 
the mucous membranes will be affected. 

According to the view of many writers, refrigeration of the body 
increases the susceptibility to infection, so that, for example, the patho- 
genic bacteria which may be present in those cavities of the body acces- 
sible from without may, after such refrigeration, be able to exert their 
injurious influences upon the tissues. 


According to Pflüger and others, all the vital processes may be brought to a stand- 
still through refrigeration, without its being impossible fora recovery to take place 
from the apparent death. This may happen even when the animal is frozen to a solid 
mass. Preyer also holds the opinion that the continuity of life may be wholly inter- 
rupted by refrigeration, and designates subjects who are thus “lifeless,” but still capa- 
ble of living, as anabiotic. Frogs are said to remain capable of life for many hours 
even though the temperature be reduced to —2.5° C., at which temperature the heart 
is frozen. According to the investigations of Koch, such anabiosis of solidly frozen 
animals is possible when only a portion of the water contained in the body ef the ani- 
mal is frozen and when the thawing process takes place slowly. In the case of rapid 
thawing strong diffusion currents are set up between the water coming from the ice- 
crystals and the concentrated albuminous solutions of the blood and the tissues; and 
these currents may exert a damaging effect upon the latter. 

According to the investigations of J. Dewar (Proc. of the Royal Soe., London, 1900), 
the seeds of wheat, barley, mustard, peas, and pumpkins do not lose their germina- 
tive power when put into liquid hydrogen; that is, in a temperature of —250°. 
Further, the protoplasm under these conditions was not changed by the cold. 


Literature. 


(Effects of High and Low Temperatures.) 


Alonzo ; Alteraz. delle fibre nervose in seg. al congelamento. A. p. le Sc. Med., xiii., 
1 


Ansiaux: La mort par le refroidissement, Bruxelles, 1889. 
Bardeen: A Review of the Pathology of Superficial Burns, Johns Hopkins Hosp. 
ep., vol. vii. 
Dittrich: Ueber Hitzschlag. Zeitschr. f. Heilk., xiv., 1893 (Lit.). 
Fraenkel: Befunde bei acut. Todesfällen nach Hautverbrennung. Deut. med. 
Wochenschr., 1889. 


12 THE EXTRINSIC CAUSES OF DISEASE. — 


Fuerst: Veränd. d. Epidermis durch leichte Wärme- und Kälteeinwirkung. Beit. v. 
Ziegler, xxiv., 1898. 

Gottstein: Klimatische Einflüsse als Krankheitsursache. Ergebn. d. allg. Path., iv., 
Wiesbaden, 1899. 

Grawitz: Widerstandsfähigkeit lebender Gewebe. Deut. med. Wochenschr., 1897. 

Heidenhain, B.: Inspiration erwärmter feuchter Luft. Virch. Arch., 70 Bd., 1877. 

Hochhaus: Gewebsveränd. nach Kälteeinwirkung. Virch. Archiv, 154 Bd., 1888. 

Horvath „erbkühlungsversuche. Cent. f. d. med. Wiss., 1873; Arch. f. d. ges. Phys., 
xii., 1875. 

Jacubasch: Sonnenstich u. Hitzschlag, Wien, 1881. 

Keferstein: Der Erfrierungstod, Berlin, 1893. 

Kisskalt: Disposition, Erkältung u. Abhärtung. Münch. med. Wochenschr., 1900. 

Kochs: Wirkung der Kälte und Anabiose. Biol. Cent., 1890, u. xv., 1895. 

Kijanitzin: Ursache des Todes nach Hautverbrennung. Virch. Arch., 131 Bd., 1898. 

Köster: Hitzschlag. Berl. klin. Wochenschr., 1875. 

Kriege: Hyaline Veränderungen der Haut durch Erfrierungen. Virch. Arch., 116 
Bd., 1889. 

Laloy: Scheintod u. Wiederbelebung als Anpassung an Kälte. Biol. Cbl., xx., 1900. 

Lefévre: Réactions conséc. aux réfrigérations. Journ. de phys., ii., 1900. 

Le Noir: Agents physiques. Pathol. gen. publ. par Bouchard, i., 1895. 

Lesser: Ueber die Todesursachen nach Verbrennungen. Virch. Arch., 79 Bd., 1830. 

Masehold: Sonnenstich u. Hitzschlag. Eulenburg’s Realencyklopädie, xxii., 1899. 

Markusfeld u. Steinhaus: Todesursache nach Verbrühung. Cent. f. allg. Path., vi., 
1895. 

Naunyn: Kritisches u. Experimentelles z. Lehre v. Fieber. Arch. f. exp. Path., 
xviii., 1884. 

Obernier: Der Hitzschlag, Bonn, 1889. 

Parascandolo: Altérat. du syst. nerveux dans les brülures. Arch. de phys., x., 1898 

Pflüger: Die allgemeinen Lebenserscheinungen, Bonn, 1889. 

Ponfick: Todesfällenach Hautverbrennungen. Berl. klin. Woch., 1876, 1877, u. 1883. 

Pictet: L’Emploi des basses temper. Jahresber. über 1893 v. Hermann, ii., 1895. 

Preyer: Ueber Anabiose. Biol. Centralbl., xi., 1891. 

Rischpler: Histol. Veränderungen nach der Erfrierung. Beitr. v. Ziegler, xxviii., 

1900. 

Ruhemann: Ist Erkältung eine Erkrankungsursache? Leipzig, 1898. 

Salvioli: Causa della morte per scoltatura. Virch. Arch., 125 Bd., 1891, u. Arch. ital. 
de Biol., xv., 1891. 

Silbermann: Ursachen d. Todes nach Hautverbrennungen. Virch. Arch., 119 Bd., 
1890. 

Sonnenburg: Verbrennungen. Deutsch. Chirurgie, Lief. 14, Stuttgart, 1879. 

Uschinsky: Wirkung der Kälte auf verschiedene Gewebe. Beitr. v. Ziegler, xii., 
1892. 

Werhovski: Wirkung erhöhter Eigenwärme. Beitr. v. Ziegler, xviii., 1895 (Lit.). 

Wegner: Abkühlung blossgelegter Organe. v. Langenbeck’s Arch., xx., 1876. 

Welti: Todesursache nach Hautverbrennungen. Beit. v. Ziegler, iv., 1889; Cent. f. 
allg. Path., 1890. 

Ziegler: Wirkung erhöhter Eigenwärme. Verh. d. Congr. f. inn. Med., 1895. 


& 4. A sudden lowering of atmospheric pressure, as in the case of 
mountain-climbing and balloon ascents, may cause conditions of great 
exhaustion, with marked palpitation of the heart, unconsciousness, ir- 
regular breathing, and sometimes vomiting, and bleeding from the gums 
and lips. These symptoms depend most probably upon a lack of oxygen 
(P. Bert), the capillaries of the lung being unable to take up sufficient 
oxygen from the highly rarefied air. According to the investigations of 
Schumburg and Zuntz, it appears that a given amount of labor calls for 
a greater amount of oxygen at an increased elevation than at a lower 
level. The symptoms of mountain-sickness appear at a lower elevation 
than those of balloon-sickness, owing to the demands made wpon the 
muscles in the former case during the climbing. During the building of 
the Gorner Grat Railway it was found that at a height of 2,700-3,000 
metres the capacity of the laborers was diminished to a third. The oc- 
currence of hemorrhages is probably due to the formation of fissures in 


CHANGES OF ATMOSPHERIC PRESSURE: ELECTRICITY. 13 


the mucous membranes, caused by drying due to the rapid evaporation 
(Hoppe-Seyler, von Recklinghausen). 

According to the researches of Egger, Miescher, and others, a sojourn 
in high altitudes leads, after a short time, to an increase in the number 
of red cells and a greater hemoglobin-content of the blood. 

Schaumann and Rosenquist hold that the same phenomenon may be 
observed in animals confined for some time in bell-jars at a lower atmos- 
pheric pressure. Other authors (Schumburg, Zuntz, Gottstein) oppose 
this view, and maintain that the phenomenon is due either to a thicken- 
ing of the blood from loss of water and to changes in the distribution of 
the blood, or to changes in volume of the measuring-apparatus; they 
endeavor to explain the favorable effects which many individuals expe- 
rience from a residence at high altitudes by certain stimulating influ- 
ences (greater exposure to sun’s rays) which affect the nervous system 
and cause increased metabolism. According to Marti, intense and pro- 
longed irradiation of the body stimulates the formation of red blood-cells 
and to a lesser degree also that of the hemoglobin. 

A sojourn in diving-bells or caissons, such as are employed in build- 
ing operations beneath the water, in which the atmospheric pressure is 
increased, under certain conditions, as high as four atmospheres or even 
greater, causes a slight difficulty in breathing and a relatively unimpor- 
tant increase of the pulse-rate. If a change be made quickly from the 
compressed atmosphere to air of ordinary pressure, there may occur 
within an hour a condition of great fatigue, tightness of the chest, ring- 
ing of the ears, cramps in the muscles, pains in the joints and limbs, 
hemorrhages from the nose, ears, and lungs, dilatation of the pupils, and 
under certain conditions paralysis, coma, delirium, and even death after 
an interval of from one to twenty days. The cause of these phenomena 
is probably to be found in the sudden escape from the blood of nitrogen 
which had been absorbed under the high pressure (von Leyden), or in an 
obstruction of the blood-vessels of the spinal cord through the formation 
of gas-bubbles (Hoche). According to experimental investigations of 
Heller, Mager, and von Schrotter, the blood, after rapid removal of 
pressure, contains free gas (almost exclusively nitrogen), so that free gas 
circulates in the blood. The researches of von Leyden and von Niki- 
foroff show that in fatal cases associated with paralysis areas of de- 
generation are found in the white columns of the spinal cord, in which 
individual nerve-fibres are torn apart, presenting marked changes in the 
form of swelling of the axis-cylinders, disintegration of the medullary 
sheaths, and the formation of vacuoles in the place of the nerve-fibres. 
These disturbances are regarded as due to the production of gas-bubbles 
within the spinal cord. If the gray matter is involved, the ganglion- 
cells may also degenerate. 

Changes in the electrical condition of the atmosphere and in the 
magnetic state of the earth produce no demonstrable changes in the hu- 
man body; on the other hand, electric discharges, as lightning-stroke, 
may cause, in part, local burns (Fig. 1), and, in part, lesions of the 
whole body. Under certain circumstances lightning-stroke causes lacer- 
ation of internal organs, as, for example, of the heart and liver. The 
most frequent and important effect of lightning-stroke is a paralysis of 
the nervous system, which gives rise to a severe dyspnea, which may 
be fatal after a few minutes or hours or which may gradually pass away 
after several hours, days, or weeks. Only rarely do individual nerve- 
trunks remain permanently paralyzed. A transitory paralysis may oc- 


14 THE EXTRINSIC CAUSES OF DISEASE. 


cur when the electrical discharge has not pasged through the body but 
has descended in its neighborhood. 

In individuals who have been struck by lightning there may be found 
slight or severe burns of the skin corresponding to the points of entrance 
and exit of the current, and various injuries to the tissues in the course 
of its path through the body. The marks of the burn are for the greater 
part red, and form peculiar branching 
zigzag lines, the so-called lightning jig- 
ures (Fig. 1), which are essentially a hy- 
peremia, and soon disappear if the burns 
are not severe. 

The passage of powerful electric 
currents of high tension, such as are 
generated by dynamos, through the hu- 
man body, as may happen when an in- 
dividual is placed in a circuit or comes 
into contact with an uninsulated con- 
ductor, may give rise to severe disturb- 
“ ances or cause death. According to 

. Kratter, the lower limit of danger occurs 
at a tension of about five hundred volts. 
Alternating currents are much more 
dangerous than continuous ones of the 
same strength and tension. When the 
effects are not fatal, the injured person 
is suddenly rendered unconscious, this 
condition lasting for a few minutes or 

Fig, 1.—Lightning-ügures on the shoul. Several hours, and for several days after- 
figtmmcg' Sd Arm of a woman struck by ward symptoms of vertigo, prostration, 

headache, and palpitation of the heart 
may persist (Kratter). At the points of contact more or less severe 
burns are produced. 

In fatal cases, death takes place suddenly or rarely after ten or thirty 
minutes. The autopsy findings, aside from the burnsat the points of con- 
tact, are evidences of suffocation and hypervenosity of the blood, stasis 
of the blood within the thoracic vessels, and often small scattered 
hemorrhages which are due partly to suffocation, and partly to the 
direct action of the current. The cause of death is paralysis of the cen- 
tre governing the respiration or the heart’s action. 





Literature. 
(Effects of Changes of Atmospheric Pressure and of Solarization.) 


Bert, P.: La pression barométrique, Paris, 1878. 

Egger: Veränderungen d. Blutes im Hochgebirge. Congr. f. inn. Med., Wiesbaden, 
1893; u. Arch. f. exp. Path., 39 Bd., 1897. 

Gottstein: Klimat. Einflüsse als Krankheitsursachen. Ergebn. d. allg. Path., iv., 
Wiesbaden, 1899: Vermehrung der rothen Blutkörp. im Hochgebirge. Minch. 
med. Woch., 1899. 

Heller, Mager, Schrötter: Mitth. über Caissonarbeiter. Klin. Woch., 1895; Unter- 
such. über d. Wirkung rascher Veränderungen d. Luftdruckes. Pfüger’s Arch., 
67 Bd., 1897; Luftdruckerkrankungen, Wien, 1900. 

Hirsch: Handbuch der histor.-geogr. Pathologie, Stuttgart, 1882-1888. 

Hoche: Luftdruckerkrankung d. Centralnervensystems. Berl, klin. Wochenschr., 
1897 


MECHANICAL INFLUENCES. 15 


Hoppe-Seyler: Müller’s Arch., 1857; und Physiol. Chemie, Berlin, 1877. 

Jourdanet: L’Intiuence de la pression de l’air, 1875. 

Leyden: Durch plötzl. Verminderung d. Barometerdrucks entsteh. Rückenmarksaffec- 
tion. Arch. f. Psych., ix., 1879. 

Loewy u. Zunz: Einfluss d. verdünnt. Luft. Pflüger’s Arch., 1897. 

Marti: Wirkung der Hautreize und Belichtung. Verh. d. Congr. f. inn. Med., Wies- 
baden, 1897. 

Mercier: L’Influence de l’altitude. Arch. de phys., vi., 1894. 

Miescher: Bezieh. zwisch. Meereshöhe u. Beschaftenh. d. Blutes. Corrbl. f. schweiz. 
Aerzte, 1893. 

Mosso: Der Mensch auf den Hochalpen, Leipzig, 1899. 

Nikiforoff: Veränderungen d. Rückenmarks in Folge schneller Herabsetzung des 
baromcetrischen Druckes. Beitr. v. Ziegler, xii., 1892. 

Schaumann u. Rosenqvist: Blutveränd. im Höhenklima. Zeit. f. klin. Med., 35 
Bd., 1898. 

Schumburg und Zunz: Einwirkung des Hochgebirges. Pflüger's Arch., 63 Bd., 1896. 

Snell: Compressed-Air Illness, London, 1896. 

Wolff: Einfluss des Gebirgsklimas auf d. Menschen, Wiesbaden, 1895. 

Zunz on athogenese der durch Luftdrucksänderungen erz. Krankheiten. Fortschr. d. 
Med., xv., 1897. 


(Effects of Lightning and of Electrical Currents.) 


D’Arsonval: L’énergie électrique. Path. gen. publ. par Bouchard, i., Paris, 1895. 

Dillner: Ueber die Wirkung des Blitzes. In.-Diss., Leipzig, 1865. 

Ebertz: Ueber Blitzverletzungen. In.-Diss., Tübingen, 1892. 

Haberda: Tödtung durch Blitzschlag. Wiener klin. Wochenschr., 1891. 

Kratter: Wirkung d. Blitzes. Vierteljahrsschr. f. ger. Med., 1891; Tod durch Elek- 
tricitat, Wien, 1896 (Lit.); Elektrische Verunglückungen. Eulenb. Jahrb., vi., 1896 
(Lit.). 

Liman: Blitzschlag. Deutsch. med. Wochenschr., 1885. 

Mills and Weisenburg: The Effects on the Nervous System of Electric Currents of 
High Potential. Univ. of Penn. Med. Bull., 1903. 

Oesterien: Blitzschlag. Maschka’s Handb. d. ger. Med., i. 

Prevost et Battelli: mort par les décharges électriques. J. de phys., i., 1899. 

Vincent: Contrib. a l’hist. medicale de la foudre, Paris, 1875. 


2. The Origin of Disease through Mechanical Influences. 


“ §5. Traumatic influences of various kinds leading to concussion, 
bruising, and laceration of tissue are of very frequent occurrence, and 
act partly through the tearing and destruction of tissue, partly through 
changes in tissue-organization not recognizable to the naked eye, and 
partly through lesions and ruptures of the blood- and lymph-vessels, and 
through irritation and paralysis of nerves. The sequel are partly 
necrosis and destruction of tissue, partly disturbances of circulation, inflam- 
mation, and regenerative proliferations. Frequently repeated mechanical 
traumatisms of slight degree, such as rubbing, may give rise to congestive 
hyperemia and inflammations, which may lead further to hyperplastic 
growths of tissue. If large quantities of insoluble dust particles are con- 
tinuously taken into the lungs, extensive changes may occur in these or- 
gans and, under certain circumstances, in other organs. As a result of 
prolonged pressure and diminution of space, atrophy of an organ or tissue 
may occur (corset-liver). 

After a single or after frequently repeated trauma, there may de- 
velop under certain conditions at present unknown to us, malignant new- 
formations of tissue called tumors. Trauma may further pave the way 
for an infection, either in that the wound caused by the trauma is in- 
fected at the time of injury or is secondarily infected from without ; or that 
micro-organisms were previously present in the body under conditions in- 
hibiting their growth, and these find in the injured tissues a suitable soil for 
grouth, so that to the trauma an infection is joined. 


16 THE EXTRINSIC CAUSES OF DISEASE. 


Traumatic influences affect, first of all, the external parts of the 
body ; but it may happen, either with or without visible injury to ex- 
ternal parts, that internal organs may be injured, and the internal 
lacerations, necroses, and hemorrhages thus produced may be followed, 
not only by inflammations and reparative tissue proliferations, but also 
by malignant neoplasms (as, for example, after fractures of bones), and 
by infective processes. 

Mechanical lesions (also thermal, electrical, and corrosive) run a spe- 
cial course, if through the local injury the nervous system becomes in- 
volved. Such involvement occurs either through the direct action of 
the trauma upon the central nervous system; or, by the stimulation of 
the sensory or sympathetic nerves, the central nervous system may be 
so affected that a number of additional nervous symptoms follow. 

If the direct concussion of the cranium is followed by paralysis of 
the cerebral function and unconsciousness, the condition is termed 
commotio cerebri or cerebral concussion. This term is especially used 
when the trauma has produced no visible changes in the structure of the 
brain, or at least none of any size or importance. 

Excessive stimulation of the peripheral nerves may cause a reflex in- 
hibition or paralysis, involving chiefly the functions of the heart and 
respiratory apparatus; the symptoms thus produced being collectively 
designated as shock. The most frequent causes of shock are injuries to 
the spinal column, abdominal cavity, and scrotum, less frequently to 
the extremities and thorax. Further, shock may be caused by light- 
ning-stroke, burns, corrosions of the skin, fear, and psychical emotions 
through whatever avenue of perception they may be called forth. In- 
dividuals whose nervous systems are in a certain condition of excitement 
are especially liable to shock; conditions of narcosis and drunkenness 
inhibit its occurrence. 

Shock is characterized chiefly by weakened energy on the part of the 
heart and irregular breathing, which lead to a decrease in the inter- 
change of gases in the tissues and to a lowering of the temperature; as a 
result, the venous blood in persons dying of shock is lighter in color than 
the normal venous blood (Roger). The consciousness is usually pre- 
served, the skin and visible mucous membranes are pale, the pulse 
is small and markedly quickened, often irregular and intermittent. 
Further, the individual suffering from shock may be either excited, 
groan, shriek, and complain of a fearful anxiety associated with 
dyspneea (erethistic shock); or he may lie quiet, with sunken countenance 
and exhibit evidences of great weakness of both sensory and motor func- 
tions (torpid shock). Insevere cases death takes place from the stoppage 
of the heart and cessation of respiration. 

Shock, in being due to the over-stimulation of the peripheral nerves, 
is closely allied etiologically to the phenomenon known as syncope; but 
the last-named condition differs essentially from shock in that its chief 
symptom is a transitory loss of consciousness, while the functions of the 
heart and respiration show no marked disturbance. Syncope is, further, 
usually preceded by prodromal symptoms, such as dizziness, ringing in 
the ear, and darkening of the visual field, these being absent. in shock. 

Not infrequently, following an injury to some part of the body, there 
may arise a more or less pronounced functional disturbance of the ner- 
vous system, which may often persist long after the local injury has 
healed, so that such disturbance is in no way dependent upon anatomical 
changes in the peripheral or central nervous system, but must be re- 


EFFECTS OF TRAUMA. 17 


garded as a purely functional disturbance of psychical origin. Such condi- 
tions are termed traumatic neuroses or accident nervous diseases, and 
are characterized chiefly by subjective but in part also by objective symp- 
toms. To the first belong especially pains not definitely localized at 
the seat of injury, as headache, pain in the chest, backache, difficulty 
in movement, general lassitude, inability to perform mental labor, dul- 
ness of perception, disturbances of sight, flashes before the eyes, dizzi- 
ness, restless sleep, loss of appetite, and disturbances of digestion. With 
these last symptoms are associated (Oppenheim, Strimpell) psychical 
depression of a hypochondriacal or melancholic character, irregularly 
placed areas of cutaneous anesthesia, enfeeblement of the senses of taste, 
hearing, and smell, motor paralysis, cramps, and hyperzsthesia, concen- 
tric narrowing of the visual field, pareses, muscular spasms, tremors, 
acceleration of the pulse, and tendency to sweating. 

According to the opinion of various writers, these phenomena de- 
pend essentially upon a psychical shattering of the perceptive life, a 
psychoneurosis which is less often due to the trauma and the associated 
psychical shock than to the resulting anxiety over health and business 
matters. The condition in part partakes of the nature of hysteria, as 
characterized by a disturbance of the normal relation between the men- 
tal and bodily processes; in part of hypochondria, as recognized by the 
spontaneous occurrence of abnormal sensations; and in part of a neuras-: 
thenia, which reveals itself by the production of abnormal pathological 
sensations through slight stimulation or exertion. If the will no longer 
controls the motor centres, hysterical paralyses arise; if the normal con- 
trol and inhibition of the will are lost, so that unreasonable will-stimuli 
are created and influence the muscles, hysterical twitchings, contract- 
ures, or convulsions take plaee. If a nervous stimulus arising in the 
sensory tract fails to reach the consciousness, there follows a hysterical 
anesthesia; if there arise in the consciousness the images of expected 
or feared sensations, and if these images are intensified into actual sub- 
jective stimuli of consciousness, hysterical pains and neuralgias result 
(Strümpell). 


Rosenbach designates as kinetoses those diseases which arise when energetic and 
continuous movements of the body in one direction are changed into the opposite direc- 
tion. so that a shifting of the internal organs results. In this class belong the patho- 
logical phenomena observed in seasickness, and in the conditions caused by see-sawing, 
whirling, mocement in a vertical direction, and sudden stoppage of motion. Asa result of 
the rapid change in direction of bodily motion, the molecules which are moving in the 
line of the primary direction are forced to move in the opposite direction; and, ac- 
cording to Rosenbach, such a change is sufficient to cause more or less important molec- 
ular disturbance. He explains the symptoms of seasickness, as, for example, the ab- 
normal secretion of the stomach, the increase of intestinal peristalsis, the vomiting, etc., 
as the results of purely mechanical influences on the tissues, and belicves that the 
liver, intestine, brain, and nerve-plexuses are similarly affected through mechanical in- 
fluences acting upon their protoplasm. Further, purely psychical influences excited 
by feelings of discomfort may aid in the production of seasickness, just as disgust, 
fright, or fear may cause dizziness. 


Literature. 


(Effects of Trauma.) 


v. Bergmann: Die Lehre von den Kopfverletzungen, Stuttgart, 1880. 

Bruns: Unfallsneurosen. Eulenburg’s Jahrb., viii., 1898 (Lit.). 

Fischer: Ueber den Shock. Sammi. klin. Vortr. v. Volkmann, No. 10, 1870. 

Freund: Traumatische Neurosen. Samml. klin. Vortr., No. 51, Leipzig, 1892. 
2 


LANE LIBRARY. STANFORD UN 


18 THE EXTRINSIC CAUSES OF DISEASE. 


Groeningen: Teber den Shock. Wiesbaden. 1585. 
Höber. sbock durch Reizung seröser Haute. Arch f. exp. Path. 40 Bd, 1897. 
Jolly: Traumatische Epilepsie. Char.-Ann.. xx.. 1885. 
Lejars: Lis agents mécaniques. Path. gen publ par Bouchard. i.. 1995. 
im: Die traumatischen Neurosen. Berlin. 1°92. 
Roger: Choc nerveux. Arch. de piys.. v.. 18G3_ vi.. 1°04. 
Bosenbach: Die Seekrankbeit, Wien. 19966: u. Eulenburg’s Realencykiop.. xxii. 
1,99. 


Sachs u. Freund: Die Erkrankungen des Nervensystems nach Unfällen. Berlin. 1899. 

Schultze: Ueber Nervenkrankbeiten nach Trauma D. Zeitschr. f. Nervenheilk.. i. 
igmüller: Unfallnervenkrankbeiten. Encvklop. Jahrb. der ges. Heilkunde. 1893 
(Lit. ). 

Stern: Die traumatische Entstehung innerer Krankheiten. Jena. 1960 , Lit.). 

Strümpell: Traumat. Neurosen. Münch. med. Woch.. 1889: Verl. d. XIL Congr. f. 
iun. Med., 1893. 


3. The Origin of Disease through Intorication. 


§ 6. By poisoning or intoxication is meant that impairment of health, 
caused by the injury to a tissue, which certain substances. by virtue of their 
chemical nature, are able to produce under certain conditions. Such sub- 
stances are termed poisons, and are derived partly from the mineral 
kingdom, partly from the vegetable, and partly from the animal king- 
dom. They may occur in a natural state or they may be produced ar- 
tificially from inorganic or organic substances, which may be either 
non-poisonous or possess quite different properties’ Many of the most 
important poisons are products of either plant or animal life, and are 
formed either within the tissues of the plant or animal, or from their 
food-supply by the transformation of substances which are either inert 
or possess an entirely different action. 

The most important poisons belonging to the mineral kingdom or which are 
produced from minerals are: metallic mercury, chlorine, bromine, iodine, 
sulphur, and various combinations of these substances, different combi- 
nations of arsenic, antimony, lead, barium, iron, copper, silver, zinc, 
potassium, sodium, chromium, ete. Of the poisons containing carbon, 
which are artificially produced, the most important are: chloroform, 
chloral hydrate, ether, alcohol, iodoform, carbon bisulphide, hydro- 
cyanic acid, potassium cyanide, oxalic acid, nitroglycerin, amyl nitrite, 
petroleum, carbolic acid, nitrobenzole, picric acid, and aniline. It may 
be observed in this connection that modern chemistry is constantly pro- 
ducing new substances, some of which are poisons. 

Of the poisons produced by plants of the higher order, those of chief im- 
portance are: the vegetable alkaloids, such as morphine, quinine, colchicine, 
atropine, hyoscyamine, veratrine, strychnine, curarine, solanine, nico- 
tine, digitaline, santonin, aconitine, cocaine, coniine, muscarine, and 
ergotine, all of which in relatively small doses may cause poisoning. 

The lower forms of plant life, especially bacteria, produce an extraordi- 
nary variety of both poisonous and non-poisonous substances, out of the food 
material (albuminous bodies) in which they develop. Some of these sub- 
stances are similar to the vegetable alkaloids, others to the ferments, 
and are therefore designated toric cadareric alkaloids, toxic ptomains, 
toxins, toxalbumins, and torenzymes (compare § 10). It may happen that 
the blood, flesh, or any organ of a healthy animal may acquire poisonous 
properties as a result of changes set up in it through the growth of bac- 
teria. Such diseases due to bacterial poisons in the food are known as 
botulismus, sausage, meat, fish, and cheese poisoning. These conditions are 
to be explained, in part, by the growth of germsin the food-stuff and 


INTOXICATION. 19 


the formation of toxic products out of the albuminous bodies; in part by 
the fact that germs were present in the tissues of the animal before 
death, the animal being slaughtered while diseased, and the use of its 
flesh as food causes either poisoning or the same disease as that affect- 
ing the animal. Under certain conditions foods which are not spoiled 
may already contain bacteria, and these may develop in the intestine of 
the individual eating the food and cause poisoning through the produc- 
tion of toxins, toxalbumins, or enzymes. ' 

According to Lombroso, the disease pellagra, which is of common oc- 
currence in Italy, Roumania, and Greece, is caused by the eating of 
decomposed corn. The disease kakké or beri-beri, which is endemic in 
Japan, is regarded by Miura and Yamagiva as due to the extended use 
of rice which has been spoiled in drying. 

Among the animals which normally produce poisons within certain tissues 
of their bodies, the best known are: serpents, toads, salamanders, fish, 
mussels, oysters, scorpions, Spanish flies, and many stinging insects. 
Certain forms of sea-fish are poisonous at all times, others only at cer- 
tain periods, and observations have been made particularly of such fish 
found in Japanese waters. According to Saotschenko, the poison of 
many poisonous fishes is secreted by certain skin-glands found at the 
roots of the dorsal and caudal fins, and may be found also in the eggs 
of such fish. According to Remy, Miura, and Takesaki, the poison is 
secreted in the sexual glands alone in the case of the poisonous fish be- 
longing to the family Gymnodontes (tetrodons). According to Mosso, 
there is found in the blood-serum of eels a toxic substance (ichthytoxin) 
which, when introduced into the small intestine of animals experimen- 
tally, causes symptoms of poisoning and may kill the animal. The ob- 
servations made of cases of poisoning from the eating of mollusks occur- 
ring some years ago at Wilhelmshafen excited general interest; in these 
cases it was found that the eating of mussels (Mytilus edulis) caused severe 
illness, resulting in some cases in death. 

According to M. Wolff, the liver of mussels contains the poison; its 
action, according to Schmidtmann, Virchow, Salkowski, and Brieger, is 
similar to that of curare. Brieger has also shown that from the poison- 
ous mussels there can be obtained basic substances closely related to 
ptomains, the basic products of decomposition. To what extent the 
causes of the production of poisons in poisonous fishes and mollusks are 
to be ascribed to normal, and to what extent to pathological processes 
of life, cannot at the present time be always decided. From the fact 
that the mussels and oysters are poisonous only in certain places where 
the water is impure, and as the starfish found in the same localities are 
similarly affected, it is probable that the poisonous action of these mol- 
lusks may in part be due to their contamination with bacteria or to the 
occurrence of certain diseased conditions. 

It is difficult to give an exact definition of poison and poisoning, since the action 
of the substances considered in this connection varies greatly according to the dose and 
attenuation, as well as the method of introduction into the tissues of the body. The 
most powerful poisons when introduced in minute doses may not only be harmless, 
but may exert a beneficial or curative effect. On the other hand, substances which are 
not usually classed with the poisons, such as the non-corrosive sodium salts, when in- 
troduced into the body in large quantities or in concentrated solutions, may produce 
effects which must be regarded as of the nature of poisoning. Further, poisons in cer- 
tain dilutions (phenol) may serve as food-material. In the definition given above I 
have followed Kobert, and in the brief survey over the action of poisons contained in 
the succeeding , paragraphs I have made ınuch use of his “Textbook on Intoxications,” 
published in 1893. 


20 “THE EXTRINSIC CAUSES OF DISEASE. 


Snake-poison is formed exclusively in the poison-glands located above the angle of 
the mouth. It is a greenish or yellowish fluid, the virulency of which is not affected by 
desiccation or preservation in alcohol. The active principle is a toxalbumin. 


Literature. 


(Intoxication. ) 


Binz, Bohm, Liebreich: Arbeiten deutsch. Pharmakologen a. d. J. 1865-1889, Ber- 
lin, 1890. 

Boehm, Naunyn, v. Boeck: Intoxicationen. v. Ziemssen's Hdb. d. spec. Path., xv., 
1880 


Fröhner: Lehrb. d. Toxicologie f. Thierärzte, Stuttgart, 1890. 

Hofmann: Lehrb. d. gerichtl. Medicin, Wien, 1895. 

Hildebrandt: Compendium der Toxicologie, Freiburg, 1893. 

Kobert: Lehrb. der Intoxicationen, Stuttgart, 1898; Compend. d. Toxicologie, Stutt- 

rt, 1894. 

Kunkel: Handb. d. Toxicologie, i., Jena. 1899. 

Lewin: Nebenwirkung d. Arzneimittel, Berlin, 1899; Die Pfeilgifte. Virch. Arch., 
138 Bd., 1894; Toxicologie, Wien, 1897; Cumulative Wirkung. Deut. med. 
Woch., 1899. 

Loew: Natürliches System der Gifte, München, 1898. 

Roger: Intoxications. Path. gen. publ. par Bouchard, i., Paris, 1895. 

Richardiöre: Intoxications. TTrait¢ de Médecine, ii., 1892. 

v. Wyss: Lehrbuch der Toxicologie, Wien, 1895. 


(Poisoning by Spoiled Foods. ) 


Albrecht: Fleischvergiftung im Bezirk Sonthofen. Wochenschr f. Thierheilk., 1878. 

Bollinger: Ucber Fleischvergiftung. Zur Aetiologie d. Infectionskrankheiten, Mün- 
chen, 1881. ; 

Butter u. Huber: Die Massenerkrankungen in Wurzen, 1877. Arch. d. Heilk., xix. 

v. Düring: Pellagra. Eulenburg’s Realencyklop., xviii., 1898. 

van Ermengem: Des intoxications alimentaires, Bruxelles, 1895; Botulismus. Zeit. f. 
Hyg., 26 Bd., 1897. 

Flinzer: Massenerkrankung in Chemnitz, 1879. Vierteljahrsschr. f. ger. Med., 
xxxiv., 1881. 

Husemann : Ostreismus (Austernvergiftung). Eulenburg’s Jahrb., vii., 1897 (Lit.). 

Kaensche: Krankheitserreger bei Fleischvergiftung. Zeit. f. Hyg., xxii., 1896. 

Kussmaul: Vergiftung mit Schwartenmagen. Deut. Arch. f. klin. Med., iv., 1868. 

Lombroso: Die Lehre von der Pellagra, Berlin, 1898. 

Müller: Wurstvergiftung. Deut. Zeitschr. f. prakt. Med., 1875. 

Nauwerck: Wurstvergiftung. Deut. med. Wochenschr., 1886; Württ. Correspbl. f. 
Aerzte, 1886. 

Schneidemühl: Botulismus. Centralbl. f. Bakt., xxiv.. 1898 (Lit.). 

Siedamgrotzky: Ueber Fleischvergiftung. Vortr. f. Thierärzte, iii. ser., 2. H., 1880. 

Silberschmidt: Fleischvergiftung. Zeitschr. f. Hyg., 30 Bd., 1899. 

Vaughan: Milk and Cheese-poisoning. Zeit. f. phys. Chem., 1886: Journ. of Amer. 
Med. Assn., 1887. 

Walder: Dic Typhusepidemie in Kloten. Berl. klin. Woch., 1878. 

Yamagiva: Zur Kenntniss der Kakké. Virch. Arch., 156 Bd., 1899. 

Zangger: Vergiftung durch Kalbfleisch. Arch. f. Thierheilk., 24 Bd., 1871. 


(Animal Poisons.) 


Aron: Experimentelle Studien über Schlangengift. Zeitschr. f. klin. Med., 1883. 

Arustamoff: Ueber die Natur des Fischgiftes. Centralbl. f. Bakt., x., 1891. 

Brenning: Die Vergiftung durch Schlangen, Stuttgart, 1895 (Lit.). 

Brieger: Miesmuschelvergiftung. Biol. Centralbl., vi., 1886, u. Deut. med. Woch., 
1885. 

Calmette: Venin des serpents. Ann. de l’Inst. Past., vi., 1892; viii., 1894; ix., 1895. 

Fischel u. Enoch: Zur Lehre von den Fischgiften. Fortschr. d. Med., x., 1898. 

Husemann: Fischgifte. Eulenburg's Realencyklop., 1895; Schlangengifte, t., xxi., 
1899; Thiergifte, 15., xxiv., 1900. 

Karlinski: Zur Pathologie der Schlangenbisse. Fortschr.-d. Med., viii., 1890. 


POISON PRODUCING LOCAL TISSUE CHANGES. Si 


Kaufmann: Ueber 68 Fälle von Giftschlangenbissen. Correspbl. f. Schweiz. Aerzte, 
1893. 

Langer: Das Gift der Honigbiene. Arch. f. exp. Path., 38 Bd., 1897. 

v. Linstow: Die Giftthiere, Berlin, 1894. 

Lustig: I microorganismi del Mytilus edulis. A. p. le Scienze Med., xii., 1883. 

Mitchell: Researches upon the Venom of the Rattlesnake, Washington, 1884. 

Mitchell and Reichert: Venoms of Poisonous Serpents, Washington, 1886, ref. Biol. 
Central.. vii., 1888. 

Miura u. Takesaki: Zur Localisation des Tetrodongiftes. Virch. Arch., 122 Bd., 1890. 

Mosso: Un venin dans le sang des murénides. Arch. it. de Biol., xii., 1888; u. Arch. 
f. exp. Path., xxv., 1888; Du venin qui se trouve dans le sang de l’aiguille. 
Arch. it. de Biol., xii., 1889. 

Nowak: Et. des altér. prod. par les venins des serpents et des scorpions. Ann. de 
IInst. Past., 1898. 

Ragotzi: Wirkung des Giftes der Naja tripudians. Virch. Arch., 122 Bd., 1890. 

Roger: Intoxications. Path. gén. publ. par Bouchard, i., Paris, 1895. 

Salkowski: Miesmuschelvergiftung. Virch. Arch., 102 Bd., 1885. 

Saotschenko: Atlas des poissons venéneux, St. Petersburg, 1887. 

Schmidt: Ueb. d. Natur des Fischgiftes. Verhandl. d. X. int. med. Congr., ii., Ber- 
lin, 1891. 

Starcke: Gift der Larven des Käfers Diamphidia locusta (Blut auflösendes Pfeilgift 
der Kalachari). Arch. f. exp. Path.. 38 Bd., 1897. 

Virchow, Martens, Lohmeyer, Schulze, u. Wolff: Miesmuschelvergiftung. 
Virch. Arch., 104 Bd., 1886. 

Virchow: Miesmuschelvergiftung. Berl. klin. Woch., 1885. 

Vollmer: Ueb. d. Wirkung d. Brillenschlangengiftes. Arch. f. exp. Path., 31 Bd., 
1892. 

Wehrmann: Et. du venin des serpents. Ann. de l’Inst. Past.. xii., 1898. 

Wolff, M.: Miesmuschelvergiftung. Virch. Arch., 108 Bd., 1886; u. 110 Bd., 1887. 
See $ 12 for literature of Ptomains and Toxins. 


$ 7. Poisons may be divided according to their action into three 
groups: first, those producing local tissue-changes; second, those acting 
injuriously upon the blood; third, those affecting chiefly the nervous 
system and the heart without producing recognizable anatomical lesions. 

The poisons which cause marked local lesions injure primarily the 
tissues with which they first come into contact upon entering the body. 
If such poisons are diffused by means of the body-fluids, the most 
diverse organs and tissues may be injured; but their action is usually 
limited to that organ in which they are stored up or through which 
they are excreted, especially the liver, intestine, and kidneys. 

The primary seat of injury is most often the mucosa of the upper 
portion of the intestinal tract and the respiratory passages, but in many 
cases the skin is first affected. Very frequently poisons, which are em- 
ployed for disinfecting, are brought into contact with wounds for the 
purpose of killing bacteria or preventing their growth, and in this way 
may cause local changes or may be absorbed and damage the internal or- 
gans or the entire body. 

The first great. group of poisons belonging to this class are those which 
cause ınarked tissue-changes at the primary point of contact, which are 
similar to those of burns, and for this reason have been designated 
caustics or corrosives. If the action of a caustic reaches its most char- 
acteristic severity, the affected tissue will be wholly destroyed and con- 
verted into either a dry, hard eschar, or under certain conditions into a 
moist, soft one. Ifthe action is of moderate intensity as the result. of 
a less concentrated solution of the caustic agent, or of incomplete action 
of the chemical even when applied in strong solution or in substance, 
or because the tissue itself is more resistant as in the case of the skin, the 
changes produced are much less severe, and are characterized by red- 
ness, swelling, inflammation, and hemorrhages. Very diverse changes 


22 THE EXTRINSIC CAUSES OF DISEASE. 


are often found in the same organ, such as local sloughing (necroses), 
hemorrhages, inflammations, and small swellings due to local hyperzemia. 
If the changes have existed for some time, the local eschars are sur- 
rounded by a more or less marked inflammatory zone, which in the case 
of certain caustics may be of very limited exent. 

The substances belonging to the class of caustic poisons are: first, the 
corrosive acids, sulphuric, nitric, hydrochloric, phosphoric, oxalic, arse- 
nic, arsenious, osmic, acetic, lactic, trichloracetic, carbolic, and salicylic 
acids; and further, the corrosive combinations of the alkalies and alka- 
line earths, potassium and sodium hydroxide (watery solutions of KOH 
and NaOH), caustic ammonia (solution of NH, in water), ammonium 
carbonate, caustic lime, and barium sulphate. Belonging in this class 
are also certain corrosire salts, chiefly of the heavy metals, such as salts 
of antimony (tartar emetic and antimony trichloride), salts of mercury 
(corrosive sublimate and red precipitate), nitrate of silver, zinc chloride, 
zinc sulphate, copper sulphate and copper acetate, aluminum acetate, 
potassium chromate and bichromate, and chloride of iron. 

The poisons belonging to this class derived from animals are: cantharidin, 
from the beetle Lytta vesicatoria ; phrynin, the secretion from the cutane- 
ous glands (parotid) of the toad; the secretions from the poison-glands 
of snakes and scorpions; the secretion of the sting-glands of bees, wasps, 
and hornets; the secretion of the salivary glands of stinging-gnats, flies, 
and gad-flies; and the secretion of the poison-glands of the maxillary 
palpz of spiders (tarantula)—all of which cause local necrosis or in- 
flammation. Many of the higher plants produce in their blossoms, seeds, 
stems, or roots substances which, when brought into contact with the 
tissues, cause local irritation and inflammation, as, for example, daphne, 
different forms of Ranunculus, varieties of anemone, marsh-marigold, 
different varieties of Calla, dragon-root, Croton tigli (from the seeds of 
which croton-oil is obtained), buckthorn (Rhamnus cathartica), black 
elder (Rhamnus frangula). 

The nature of the local changes which these substances and many 
others not mentioned here produce is naturally very varied, and is 
dependent partly upon the activity of the poison, and partly upon the 
location and manner of application. The mineral acids, solutions of 
caustic potash and mercuric chloride, when concentrated, cause marked tis- 
sue-eschars, associated with hemorrhagic inflammations, especially when 
taken into the stomach. Through the action of acids there is a marked 
withdrawal of the alkaline constituents of the body fluids, leading to dis- 
turbances of respiration and circulation. The venom of snakes, which 
belongs to the toxalbumins, causes usually severe local inflammations 
and hemorrhages, which often extend far beyond the region of the bite; 
and sometimes may cause also a widespread gangrene. There are also 
snake-venoms which produce only insignificant. local changes, the general 
symptoms of poisoning being much more prominent. The volatile or 
gaseous poisons, which in the form of gas or vapor cause local irritation 
of the tissues, affect chiefly the mucous membranes of the eye and 
respiratory tract (irrespirable gases). To this class belong especially the 
fumes of ammonia, chlorine, sulphurous acid, nitric oxide, nitric diox- 
ide, nitric trioxide, osmic acid, and mustard oil. The intensity of action 
of these poisons is very varied, often causing only atransitory hyperemia, 
but being able also to give rise to tissue necrosis and severe inflamma- 
tion. The irritation of the respiratory tract gives rise to coughing and 
a spasmodic narrowing of the glottis which may interfere with breathing. 


POISONS PRODUCING LOCAL TISSUE CHANGES. 23 


To the local irritation and inflammation caused by these poisons at 
the primary seat of contact may be added further effects upon internal 
organs. After the absorption of these poisons into the fluids of the 
body, those organs suffer most in which the poison is stored up or 
elaborated, though organs of the most varied structure may be affected, 
as well as those not concerned in the excretion of the poison. In the case 
of certain poisons, the changes at the point of entrance are very slight and 
often not recognizable, the important anatomical lesions occurring first 
in other tissues, to which the poison has been carried by the blood. 
Finally, a given poison may act also as a nerve and heart poison, so that 
clinically the effects of this action are much more prominent than the 
local lesion. In poisoning with corrosive sublimate, cell necrosis takes 
place in the secreting part of the kidneys, and there is also severe in- 
flammation of the colon. The salts of chromic acid, cantharidin, and 
many acids cause more or less marked degeneration and inflammation in 
the secreting portion of the kidney and in the urinary passages. 

Phosphorus, arsenic, antimony, and pulegon, which have but slight 
corrosive action, produce tissue-degenerations, particularly fatty degen- 
eration, and also hemorrhages, in the liver, heart, muscles, bone-mar- 
row, and capillaries of different organs, these changes being particularly 
marked in cases of phosphorus poisoning. 

If an individual is exposed for months or years to the fumes of yellow 
phosphorus, there may take place an inflammation of the jaw bones lead- 
ing to necrosis, but only when the occurrence of inflammatory changes 
is favored by other causes, such as putrid decomposition in the mouth or 
the presence of decaying teeth. 

The long-continued use of silver nitrate may be followed by a deposit 
of black granules of silver in the most diverse tissues, the skin, kidneys, 
intestinal villi, and the choroid plexus. 

The venom of snakes possesses, in addition to its local effects, a para- 
lyzing action upon the nervous system and heart, and may cause death 
through paralysis of the respiratory centre. 

Soluble salts of lead when ingested may cause irritation and inflam- 
mation of the intestine, with such symptoms as vomiting, diarrhea, 
constipation, cramps in the stomach, associated with such nervous phe- 
nomena as anesthesia, motor paralysis, convulsions, vertigo, and loss 
of consciousness. When ingested continuously for a long time, lead 
gives rise to general disturbances of nutrition, intestinal colic, pains in 
the limbs, anesthesias, motor paralyses, cerebral disturbances, and kid- 
ney disease. These disturbances are without doubt dependent upon the 
distribution and deposit of lead throughout the body, leading to anatom- 
ical lesions of varied nature. 

The active principles of ergot (Secale cornutum), sphacelinie acid and 
cornutin, when taken in large doses, as when eaten in bread, cause itch- 
ing, pain, and cramps in the limbs, followed by numbness and feeling 
of cold in the toes and finger-tips, and finally there may occur a more 
or less extensive gangrene of these parts (ergotism, “‘ Kribbelkrankheit”) ; 
at the same time ulceration of the intestine may occur. In cases of 
chronic poisoning, degenerations of the spinal cord take place (Tuczek). 
The feeding of chickens with ergot causes gangrene of the comb through 
the production of stasis and hyaline thrombosis in the blood-vessels. In 
animals fed for along time with ergot degenerative changes are found 
in the central and peripheral nervous system, in the blood-corpuseles, 
and in the endothelium of the blood-vessels (Grigorjeff). 


24 THE EXTRINSIC CAUSES OF DISEASE. 


Literature. 


(Poisons Producing Local Tissue-Changes. ) 


Bettmann: Wirk. d. Arseniks auf Blut und Knochenmark. Beitr. v. Ziegler, xxiii., 
1898, 

Brouardel: Les paralysics arsenicales. Arch. de méd. exp., viii., 1896 (Lit.). 

Coén e D’Ajutolo: Avvelenamento cronico di piombo. Beitr. v. Ziegler, iii., 1888. 

Eichhorst: Ueber Bleilähmung. Virch. Arch.. 120 Bd., 1890. 

Erlicki u. Rybalkin: Arseniklähmung. Arch. f. Psych., xxiii., 1892. 

Fraenkel u. Reiche: Nierenveränd. nach Schwefelsäurevergiftung. Virch. Arch.. 
131 Bd., 1893. 

Geyer: Ilautveränd. bei Arsenicismus. Arch. f. Derm., 43 Bd., 1898 (Lit.). 

Goetze: Die Bleivergitfung, Würzburg, 1893. 

Grigorjeff: Mutterkornvergiftung. Beitr. v. Ziegler, xviii., 1895. 

Grünfeld: Mutterkornvergiftung. Dorpater Arbeiten, herausgeg. v. Kobert, viii., 
1892, 

Hartmann. Exper. Untersuchungen über Chromsiurenephritis. Inaug.-Diss., Frei- 
burg, 1891. 

Husemann: Arsenausschläge u. Arsenvergiftung. Encyklop. Jahrb., v., 1895; 
Bleigicht, ¢b., 1897. 

Ipsen: Salpetersäurevergiftung. Vierteljahrsschr. f. ger. Med., vi., 1898. 

Jacobj: Das Sphacelotoxin. Arch. f. exp. Path.. 39 Bd., 1897. 

Janowski: Die Ursachen der Eiterung. Beitr. v. Ziegler, xv., 1894. 

Kaufmann: Die Sublimatintoxication, Berlin, 1888; u. Virch. Arch., 117 Bd., 1889. 

v. Kahlden: Die Aetiologie und Genese der acuten Nephritis. Beitr. v. Ziegler, xi.. 
1592. 

Kobert: Lehrbuch der Intoxicationen, Stuttgart, 1893. 

Kocher: Zur Kenntniss der Phosphornekrose, Berlin, 1893. 

Kockel: Wirk. v. Dämpfen salpeteriger u. Untersalpetersäure. Vierteljahrsschr. f. 
ger. Med.. 1898. 

Krysinski: Pathol. u. klin. Beiträge zur Mutterkornfrage, Jena, 1888 (Lit.). 

Langerhans: Vcränd. der Luftwege nach Carbolsäurevergiftung. Deut. med. Woch., 
1893. 

Lanz: Pathogenese der mercuriellen Stomatitis, Berlin, 1897. 

Lesser: Veriind. des Verdauungskanals durch Aetzgifte. Virch. Arch. 83 Bd., 1881. 

Leutert: Sublimatvergiftung. Fortschr., xiii., 1895. 

Lewin: Arsen. Eulenburg’s Realenceyklopädie, ii., 1894. 

Lindemann: Veränd. des Stoffwechsels durch Pulegon. Zeit. f. Biol., 39 Bd., 1900. 

Maier: Bleivergiftung. Virch. Arch., 90 Bd.. 1882. 

Meiser: Wismuthvergiftung. Inaug.-Diss.. Freiburg, 1892. 

Meyer: Wirkung des Phosphors. Arch. f. exp. Path., xiv., 1881. 

Müller: Arsenmelanose. Arch. f. Derm., 25 Bd., 1882. 

Neuberger: Wirkung des Sublimates auf die Nieren. Beitr. v. Ziegler, vi. 1889. 

Pistorius: Acute Arsenikvergiftung. Arch. f. exp. Path., 16 Bd., 1882. 

Riess: Phosphorvergiftung. Eulenb. Realeneyklop.. xix., 1899. 

Schulz: Giftigkeit der Phosphorsauerstoffverbindungen. Arch. f. exp. Path., xviii., 
1804. 

Schultze: Ueber Bleilihmung. Arch. f. Psych., 16 Bd., 1885. 

Stadelmann: Ucber den Ikterus bei Phosphorvergiftung. Arch. f. exp. Path., xxiv., 
ISSN. 

Steinhaus: Veriind. d. Netzhaut durch Phosphor. Beitr. v. Ziegler, xxii., 1897. 

Tirelli: Empoisonnement par le sublime. Arch, ital. de Biol, xxvi., 1896. 

Ullmann: Localisation dl. Quecksilbermetalle im Orranismus. Arch. f. Derm., Er- 
ränzh., 1899. 

Welander. Absorption und Elimination des Quecksilbers. Arch. f. Derm., 25 Bd., 
1893. 

Westphal: Ueber Encephalopathia saturnina. Arch. f. Psych., 19 Bd.. 1888. 

Winternitz: Allgemeinwirkung örtl. reizender Stoffe. Arch. f. exp. Path., 35 Bd., 
INYn. 

Ziegler u. Obolonsky: Wirkung des Arseniks u. des Phosphors. Beitr. v. Ziegler. 


ii., ISS8. See also S 6. 


88. The poisons which affect the blood chiefly, and are therefore termed 
blood-poisons, are partly gases and partly fixed substances. The latter 


POISONS AFFECTING THE BLOOD. 25 


are absorbed chiefly from the intestine, but they may also enter the body 
through wounds, or they may be injected directly into the blood-vessels. 
Some of the blood-poisons may also produce local lesions in the tissue at 
point of entrauce; further, there may be joined to the action on the 
blood a direct effect upon the nervous system, which under certain con- 
ditions may cause death before the action upon the blood is recogniz- 
able. Finally, it should be emphasized that the blood-changes produced 
by the poison may cause numerous secondary changes in different or- 
gaus, for instance, in the kidneys, liver, intestine, and brain. 

The most important blood-poison is carbon monoxide gas, in that it 
very frequently leads to more or less serious or fatal poisoning, through 
its action on the blood. Such poisoning most often results from the car- 
bon monoxide in coal- or illuminating-gas, but may occur under other 
conditions, as in the case of the vapors produced by gun-powder or gun- 
eotton. 

The effects of the inhalation of carbon monoxide result from the com- 
bination of the gas with the hemoglobin of the blood and the formation 
of carbon-monoxide-hemoglobin. The amount of oxygen combined 
with the hemoglobin is thereby decreased, and the taking up of oxygen 
is reduced, even when the respired air contains only 0.05 per cent or 
even 0.02 per cent of CO (Gruber). The red blood-cells themselves 
present no changes. A sudden supply of carbon monoxide to the ner- 
vous system may cause direct injury to the nerves, giving rise to convul- 
sions and later to paralysis (Geppert). In cases of long-continued 
poisoning the displacement of the oxygen from the greater portion of 
the red cells leads to tissue-asphyxia. If the affected individual does 
not die, there may result, in addition to the poisoning, severe disturb- 
ances of nutrition, occurring especially in the nervous system. The 
poisoning itself is characterized by headache, tinnitus aurium, vertigo, 
malaise, vomiting, fainting, convulsions, paralysis, and coma. The 
blood, as a result of the presence of carbon monoxide, becomes a bright 
violet or cherry-red color, so that the hyperemic skin and internal or- 
gans also appear bright red. 

A second not infrequent form of poisoning is that caused by hydro- 
cyanic acid (CNH ) and potassium cyanide (CNK ), the latter being much 
used in certain technical arts. In general, hydrocyanic acid is found in 
unstable combination in the leaves, bark, and seeds of many plants (bit- 
ter alınonds, cherry- and peach-stones, apple-seeds, leaves of the laurel, 
bark of Prunus padus, tubers of many of the Euphorbiacez, flaxseed, 
ete. ). 

Hydrocyanic acid possesses a double action. In relatively small 
doses it exerts a paralyzing action upon the central nervous system, 
death following in a very short time, even after a few seconds, from the 
paralysis of the centres of respiration and circulation. In addition, 
there is an effect upon the blood and tissues, depriving them of their 
power to combine and use the oxygen brought to them (Geppert), so 
that the organs suffocate in the presence of oxygen. According to 
Kobert, a cyan-methemoglobin is formed which is of a bright-red color, 
and gives to the hypostatic spots of the cadaver a bright red ap- 
pearance. 

A third substance belonging to this group of poisons is hydrogen 
sulphide (H,S), which may be present in the gas of sewers and dung-pits. 
When inhaled in large amounts, it may cause sudden death from paraly- 
sis of the nervous system. When hydrogen sulphide is for some time 


26 THE EXTRINSIC CAUSES OF DISEASE. 


brought into contact with blood containing oxygen (as is usually the case 
in decomposing cadavers), a sulphur-methemoglobin is formed, which 
gives to the blood a greenish color. 

Carbon monoxide, hydrocyanic acid, hydrogen sulphide, aside from 
their direct action on the nervous system, produce deleterious effects, 
chiefly, according to the statements made, in decreasing the functional 
powers of the red blood-cells, by combining with their heenioglobin. 

Another large group of poisons affect the blood chiefly, by the destruction 
of the red blood-cells, and the formation of methemoglobin, a combination of 
oxygen with the hemoglobin in the same proportion as in oxyhsmo- 
globin, but in which the oxygen is much more firmly held than in the ease 
of the latter. Such an action is produced by various oxidizing sub- 
stances (ozone, iodine, sodium hypochloride, chlorates, nitrites, and ni- 
trates); by reducing agents (nascent hydrogen, palladium hydride, pyro- 
gallol, pyrocatechin, hydrochinon, and alloxanthin); also by substances 
which have neither a reducing nor oxidizing action (salts of aniline and 
toluidin, acetanilid). In the change from hemoglobin to methzmo- 
globin, oxyhemoglobin is present as an Intermediate stage. 

The formation of methemoglobin can occur either in the red blood- 
cells or in the hemoglobin which has escaped into the blood-plasma; but 
the destruction of the blood-cells and the escape of hemoglobin into the 
plasma are not always followed by the formation of methemoglobin. 
In the case of a marked destruction of red cells, as in poisoning from 
phallin, helvellic acid, arseniuretted hydrogen, only a portion of the 
hemoglobin is changed into methemoglobin. Hemoglobin and oxyhe- 
moglobin have a red color, methemoglobin a sepia- brown. 

Dissolution of the red blood-cells and the formation of methsemo- 
globin oceur in the case of a part of those poisons causing local tissue- 
changes, as in poisoning with acids, metallic salts, phosphorus, and 
arsenie, but the property of attacking the red cells and changing the col- 
oring-matter belongs also to a large class of other substances. 

Phallin, a toxalbumin present in certain mushrooms (Amanita 8. 
Agaricus phalloides), helvellie acid, contained in the fresh morel, Helvella 
esculenta (the poison is lost through drying), arseniuretted hydrogen 
(AsH,), the ethereal extract of male fern, cause destruction of the red cells 
with a resulting increased formation of bile-pigment and a deposit of 
derivatives of the blood-pigment in the liver, kidneys, and bone-marrow. 
Potassium chlorate (KCIO,), pyrogallol (C,H,[OH],), hydrazin (H,N—NH,), 
toluylendiamin (C,H, {[NH,],CH,), vitrobenzol (C,H,NO,), nitroglycerin 
(C,H, [NO,],), amyl nitrite (C,H, NO,), pieric acid (C,H,[NO,],OH), aniline 
(CLH,NH,), carbon disulphide (CS,), are distinctive in their action, in that 
they cause formation of methemoglobin, sometimes with destruction of 
the red cells, at other times without. 

Large doses of potassium chlorate may cause death in a few hours, 
through the destruetion of the red blood-cells and through the action of 
the potassium, with the occurrence of vomiting, diarrhea, dyspnaa, 
eyanosis, and cardiae insufficiency. The blood becomes chocolate-brown 
in color. In more protracted cases of poisoning by smaller doses the 
products of blood destruction are found in the spleen, liver, bone-mar- 
row, and kidneys. The urine in these cases may vary in color from a 
reddish-brown to black (methemoglobin). Delirium, numbness, coma, 
and convulsions occur, showing the marked involvement of the central 
nervous system. Pvrogallol produces similar symptoms. Hydrazin 
and phenylhydrazin produce multiple thrombosis, in addition to the de- 


POISONS AFFECTING THE BLOOD. 27 


struction of red cells and formation of methzmoglobin. In poisoning 
with toluylendiamin the essential feature is a destruction of the red cells, 
with a deposit of iron-containing pigment in spleen, liver, and bone-mar- 
row. Incats hemoglobin may be excreted by way of the urine (Biondi). 
In picric-acid poisoning there occurs, in addition to the destruction of 
blood-cells and formation of methemoglobin, a severe irritation of the 
central nervous system, characterized by violent corvulsiors. Aniline 
and carbon disulphide not only injure the blood, but also give rise to ir- 
ritation and paralysis of the nervous system. 


According to Kobert, ricin derived from the seeds of the castor-bean, and udrin 
from the seeds of abrus precatorius, should be classed with the blood-poisons, in that 
in the test-tube they cause an agglutination of the red cells and the formation ofa 
flocculent precipitate. In animals poisoned experimentally, local irritations, tissue- 
degenerations and inflammations, similar to those caused by certain bacterial toxins, are 
produced, as well as disturbances in the centres of the medulla oblongata, leading to 
cessation of respiration with progressive falling of blood-pressure. Tissue-degenera- 
tions, inflammation, and hemorrhage sare found, after longer action, at the point of 
application and in the intestine, where the poison is excreted. Degenerative changes 
are also found in lymphocytes, liver and kidney cells, and heart muscle. 


Literature. 


( Blood- Poisons ; Abrin and Ricin.) 


Afanasiew: Vergiftung mit Toluylendiamin. Zeitschr. f. klin. Med., 6 Bd., 1883. 

Belky: Zur Kenntniss der Wirkung der gasförmigen Gifte. Virch. Arch., 106 Bd., 
18886. 

Berkley: Ricin-poisoning. Trans. of the Path. Soc. of Philadelphia, xviii., 1898. 

Biondi: Experimentelle Untersuchungen über Ilämatolyse. Beitr. v. Ziegler, x viii., 
1895. 

Böhm u. Külz: Giftiger Bestandtheil d. Morchel. Arch. f. exp. Path., 19 Bd., 1885. 

Bostroem: Intoxication durch die essbare Morchel, Leipzig, 1882. 

Cramer: Befund im Gehirn bei Kohlenoxydvergiftung. Centralbl. f. allg. Path., iv., 
1894. 

Cruz: Alt. hist. dans l’empois. par la ricine. Arch. de med. exp.. xi., 1899. 

Dittrich: Ueber methämoglobinbildende Gifte. Arch. f. exp. Path., 29 Bd., 1892. 

Dreser: Zur Toxikologie des Kohlenoxyds. Arch. f. exp.-Path., 29 Bd., 1891. 

Dütting: Vergiftung durch Inhalation von Arsenwasserstoff. Inaug.-Diss., Freiburg, 
1888. 

Ehrlich: Veratrin- und Sublimatvergiftung. Charité-Ann., x., 1885. 

Falkenberg : Vergift. durch Anilin, chlorsaure Salze u. Sublimat. Virch. Arch., 123 
Bd., 1891. 

Flexner: Hist. Chang. prod. by Ricinand Abrin. Jour. of Exp. Med., 1897, ref. Cent. 
f. a. Path., 1899. 

Georgiewsky: Wirkung des Extract. filicis marisaeth. Beit. von Ziegler, xxiv., 1898. 

Geppert: Leber das Wesen der Blausäurevergiftung. Zeitschr. f. klin. Med., 15 Bd., 
1889. 

Geyer: Chron. Hautveränderungen bei Arsenicismus. Arch. f. Derm., 43 Bd., 1898 
(Lit.). 

Huber: Giftwirkung des Dinitrobenzols. Virch. Arch., 126 Bd., 1891. 

Husemann: Pilzvergiftung. Eulenb. Realencyklop., xix., 1898 (Lit.). 

Katayama: Neue Blutproben bei Kohlenoxydvergiftung. Virch. Arch., 114 Bd., 
INSS. | 

Kobert: Lehrbuch der Intoxicationen, Stuttgart, 1893. 

Koch: Schwarzwasserficber (Chininvergiftung). Zeit. f. Hyg., 30 Bd., 1899. 

Lebedeff: Morchelvergiftung. Virch. Arch., 91 Bd., 1883. 

Lewin: Nebenwirkung d. Arzneimittel, Berlin, 1899; Toxikologie, Wien, 1897. 

Marcacci: Empoisonnement par l’oxyde de charbon. Arch. ital. de Bioi., xix.. 1898. 

Marchand: Wirkung chlorsaurer Salze. Arch. f. exp. Path., 22 Bd., 1886; u. 28 Bd., 
1887. 

v. Mering: Das chlorsaure Kali, Berlin, 1885. 

Müller: Ricinvergiftung. Arch. f. exp. Path., 42 Bd.; u. Beit. v Ziegler, xxvii., 
1990. 


28 THE EXTRINSIC CAUSES OF DISEASE. 


Petrone: Avvclenamento da acido pirogallico, Catania, 1895. 

Ponfick: Morchelvergiftung. Virch. Arch., 88 Bd., 1886. 

Poelchen: Gehirnerweichung nach Kohlendunstvergiftung. Virch. Arch., 112 Bd., 
1888. 

Silbermann: Blutgerinnung dureh chlors. Salze, Arsen, Phosphor, etc. Virch. Arch., 
117 Bd., 1889. 

Stadelmann: Vergiftung mit Toluylendiamin. Arch. f. exp. Path., 14 Bd., 1881, 16 
Bd., 1883, 23 Bd., 1887: Der Ikterus, Stuttgart, 1891. 

Stephens: Hämolytic Action of Snake Toxins. Jour. of Path., vi., 1900. 

Stockvis: Vergift. mit chlorsaurem Kali. Arch. f. exp. Path., 10 Bd., 1897; u. 21 
Bd., 1886. 

Uschinsky: Schwefelwasserstoffvergiftung. Zeitschr. f. phys. Chem., 17 Bd., 1892. 

Werhovsky: Abrinvergiftung. Beit. v Ziegler, xviii., 1895. 


§ 9. The last group of poisons, generally classed together as nerve 
and heart poisons, is characterized chiefly by the fact that, in spite of the 
severity of the symptoms, as shown in the form of irritations and paraly- 
ses, anatomical changes either cannot be recognized at all or are confined 
to structural changes in the protoplasm of individual nerve-cells, which 
are of similar character in the case of different poisons. This is espe- 
cially the case when the poison is quickly fatal, while if the poisoning 
runs a protracted course, or in the case of chronic poisoning from small 
doses, extending over months and years, there are very often found 
marked anatomical changes—a fact which may be taken as evidence that 
these poisons do not produce solely functional disturbances of the ner- 
vous system, but cause injury to the cell-protoplasm which may be mani- 
fested in the form of degenerations. 

Of the very great number of poisons which act especially upon the ner- 
vous system and may cause death through its paralysis, the most impor- 
tant are: chloral hydrate, opium and its alkaloid morphine, cocaine, 
atropine, hyoscyainine, daturine (stramonium-atropine), nicotine, 
coniine, eicutoxin, santonin, camphor, quinine, veratrine, colchicine, 
aconitine, strychnine, cytisin, curarine, and samandarine (salamander- 
poison). 

Of the heart-poisons, digitalin, helleborin, muscarine, and phrynin 
(poison of toads) are of special importauce. 


Chloroform (CITC), when applied directly to the mucous membranes, causes 
local irritationand may produce transitory inflammation. When conveyed to the blood 
through inhalation or by absorption from the intestinal tract, it gives rise, after a 
short period of stimulation, to a condition of diminished irritability of the cerebral gray 
and white matter. According to Binz, the protoplasm of the ganglion-cells suffers a 
slight coagulation, Death may be caused by paralysis of the central nervous system, 
as well as by a premature heart-failure: the latter. however, occurring only when the 
heart is abnormally weak or degenerated, or possibly when the irritation produced by 
the chloroform upon the mucous membrane of the nose causes a strong reflex stimula- 
tion of the inhibitory nerves of the heart. The long-continued use of chloroform may 
cause degenerative changes in different organs, as the heart, kidneys, liver, muscles, 
and blood. 

Ether (dicthyl ether CoHl,OC,H,) acts similarly to chloroform, but is less poisonous, 
and acts less detrimentally upon the heart. 

Nitrona oride (NO acts chiefly upon the cerebrum, lowers the sensibility of pain, 
and paralyzes consciousness; later, the action may extend to the spinal cord, the 
medulla oblongata, and the heart. 

Aleohol (OH,OLH), after a transitory stimulation, has a depressing and paralyzing 
action upon the brain, at the same time causing a dilatation of the arteries of the skin, 
so that in intoxicated individuals severe chilling threugh the skin may easily occur. 
Death may take place suddenly, with symptoms similar to those of apoplexy ; more 
frequently there isa gradual loss of consciousness and of sensory perception, the respira- 
tion becomes slower, the pulse small. the face cvanotic: complete coma and general 
paralysis forming the closing symptoms. The immoderate use of alcohol for months 


NERVE AND HEART POISONS. 29 


or years may, on the one hand, give rise to pathological deposits of fat in those regions 
where fat is normally found; on the other hand, to fatty degeneration of glandular or- 
gans, particularly of the kidneys and liver; also degenerative atrophies of liver and kid- 
neys associated with increase of connective-tissue; further, sclerosis and atheroma of 
the arteries, degeneration of the brain, etc., are ascribed to the action of alcohol. At 
the present time it is impossible to say in what manner, how often, and to what extent 
these changes are dependent upon the use of alcohol. It is certain, however, that 
drunkards suffer frequently from disturbances of digestion and circulation, catarrhal 
inflammations of pharynx, larynx, and bronchi, and disturbances of cerebral function; 
and that the disease of the brain known as delirium tremens, which is characterized by 
general muscular tremors, obstinate insomnia, anxiety, and hallucinations, is especially 
to be ascribed to alcoholisın. 

Chloral hydrate (CCl, CHO. H,0) causes local irritation of mucous membranes, and 
through the blood produces paralysis of the brain, spinal cord, and heart, and thus in- 
duces sleep. In fatal doses, death follows deep coma as a result of adema of the lungs 
due to the general relaxation of the tissues. 

Optum and Morphine (C,:H,,.VO,) depress the cerebral functions, thereby inducing 
sleep; in individual cases there may be a preceding period of stimulation. Large doses 
lead to unconsciousness, paralysis of muscles, slowing and weakening of the heart’s 
action, contraction of the pupils, slowing of intestinal peristalsis, diminution in the ex- 
change of gases in the blood dependent upon diminished excitability of the respiratory 
centre. There is no characteristic autopsy finding; the blood is usually dark and fluid. 
The chronic use of opium may give rise to digestive disturbances, emaciation, vertigo, 
sleeplessness, neuralgias, imbecility, impotence, weakness of the bladder, hallucination, 
tremors of the hands and feet, fever, etc., yet these symptoms may vary much in 
different individuals. In chronic morphinism the organism becomes accustomed to 
increasingly larger doses; withdrawal of the drug causes severe nervous disturbances, 
and under certain conditions dangerous collapse. 

Cocaine (C\;H,,NO,) produces peripherally a dulling of the excitability of the 
sensory nerve-endings; centrally, first a stimulation and later a paralysis. The chronic 
use of cocaine gives rise to symptoms similar to those of chronic morphinism. 

Atropine and hyoscyamine (Ci:Hs:NO;), the alkaloids which are found in the 
Solanacee (deadly nightshade, thornapple, and henbane), cause paralysis of the periph- 
eral nerve-organs and a central stimulation, followed later by paralysis. Solutions 
of atropine introduced into the eye produce dilatation of the pupil and paralysis of ac- 
commodation for near vision, through its paralyzing action on the endings of the motor 
oculi in the iris. Atropine may further cause suppression of the secretion of certain 
glands (as the submaxillary); it also inhibits intestinal peristalsis. Asa result of the 
action of this poison upon the brain, a condition of excitement, gayety, inclination to 
laugh, leading even to insanity and frenzy, may be produced, followed by paralysis. 
The autopsy findings are negative. 

Nicotine (CioH,,Ns), a volatile alkaloid found in the tobacco plant, acts upon both 
peripheral and central nervous systems, causing nausea, salivation, vomiting, diarrhea, 
vertigo, muscle weakness, headache, convulsions, delirium, and paralysis. Chronic 
nicotine poisoning may give rise to nervous affections and disturbances of the heart’s 
action. According to Vaa, there is in both chronic nicotine and alcohol poisoning a 
degeneration of the ganglion-cells characterized by a homogencous appearance of the 
chromatin. 

Coniine (C.H,,N), the alkaloid present in hemlock, causes paralysis of the periph- 
eral motor nerve-endings, first stimulating and then paralyzing the central nervous 
system. (icutorin, a poisonous resin obtained from the water-hemlock (Cicuta ttrosa) 
produces nausea, vomiting, attacks of colic, cardiac palpitation, convulsions, and un- 
consciousness. 

Suntonin (C,./1,,03) causes convulsions by its action on the brain and spinal cord, 
with benumbing of the sensorium, vertigo, vomiting, salivation, and yellow vision or 
xanthopsia, in which white is seen as yellow and blue as green. 

Quinine (CseHy,N303), the most important of the numerous alkaloids contained in 
the bark of cinchona and other closely related plants, has a paralyzing action upon 
living protoplasm, and in relatively small doses lowers the functional capacity of the 
brain. Large doses produce death through paralysis of the centre of respiration and of 
the heart. 

Aconttine, colchicine, and veratrine produce local irritations and, later, benumbing 
of the peripheral endings of the sensory nerves. On the central nervous system they 
have first a stimulating action, later a paralyzing. 

Strychnine (C3:Hss.N203), obtained chiefly from the plant nux vomica, causes an 
increased reflex excitability of the nerve centres, so that the slightest external stimu- 
lus may produce tetanic convulsions. Death may occur in from ten to thirty minutes 


30 THE EXTRINSIC CAUSES OF DISEASE. 


after the first convulsion, and is the result of central paralysis, namely, of the vaso- 
motor centre. 

Curarine (CoAssN), the active principle of the arrow-poison curare, is probably 
derived from the cortical portion of the roots of different plants of the strychnia family. 
Wlien used in small doses it paralyzes the endings of the motor nerves of the muscles. 
Larger doses cause paralysis of the central nervous system and of the vasomotor 
nerves, after a temporary stimulation. 

Digitalin and digitalein, two glucosides obtained from the foxglove, act as local 
irritants; after absorption they stimulate the heart, vagus-centre, and the musculature 
of the blood-vessels, so that with a slowing of the heart-beats there is an increase of 
blood-pressure. Large doses cause headache, delirium, tinnitus aurium, irregular in- 
crease in the frequency of the heart’s action, convulsions, and coma. 

ed Helleborin, a glucoside obtained from hellebore, acts similarly to the preparations 
of digitalis. 

Muecarine (C; 7,503), the poison of the fly-agaric, acts as a stimulant to those 
nerve-endings which are paralyzed by atropine. The intense excitation of the inhib- 
itory centres of the heart causes stoppage of the unparalyzed heart, and death is 
thereby produced. The general symptoms of muscarine poisoning are salivation, ver- 
tigo, anxiety, nausea, vomiting, diarrhwa, convulsions, and finally unconsciousness. 
Small doses produce a condition of excitation similar to that of drunkenness. 


The above summary of poisons, which is of necessity confined to a limited number, 
I have based upon the generally accepted classification, which Kobert has also retained 
in his text-book on intoxications. A more exact knowledge of the action of poisons 
than we now possess will surely in the future be made a basis for a different classifica- 
tion. veiw (see literature to 8 6) has recently attempted to make a classification of 
poisons according to their action upon the living organism, that is, upon the living 
protoplasm. He distinguishes two great groups, namely, general potsons, which in 
moderate concentration are fatal to all living organisms; and special potsona, which 
have no injurious effect upon certain classes of organisms. The general poisons are 
characterized chiefly by their power to change the chemical character of the active 
protein-bodies, out of which living protoplasm is formed. They may be classed as 
follows: (1) Oridizing poisons (ozone, chromic acid, manganic acid, hy permanganic 
acid, hypochlorites, hydrogen peroxide, chlorine, bromine, iodine, phosphorus, arse- 
nious acid); (2) potsons haring a catalytic action (ethyl ether, chloroform, chloral, many 
hydrocarbons, etc.), which transfer to the protoplasm the unstable condition of their 
molecules, and so lead to chemical changes in the unstable albumin; (8) potsons acting 
by the production of salts (acids, soluble mineral bases, and corrosive alKalies, alkaline 
earths, salts of the heavy metals), which form with the protein-bodies chemical com- 
binations of the nature of salts; (4) substitution poisons (hydroxylamin, diamide, 
phenylhydrazin, ammonia, phenol, hydrocyanic acid, etc.), which even when greatly 
diluted interfere with the aldehyde or amido-groups. The special potsons are classified 
as follows: (1) Toric proteids. i.e., (a) torulbumins (produced by bacteria and poisonous 
to animals); (b) alerins and tmmunitorins (produced in animals physiologically or 
pathologically, and poisonous for bacteria): (c) regetable enzymes (abrin. ricin, produced 
from phancrogams and the higher fungi, and poisonous to animals); (d) antmal enzymes 
(produced by certain animals, snakes, fishes, and spiders, and poisonous to other ani- 
mals); (2) organic buses (strychnine, atropine, curare, etc.), having an unexplained ac- 
tion; (3) poisons acting indirectly, which interfere with the processes of respiration 
(carbon monoxide, sulphites), or which act as pdisons through decomposition (nitrites, 
iodine combinations), or which cause structural alterations through changes in the 
tumidity (“Quellungszustand ”) of certain organized tissues (neutral alkaline salts, 
alkaline earths, oxalates). 


Literature. 


(Nerve and Heart Poisons. ) 


Afanasiew: Zur Path. des acuten u. chron. Alkoholismus. Beitr. v. Ziegler, viii., 
1890. 

Ambrosius: Tod nach Chloroforminhalation. Virch. Arch., 188 Bd., Suppl., 1894. 

Binz: Das Chinin. Berlin, 1875; Alkohol. Eulenburg’s Realencyklop., iii. Aufl., 1888. 

Braun: Veränd. d. Nervensystems durch chron. Alkoholintoxication, Tübingen, 1899. 

Brouardel: Les paralysies arsénicales. Arch. de med. exp., viii., 1896 (Lit.). 

Demme: Ueber den Einfluss des Alkohols auf den Organismus des Kindes, Stuttgart, 
1890. 


ORIGIN OF DISEASE THROUGH INFECTION. 3. 


Denys: Zur Kenntniss der Wirkung desStrychnins. Arch. f. exp. Path., 20 Bd., 1886. 

Faust: Zur Kenntn. d. Samandarins. Arch. f. exp. Path., 41 Bd., 1898. 

Fraenkel, E.: Veränderungen durch Chloroformnachwirkung. Virch. Arch., 127 Bd., 
1892. 

Garré: Die Aethernarkose, Tübingen, 1898. 

Goldscheider u. Flatau: Normale u. pathol. Anatomie der Nervenzellen, Berlin, 
1898. 

Husemann: Pfeilgifte. Eulenburg’s Realencyklop., xviii., 1898. 

Jacottet: Et. sur les alterations des cellules nerveuses. Beitr. v. Ziegler, xxiv., 1897. 

Jakobj: Pharmakol. Unters. über das Colchicumgift. Arch. f. exp. Path., 27 Bd., 
1890. 

v. Kahlden: Wirkung des Alkohols auf Leber u. Nieren. Beitr. v. Ziegler, ix., 1881. 

Kappeler: Chloroform. Deutsch. Chir., Lief. 20; Arch. f. klin. Chir., 87 Bd., 
1387. 

Kobert: Muscarinwirkung. Arch. f. exp. Path., 20 Bd., 1886; Intoxicationen, Stutt- 
gart. 1898. 

Kraepelin: Psych. Wirkung des Alkohols. Münch. med. Woch., 1899. 

Lewin: Die Nebenwirkung d. Arzneimittel, Berlin, 1899; Pfeilgifte. Virch. Archiv, 
136 Bd., 1894. 

Lissauer: Unters. über die Wirkungend. Veratrumalkaloide. Arch. f. exp. Path., 28 
Bd., 1887. 

Mosso: Wirkung des Cocalns. Arch. f. exp. Path., 23 Bd., 1887; Pflüger’s Arch, 2’ 
Bd., 1892. 

Ostertag: Die tödtliche Nachwirkung des Chloroforms. Virch. Arch., 118 Bd., 1889. 

Poroschin: Veränd. durch Chloroformnarkose. Cbl. f. d. med. Wiss.. 1898. 

v. Schröder: Unters. über Morphin. Arch. f. exp. Path., 17 Bd., 1883. 

Spitzer: Darmwirkung des Opiums u. Morphins. Virch. Arch., 123 Bd., 1891. 

Strassmann: Tödtliche Nachwirkung des Chloroforms. Virch. Arch., 115 Bd., 1889. 

Strümpell: Die Alkoholfrage vom ärztl. Standpunkt aus. Münch. med. Woch., 
1893. 

Tillie: Ueber d. Wirkung des Curare u. seine Alkaloide. Arch. f. exp. Path., 27 Bd., 
1890. 

Tuman: Wirkung des Cocains auf psychomotor. Centren. Arch. f. exp. Path., 22 Bd., 
1887. 

Vas: Chron. Nicotin- u. Alkoholvergiftung. Arch. f. exp. Path., 83 Bd., 1894. 

Vollmer: Wirkung v. Morphin u. Atropin auf d. Athmung. Arch. f. exp. Path., 30 

1892. 


4. Origin of Disease through Infection or Parasitism. Miasms and Conta- 
gion. Vegetable and Animal Parasites. 


810. As seen in the last sections (§ 6 to § 9), there occur in the in- 
toxications certain morbid vital phenomena, which are caused by definite 
chemical] substances, the mode and severity of whose action, in so far as 
the idiosyncrasy of the poisoned individual and the especial manner of 
application of the poison are not considered, depend not only upon the 
character of the poison but also upon the size of the dose employed. 

In those diseases which arise from infection and which are called 
infectious diseases, we have, on the contrary, to deal with morbid vital 
phenomena, which, if we disregard the susceptibility of the infected indi- 
vidual and the especial mode of entrance of the infecting material into 
the body, are dependent solely upon the character of the infecting agent, 
while the dose is of little or no significance. 

The essential difference between intoxication and infection lies in the 
fact that in the first case there is no increase of the poison within the 
body, while in infection the harmful agent increases after its entrance into 
the organism, so that the smallest possible amount of the infective mate- 
rial may give rise to the most severe and fatal disease. The size of the 
dose of the infecting agent has an influence upon the succeeding illness 
only in so far as the probability of infection (that is, reproduction of the 
injurious agent within the body) is increased with the amount of the 


32 THE EXTRINSIC CAUSES OF DISEASE. 


same taken into the body, and that consequently the reproduction of the 
infective agent may in shorter time reach such proportions as to give 
rise to pathological tissue-changes and symptoms of disease. 

The injurious agents causing the infectious diseases enter the human 
organism from the external world and give rise to an ilness which may 
run a pathognomonic course; and from the peculiarities of this course it 
may be possible to conclude that the disease is due to a specific organism 
possessing a characteristic action. In the case of pregnant women the 
infective agent may be transmitted from the organism of the mother to 
the foetus in utero. 

If an infectious disease attacks a great number of individuals in a 
given locality, it becomes a pestilence or an epidemic. | 

Experience based upon clinical observation teaches us that in some 
cases the injurious agent which causes a certain infectious disease is 
active only in certain regions and infects (that is, makes ill) individuals 
who live in this region. In other cases it is seen that contact with a dis- 
eased individual, or proximity to such, or the use of some object touched 
by the affected person or contaminated in other ways—for example, 
through dejecta or through sputum—may produce the disease. Finally, 
it may also be noted that infective material develops only at certain 
times in a given locality, and only when an infected individual visits 
that pzrticular region and through his presence leads to the production 
there of the infective material. 

From these varying conditions occasion has been taken to divide the 
agents capable of causing infection into different groups and to desig- 
nate these by particular names. If the infective agent is connected with 
a certain locality it is termed a miasm, the conception underlying this 
being that the affected region produces the injurious material. If only 
a particular region produces the infective agent, the term local miasm is 
used; but if universally present, a ubiquitous miasm. To the miasmatic 
diseases belong especially malaria, croupous pneumonia, articular rheu- 
matism, many wound. infections, septic osteomyelitis, and ulcerative endo- 
carditis. 

The conveyal of an infection from man to man directly or indirectly 
and its spread through houses, villages, cities, and countries is termed a 
contagium ; and it is thereby understood that the production of the in- 
fective agent takes place only in the human body, or in some lower ani- 
mal, its development and increase outside of these being impossible. To 
such contagious diseases belong smallpox, measles, scarlatina, diphtheria, 
typhus fever, recurrent fever, anthrax, hydrophobia, gonorrhea, whoop- 
ing-cough, influenza, many catarrhs of mucous membranes, tuberculosis, 
syphilis, glanders, and leprosy. 

If an infective agent develops in a certain locality only when an in- 
fected person visits the region and thereby gives rise to an epidemic, the 
term miasmatic contagious disease is used, with the assumption that 
{he infective agent had spread from the body of the first patient into the 
outer world, and had somewhere multiplied, and either alone or through 
the aid of special local influences had been able to produce in the inhab- 
itants of the region an epidemic spread of the disease. To such mias- 
matic-contagious diseases belong cholera, typhoid fever, dysentery, yel- 
low fever, and bubonic plague. 

The nature of miasmatic and contagious diseases was unknown to the 
older practitioners. The occurrence of an infectious disease as a plague 
or epidemic was explained by causes sought in peculiar cosmic or telluric 


PARASITES. 33 


conditions, and these were designated constitutio epidemica or constitutio 
pestilens. Only in the last decade has our knowledge of the causes and 
nature of the infectious diseases made true advances, and it has been 
demonstrated that the infectious diseases are parasitic diseases, the origin 
of which is to be attributed to the increase of small living organisms within the 
human body. It is true that the parasitic cause has been positively demon- 
strated in only a part of the infectious diseases, but it is highly proba- 
ble that all are caused by parasites. To the hypothesis that the causes 
of infectious diseases were to be sought in living organisms, capable of 
reproduction, in a contagium animatum, the earlier investigators were led 
chiefly by the fact that the infective agent causing a certain disease 
could, when once present, constantly renew itself and indefinitely in- 
crease, so that from a single case of the disease an endless number might 
be infected ; and further that extremely small and imponderable quanti- 
ties of the infective material were sufficient for the infection of an indi- 
vidual, so that the intense effects of an infection upon the human organ- 
ism could be explained only by the assumption of an increase of the 
infective agent within the body. 

The attempt has also been made many times to explain the phe- 
nomena of infection through the action of injurious gases or soluble fer- 
ments. Such hypotheses are wholly unsatisfactory, inasmuch as they 
leave unexplained the chief phenomena of the spread and course of epi- 
demics, or the explanations adduced are open to well-founded objections. 

The parasites which cause infectious diseases belong to the lowest 
forms of plant and animal life. Among the plants the schizomycetes 
or bacteria, among the animals the minute organisms belonging to the 
protozoa, play the most important role in the production of disease. Of 
the more highly organized plants the saccharomycetes and hypho- 
mycetes may act as infective agents, but their pathological significance 
is much less than that of the bacteria. Among the animals, numerous 
worms (Nematodes, Trematodes, Cestodes) and arthropoda (Arachnida 
and Insects) occur as human parasites, but their action is much more 
limited, and the pathological conditions produced by them are not ordi- 
narily classed as infectious diseases in the narrow sense of the term. 

For the production of a true infection, it is necessary that a given 
parasite must increase in the human body and produce a number of gen- 
erations, which spread more or less widely through the tissues. If the 
itch-mite, which produces many generations in the epidermis, be ex- 
cluded, the parasitic Schizomycetes, Saccharomycetes, and Protozoa 
alone are to be regarded as fulfilling the above condition; the higher 
animal parasites passing only a part of their life within the human body 
—that is, within the same host. Those parasites which multiply within 
the invaded organs, through the production of eggs or of matured em- 
bryos or of larvz, do not become sexually reproductive in the same 
host. 

Parasitic infection, that is, the entrance of parasites into the human 
body, and their increase, can occur in almost every part of the body. The 
most common avenues of infection are the mucous membranes which admit 
of access from without, especially the respiratory and intestinal tracts, 
which in particular favor the entrance of parasites. In many cases the 
parasites are contained in the food and drink, especially in water. Since 
the pathogenic organisms are for the greater part very small, and when 
suspended in the atmosphere may be carried about everywhere by means 
of the air-currents, they are often present in the respired air and so 

3 


34 THE EXTRINSIC CAUSES OF DISEASE. 


reach the air-passages or alveoli of the lungs, where they may become at- 
tached to the walls and frequently obtain entrance into the tissues. 

Further, wounds form a favorable place for the entrance of small 
parasites, and may be the starting-point of an infection through the en- 
trance of the latter, either from the air or through contact with con- 
taminated fluids or objects. Finally, parasites may establish them- 
selves in the uninjured skin, and, increasing, give rise to an infectious 
disease. 


The view that certain discases, particularly the plague, were of parasitic origin, is 
very old, and found expression in the works of Kircher (1602-1680), Lancist (1654-1720), 
Linne (1707-1778), and others. It has been left to very recent times, however, to place 
the theory of the parasitic origin of disease upon a secure foundation. Though several 
decades ago Jlenle, Liebermeister, and others asserted that the peculiarities of infectious 
diseases could be explained only by the assumption of a contagium animatum, the es- 
tablishment of this doctrine is due to the results of the investigations of the last thirty 

rears. 

’ The influence which climate exerts upon man is, if the influence of temperature 
be not considered, essentially dependent upon the conditions of the soil of a given re- 
ion with respect to the development of micro-organisms which are capable of causin 
isease. A rough windy climate may therefore be healthy, while one that is mild an 
subject to slight variations of temperature may be unhealthy. In the case of inhabited 
regions, the question naturally arises as to the prevalence of epidemics among the in- 
habitants. Temporary changes in the injurious influences of a certain climate are de- 
pendent partly upon the fact that the pathogenic organisms do not at all times increase 
in the same ratio, and partly that the micro-organisms present in the earth do not al- 
ways get into the drinking-water or into the atmosphere, or at least obtain entrance 

into the human organism only at times. 


According to Pettenkofer, the spread of miasmatic-contagious diseases, as, for in- 
stance, cholera, cannot be explained by the fact that bacteria from the dejecta ofa 
cholera patient are able to survive outside of the body fora given length of time, and 
under favorable circumstances to increase, obtain entrance into the mouth by means of 
drinking-water, food, or unclean hands, reach the intestines, and again produce an in- 
fection. On the other hand, he believes that the disease-germs on reaching the soil are 
able to form their characteristic poisons only when certain temporary local conditions 
are present in the affected region, so that the disease germs combining with an unkown 
something. that is, under the influence of the soil, must acquire a higher virulence in 
order to form the characteristic poison of the disease. The latest researches concerning 
the etiology and spread of typhoid fever, cholera, and the plague do not support this 
theory ; on the contrary, they show that the bacteria of cholera, typhoid fever, and the 

lague are sufficient in and of themselves in given cases to produce an infection. It 
ollows from what has already been said that cholera germs, when introduced into the 
intestinal canal of man or of certain experimental animals, are able to cause cholera. 


Literature. 
(Infections. ) 


Aoyama: Mitteil. über die Pestepidemie in Hongkong, Tokio, 1895 (ref. Cent. f. Bakt.. 
xix.). 

Bouchard: Les microbes pathogénes, Paris, 1892. 

Charrin: L’infection. Path. gen. publ. par Bouchard, ii., Paris, 1896. 

Däubler: Grundzüge der Troperhygiene, Berlin, 1900. 

Duclaux: Le microbe et la maladie, Paris, 1886. 

Feer: Scharlach, Masern, Rötheln. Ergebn. d. allg. Path., iv., 1899. 

Flügge: Die Mikroorganismen, Leipzig, 1896; Verbr. d. Cholera. Zeit. f. Hyg., xiv.. 
18938 (Lit.). 

Galtier: Traité des maladies contagieuses des animaux domestiques, 2d éd., t. i.. 
Paris, 1891. 

Grancher, M.: Pasteur et la médecine contemporaine. Arch. de méd. exp., vi., 1894. 

Haeser: Geschichte der Medicin u. der epidemischen Krankheiten, i1.-iii., Jena, 1875- 
1882. 


BACTERIA. 35 


Hanking: La propagation de la peste. Ann. de l’Inst. Past., xii., 1898. 

Hecker: Die grossen Volkskrankheiten des Mittelalters, her. von A. Hirsch, Berlin, 
1865. 

Henle, J.: Pathol. Untersuchungen, Berlin, 1840; Rationelle Pathologie, Braun- 
schweig, 1853. 

Hirsch, A.: Handb. der historisch-geogr. Pathologie, i. and ii., Stuttgart, 1881-1886. 

Hueppe: Die Choleraepidemie in Hamburg, 1892, Berlin, 1893; Einführung in d. 
Bakteriologie, Wiesbaden, 1896. 

Koch: Conferenz zur Erörterung der Cholerafrage. Deut. med. Woch., 1884, 1885, 
1886; Die Cholera in Deutschland während des Winters 1892-1893. Zeit. f. Hyg., 
xv., 1893. 

Koch und Gaffky: Ber. üb. d. Thatigkeit der zur Erforschung der Cholera im Jahre 
1883 nach Egypten u. Indien entsandten Kommission. Arb. a. d. K. Gesundheit- 
sanite, iii., Berlin, 1887. 

Laveran: Les maladies épidémiques. Path. gen., ii., Paris, 1896. 

Liebermeister: Ueber die Ursachen der Volkserkrankung., Basel, 1865. 

Löffler: Ueber die geschichtliche Entwickelung der Lehre von den Bakterien, Leipzig, 
1887. 

Lubarsch: Zur Lehre v. d. Geschwülsten u. Infektionskrankheiten, Wiesbaden, 1899. 

Mannaberg: Die Malariakrankheiten, Wien, 1899. 

Marchiafava and Bignami: Malaria. Twent. Cent. Pr., xix., New York, 1900. 

Martius: Pathogenese innerer Krankheiten, i., Leipzig, 1899. 

v. Pettenkofer: Aufsätze über Cholera u. Typhus in d. Zeitschr. f. Biol. seit 1864; 
Arch. f. Hyg. seit 1883; Ueber Cholera. finch. med. Woch., 1892. 

Rumpf: Die Cholera indica und nostras, Jena, 1898. 

Scheube: Die Krankheiten der warmen Länder, Jena, 1900. 

Schneidemühl: Vergleichende Pathologie d. Menschen u. d. Thiere, Leipzig, 1895- 


1899. 

Virchow: Ges. Abhandl. a. d. Gebiete d. off. Med. u. d. Seuchenlehre, i. and ii., Berlin, 
1879. 

Weichselbaum: Epidemiologie, Jena, 1899. 
See also § 12. 


§11. The disease-producing bacteria are extremely small, uni- 
cellular organisms, which appear in the form of little spheres (cocci), 
and fine, straight, or curved rods (bacilli and spirilla), frequently unit- 
ing in peculiar combinations. Some multiply in the external world, and 
only occasionally enter the human body; others, on the contrary, are so 
constituted that they cannot reproduce in the outer world and are able to 
multiply only when in the human or animal body. The pathogenic bac- 
teria are therefore divided into two classes, ectogenic and endogenic; the 
first is identified with the miasmatic diseases, the latter with the conta- 
gious. There is, however, no sharp division-line between these two 
classes, inasmuch as certain bacteria which ordinarily multiply only in 
the human or animal organism, may, under certain conditions, develop 
in the outside world; so that in a certain sense a contagium becomes a 
miasm. 

On the other hand, it is not necessary for the spreading of a disease 
caused by ectogenic organisms that the Schizomycetes develop outside of 
the human body; more frequently a direct infection from individual to 
individual takes place. For example, the bacilli of anthrax can mul- 
tiply as well in the outer world as in the animal body, and the disease 
may be spread by direct transmission from man to man or from an ani- 
mal to man, as well as by the entrance of the bacilli into the human or 
animal body through some infected culture-medium. The cocci which 
produce suppuration, or those causing inflammation of the lungs, can 
likewise infect a healthy individual directly from the outer world where 
they have multiplied, or from another diseased individual. 

It follows therefore that no sharp line can be drawn between miasms 
and contagions or between ectogenic and endogenic bacteria. The distinction 


36 THE EXTRINSIC CAUSES OF DISEASE. 


is of value only in that in many infectious diseases one of the two forms 
of spreading predominates, and there are also infections in which, so far 
as our knowledge goes, there is but one mode of dissemination. For ex- 
ample, small-pox and measles, the infective agents of which have not yet 
been discovered, spread only by direct and indirect contagion; and it is 
also assumed that the poison of syphilis is not able to increase outside 
of the human body. 

Pathogenic bacteria may be found outside of the human body, in 
solids, liquids, and in the atmosphere. Those forms which are able to 
multiply outside of the body (bacteria of cholera, typhoid, anthrax, sup- 
purations, actinomycosis) are found especially in water fouled by organic 
substances, or in damp earth rich in organic material or in dead animal 
or vegetable tissue containing moisture. They are besides often present 
in dry earth and dried tissue, and can pass from these, as well as from 
fluids, into the air, their distribution being favored by dust, strong cur- 
rents of air, and excessive sprinkling. In the drying of substances con- 
taining bacteria, a portion of the bacteria are killed, since they are not 
able to survive complete desiccation. Many of the pathogenic bacteria 
produce resistant forms (spores) which are able to bear long-continued and 
complete drying, and therefore to retain their vitality in the air. If these 
come into contact with firm bodies or fluids and remain attached to them, 
they may survive for a long period, and under favorable conditions—that 
is, if they find proper nourishment and sufficient moisture, and if the tem- 
perature reaches the height necessary for their development—they may 
again multiply. 

Bacteria, which are not able to multiply outside of the human or 
animal body, or at least do so only under very special and rare condi- 
tions, are able to preserve themselves outside of the body for a length of 
time, only when they produce forms which survive desiccation, or are 
not killed by the chemical influences of their environment in the fluids, 
damp earth, and tissues in which they are found. For a limited time 
they may cling to the most varied substances and retain their vitality, so 
that for a certain length of tine contaminated objects are capable of 
causing infection. Bacteria which are able to survive drying may be 
found in the dust of the streets, of the floors and walls of houses, as well 
as in the air itself, particularly so when the bacteria are thrown off in 
great abundance from the diseased individual in whom they have multi- 
plied. This is especially true of the bacillus of tuberculosis, in that in 
pulmonary tuberculosis the sputum, in intestinal tuberculosis the feces, 
and in case of tuberculosis of the urogenital tract the urine, may contain 
great numbers of the bacilli. 


Literature. 
(Distribution of Bacteria.) 


Bolton: Verhalten verschied. Bakterien im Trinkwasser. Zeit. f. Hyg., i., 1886. 

Braem: Degeneration pathogener Bakterien im Wasser. Beitr. v. Ziegler, ii., 1890. 

Chantemesse: Le sol, l'eau et l’air. Traite de Path. gén., ii., Paris, 1896. 

Cornet: Die Verbreitung der Tuberkelbacillen ausserhalb d. Körpers. Zeit. f. Hyg., 
v., 1889. 

Cramer: Die Wasserversorgung von Zürich, Zürich, 1885. 

Emmerich: Verunreinigung der Zwischendecken. Fortschr. d. Med., i., 1883 

Esmarch: Der Keimgehalt der Wände. Zeit. f. Hyg., ii., 1887. 

Flügge: Die Mikroorganismen, 1896: Hygiene, Leipzig. 1894. 

Fodor. Ilygien. Unters. über Luft, Boden u. Wasser, Braunschweig, 1882. 


t 


BACTERIAL INFECTION. 37 


Frankel: Bakteriengehalt des Eises. Zeit. f. Hyg., i., 1886; Bakt. in verschiedenen 
Bodenschichten, ibid., ii.. 1887: Keimgehalt des Grundwassers, ibid., vi., 1889. 

Germano: Uebertraguny d. Infection durch d. Luft. Zeit. f. Hyg.. 26 Bd., 1897. 

Giacosa: Les corpusc. organisés de lair des hautes montagnes. Arch. ital. de biol., iii., 
1886. 

Grancher ct Deschamps: Rech. s. le bacille typhique dans le sol. Arch. de méd. exp., 
i., 1889. 

Haegler: Die chirurg. Bedeutung des Staubes. Beitr. v. Bruns, ix., 1892. 

Hesse: Bestimmung der i. d. Luft enthalt. Mikroorganismen. Mitth. a. d. K. Ges.- 
Amte. ii., Berlin, 1884; Nahrungsmittel als Nährböden f. Typhus u. Cholera. Zeit. 
f. Hyg., v., 1889. 

Kammerer u. Giacomi: In der Luft enthalt. Keime. Arch. f. exp. Path., xxi., 1886. 

Koch: Nachweis der Bakterien in Luft, Boden u. Wasser. Fortschr. d. Med., i., 1883. 

Lustig: Diagnostik der Bakterien des Wassers, Jena, 1898. 

Petri: Ueber Nachweis u. Bestimmung pflanzl. Mikroorganismen i. d. Luft. Cent. f. 
Bakt., ii., 1887. 

Sawtschenko: Beziehung d. Fliegen z. Verbreitung d. Cholera. Cent. f. Bakt., xii., 
1393. 

Soyka: Der Boden. Handb. d. Hyg. von Pettenkofer, i., 1889. 

Straus et Dubrarry: Durée de la vie des microbes pathogenes dans l'eau. Arch. de 
med. exp., i., 1889. 

Winogradsky: Les organismes de la nitrification. Ann. de l’Inst. Pasteur, iv. and 
v.. 1890 and 1891. 

Wolffhügel u. Riedel: Vermehrung d. Bakt. im Wasser. Arb. a. d. K. Gesundheits- 
amte, 1886. 


$ 12. The avenues of entrance for bacteria are, in general, the 
mucous membranes of the intestinal canal, respiratory tract, and the 
middle ear, the conjunctiva, the alveoli of the lungs, and open wounds. 
Through recent wounds, both pathogenic and non-pathogenic bacteria 
are rapidly taken up into the lymph and blood; while through wounds 
showing healthy, granulating, uninjured surfaces, the entrance of many 
bacteria into the tissues is hindered. Pathogenic bacteria not infre- 
quently enter through the uninjured skin, either by way of the hair-fol- 
licles or through the sebaceous or sweat glands. Under especial condi- 
tions (coitus, surgical operations, dribbling of urine) the infection may 
take its start from the mucous membranes of the urogenital tract. Some 
infections may be transmitted by insects, which have taken up bacteria 
with the blood or secretions of «a diseased individual or animal, or, hav- 
ing become contaminated externally by such, may infect an open wound 
by scraping the bacteria off their legs upon the exposed surface, or by 
the direct introduction of gerins into the skin or aecessible mucous mem- 
branes during the act of stinging or sucking. If meat containing bac- 
teria be eaten, and if the animal while alive was affected by an infee- 
tious disease which also occurs in man, this particular disease may be 
transmitted to man, in case the bacteria had not been previously de- 
stroved. 

Bacteria arrive at the point of entrance, sometimes in association 
with chemically active substances, sometimes without such; the first is 
more likely to occur in the intestinal tract, the second in the respiratory 
passages and in the lungs; yet chemical substances may also find their 
way into the lungs with bacteria, and bacteria may enter the intestinal 
canal without the association of chemically active material. 

The harmful chemical substances which accompany the bacteria 
may be either an accidental admixture of the food, or of the water used 
for drinking or washing or for the cleansing of wounds, or of the re- 
spired air; but they are more frequently the products of the bacteria 
themselves. All bacteria, even the non-pathogenic, produce within the 
medium in which they grow certain changes designated as fermentation 


38 THE EXTRINSIC CAUSES OF DISEASE. 


or decomposition processes, which stand in the closest relationship to 
their life-activity and reproduction. Among these products of chemical 
inetamorphosis are many which are injurious to the organism of man and 
the higher animals, in that they are able to cause, in a manner similar to 
that of the poisons already mentioned, partly local tissue-degenerations 
and inflammations, partly blood-changes, and partly symptoms of gen- 
eral poisoning, which may be manifested in functional disturbances of 
the nerves, heart, or respiratory apparatus. The most important of 
these substances are the decomposition-products of albuminoid bodies, 
the cadaveric alkaloids or ptomains, basic bodies, of which many are 
poisonous for man and are consequently called toxins. Further, actire 
albuminoid bodies, the toxalbumins, occur, which are probably formed 
and cast off by the bacteria themselves (Buchner). For example, in 
decomposing meat the basic products, neuridin, cadaverin, putrescin, 
neurin, and methylguanidin, are formed; of these the last three are very 
poisonous toxins. The bacillus of typhoid fever forms a toxin (typho- 
toxin), which produces paralysis and stimulates the intestinal and 
salivary secretions; cholera bacteria form, in addition to penta- and 
trimethylendiamin and methylguanidin, also specific toxins, which irri- 
tate the intestine, destroy the coagulability of the blood, and cause mus- 
cular spasms. The tetanus bacillus produces tetanotoxin, a toxalbumin 
which causes violent musele spasms; according to Roux, Yersin, 
Brieger, and C. Frankel, the diphtheria bacillus, anthrax bacillus, 
typhoid bacillus, cholera spirillum, and the pus-cocei form toxalbumins. 

When bacteria develop in large numbers in the tissues, and finally 
die, the soluble substance of the bacterial cell, mycoprotein, may cause 
irritation of the surrounding parts. 

If toxic bacterial products are introduced in considerable quantity 
into the intestinal canal or into wounds at the same time with bacteria, 
symptoms of poisoning may be produced without a coincident. infection, 
that is, without an increase of bacteria in the tissues. The same thing 
may also happen when poison-producing bacteria develop in the contents 
of the intestine or in wound-secretions or in necrotic lung-tissue, and so 
multiply as saprophytes. Such cases cannot strictly be regarded as infec- 
tions, the disease is much more to be regarded as an intoxication; but in 
such cases a sharp line between infection and intoxication cannot be 
drawn, since bacteria originally growing as saprophytes not infrequently 
enter the tissues and multiply there. 

Intestinal intoxications caused by bacterial toxins and toxalbumins oc- 
eur especially when animal tissues or fluids are eaten in a state of de- 
composition due to the presence of bacteria; and to these intoxications 
belong the greater part of the affections termed meat-, sausage-, fish-, and 
cheese-poisoning. In these cases the particular poison is either taken as 
such with the food into the intestinal canal, or else is formed there. 
Likewise, decomposition and fermentation of the vegetable constituents 
of diet—as, for example, fermenting fruit-juices, cabbage, peas, beans, 
maize, rice, ete. —may have an injurious effect upon the intestine or even 
upon the entire organism, especially when eaten in large quantities or 
for a long period of time. The chronic disease known as pellagra or 
* maidismus,” occurring especially in Italy, Spain, Southwest France, and 
Roumania, is an example of such a condition. It is due to the eating of 
spoiled maize (Lombroso, Tuezek); and is characterized by gastro-intes- 
tinal disturbances, changes in the skin, disturbances of spinal and 
cerebral functions, and general marasmus, 





\ 


LACTERIAL INFECTION. 39 


If the bacteria which have entered the body through one of the 
above-mentioned avenues of infection are in a strict sense pathogenic, so 
that they give rise to an infection, they may increase first at the point 
of entrance, in the intestinal mucous membrane, in a wound, in the 
skin, ete. The local effects of their growth are dependent primarily 
upon the individual characteristics of the bacteria, as well as upon the 
peculiarities of the affected tissue. In general, the local action is char- 
acterized by tissue-degenerations, necrosis, inflammations, and new-for- 
mation of tissue, so that it is possible in many cases to determine the na- 
ture of the infection, that is, the species of bacteria causing the 
infection, from the character of the local changes. It is, however, 
difficult or impossible to determine in every case the exact mode of ac- 
tion of the multiplying bacteria; in general, it may be said that the 
processes of chemical metamorphosis excited by the multiplication of the 
bacteria produce certain changes in the tissue-cells, in that different sub- 
stances of active chemical nature either kill the cells, or at least induce 
degenerative changes in them, or in part excite increased cell-activity. 
In the further development of the process the substances derived from 
dead and dissolving bacteria may also produce effects upon the surround- 
ing tissue. In a certain sense, therefore, there occurs through the local 
growth of bacteria a local intoxication, which is of far greater significance 
than the withdrawal of nutritive material through the consumption by the 
bacteria of food substances. The latter is, however, not wholly without 
significance, inasmuch as the chemical changes produced by the bac- 
teria in the tissue juices often render these unfit for the nourishment of 
the tissue-cells, so that the cells suffer even when no poisonous substances 
are produced. 

the participation of the entire organism in a local bacterial infec- 
tion may be very slight or wholly absent, so that the disease appears as 
a purely local affection (tubercuiosis). In other cases the toxins and 
toxalbumins formed in the local focus of infection are absorbed into the 
body fluids (i.e., into the blood), and a general intoxication (toxinemia) 
is produced; that is, poisonous effects are exerted upon the nervous sys- 
tem, sometimes upon the blood itself and upon the heart; and the 
poisons thus taken into the body may produce demonstrable changes in 
the internal organs, particularly in the extretory glands, at times also in 
the skin. In many diseases (tetanus, typhoid fever, streptococcus and 
staphylococcus infection, diphtheria) the symptoms of poisoning are es- 
pecially prominent. 

If healing does not take place in the primary seat of infection, the 
neischboring tissues may be involved by an invasion of bacteria by con- 
tinuity. Very often the bacteria gain entrance to the lymph-vessels 
or blood-channels (bacteriemia), and in this way are transported and 
spread over the entire body. The result of this metastasis of bacteria is 
the production of a lymphogenous or hematogenous infection ; that 
is, secondary foci of disease identical in character with the primary seat of 
infection are formed at a distance from the primary focus. In certain 
diseases (tuberculosis, suppurations, plague) the number of metastases 
is usually very great, so that many parts of the body (lymph-glands, 
liver, lung, brain, muscles, bones, kidneys, etc.) may contain diseased 
areas. On the other hand, in other infections metastasis of bacteria 
from the original focus to other organs does not occur (tetanus, diph- 
theria), or the transported bacteria cause only changes of a milder type 
(typhoid fever). | 


~ 


40 THE EXTRINSIC CAUSES OF DISEASE. 


During the transportation of bacteria through the blood-vessels, there 
is usually no increase of the bacteria in the circulating blood, the blood 
serving only as a vehicle to carry the bacteria to other parts of the body, 
multiplication occurring first at those points where the bacteria have 
come to rest. Nevertheless, in certain infections (anthrax) the bacteria 
increase enormously in the circulating blood, and in this way may cause 
damage to the blood itself. Through the obstruction of small blood-ves- 
sels by the multiplying bacteria, there may be added to the intoxication 
also local disturbances of circulation. 

The metastasis of bacteria or toxic substances, or both, from a local- 
ized seat of infection, and the production thereby of secondary foci and 
syınptoms of intoxication, give rise to the condition which is generally 
termed sepsis. Aceording to the predominant symptoms there may be 
distingushed a septemia or septicemia, a pyemia and a lymphangoitis. 
Through the combination of both the latter with septsaemia, septicopyemia 
is produced. Originally the designation septicemia was applied to 
those cases in which a localized infection was associated with a putrid 
intoxication caused by bacterial poison or a toxrinemia without the spread 
of bacteria through the body. At the present time, according to the 
precedent set by Koch, Gaffky, and others, septicemia is used to desig- 
nate the condition characterized by the entrance of both bacteria and 
their poisons into the blood, a coincident torinemia and bacteriemia ; 
indeed, by many authors the pure putrid intoxication or toxinemia is 
separated from septicemia. 

The term pyzmia, originally signifying a metastasis of pus through 
the blood, is at present employed to designate the condition in which 
the metastasis of bacteria gives rise to the formation of metastatic ab- 
8CE88ES. 


In septicopyemia the symptoms of toxinemia and bacterisemia are 
combined with the formation of metastatic foci. Lymphangoitis is an 
inflammation of the lymph-vessels and their surroundings caused by trans- 
ported bacteria. 

Sepsis in its different forms is most frequently caused by the true 
pyogenic organisms, staphylococcus pyogenes aureus, and the streptococcus 
pyogenes, but similar conditions also occur in infection with the pneu- 
mococeus, gonococeus, typhoid bacillus, colon bacillus, plague bacillus, ete. 

If bacteria are deposited secondarily in the body-passages which are 
lined with mucous membrane, as in.the respiratory or urogenital tract, 
they may multiply within these tracts and produce their characteristic 
pathological changes. Likewise, they may multiply also within the 
large body-cavities, in the peritoneal, pleural, and subarachnoid 
spaces. In the case of an infection occurring in a pregnant woman, 
many varieties of bacteria (anthrax, symptomatic anthrax, glanders, 
recurrent fever, typhoid, pneumonia, the pyogenic bacteria) may be 
transmitted to the foetus. 

The deseription given above of the course of an infection may be 
taken as a general type, and many infections run such a course (typhoid, 
pyiemia, erysipelas, plague, diphtheria, tetanus, tuberculosis, syphilis, 
leprosy, glanders, actinomycosis, ete.); but there are also many devia- 
tions from this scheme. In the first place, it not infrequently happens 
that in an infection which in general runs a typical course, the primary 
seat of infection is not demonstrable, either because no changes occurred 
at the point of entrance, or the changes produced have since disap- 


BACTERIAL INFECTION. 41 


peared. Such forms of infection are known as cryptogenic; they may. 
be lymphogenous or hematogenous. It is typical of many infections 
that the primary localization of the cause of the disease is not recogniz- 
able, so that general symptoms occur before local changes are demonstrable, 
and the tissue-changes occurring later have more the character of a sec- 
ondary localization of the poison of the disease. This occurs especially in a 
number of infectious diseases, the causes of which are unknown to us; 
for example, in scarlet fever, smallpox, and measles; yet in many in- 
fections whose causes are known we are not always able to discover at 
what point the first multiplication of the bacteria occurs. Thus we 
know that in relapsing fever the spirilla are found in the blood in large 
numbers at the time of the fever, but the place of their multiplication is 
unknown to us. 

Not infrequently a secondary infection may be joined to one already 
present. In many cases the association is entirely accidental, in other 
cases the anatomical changes produced by the first infection cause a 
local predisposition to the new invasion. To the first group would be- 
long, for instance, a croupous pneumonia occurring in an individual 
suffering with tuberculosis; while the occurrence of an infection with 
cocei causing suppuration and septic intoxication, as in the case of 
wound-infections, in the course of typhoid, diphtheria, scarlet fever, 
dysentery, caseous ulcerating tuberculosis, etc., may be regarded as due 
to the production of local tissue-changes favoring the entrance of bac- 
teria. According to the characteristics displayed by the recent epi- 
demics of influenza in Europe, influenza is a disease which predisposes 
in a marked degree to secondary infection. In certain infections, as, 
for example, in many forms of purulent processes, the tissues may con- 
tain, even at an early stage, two or more varieties of bacteria—an asso- 
ciation of bacteria or double infection. 


It has been known for many years that during decomposition poisonous substances 
are formed. As early as 1852 Beck observed that ammonia hydrothionate, which oc- 
curs in pus and putrid ichor, possessed septic properties when injected into animals. 
Panum, in 1863, obtained from decomposing material a putrid poison, that is, a body 
not destroyed by boiling and evaporation, which possessed an action similar to that 
of snake-poison and the vegetable alkaloids and caused in dogs salivation, dilatation of 
the pupils, diarrh@a, fever, and severe prostration. Fon Bergmann and Schiniedeberg 
obtained from decomposing ycast a crystalline body, sepein, which in animals produced 
the symptoms of a putrid Intoxication. Senator, Hiller, and Mtkulicz extracted from 
decaying tissue-masses by means of glycerin a substance which likewise possessed a 
septic action. Billroth called this poisonous substance putrefactire zymoid. Selmi en- 
deavored to characterize all these substances more minutely, and obtained from differ- 
ent constituents of cadavers extracts, partly soluble in ether, partly in water, which he 
recognized as fixed bases of alkaloid-like character, and which he designated as 
cadaveric alkaloids or ptomains. Guantier, Etard, Zuelzer, Sonnenschein, Bechamp, 
Schmiedeberg, Harnach, v. Nencki, Otto, Angerer, and others also found in decomposing 
tissues similar cadaveric alkaloids, which in experiments upon animals were partly in- 
ert, and partly toxic, producing in the latter case symptoms of poisoning similar to 
curare, morphine, and atropine. To von Nencki (1876) is due the honor of being the 
first to obtain a cadaveric alkaloid in its pure form and to establish its formula; this 
was accomplished in the case of collidin, obtained from decomposing glue and albumin, 
its platinum salt crystallizing in flat needles. Following ¢c. Neneki, Etard, Gautier, 
and Baumann, and especially Drieyer, have studied ptomains, the last named having 
obtained a large number of them in a pure state and determined their physiological 
action. For instance, Brieger obtained from fibrin peptone a poison (peptotoxin) 
which in animals causes symptoms of paralysis and ultimately death. From decom- 
posing horse-flesh he extracted three substances crystallizing in needles, aamely, 
neuridin, neurin, and cholin, the second of which is markedly poisonous, and, like 
muscarine, causes salivation, disturbances of circulation and respiration, contraction of 
the pupils, and clonic convulsions. From fish-flesh he obtained, besides neuridin, three 


42 THE EXTRINSIC CAUSES OF DISEASE. 


other poisonous bodies: ethylendiamin, a substance similar in its action to muscarine, 
and a substance called gadinin. From decomposing glue and cheese he obtained the 
poison neurin, and from decomposed yeast dimethy lamin. 

The majority of ptomains are not found in fresh tissues, and it is therefore very 
probable that they are derived from the splitting of chemical combinations present in 
the tissues. Thus it is probable that cholin is formed from the splitting of lecithin. 
and by the further decomposition of cholin the poison neurin is formed. Cholin and 
neuridin are, according to Brieger, demonstrable even in the fresh human brain. 

After the poisonous nature of part of the ptomains had been made known through 
the researches mentioned above, there was developed the Aypothesis that the toxic symp- 
toms observed in infectious diseases could be entirely, or in a great measure, ascribed 
to the action of the substances called toxins. Through the investigations of recent 
years (Rouz, Yersin, Buchner, Brieger, C. Frankel) it has been shown that toxalbumins 
play a more important role than the toxins, and can therefore be regarded as the pecul- 
tar specific bacterial-poisons, Our knowledge of active albuminoid bodies had been 
previously confined to the enzymes (pepsin, trypsin, ptyalin, diastase), which produce 
a hydrolytic splitting. The active poisonous albuminoids, the toxalbumins, have been 
made known for the first time through recent investigations of the infectious diseases. 
Brieger and Fränkel hold the view that the toxalbumins which produce symptoms of 
intoxication are formed by the action of bacteria from the albumins of the body juices. 
Buchner, on the contrary, believes that they are produced by the bacterial cell itself. 
and supports this view by the fact that the diphtlieria bacillus in urine containing no 
albumin (Guinochet), and the tetanus bacillus in a solution of asparagin with mineral 
salts, are able to produce their characteristic toxalbumins. Asin the case of the en- 
zymes, the toxalbumins in solutions lose their activity at temperatures of 55° to 70° C. 
In the dry state they are able to withstand much higher temperatures. After injection 
into the tissues of an animal, toxalbumins do not act immediately, but after some hours 
or even after several days. In this respect they differ from ordinary poisons. 

According to the experimental investigations of Parclowsky, staphylococci injected 
subcutaneously into guinea-pigs puss very quickly into the blood, and are found within 
a quarter of an hour in the liver, spleen, and kidneys, They remain in the blood for 
from six to twelve hours, and then disappear. In the organs where they multiply they 
may remain as long as fourteen days. Four to ten days befere death they again appear 
in the blood. Streptococci produce in rabbits a general streptomycosis resulting fa- 
tally in from twenty to twenty-four hours. 

Should the composition of the blood be altered and the blood and tissue-juices be 
contaminated by the continuous introduction of harmful substances, a condition may 
be produced which may be designated as a dyscrasia produced by bacteria. It is to be 
noted, however, that the term dyscrasia, which was formerly much used to designate 
changes in the constitution of the blood and lymph, finds at the present time but little 
usage. 


Literature. 


(Origin of Diseases through Bacteria and Bacterial Products. ) 


Baumgarten: Der gegenwiirtige Stand der Bakteriologie. Berlin. klin. Woch., 1900. 

Behring: Die Geschichte der Diphtherie m. Berücksichtig. d. Immunitätslehre, Leip- 
zig, 1893. 

v. Bergmann: Das putride Gift und die putride Intoxication, Dorpat, 1868. 

Blumberg: Putride Intoxication. Virch. Arch., 100 Bd., 1885. 

Bouchard: Actions des produits séerétes par les microbes pathogenes, Paris, 1890: 
Theorie de l’intection. X. intern. med. Congr., i., Berlin, 1891; Les microbes 
pathogenes, Paris, 1892. 

Brieger: Actiologie des Wundstarrkrampfs. Biol. Cbl., vii., 1887; Tetanin und 
Mytilotoxin. Virch. Arch., 112 Bd. ; Zusammensetzung des Mytilotoxins nebst einer 
Uebersicht der bisher bekannten Ptomaine u. Toxine, ib., 115 Bd.; Ueber Ptomaine, 
i.-iii., Berlin, 1885-1886; Bakterien und Krankheitsgifte. Biol. Cbl., x., 1890; 
Bakteriengifte. Zeit. f. Hyg., xix., 1895; Diphtherie u. Tetanus. Deut. med. 
Woch., 1890; Fleischvergiftung, ib., 1897. 

Brunner: Der Begriff Prämie u. Septhämie, Frauenfeld, 1899. 

Buchner: Durchtritt von Infectionserregern durch aie intacte Lungenoberflic he. 
Arch. f. Hyg., 1888: Münch. med. Woch., 1888; Ueber Bakteriengifte, ibid. , 1893. 

Charrin: L’infection. Traite de Path. gen. publ. par Bouchard, ii., Paris, 1896. 

Debierre: Les maladies infecticuses, mierobes, ptomaines, leucomaines, Paris, 1888. 

Duclaux: Ferments et maladies. Paris, 1882; Le microbe et les maladies, Paris, 1886: 
Phenomenes généraux de la vie des microbes. Ann. de l’Inst. Pasteur, i., 1887; 
Les mati¢res albuminoides, ibid., v.. 1891; Trait¢ de Mikrobiologie, Paris, 1899. 


PATHOGENIC MOULDS AND FUNGI. 43 


van Ermengem: Les intoxications alimentaires, Bruxelles, 1895. 

Flexner: Tue Pathology of Toxalbumins, Baltimore, 1897. 

Flügge: Die Mikroorganismen, Leipzig, 1896. 

Friedrich: Asept. Versorgung frischer Wunden. Arch. f. klin. Chir., 57 Bd., 1898. 

Gaffky u „aak: Wurst- u. Fleischvergiftung. Arb. a. d. Kais. Gesundheitsamte, 
vi., 1890. 

Gamaleia: Les poisons bacteriens, Paris, 1892. 

Gautier: Sur les alcalofdes dcrives de la destruction bactérienne ou physiologiques des 
tissus animaux, ptomafnes et leucomaines, Paris, 1886. 

Grancher: M. Pasteur et la médecine contemporaine. Arch. de med. exp., vi., 1892. 

Halban: Resorpt. d. Bakt. bei localer Infection. Jahrb. d. K. Akad., Wien, 1896. 

Hildebrand: Eindringen pathog. Mikroorganismen von d. Lunge aus. Beit. v. Zieg- 
ler, ii., 1887. 

Hueppe: Naturwissensch. Einführung in die Bakteriolugie, Wiesbaden, 1896. 

Husemann: Fleischvergiftung. Encykl. Jabrb., v., 1895; Ptomaine. Eulenb. 
Eucykl., xix., 1898. 

Janowski: Die Ursachen der Eiterung (Lit.). Beitr. v. Ziegler, xv., 1894. 

v. Kahlden: Sepsis. Eulenburg’s Realencyklop , xxii., 1899 (Lit.). 

Koch: Untersuchungen tiber Wundinfectionskrankheiten, Leipzig, 1887. 

Kruse: Die Krankheitserregung, Leipzig. 1896. 

Levy: Sepsinvergiftung. Arch. f. exp. Pathol., 34 Bd., 1894. 

Löffler: Die geschichtliche Entwickelung der Lehre von den Bakterien, Leipzig, 1887. 

Neisser: Duichgängigk. d. Darmwand f. Bakterien. Zeit. f. Hyg., xxii., 1896 (Lit.). 

Neusser: Die Pellagra, Wien, 1887. 

Notzel: Infection granulirender Wunden. Fortsch., xvi., 1898. 

Orloff: Eintrittswege der Mikrobicn in den thier. Organismus. Cent. f. Bakt., iii., 1888. 

Paltauf u. Heider: Der Bacillus maidis u. seine Beziehungen zur Pellagra. Med. 
Jahrb., 1889. 

Panum: Das putride Gift. die Bakterien, die putride Infection und die Septikümie. 
Virch. Arch., 60 Bd., 1874. 

Pawlowsky: Zur Frage der Infection. Zeit. f. Hyg., 33 Bd., 1900. 

Roth: Durchlässigkeit d. Schleimhäute u. d. äuss. Haut für Bakterien. Zeit. f. Hyg., 


iv.. 1888. 
Roux «t Vaillard: Contr. A l’et. du tétanos. Ann. de l’Inst. Pasteur, 1893. 
Roux ct Yersin: Contr. ä l’et. de Ja diphthérie. Ann. de l’Inst. Pasteur, 1888 and 


1890. 
Romer: Infection vom Conjunctivalsack aus. Zeit. f. Hyg.. 32 Bd., 1899. 
Bunge: Die Krankheiten der ersten Lebenstage, Stuttgart, 1893. 
Schimmelbusch u. Ricker: Bakterienresorption frischer Wunden. Fortschr. d. Med., 
1895. 
Tuczek: Klin. u. anat. Studien über Pellagra, Berlin, 1893. 
Vaughan and Novy: The Cellular Toxins, 1902 (Lit.). 
Virchow: Traumatismus u. Infection. Virch. Arch., 162 Bd., 1900. 
Weiss: Actiologie der Otitis media im Säuglingsalter. Beitr. v. Ziegler, xxvii., 1900. 
Woodhead: Bacteria and their Products, London, 1891. 
See also § 6 and § 10. 


3 13. The pathogenic moulds and fungi belong, as do the Schizomy- 
cetes, to the non-chlorophyllaceous thallophytes. They occur in the 
human organism in the form of jointed or unjointed and sometimes 
branching threads or hyphae, and short oval cells, the so-called conidia. 
At times they form fructification organs of peculiar structure. The sin- 
gle cells are much larger than those of the Schizomycetes, so that they 
may be seen with lower magnifying power. Outside of the body the 
moulds (.Mucorini) develop as velvety films of different colors, on the 
surface of many organic substances and fluids, from the carbon-com- 
pounds and salts of which they derive their nourishment. The yeast- 
fungi (Saccharomycetes) are found chiefly in fluids containing sugar, and 
are the cause of the alcoholic fermentation of the same. 

The spores or conidia, which are for the greater part formed in spe- 
cial organs of fructification, but may also be developed by a simple proc- 
ess of constriction of the ends of the hyph, pass into the air from the 
surface of the mould-film aid may be widely scattered by the air cur- 


44 THE EXTRINSIC CAUSES OF DISEASE. 


rents. Likewise, yeast-cells may be carried about in the air, in the case 
of the evaporation of a fermenting fluid and the conversion of its residue 
into dust. 

The Mucorini and the Saccharomycetes have a much less pathological 
significance than the Schizomycetes, in that only a few forms are able to 
multiply within the body, and those which do so multiply develop only 
in a very limited area, so that the disease remains a purely local one. 
Finally, they produce no poisons capable of affecting the organism as 
a whole through the blood or nervous system, but at the most only sub- 
stances which cause changes in the tissues in the immediate neighbor- 
hood of the hyphe. They can therefore produce only local infectious 
diseases. 

The avenues of entrance for these organisms are, in general, the same 
as those for the bacteria. The development of moulds is almost entirely 
restricted to regions accessible from without. Very frequently they de- 
velop only in the necrotic material lying on the surface of the affected 
area of skin or mucous membrane or wound. Thus, for example, the 
external ear, through uncleanliness, presence of cerumen, or of oil which 
has been dropped into the canal, may become the seat of a growth 
of moulds. These may develop also in necrotic areas in the lungs 
or in desquamated epithelium and food-remains in the mouth-eavity. 
Through the ingestion of fermenting fruit-juices, a further development 
of yeasts may take place in the stomach. Not infrequently, under 
other conditions, the stomach may contain yeasts in small numbers. The 
changes produced by the saprophytic development of the moulds and 
yeasts are in general insignificant, that of the latter being practically nd. 
Inflammatory changes may be set up by the moulds, as a result of the 
chemical changes produced in the materials affording them nutriment. 
The local action may be increased through the penetration of the hyphe 
into the living epithelium, in that the hyphie in this way enter into close 
relations with the epithelium and thereby take on the nature of a para- 
sitice growth. Under certain conditions the moulds may even penetrate 
into the connective tissue, but their development. there is of a very lim- 
ited character. Only in very rare cases and under special conditions 
has a metastasis of conidia through the blood or lymph been observed. 
The deposit of conidia in other organs may be followed by a develop- 
ment of hyohe, which may give rise to local degenerations and inflam- 
mation. From these secondary foci no further spread of the mould oc- 
curs. 

The parasitic röle of the moulds is most pronounced in the case of a 
few forms which are found in the skin, developing in the epidermis and 
its adnexa, the hair and nails, and giving rise to peculiar epithelial de- 
generations and inflammations of the papille and corium (favus, herpes 
tonsurans, pityriasis versicolor). Im rare cases yeasts may also develop 
in the deeper tissues, and cause inflammation and tissue-proliferations. 


Literature. 
(Infeetion by Moulds and Yeasts.) 


Baumgarten: Lehrb. d. Mykologie. Braunschweig, 1886-1889, 

Bezold: Otomykosis. Zur Actiologie der Infectionskrankheiten, München, 1881. 
Buschka: Ueber IIefeninykosen. Klin. Vortr.. No. 18, Leipzig. 1898. 

Busse: Pathogene Hefen und Schimmelpilze. Ergebn. d. allg. Path., v., 1900. 
Cao: Oidien u. Oidionykosen. Zschr. f. Hvg., 34 Bd., 1900 (Lit.). 


ANIMAL PARASITES. 45 


Dubreuilh: Les moisissures parasitaires de l'homme. Arch. de med. exp., 1891 (Lit.). 
Duclaux: Ferments et maladies, Paris, 1882; Le microbe et la maladie, Paris, 1886. 
v. Düring: Dermatomykosen. Eulenb. Jahrb., 1890 (Lit.). 

Flügge: Die Mikroorganismen, Leipzig, 1896. 

Kehrer: Der Soorpilz, Heidelberg, 1883. 

Leber: Die Entstehung der Entzündung, Leipzig, 1891. 

Pick: Stand der Dermatomykosenlehre. Arch. f. Derm., xxix., 1894. 

Podak: Aspergillusmykosen. Virch. Arch., 139 Bd.. 1895 (Lit.). 

Sanfelice: Pathogene Blastomyceten. Zeit. f. Ilyg., xxi., 1896. 

Saxer: Pneumonomykosis aspergillina, Jena, 1900. 

Schmorl: Soormetastase in der Niere. Centralbl. f. Bakt., vii., 1890. 
Siebenmann: Die Schimmelmykosen des Ohres, Wiesbaden, 1890. 

Toulerton: Pathogen. Action of Blastomycetes. Journ. of Path., vi., 1899. 


§ 14. The production of disease by animal parasites is most fre- 
quently brought about by the introduction of mature parasites, larve, 
or eggs into the intestinal tract through the medium of the food and 
drink or by unclean fingers. This is particularly true of those parasites 
whose habitat is in the intestine or the tissues located within the body; 
such parasites are accordingly designated as Entozoa. Parasites living 
in the outer tissues, as the skin, are termed Epizoa; they remain either 
on the surface of the skin or penetrate into the same from without. 
The passage of parasites from the intestine into the internal tissues and 
the changes thereby produced constitute the condition which is usually 
called, after the designation first used by Heller, an invasion-disease. 
The animal parasites for the greater part produce only local changes, 
but they can also cause symptoms of a general disease, particularly when 
the parasites increase in the body and are present in great numbers in 
the blood or certain tissues, or when they produce toxic substances. 

The parasitic protozoa are partly harmless parasites, which develop 
in the secretions of the mucous membranes without causing pathological 
changes. Other forms, on the contrary, can penetrate into the living 
tissues, increase inside of cells, and give rise to local morbid changes, 
characterized chiefly by peculiar new-formations of tissue (coccidia-dis- 
ease of the rabbit’s liver, epithelioma contagiosum). Certain forms, 
which are probably to be classed as Sporozoa, increase in the blood, as 
inhabitants and destroyers of the red blood cells, and are the cause of 
the infectious disease known as malaria. It is not impossible that other 
infectious diseases, for example, small-pox, are caused by parasites be- 
longing to the Protozoa. 

The parasitic worms (Nematodes, Cestodes, Trematodes) occur in 
man, partly in the adult and fully developed sexual state, and partly in 
the larval state. In the first case they are for the greater part intestinal 
parasites, which obtain nourishment from the intestinal contents, rarely 
sucking the blood from the intestinal mucosa. Fully developed worms 
are also found in other regions, as in the blood- and lymph-vessels, bile 
passages, lung, pelvis of the kidney, and in the skin. The eggs or fully- 
developed larvz produced in the body by parasitic worms are either cast 
out with the dejecta or, through active wandering or metastasis through 
the blood or lymph, finally reach other organs of the body, where they 
pass the first stage of their development. Here they remain, however, 
in a larval condition, and do not reach sexual maturity. The larvs are 
capable of further development only when they have been taken into a 
new host. 

The worms which reach their sexual maturity in the human body are 
taken in as larve through the food and drink. Their first stage of de- 


46 THE EXTRINSIC CAUSES OF DISEASE. 


velopment is passed in the great majority of cases in animals whose flesh 
is used for food; in other cases in certain of the lower animals not used 
as food. Others develop in water or damp earth or even in the human 
intestine, so that the embryos or eggs, which pass off with the dejecta, 
develop at once in case they are again introduced into the intestinal 
tract of man. 

The worms which occur in man only in the larval condition (hydatids) 
develop from eggs which have come from sexually mature worms, which 
inhabit different animals. They are taken into the intestinal tract. usu- 
ally in the food or drink, but under special conditions eggs capable of 
development may be contained in the dust of the air, and, being inhaled 
and finally reaching the intestinal tract, complete the first stage of de- 
velopment. 

The intestinal parasites for the greater part produce only slight dis- 
turbances, though they may cause mechanical irritation of the intestine. 
The presence of blood-sucking worms in large numbers (Anchylostoma 
duodenale) can cause anzemia. Those parasites which enter the tissues 
may cause in their vicinity mild inflammation and proliferation of tis- 
sue, which may produce more marked clinical symptoms when the num- 
ber of the parasites (trichina-larve) in the tissues is very great. Others 
are of pathological importance, in that they reach a large size (echino- 
coccus cysts) and thereby crowd aside and compress the neighboring 
structures. 

Otherwise their pathogenic significance depends essentially upon their 
location. A parasite situated in the muscles or subcutaneous tissue may 
cause very slight symptoms, while one in the eye, medulla oblongata, 
heart, or blood-vessels may cause severe disturbances, and under certain 
conditions death. 

The parasitic arthropoda (Arachnida and Insects) come to the human 
body partly from the outer world, partly from infected animals, and 
partly from infected human beings. They belong almost wholly to the 
Epizoa, which have their habitat in and upon the skin and accessible 
mucous membranes (lice, bedbugs, fleas, mites) or only occasionally take 
their nourishment from the skin (gnats, gad-flies, flies), a few multiply 
either in the skin (itch-mite) or upon its surface (lice). Flies and gad- 
flies occasionally lay their eggs upon the mucous membranes or surfaces 
of wounds, and from the eggs so laid larv may develop. The larva of 
an arachnoid (Pentastoma denticulatum) is alone found in the internal 
organs. In so far as the Arachnida penetrate into the tissues (epider- 
mis, hair-follicles, and sebaceous-glands), they cause irritation and in- 
flammation; the bite of insects that suck blood 1s also followed by an in- 
flammation in the neighborhood of the puncture. 

Attention has recently been directed to the possibility that mos- 
quitos, stinging flies, gad-flies, bed-bugs, lice, etc., may be the conveyers 
of an infection, in that bacteria or protozoa may by chance be attached 
to their bodies, or that in the act of sucking blood of an infected man or 
animal they may take up into their bodies either bacteria or protozoa 
and later convey them to other individuals. So far as experience goes, 
the danger of such conveyal is not very great in the case of the majority 
of the infectious diseases, since the bacteria thus taken up die after a 
time; yet it is probable that such conveyal does take place, as, for ex- 
ample, in plague, infection with pus-cocci, and anthrax. This method 
of conveyal is of chief importance in malaria, in that the plasmodia taken 
from the blood of infected individuals by mosquitos (anopheles) undergo 


ANIMAL PARASITES: INTRINSIC CAUSES OF DISEASE. 47 


further development in the body of the mosquito and produce a new generation, 
which through the bite of the mosquito is transferred to another individual, 80 
that the spread of malaria is accomplished through mosquitos. Similar 
conditions exist also in the case of the tsetse-fly disease and Texas fever 
of cattle, the latter being conveyed by ticks. Further, it is claimed by 
Manson, Sonsino, and others that the infection of man with the filaria is 
also brought about through the agency of mosquitos. 


Literature. 


(Origin of Disease through Animal Parasites. ) 


Barbacci: Die Aetiologie der Malariainfection. Cent. f. path. Anat., iii., 1892. 

Blanchard: Parasites animaux. Path. gén., ii., Paris, 1896. 

Braun: Die thierischen Parasiten des Menschen, Würzburg, 1893. 

Celli: Die Malaria, Berlin, 1900. 

Davaine: Traité des entozoaires, Paris, 1877. 

Golgi: Malariainfection. Arch. per le Sc. med., x., 1886, and xiii., 1889; Arch. ital. de 
biol., ix. and xiv., 1890; Beitr. v. Ziegler, iv., 1889, and vii., 1890; Zeitschr. f. 

x.. 1891. 

Howar ye: Mosquitos, New York, 1901. 

Huber: Bibliographie der klin. Helminthologie, München, 1891-1895. 

Kitt: Bakterienkunde, Wien, 1899. 

Küchenmeister u. Zürn: Die Parasiten des Menschen, Leipzig, 1882. 

Laveran: Du paludisme et de son hématozoaire, Paris, 1891. 

Leuckart: Die thierischen Parasiten des Menschen, 2 Aufl., 1879-1897. 

Lühs oe sebnisse der neueren Sporozoenforschung Cent. f. Bakt., xxvii. and xxviii., 


Mannaber Die Malariaparasiten, Wien, 1898; Die Malariakrankheiten, Wien, 1899. 

Mühling: Tevertragung von Krankheitserregern durch Wanzen u. Blutegel. Cent. 
f. Bakt., xxv., 1899. 

Nuttal: Die Mosquito-Malariatheorie. C. f. Bakt., xxv. and xxvi., 1899; die Rolle der: 
Insecten, Arachnoiden u. Myriapoden als Träger bei der Verbreitung von durch 
Bakterien u. thier. Parasiten verursachten Krankheiten. Hygien. Rundschau, ix., 
1899, ref. Cent. f. Bakt., xxvi., 1899. 

Perroncito: I parassiti dell’ uomo e degli animali utili, Milano, 1882. 

Reed: Etiology of Yellow Fever. Pan-Amer. Cong., 1901; Amer. Med., 1901; Med. 
Rec., 1901. 

Schneidemühl: Die Protozoen als Krankheitserreger, Leipzig, 1898. 

Uhlworm: Centralbl. f. Bakt. u. Parasitenkunde, 1887-1900. 

Zürn: Die Schmarotzer auf und in dem Körper der Haussäugethiere, Weimar, 1822-1889. 


ll. The Intrinsic Causes of Disease. Predisposition, Idiosyncrasy, 
and Immunity. Inheritance of Pathological Conditions and 
Diseases. 


§ 15. The view is very frequently advanced that all pathological con- 
ditions are ultimately to be referred back to external causes. This is 
correct only in so far as the development of the human species, as well 
as that of the human individual, is not the result of a definite scheme of 
evolution of successive forms of animal life, but rather has been, and is 
still, purely the result of the action of external influences. If, on the 
other hand, the life of a single individual be alone regarded, there can 
be no doubt that for the origin of many pathological changes and diseases, 
certain qualities originating, partly in the congenital anlage and partly ac- 
quired in the course of life, play a réle of very great importance. 

The peculiarity of somatic qualities is shown in one of two ways: 
either in a changed condition of the power of the organism to resist ex- 
ternal influences, or in that pathological changes of tissue or disturb- 


48 THE INTRINSIC CAUSES OF DISEASE. 


ances of function arise independently of external influences. The first 
finds expression in those qualities of the body designated as predisposi- 
tion, idiosyncrasy, and immunity; the latter in certain inheritable, patho- 
logical conditions and functions of single tissues and organs or of the entire 
organism, which develop from congenital anlage without the aid of external in- 
fluences. 

Predisposition and immunity play an especially important röle in 
the origin of the infectious diseases. Man possesses an absolute im- 
munity or insusceptibility to many of the micro-organisms pathogenic 
for animals; as, for example, the bacteria of swine-plague, swine- 
erysipelas, symptomatic anthrax. It is, therefore, to be inferred that 
the character of his tissues and tissue-juices does not favor the entrance 
and multiplication of the organisms causing these diseases. 

On the other hand, the human race shows an especial predisposition 
or susceptibility for other diseases, such as small-pox, vaccinia, measles, 
and influenza, so that the great majority of human individuals in the 
course of life acquire these diseases. In the case of other diseases, as 
scarlet fever, pneumonia, typhoid fever, diphtheria, the susceptibility 
seems much less, but it is not possible to determine exactly to what ex- 
tent the greater rarity of these diseases is dependent upon the fact that 
the individuals not affected are not exposed to the infection. 

In the case of many infectious diseases, there is a greater suscepti- 
bility shown in childhood than in old age; as, for example, diphtheria, 
whooping-cough, and scarlet fever. Further, there are also variations 
in the degree of susceptibility at different times, as, for example, an in- 
dividual may be exposed at certain times to measles without becoming 
infected, while at other times under similar conditions he may contract 
the disease. 

In the case of many pathogenic organisms there appears to be neces- 
sary for the entrance of infection a certain favoring condition or temporary 
increase of susceptibility. As evidence of this may be taken the fact that 
in the human intestinal canal, and especially in the mouth and throat, 
as well as in the respiratory tract, pathogenic organisms (streptococci, 
staphylococci, pneumococci, tubercle bacilli) may be present without the 
occurrence of an infection. It may also happen that cholera spirilla 
may increase abundantly in the intestine without causing marked symp- 
toms. 

Such occurrences may be explained in part by a decrease or loss of 
virulence on the part of such bacteria, but this explanation cannot be 
applied to all cases. In many instances it must be assumed that the 
harmlessness of the bacteria is due to the ability of the tissues to hinder 
their entrance into the deeper parts. In some cases this may depend 
upon the structure and organization of the tissue, in other cases chemical 
substances may have a determining influence (see § 30). In favor of the 
first assumption lies the fact that tissue-lesions, which permit of the 
entrance of bacteria, bring about an infection. A wound, therefore, 
in whatever way produced, forms a local predisposition, and the disease, 
in such cases, bears the character of a wound-infection. Infections 
caused by pus-cocci, tubercle bacilli, tetanus bacilli, glanders, and an- 
thrax bacilli are often of this character. 

Other causes leading to an increased predisposition to infection are 
less easily recognized. Jt appears that severe chilling, “‘taking of cold,” 
may have this effect; also changes in the tissues due to preceding infectious 
or non-infectious local or general diseases. In the case of intestinal infec- 


PREDISPOSITION: IDIOSYNCRASY. 49 


tions (typhoid, cholera), gastro-intestinal disturbances, diminished acidity 
of the stomach contents, overloading of the intestines, retention of the 
contents, etc., play an important réle. Not infrequently it is impossible 
to determine what causes have favored the production of an infection at 
a given time. 

Special predisposition or special lessened resistance of the organ- 
ism is also not infrequently shown to other injurious agents than those 
of infectious nature. Certain individuals are less able than others to 
stand external high temperatures, particularly if at the same time bodily 
labor is performed. Of the soldiers on a march only a fraction may 
suffer from heat-stroke, although all are under the same conditions. The 
altitude at which different individuals, during mountain ascents and bal- 
loon voyages, become sensible of the deficiency of oxygen, varies greatly. 
The after-effects of chloroform anesthesia differ greatly in different in- 
dividuals. Many individuals become exhausted through physical or 
mental labor at a time when in other individuals, under like conditions, 
no trace of such exhaustion is discoverable; and such influences operat- 
ing daily upon a brain, in cases of especial predisposition, may lead to 
diseased conditions. 

Occasionally certain individuals show a sensitiveness toward particu- 
lar external influences, which is wholly anomalous to that usually ob- 
served, so that symptoms of disease may be caused by influences which 
ordinarily do not affect the majority of mankind. Such a peculiar sen- 
sitiveness is designated idiosyncrasy. It is exhibited particularly in 
reference to certain chemical substances, in that certain articles of food 
or drink regarded as harmless act upon such persons as poisons. The 
eating of fresh fruit or sugar or salad produces, m certain individuals, 
nausea and vomiting. Others have an aversion to partaking of dishes 
prepared from liver or kidneys, and become ill if they overcome this 
aversion and eat these foods. Others still, after eating crawfish, lobster, 
strawberries, raspberries, morels, or asparagus, are affected with urti- 
caria, a disease characterized by an eruption of itching wheals, colic, and 
vomiting. Not a few persons are unable to drink boiled milk without 
unpleasant results therefrom. Alcohol, even in very small doses, may 
in certain individuals cause marked excitation, or narcosis, or remarka- 
ble disturbances of the vaso-motor system. The drinking of cocoa may 
cause cardialgia and dyspeptic symptoms. Doses of morphine or chloro- 
form, which are borne by the majority of mankind without injury, may 
cause in certain individuals severe symptoms or even death. Some in- 
dividuals show a high degree of sensitiveness, on the part of the mucous 
membranes of the respiratory tract, to the pollen of certain grasses, so 
that during the time of the hay-barvest the inhalation of the pollen 
which is widespread through the air gives rise to a catarrhal condition 
of the nose and conjunctiva, often of the larynx, trachea, and bronchi, 
which in severe cases may be associated with asthma and fever. These 
conditions are known as hay-fever, hay-asthma, or as pollen- diseases. 
Disinfecting fluids, corrosive sublimate or carbolic acid, in solutions 
which are ordinarily borne without discomfort, may, when applied to 
the skin of certain individuals, cause not only local disturbances of sen- 
sation and inflammation, but under certain conditions may excite an 
eczema which spreads over a large part of the body. 

On what the peculiar idiosyncrasy in individual cases depends i is not 
clear. Im many cases an especial excitability of the nervous system or 
of certain parts of the same may be regarded as the cause of the phe- 

4 


50 THE INTRINSIC CAUSES OF DISEASE. 


nomenon. In acquired idiosyncrasy, as, for instance, that exhibited 
toward certain articles of food, psychical factors may play a part. 


The great importance of the part played by natural predisposition and immunity 
in the origin of infectious diseases has not only been made evident by the study of the 
spread of epidemics among men and animals, but has received also abundant contirma- 
tion by numerous experimental investigations. If, for example. a mixture of different 
bacteria be injected into an animal, only a part of these will develop and produce tissue- 
changes; the others die. If the same mixture be injected into an animal of a different 
species, the bacteria which develop are not the sameas those in the first case. Further, 
a certain form of bacteria which when inoculated into a certain species of mouse in- 
variably causes death, may, when inoculated into another mouse of different species, 
be without effect. Mice are very susceptible to anthrax, rats are nearly immune. The 
poison of the so-called septicemia of rabbits kills with absolute certainty rabbits and 
mice; guinea-pigs and rats are immune to it, while sparrows and pigeons are suscepti- 
ble. he spirilla of relapsing fever may be successfully inoculated only into apes. 
Gonorrhea, syphilis, and leprosy cannot be successfully inoculated into any of the 
lower animals. 

In the same species, different animals of different ages exhibit differences of sus- 
ceptibility toward certain organisms. Young dogs are easily infected with anthrax 
(Koch), old ones are not. 

Different experiments have shown that an immunity toward a certain infection 
may be destroyed by suitable action upon the tissue (Sirotinin, “ Die Vebertragung von 
Typhusbacillen auf Versuchsthiere,” Zeitschr. f. Hyg., i., 1886). According to Roger 
(“Contribution A l’etude expérimentale ducharbon symptomatique,” Rerue de méd., ' 
1891), the natural immunity of rabbits and pigeons against symptomatic anthrax may be 
overcome, if the non-pathogenic Bacillus prodigiosus be inoculated at the same time with 
the bacillus of the disease. According to this investigator, the decomposition product 
of the prodigiosus that is soluble in glycerin exertsa modifying action upon the organism. 

According to Gottstein (“ Beiträge zur Lehre von der Septikämia,” Deut. med. Wochen. 
schr., 1890), guinea-pigs may be made susceptible to the subcutaneous inoculation of 
chicken-cholera bacilli, to which they are naturally immune, through the injection of 
substances which destroy the red blood-cells, such as hydracetin or pyrogallol. This 
investigator concludes, therefore, that toxic substances, which render either man or ani- 
mals more susceptible to infection, act chiefly through a dissolution of the red cor- 
puscles. According to Leo (“ Beiträge zur Immunitätslehre,” Zeitschr. f. Hyg., vii., 1890), 
white mice which are immune to glanders may be made susceptible to inoculations with 
the bacilli of this disease by mixing with their food a small quantity of phloridzin, 
which causes a toxic diabetes. 

According to Canalis and Morpurgo, pigeons may be made susceptible to anthrax 
through starvation. According to Lede, chilling of the body increases the suscepti- 
bility to infection. 


The especial diseases to which the new-born so frequently succumb are, aside from 
the conditions acquired during intra-uterine life, dependent partly upon a pathological 
weakness of the entire organism (especially in case of premature birth), and partly upon 
the surrounding conditions. Asphyxia, which is of such frequent occurrence, may 
arise either as the result of bodily weakness or of pathological influences exerted dur- 
ing delivery. Infectious diseases may be acquired through the stump of the cord or 
through the accessible mucous membranes and respiratory tract during birth. H«xmor- 
rhages are dependent partly upon traumatic influences exerted during birth, partly 
upon disturbances of circulation and upon infections. 

Children are, as has been shown by medical experience, more suaceptible to many tn- 
fections than adults; particularly so in the case of whooping-cough, diphtheria, measles, 
and scarlet fever. The skin of infants also offers less resistance to the entrance of pus- 
cocci than that of older individuals. In this connection it should be noted that the 
slight susceptibility or the immunity of many adults is dependent upon the fact that 
they owe their immunity to attacks of such diseases during childhood. Further, it 
should be remarked that children are more exposed to certain infections, for instance, 
tuberculosis, than are adults. 

In later life hemorrhages, softening of the brain, cardiac degenerations, cancerous 

owths, and the formation of gall-stones are of especially frequent occurrence. The 
disense of the arteries known as arteriosclerosis, and also gout, may appear even in the 
late years of middle life. The predisposition in old age to certain diseases depends in 
part upon degencrative processes, associated with premature senility of the tissues; in 
part also upon the fact that certain intluences, which the years bring with them, grad- 


PREDISPOSITION AND IMMUNITY. 51 


ually accumulate, so that finaliy the changes which they produce become so prominent 
that they lead to functional disturbances, and thereby to recognizable morbid condi- 
tions. Moreover, it is to be remarked that many pathological symptoms of old age are 
secondary diseases, which become apparent only after other tissue-changes have 
reached a certain degree. For example, senile hemorrhages, senile gangrene, degenera- 
tions of the brain and heart are dependent upon disease-processes occurring in the 
arteries. 

The predisposition of the sexes to certain diseases depends, in the first place, upon 
the especial structure and function of the sexual apparatus. The conditions of preg- 
nancy and the puerperium offer an especially favorable field for many diseases, as, for 
example, for infection through wounds. Moreover, the different relations of the sexes 
to many diseases may be explained by differences in the modes of labor and in the hab- 
its of living of the two sexes. 

Differences of predisposition of different races are shown particularly in regard to 
malaria and dysentery, toward which the negro in general shows less susceptibility 
than the European. The Japanese are said to be more susceptible than the European 
toward beri-beri. 


Literature. 
(Predisposition and Immunity. ) 


Bourcy: Prédisposition et immunité. Pathol. gén., i., Paris, 1895. 

Canalis u. Morpurgo: Eintluss des Hungers auf die Empfänglichkeit für Infections- 
krankheiten. Forschr. d. Med., viii., 1890. 

Charcot: Lecons sur les maladies des vieillards, 1868. 

Ehrlich: Experimentelle Untersuchungen über Immunität. Deut. med. Wochenschr., 
1891. 

Emmerich: Die Ursachen der Immunität. Arch. f. Hyg., xii., 1891. 

d’Espine et Picot: Manuel pratique des maladies de l’enfance, Paris, 1889. 

Galli-Valerio: Immunitä e resistenza alle malattie, Mil., 1897. 

Goenner: Heufieber. Correspbl. f. Schweizer Aerzte, 1897. 

Henoch: Verlesungen über Kinderkrankheiten, Berlin, 1890. . 

Hirsch: Handbuch der historisch-geographischen Pathologie, Berlin, 1881-1886. 

Hueppe: Naturwissensch. Einführung in die Bakteriologie, Wiesbaden, 1896. 

Jousset: Traite de l’acclimatement et de l’acclimatation, Paris, 1884. 

Lode: Beeinflussung d. Disposit. z. Infect. durch Wärmeentziehung. Arch. f. Hyg., 
28 Bd., 1896. 

Lubarsch: Untersuch. üb. d. Ursachen d. angebor. u. erworbenen Immunität, Berlin, 
1891; Zur Lehre von den Geschwülsten u. Infectionskrankheiten, Wiesbaden, 1899. 

Maggelsen: Ueber die Abhängigkeit der Krankheiten von der Witterung, Leipzig, 
1890. 

Marfan: Le surmenage. Pathol. gén. de Bouchard, i., Paris, 1895. 
‘Martius: Pathogenese innerer Krankheiten, Leipzig, 1899 and 1900; Krankheitsursache 
u. Krankheitsanlage. Verh. der Dtsch. Ges. d. Naturforscher, Leipzig, 1898. 
Müller: Die Krankheiten d. weibl. Körpers in ihren Bezich. z. d. Geschlechtsfunc- 
tionen, 1888. 

Runge: Die Krankheiten der ersten Lebenstage, Stuttgart, 1893. 

Riess: Heufieber. Realencylop., 1896 (Lit.). 

Stockvis: Vergleichende Rassenpathologie und Widerstandsfähigkeit des Europäers 
in den Tropen. Verh.d. X. internat. med. Congr., i., Berlin, 1891. 

V : Lehrbuch der Kinderkranheiten, Stuttgart, 1890. 
uisen: Ueber Immunität und Idiosynkrasie. Arch. f. exp. Path., 85 Bd., 1895. 


$16. Among the morbid conditions originating from intrinsic 
causes, that is, without the aid of specific extrinsic influences, and 
which either appear spontaneously or are developed through any ex- 
ternal influence whatsoever, there may be distinguished different groups; 
namely, one in which the body as a whole—the constitution—is in- 
volved; another in which only a part of the body as a system or an or- 
gan is affected; and, finally, a third in which only a part of an organ 
presents functional or anatomical changes of a pathological nature. It 
must be noted that there is no sharp dividing line between these groups, 
inasmuch as local pathological changes may be associated with constitu- 


52 THE INTRINSIC CAUSES OF DISEASE. 


tional conditions. Further, it is often very difficult or impossible to de- 
termine exactly what part intrinsic and what part extrinsic causes have 
taken in the production of such pathological conditions, inasmuch as 
the force of the external influence which has called the pathological pro- 
cess into activity cannot be estimated with certainty. 

Among the constitutional diseases arising from intrinsic causes 
are to be mentioned, first, the development of dwarfs and giants, dis- 
turbances of growth, the first of which is marked by an under-develop- 
ment of all the parts of the body, both of the skeleton and the soft 
parts, while the second is characterized by a growth exceeding that of 
the ordinary individual. It cannot be doubted that both dwarf and giaut 
growths are often purely dependent upon a congeuital tendency; but the 
sume effects can be produced, at least in so far as the inhibition of 
growth is concerned, by harmful influences exerted during the period of 
development and growth. It cannot always be told with certainty 
whether an abnormal bodily growth is dependent: upon a congenital ten- 
deney or upon pathological influences during the period of growth, as, 
for example, upon disturbances of growth due to disease or loss of the 
thyroid gland. 

The same difficulty is presented in cases in which the body has at- 
tained full development of stature, but manifests a general feebleness of 
constitution, as shown by its inability to withstand a great variety of 
external influences. Such condition may arise either from congenital 
defective and weak anlage or from harmful influences which have at- 
tacked the body during intra- or extra-uterine life; or further, congeni- 
tal weak anlage and external weakening influences may have affected the 
development of the individual in an equal measure. 

A further constitutional peculiarity, which is founded upon a spe- 
cial congenital anlage, is corpulence (obesity, adipositas, lipomatosis uni- 
versalis), a condition in which fat is deposited in an excessive amount, 
either in the tissues normally containing fat, or further, in regions which 
normally contain no fat, as, for example, beneath the endocardium or 
between the muscles. The increased deposit of fat is ultimately to be 
referred to a disproportion between fat-production or fat-supply and fat- 
consumption, the pathological increase of fat being at one time depend- 
ent upon an abnormal increase of fat-production, at another on a de- 
crease of fat-consumption. Daily experience teaches that the energy 
with which metabolism goes on in the body differs greatly, and changes 
also at the different periods of life, so that the normal amount of nour- 
ishment tends at one time to fatten, at another time does not. 

In the pathological eondition termed obesity, which in part rests 
upon a congenital tendency, the energy of the protoplasmic forces of 
destructive metamorphosis is weakened, so that an abnormal amount of 
fat is deposited, even when only a moderate or even a decreased amount 
of nutritive material is supplied to the tissue. 

Gout, like obesity, is also a constitutional disease, which is chiefly 
dependent upon a congenital anlage and is produced essentially by in- 
trinsic causes. The exact. nature of the disease is not yet known. It is 
characterized by deposits of urie acid in the tissues. According to Gar- 
rod and Ebstein, the acute attacks of gout are caused by an accumula- 
tion of uric acid which has its origin either in the kidneys or in local 
conditions. On the other hand Pfeiffer holds that the essential feature 
of the gouty tendency consists in the fact that the uric acid is produced 
in a form which is soluble only with difficulty. According to von 


PATHOLOGICAL CONDITIONS DUE TO INTRINSIC CAUSES. 53 


Noorden, the formation and deposit of uric acid is only a secondary 
process, which is induced by the presence of a certain ferment having 
only a local action, and is consequently not dependent upon the amount 
or character of the uric acid formed in other parts of the body. 

Pathological changes arising in single systems and organs from 
intrinsic causes may occur in any part of the body, and may involve 
an entire system or organ, or only a part of one. 

In the skeleton there may occur abnormal development of single 
parts, as, for example, an abnormal smallness of the extremities (micro- 
melia) or of the head (microcephalus) in contrast to the size of the 
trunk; an abnormal over-development of & bone or group of bones 
(macrocephalus, macrodactylism, giant growth of a finger, entire foot, 
or of an extremity); malformations of the extremities (cleft-hand, cleft- 
foot, ete.). Occasionally supernumerary bones, as carpal bones or 
phalanges, may develop, giving rise to supernumerary fingers. Fur- 
ther, there may be developed atypical formations, such as bony out- 
growths (exostoses, hyperostoses), which may extend over the skeleton 
to a greater or less extent, originating either spontaneously or following 
some traumatism. 

In the muscular system there occur particularly pathological bony 
formations, either single or multiple (myositis ossificans), which, in the 
period of childhood, occasionally lead to a progressive stiffness of the 
muscles, through the transformation of muscle into bony plates. 

In the vascular system there occur either gross anatomical changes, 
such as abnormal branching of the arteries, pathological development 
of the heart, or finer changes, which reveal themselves through some 
abnormal action on the part of the circulatory apparatus or through a 
tendency to hemorrhages (hemophilia) which take place spontaneously, 
that is, without our being able to demonstrate the action of some in- 
jurious influence upon the heart or blood-vessels. 

During the development of the central nervous system there may 
occur primary disturbances, which in part may manifest themselves only 
through some pathological disturbance of function or some special predis- 
position to disease, while others are distinguished by gross anatomical 
changes, such as abnormal smallness of the brain (micrencephalon) or of 
the spinal cord (micromyelia), defective development or absence of par- 
ticular parts (see chapter on malformations), misplacement of the gray 
ınatter (heterotopia of the gray substance), abnormal formation of cavi- 
ties (syringomyelia), or abnormal formations of neuroglia. These dis- 
turbances may involve the functions of the sensory organs and the motor 
centres, and even to a greater extent the psychical processes. The mor- 
bid conditions known as idiocy, epilepsy, periodic and circular insanity, 
hysteria, neurasthenia, as well as paralysis, mania, melancholia, and 
dementia, may have their origin in a congenital predisposition. Re- 
cently the tendency to crime has also been ascribed to a congenital pre- 
disposition, and Lombroso, in particular, has endeavored to prove that 
the man who lives only through crime and for crime, the Homo delin- 
quens, is a congenital criminal—that is, a man who suffers from bodily 
and mental abnormalities, who possesses other physical and psychical 
characters than the normal mau or even than one who is simply men- 
tally unbalanced, in that he presents the symptoms of a form of degener- 
ation tending in a well-defined direction. According to Lombroso, a 
subnormal development of the anterior half of the cranium, associated 
with a corresponding lack of development of the anterior portion of the 


54 THE INTRINSIC CAUSES OF DISEASE. 


cerebrum, in connection with an over-development of the posterior por- 
tion, produces a feebler development of the intelligence and of the moral 
sense, and favors a strongly developed instinct-life.. Benedikt even goes 
so far as to maintain that the criminal possesses a peculiar configuration 
of the cerebral convolutions, similar in type to those of beasts of prey. 

The views of Lombroso and Benedikt have met with much opposi- 
tion, and have been attacked as incorrect. There can be no doubt that: 
there does not exist a degenerate species of the human race, which is 
characterized by such anatomical peculiarities as to make it possible for 
us to distinguish a class of Homo delinquens from that of Homo sapiens. 
All the somatic peculiarities regarded as characteristic of the criminal 
type—as, for example, the beast-of-prey type of cerebral convolutions, 
slightly developed frontal brain, receding forehead, massiveness of the 
lower jaw, prognathia, asymmetry of the cranium, marked prominence 
of the arcus superficialis and arcus frontalis, pathological conformations 
of the skull, ete. —while relatively frequent in criminals, are also far 
from being infrequent in normal men. On the other hand, it is not to 
be doubted that the tendency to crime is very frequently dependent upon 
a congenital predisposition having its seat in some special organization 
of the central nervous system. In this respect the criminal resembles 
the insane individual; further, mental diseases—for example, epilepsy 
and hysteria—are often observed in criminals. 

Pathological cerebral functions may develop primarily in individuals 
possessing such morbid predispositions—that is, witaout external influ- 
ences playing any part in the production of the disturbance, so that. the 
person concerned may manifest pathological disturbances of cerebral 
functions without the concurrence of any external injury, either during 
the period of development and growth or later. On the other hand, in 
other cases, external influences—such as mental work, sorrow, care, 
psychical irritation, disease, ete.—are the causes which give rise to the 
particular illness—that is, to the occurrence of pathological brain or 
spinal-cord functions. In these cases the inherited tendency consists 
only in an abnormal weakness, a predisposition to disease of the central 
nervous system, so that insignificant influences which would produce no 
recognizable effects upon a normal individual are sufficient to excite the 
morbid phenomena. Since many influences, as diseases, infections, 
psychical irritations, are adequate under certain conditions to produce 
mental diseases in individuals who must be regarded as normal, it is 
clear that in many instances it is difficult and often impossible to deter- 
mine what part the intrinsie causes—the inherited predisposition—and 
what part the extrinsie causes have had in the production of a disease 
of the central nervous system. 

In the case of the peripheral nerves, it is especially their connective- 
tissue elements which often take on a pathological activity of growth 
under the influence of intrinsic causes. This activity may manifest it- 
self partly in the form of diffuse thickenings (fibromatosis of the nerves), 
which are situated either along the course of those nerves large enough 
to be dissected with the knife or along the finer nerves, often in large 
numbers through the entire nervous system, and occasionally involving 
the entire territory of the peripheral nerves, the skin being most fre- 
quently affected (multiple fibromata of the skin). In individual cases 
the fibromatosis of the nerves is associated with an increase in the num- 
ber of nerve-fibres, so that within a given area of nerve-distribution 
there will be found a great Increase of nerve-fibres, thickened through a 


PATHOLOGICAL CONDITIONS DUE TO INTRINSIC CAUSES. 55 


pathological increase of the endoneurium and for the greater part twisted 
and wound into serpentine forms (cirsoid neuroma, plexiform neuroma). 

Among the pathological conditions of the visual apparatus are to 
be mentioned in particular dyschromatopsia and achromatopsia, con- 
genital partial or total color-blindness, which are frequently spoken of 
as Daltonism, and are characterized by a want of perception for certain 
colors (most frequently for red and green) or for all the colors. In this 
same category belongs further the typical pigment degeneration of the 
retina, in which there occurs a peculiar spotted, black pigmentation of 
the retina, associated with a diminution of central sharpness of vision 
and light-perception, with a narrowing of the visual field. Finally, 
certain forms of myopia, also albinism (absence of pigment in the 
choroid), the latter condition also involving the structures of the skin, 
are to be considered in this connection. 

Of intrinsic conditions of the auditory apparatus deaf-mutism is of 
chief importance; this condition, in part at least, is dependent upon a 
primary disturbance of development. Further, certain malformations 
of the external ear fall into this class. 

In the skin and subcutaneous connective tissue new-growths may 
develop from congenital anlage, consisting of proliferations, sometimes 
of connective tissue, at other times of epithelium. They often involve 
particular parts of the skin, as the cutaneous nerves, blood-vessels, 
lymph-vessels, or the adipose tissue. When occurring as extensive 
thickenings of the skin and subcutaneous tissue, they constitute the 
foundations of the conditions known as fibromatous, neuromatous, 
hemangiomatous, lymphangiomatous, and lipomatous elephantiasis. As 
circumscribed growths they are known as birth-marks, fleshy moles, 
lentigines, freckles, and tumors of the blood- and lymph-vessels. The 
epithelial hypertrophies give rise to those conditions designated as fish- 
scale disease or ichthyosis, ichthyotic warts, and cutaneous horns. 

In addition to the pathological conditions which have been mentioned, 
there are also malformations of the body (see chapter on malforma- 
tions) or also of internal organs which must be regarded as primary— 
i.e., which are not produced by injurious influences exerted upon the 
developing fcetus. Finally, many forms of tumors (see chapter on 
tumors) are to be placed in this class, particularly those which are found 
to be already developed at birth or which develop during childhood. 


Literature. 


(Diseases Arising from Intrinsic Causes. ) 


Anton: Die Aufgaben d. Psychiatrie u. d. Lehre v. d. Vererbung v. Nervenkrank- 
heiten. Wien, 1892. 

Baer: Der Verbrecher in anthropologischer Beziehung, Stuttgart, 1893. 

Benedikt: Anat. Studien an Verbrechergehirnen, Wien, 1879; Cent. f. d. med. Wiss., 
1880. 

Charcot. Maladies des vieillards, gouttes et rhumatisme. (Euv. comp!., vii., Paris, 
1890. 

Cohn: Studien über die angeb. Farbenblindheit, Breslau, 1879. 

Cohnheim: Vorlesungen Ober allgemeine Pathologie, Berlin. 1882. 

Crocq: L'unité de la diathöse et Vhérédité morbide. Rev. de méd., 1893. 

Ebstein: Die Fettleibigkeit, Wiesbaden, 1882; Natur und Behandlung der Gicht, 
Wiesbaden, 1882; Beitr. z. Lehre von der harnsauren Diathese, Wiesbaden, 1891; 
Die Stellung der Fettleibigkeit, der Gicht und der Zuckerkrankheit im nosolog. 
System. Deutsch. med Woch., 1898. 

Fere: Nervenkrankheiten und ihre Vererbung, Berlin, 1896. 


56 THE INTRINSIC CAUSES OF DISEASE. 


Le Gendre: L’hérédité. Patlıol. gen. publ. par Bouchard, i., Paris, 1895. 
Grassmann: Erblichkeit der Psychosen. Zeitschr. f. Psych., 52 Bd., 1895. 
Haeckel: Antlıropogenie, 1891. 
Kisch: Die Fettleibigkeit, Stuttgart, 1888, and Eulenburg’s Realencyklop., Art. 
Fettsucht, 1895. 
Kolisch: Wesen und Behandlung der uratischen Diathese, Stuttgart, 1895. 
Koller: Erblichkeitsstatistik der Geisteskrankheiten. Arch. f. Psych., 27 Bd., 1895. 
Kurella: Cesare Lombroso und die Naturgeschichte des Verbrechers, Hamburg, 1893. 
Lee: De l’obesite, Paris, 1886. 
Locher- Wild: Ueber Familienanlage und Erblichkeit, Zurich, 1874. 
_Lombroso: Der Verbrecher, i.-iii. (mit Bilderatlas), Hamburg, 1891-1895. 
Lombroso u. Ferrero: Das Weib als Verbrecherin und Prostituirte, Hamburg, 1894. 
v. Noorden: Pathologie des Stoffwechsels (Fettsucht, Gicht), Jena, 1893. 
Pfeiffer: Das Wesen der Gicht, Wiesbaden, 1891. 
Schaeffer: Fötale Ohrformen bei Erwachsenen. Arch. f. Anthropol., xxi., 1892. 
Sernoff: Die Lehre Lombroso’s. Biol. Centralbl., xvi., 1896. 
Virchow: Descendenz u. Pathologie. Virch. Arch., 108 Bd., 1886. 
Wagner: Die Krankheitsanlage. Deutsch. Arch. f. klin. Med., 23 Bd., 1888. 
Wiedersheim: Der Bau des Menschen, Freiburg, 1893. 
See also 8 17. 


§ 17. The origin of diseases attributed to intrinsic causes—that is, 
of diseases in which extrinsic influences are either entirely absent during 
both intra- and extra-uterine life, or are of significance only as a source 
of irritation sufficient to excite into development pathological tendencies 
already present in the body—may be explained in two ways: Hither the 
pathological peculiarities of the individual concerned are inherited from the 
ancestors, or they are developed from the seed, i.e., from the individual sexual 
nuclei that have copulated or from the segmentation nucleus resulting from 
their union. 

The inheritance of pathological qualities is a fact clearly shown by 
clinical observations, Inasmuch as many of the examples of diseases due 
to intrinsic causes which are cited in §16 also appear as inheritable 
characteristics in certain families. In some cases these characteristics 
are transmitted from the parents to the children, in other cases the 
grandchild may exhibit pathological peculiarities of the grandparents, 
the parents themselves remaining exempt; finally, in other cases the 
pathological peculiarity may be manifested in individuals of the collat- 
eral branches, as from uncle to nephew. Dwarfishness and giantism are 
pathological peculiarities which frequently characterize certain families. 
Six fingers, cleft-hand and cleft-foot, hare-lip, dextrocardia, birth-marks, 
multiple exostoses, fibromatosis of the nerves, and multiple neurofibro- 
mata may appear in families for many successive generations. 

Congenital hemophilia is also an inheritable condition, which is 
ordinarily transmitted through the daughter to a male grandchild, the 
daughter not showing the disease. There may occur, however, a direct 
transmission of hemophilia from parents to children. Partial or total 
color-blindness als occurs as an inheritable family disease, especially 
affecting the male members, and like hemophilia is transmitted through 
the female line, whieh does not: suffer, to the male descendants. The 
typical pigment-degeneration of the retina, myopia, deaf-mutism, cer- 
tain forms of progressive muscular atrophy, and polyuria (Weyl) are 
also inheritable. 

According to Gairdner and Garrod, in about ninety per cent of the 
eases of gout there is a family history of the disease. 

Of the pathological conditions of the nervous system many are in- 
heritable; to these belong especially periodic and circular insanity, 
epilepsy, hysteria, congenital insanity, and to a somewhat less extent 


THE INHERITANCE OF DISEASE. 57 


melancholia, mania, delusional insanity, and alcoholism. Progressive 
paralysis, the deliriums, and the conditions of nervous exhaustion are 
but slightly influenced by heredity (Kraepelin). Hagen estimates the 
number of hereditary insane at 28.9 per cent, Leidesdorf at 25 per cent, 
Tigges at over 40 per cent of all cases, while Forel holds that 69-85 per 
cent may be accounted for by heredity. 

In the most severe forms of hereditary degeneration the pathological 
condition itself is inherited, but more frequently the predisposition to 
disease is alone inherited and the morbid condition itself is developed 
through the action of extrinsic harmful influences upon the central ner- 
vous system. The character of the disease in the descendants may be 
the same as in the ancestors (identical heredity). More often the charac- 
ter of the disease is changed (transformational heredity), not infrequently 
in the sense that the severity of the condition increases from generation 
to generation (degenerative heredity). 

According to Morel, there may appear, for example, in the first gen- 
eration, nervous temperament, moral depravity, excesses; in the second, a 
tendency to apoplexy, severe neuroses, alcoholism; in the third, psychi- 
cal disturbances, suicidal tendency, intellectual incapacity; finally, in 
the fourth, congenital idiocy, malformations, and arrests of development. 

The occurrence of inheritable diseases is by no means remarkable; 
it is a well-known fact that ina family not only the peculiarities of race, 
but also of that particular family are inherited, and that very often the 
characteristic qualities of either parent or of both recur in the children. 
As a hypothesis for the explanation of heredity, it is only necessary to 
assume that the peculiar quality under consideration represents not 
merely a somatic change accidentally acquired during the life of the an- 
cestor, but much rather a quality of the ancestor developed from a con- 
genital anlage. Diseases which in a normal individual arise only un- 
der the influences of some external injurious influence are never in atrue 
sense inherited (compare § 19), but only those pathological conditions 
existing in the germ are to be regarded as examples of true inheritance. 
If a certain disease, as, for example, a mental disease or myopia, is the 
product of a special inherited predisposition plus the effect of injurious 
influences which have acted upon the body during life, only that part 
can be transmitted which has its seat in some peculiar congenital anlage, 
but not that caused by external influences—the acquired condition can- 
not be inherited. 

In direct inheritance—i.e., in that form of inheritance in which 
parental qualities are transmitted to the child—the transmission of nor- 
mal as well as of pathological qualities is possible only when both sexual 
cells, in the condition in which they combine, contain the potentialities 
of the characteristics of both parents, in so far as these characteristics 
are transmissible. The product. of the union of the sexual cells—the 
seymentation-cell—must, therefore, contain within itself both the pa- 
ternal and maternal qualities. Since the sexual cells do not represent 
a product of the body developing during the course of life, but are rather 
to be regarded as independent structures, which at an early period of 
development are separated from the other parts of the body (that is, from 
the somatic cells) into special organs, where, protected and nourished by 
the body to which they belong, they lead an independent existence; the 
only possible explanation for the phenomenon of inheritance is found in 
the hypothesis that the individual sexual cells contain, from the time of 
their origin onward, the potentialities of the same qualities which appear 


58 THE INTRINSIC CAUSES OF DISEASE. 


in the body in which they dwell. Both the sexual cells and the body 
itself, therefore, inherit in general the same qualities from the ancestors. 
Since in the act of fructification only the nuclei of the sexual cells—that 
is, parts of the same—come to copulation, we are compelled further to 
assuine that the nuclei are the bearers of inheritable qualities, and the 
peculiarities of the individual arising from the combination of the sex- 
ual nuclei have their foundation in the organization of the nuclei. 

The appearance in the descendants of normal or pathological char- 
acters belonging to the collateral relatives (uncle, great-aunt, or cousin), 
but which are not present in the parents, is known as collateral inheri- 
tance. This phenomenon is explained by the hypothesis that the sexual 
cells, in their origin, received characteristics which the bodies of the 
parents did not receive, or which, at least, did not undergo development 
and manifest themselves in the parental bodies, whereas in certain rela- 
tives they did become manifest. 

The appearance in an individual of normal or pathological character- 
istics which were wanting in the parents, but were present in the grand- 
parents or great-grandparents, is known as atavistic inheritance. This 
phenomenon is explained by the hypothesis that given characteristics of 
the grandparents or great-grandparents were transmitted to the sexual 
cells of the son, or of the son and grandson, without developing in the 
body of the first, while the quality thus remaining latent became again 
manifest in the grandson or great-grandson. 

The attempt has been made to give to the atavistic mode of transmis- 
sion—which is of frequent occurrence and is usually confined to the 
immediate generations of ancestors—a wider significance in pathology. 
Thus it has been proposed to explain the occurrence of many newly aris- 
ing pathological conditions, which appear similar to certain somatic 
qualities possessed by remote animal species in the ancestry of man, as a 
reversion to the type of these ancestors. For example, microcephalus 
and mierencephalus have been explained as a reversion to the ape type; 
and Lombroso is inclined to regard the homo delinquens as an atavistic 
phenomenon. There can be no doubt that certain writers have gone too 
far in this respect and have mistaken certain acquired pathological for- 
mations or new germ-variations (compare § 18) for atavistie conditions. 
Aside from the question of reversion to the type of the nearest genera- 
tions of ancestors, atavism plays but an insignificant part in pathology, 
and it can really be employed only in the explanation of pathological 
formations in which the tissues show a certain fluctuation of behavior, 
so that not rarely formations arise which in phylogeny or ontogeny rep- 
resent stages of the then normal conditions. In this category belong, for 
example, the occurrence of certain forms of the ear, supernumerary ribs, 
nipples, or mammary glands, and the development of certain muscles 
which are found in the most closely related mammals. 


It is held by many writers that da dndiriduual cases, acquired pathological conditions 
many, under certain cireumstances, be transmitted to the descendants. Some even affirm 
the possibility of hereditary transmission of deformities caused by injury, and regard 
such transmission as proved in certain cases. In support of their view they believe 
that they can refer to the hereditary transmission of birth-marks, malformations of the 
fingers, myopia, mental diseases, predisposition to tuberculosis, ete., as examples, ac- 
cording to their assumption, of diseases which appeared in the first instance as ac- 
quired, and which were then transmitted to the descendants. Further, they hold that 
they can point to observations on animals, of which numerous accounts are found in 
the literature. as giving evidence that injuries may cause deformities which are later 
transmitted to the offspring. 


THE INHERITANCE OF PATHOLOGICAL CONDITIONS. 59 


An unprejudiced examination, however, of the material collected in support of 
this view shows that observations which establish the hereditary transmission of patholog- 
seul characteristics acquired in the individual do not exist. The alleged proofs are found 
in part to be based upon inaccurate observations, in part upon incorrect inferences 
drawn from accurate observations. For example, the assumption that the occurrence 
of a birth-mark in a child in the same region of the skin as that in which the mother 
has a scar is a proof of inherited deformity is wholly in the wrong, inasmuch as birth- 
marks and scars represent two entirely different pathological processes. If, among the 
descendants of a man who suffered from some form of mental disease and who showed 
this disease only after a certain age through the perversity of his actions, there appears 
an inheritable disease of the central nervous system, or if we note a similar occurrence 
in the case of myopia, we cannot conclude from such observations that the disease of 
the ancestor was purely an acquired condition. The term acqutred, in the biological 
sense, can be applied only to that which in the course of the life of an individual arises 
purely from extrinsic influences, but not toa quality, the anlage of which existed al- 
ready in the germ-cell, although this quality did not become manifest until excited to 
development by extrinsic influences. Should there appear in a family inheritable men- 
tal diseases or hereditary myopia, the first case of such diseases may have already been 
due to some pathological alteration of the germ, although no manifestations of the dis- 
ease occurred until some of the outside influences of life excited it to activity, and so 
rendered possible the recognition of the pathological condition. The particular patho- 
logical condition in this case cannot, therefore, be regarded as a purely acquired disease. 

The observations of Brown-Séguard that guinea-pigs, in which epilepsy has been 
experimentally induced, can transmit the condition of epilepsy, have been shown by 
Sommer to be incorrect, in that the condition is not a true epilepsy, but a reflex 
epilepsy, and is not transmitted. 

Against the occurrence of an inheritance of acquired pathological conditions is the 
simple consideration that the human race, which is exposed to so many injurious influ- 
ences, and whose individual members suffer so frequently from disease and mutilations, 
would very soon arrive at a state of extreme misery and stunted growth and would 
eventually perish were only a small part of the acquired diseases transinitted to the 
descendants. Further, the origin of man and animal forms reproducing through ger- 
minal cells is in itself an argument against the possibility of the transmission of qualities 
acquired by the individual. 

The act of fructification—that is, the first step leading to the production of a new 
individual—is accomplished by the copulation of the sexual nuclei—that is, of the 
nuclei of the ovum and spermatozoén. According to the researches of the last. decades, 
there can be. no doubt that these nuclei are the bearers of the hereditary characteristica of 
the parents, and that the individuality of the copulating nuclei is inherent in the or- 
ganization of the same. It is impossible to conceive in what manner processes taking 
place in the body cells can produce in the sexual nuclei, which lie within special cells 
in the sexual glands, such alterations of organization that they shall contain in poten- 
tial form the acquired characteristics of the body and transmit them, after copulation 
has occurred, to the descendants. 

Deluge was able to fructify non-nucleated portions of the eggs of echinoderms, 
annelides, and mollusks with spermatozoa (merogony). He regards the union of the 
nucleus of the spermatozoön with the protoplasm of the egg as the essential feature of 
fructification. This is not applicable to the ordinary method of fructification, but only 
shows that in exceptional cases the entrance of the spermatozoön into the protoplasm 
of the egg is sufticient for the setting-up of further development, and that the nucleus 
of the spermatozoön entering into the egg without uniting with the nucleus of the lat- 
ter exercises an especial influence upon the protoplasm of the egg. 

Darictn in his time represented the view that acquired characteristics could be 
transmitted to the descendants, and endeavored to make such phenomena intelligible 
by the theory that molecules from all the cells of the body contribute to the formation 
of the germ-cells, and that, consequently, alterations of the organism can be trans- 
mitted to the germ-cell. Nevertheless, there occur in the writings of Darwin state- 
ments which not only do not agree with this opinion, but directly contradict it. 


Literature. 
(Inheritance of Pathological Conditions. ) 


Adami: Heredity in Relation to the Development of Morbid States. Ref. Handbook 
of Med. Sc., 1902. 

Bernhard: Familiäre Erkrankung d. Centralnervensystems. Virch. Arch., 126 Bd., 
1891. 


60 THE INTRINSIC CAUSES OF DISEASE. 


Bollinger: Ueber Vererbung von Krankheiten, Stuttgart, 1882. 
Brown-Sequard: Arch. de phys., i., 1868, ii., 1869, iii., 1870, iv., 1872 (giebt an, dass 
künstlich erzeugte Epilepsie bei Meerschweinchen auf die Jungen übergehen 


könne). 

Couvelaire: La dysostose cleido-cranienne. J. de phys., i.. 1899. 

Darwin, C. H.: Die Ehe zwischen Geschw Ssterkindem- und ihre Folgen, Leipzig, 
1876. 


Dejerine: L’heredite dans les maladies du syst&me nerveux, Paris, 1886. 

Delage: Etude sur la mérogonie. Arch. de zool. exper., 1899. 

Deutschmann: Vererbung v. erworb. Augenaffectionen. Zehender’s kl. Monatsbl., 
xviii., 1880. 

Fischer: Ueber hereditäre multiple Exostosenbildung. Dtsch. Zeitschr. f. Chir., 
xii.. 1880. 

Grandidier: Die Hämophbilie. ii Aufl., 1877. 

Griesinger: Die Pathol. u. Ther. der psych. Krankheiten, 7 Aufl.. 1892. 

Gutzmann: Vererbung v. Sprachstörungen. Deut. med. Woch., 1898. 

Hagen: Statist. Unters. über Geisteskrankheiten, 1876. Ueber die Verwandtschaft 
des Genies mit dem Irresein. Allg. Zeitschr. f. Psych., xxxiü. 

Henle: Handbuch der rationellen Pathologie, i., Braunschweig, 1846. 

Herrmann: Die Vererbung v. path. Zuständen beim Pferde. Vortr. f. Thierärzte, 
viii., 1, 1885. 

Hössli: Geschichte und Stammbaum der Bluter von Tenna, Inaug.-Diss., Basel, 1885. 

Lossen (Bluterfamilie): Deut. Zeitschr. f. Chir., vii. 

Lucas, P.: Heredite naturelle, Paris, 1850. 

Mayer: Spalthand u. Spaltfuss (durch 4 Generat. vererbt.). Beitr. v. Ziegler, xxiüi., 
1898. 

Morel: De l’hérédité morbide progressive, Paris, 1867. 

v. Nathusius: Die Vorgiinge der Vererbung bei den Hausthieren, Berlin, 1891. 

Reinecke: Erblichkeit der multiplen Wachsthumsexostosen. Beitr. v. Bruns, viii, 
1891. 

Roth: Die Thatsache der Vererbung, Berlin, 1885. Der gegenwärtige Stand der 
Frage der Vererbung erworbener Eigenschaften. Wiener Klinik, 7 H., Wien, 
1890. 

Saury: Etude clin. sur la folie hereditaire, Paris, 1886. 

Sioli: Vererbung von Geisteskrankheiten. Arch. f. Psych., xvi., 1885. 

Sommer: Die Brown-Séquard’sche Meerschw einchenepilepsie. Beitr. v. Ziegler, 
xxvii., 1900. 

Thoma: Ueber einige senile Veränderungen des Körpers, Leipzig, 1884. 

Virchow: Gesammelte Abhandlungen, Frankfurt, 1856. Virch. Arch., 103 Bd., 1886. 

Weil: Die hereditäre Form des Diabetes insipidus. Virch. Arch., 95 Bd., 1884. 

Zander: Ist die Polydaktylie theromorphe Varietät oder Missbildung? Virch. Arch., 
125 Bd., 1891. 

Ziegler: Kénnen erworbene pathologische Eigenschaften vererbt werden u. wie 
entstehen erbliche Krankheiten u. Missbildungen? Beitr. v. Ziegler, i., 1886; Die 
neuesten Arbeiten ‚über Vererbungs- u. Abstammungslehre u. ihre Bedeutung f. 
d. Pathologie, ib., iv.. 1888. 

See aiso S 16 and x is 


$18. As has been explained in § 17, inherited diseases are always such as 
have at the very first developed from intrinsic causes, that is, from certain 
anlage in the germ-cells ; or at least are diseases in which the predisposition 
thereto is a congenttal characteristic. Conversely, the statement may be 
made that all normal or pathological qualities in the germ-cells are inheritable. 

Consequently, the questions as to the primary origin of inherited dis- 
eases are identical with the questions concerning the nature of the causes 
of intrinsie diseases—i.e., concerning the origin of those pathological 
qualities which we regard, when appearing later, as arising spontane- 
ously and dependent upon some congenital anlage. 

The first appearance of new pathological characteristics which are 
inheritable may be dependent upon the fact that as a result of sexual 
procreation—i.e., of the union of two sexual nuclei, one of which is the 
bearer of the transmissible qualities of the father, the other of those of 
the mother—new variations are constantly arising, so that the child is 





THE INHERITANCE OF PATHOLOGICAL CONDITIONS. 61 


never exactly like one parent; but, on the other hand, in addition to the 
qualities which the parents offer, it possesses also new qualities. Even 
if we assume that the sexual nuclei at times contain in potential form 
exactly the same characteristics as those of the parents, the product re- 
sulting from the copulation of these nuclei would present a certain 
degree of variation. In such a case, however, the differences between 
the children of such parents would be but slight. As a matter of fact, 
the different products of the same parents may show an infinite variety, 
by reason of the fact that the germ-cells themselves contain further a 
mixture of the transmissible characteristics of the paternal and maternal 
ancestors, and that this mixture is never the same in the individual 
germ -cells. 

In accordance with this is the fact that the children of a certain fam- 
ily always present important differences in both physical and mental 
qualities. A marked resemblance occurs only in the case of twins aris- 
ing from one egg—i.e., when the process of development of both chil- 
dren has started from the same act of copulation. 

The embryonal variations resulting from the mixture of two indi- 
vidually different hereditary tendencies can find their expression in 
the most varied qualities of the body and mind of the developing child. 
If these do not deviate in a marked degree from the characteristics which 
the different members of the family show, the conditions are regarded as 
normal and ordinarily receive no especial attention. If, on the con- 
trary, important differences of character are produced, the occurrence 
attracts greater attention; and, according to the value which it has for 
the individual concerned, is regarded at one time as something favor- 
able, at another time as something unfavorable, something pathological. 
When small, weak parents produce children who develop into large and 
strong individuals, or when the intellectual capacity of the children sur- 
passes that of the parents, the occurrence is regarded as favorable. If, 
as actually happens, a genius in any branch of human knowledge or skill 
suddenly appears within a family, without any evidence of an especially 
marked mental development in the ancestors, the phenomenon would 
attract general attention and be regarded as a fortunate event. But if, 
on the other hand, strong parents beget children who are weak or 
physically defective, or if they show a mental development inferior to 
that of their parents, or if they show a complete stunting of a part of 
their mental faculties, the newly appearing variation is regarded as abnor- 
mal, pathological. oo. 

If we consider the experiences which the pathology of man and ani- 
mals furnishes, the assumption seems fully warranted that of the 
transmissible pathological conditions and predispositions, very many, 
perhaps the majority, are referable to a variation of the germ based 
upon the amphimixis. For example, the group of hereditary patho- 
logical conditions and predispositions of the central nervous system, 
hereditary myopia, hemophilia, pigmentation of the retina, and poly- 
dactylism may arise in this manner. If such abnormal characteristics 
show themselves repeatedly in the children of the parents, who are them- 
selves normal and have healthy ancestors, it may be assumed that the 
germ-cells of the parents, though individually normal, have through 
their union given rise to a pathological variation. This hypothesis be- 
comes substantiated when one or both parents produce normal offspring 
through copulation with other individuals. 

Besides the variations which are the result of normal sexual repro- 


62 THE INTRINSIC CAUSES OF DISEASE, 


duction, it is very probable that pathological germ-variations which lead 
to the development of transmissible pathological qualities may also arise 
through the action of injurious influences upon the sexual nuclei or the 
segmentation nucleus; or else that the process of copulation—that is, 
the union of the sexual nuclei—has been disturbed in some manner. 
The injurious substance may be a body-product, or it may come from 
without, and at the same time also produce its harmful effects upon the 
body. Consequently, in these cases we may speak of the acquiring of a 
transmissible pathological characteristic through the action of an extrinsic in- 
jurious influence. This does not mean, however, as has been accepted by 
many, that the tissues of the body, under the influence of extrinsic 
harmful influences, first suffer changes in themselves, and then transfer 
these changes to the germ-cells. It is to be believed, rather, that the 
harmful influence acts directly upon the sexual nuclei or the segmenta- 
tion-nucleus, producing in these a change of some kind, which later leads 
to a pathological development of the individual developing from the im- 
pregnated egg. It is a matter of no importance, so far as the nature of 
the resulting pathological variation is concerned, whether the somatic 
tissues also suffer changes, or of what nature such changes may be. 

If a transmissible pathological characteristic arises, it may, in case it 
does not. affect life or prevent reproduction, actually be transmitted, al- 
though this does not necessarily follow. The chances that a particular 
characteristic will be transmitted are greatest when both parents possess 
the same quality, as, for example, when both parents are affected with 
hereditary deaf-mutism or with near-sightedness. If the characteristic 
is wanting in one parent, there is produced most frequently a new germ- 
variation, in which the pathological characteristic fails entirely to mani- 
fest itself, and in the following generations may completely disappear. 
If several descendants are begotten, the pathological characteristic, in 
case it is not wholly lost, may show itself in only a few of the descend- 
ants, and in these in either a modified or in an aggravated form. Not 
rarely it happens that the characteristic remains latent in one generation 
—that is, is confined to the sexual cells, and appears again in the second 
generation. 


There seems to me to be no doubt that, through the copulation of two sexual 
nuclei possessing different hereditary tendencies, variations may be produced, and that 
among these there may be some which are to be regarded as pathological. It is more 
difficult to answer the question whether, besides these, there are not also transmissible 
variations of a pathological nature, which arise through influences which affect the 
sexual nuclei or the segmentation-nucleus; and further, if we accept the existence of 
such variations, with what frequency do they occur, Weismann, according to his most 
recently published statements, holds the opinion that the bssis of transmissible varia- 
tions is to be found, not in the amphimixis, but rather in the direct action of external 
influences upon the sexual nuclei. Starting from the assumption that the variable 
cells or cell-groups derived from the germ (by him designated as hereditary pieces or 
determinates) are represented in the germ-plasma by special particles, which are formed 
by the grouping together of a number of life-trophoblasts or biophores (molecular groups 
which represent the smallest units of life), and which he calls determinants or determin- 
tng pieces, he believes that he is warranted in ascribing the transmissible variation 
primarily to the changes produced by external influences in the determinants or group 
of determinants contained within the nuclear chromatin, so that finally the hereditary 
pieces or determinates derived from them also suffer changes. He believes that suc 
an influence might be exerted by excessive nourishment of a determinant, causing it to 

row more rapidly. For example, he regards it as possible that many congenital mal- 
ormations (for example, an increase in the number of fingers and toes) can be referred 
to a reduplication of the deterininant-groups caused by increased supply of nourish- 
ment. According to Weismann, the amphimixis has only a secondary influence in the 
origin of a permanent variation, in that it mixes in constantly new manner the varia- 


THEORIES OF INHERITANCE. 63 


tions dependent upon the changes in the determinants, but does not in itself produce 
new variations. “The deviations which the determinants suffer through unequal con- 
ditions of nutrition constitute the material out of which, through amphimixis in con- 
nection with selection, the visible individual variations are produced, through whose 
increase and combination new forms arise.” 

I agree with Weismann in so far as the assumption that the appearance of a new 
variation of pathological nature is in part to be referred to changes in the determinants 
contained within the sexual nuclei, due to the direct action of extrinsic influences. I 
do not, however, believe that there is sufficient ground for attributing, as does Weis- 
mann, the formation of new separate parts to an over-nourishment of single groups of 
determinants. Such a dependence of the germ-plasma upon the surrounding nutritive 
matcrial seems to me scarcely conceivable, and is opposed to all views hitherto held re- 
garding the nutrition of cells. Not only quantitative but much rather qualitative 
changes of the food-material would appear to be necessary in order to produce changes 
in the organization of the determinants. Further, I hold that the amphimixis has not 
only a secondary but much more a primary significance with regard to the origin of 
pathological variations, in the sense that it itself is able to produce new variations. 

nally, it seems to me that we cannot at the present wholly set aside the hypothesis 
of Naägeli, according to which the idioplasm is capable of altering its own condition, 
from within outward, in certain fixed directions and according to certain fixed laws, 
and thus may produce new characteristics. 


Literature. 
( Theories of Inheritance. ) 


Ackermann: Mechanismus u. Darwinismus in der Pathologie, Halle, 1884. 

Adami: New York Medical Journal, June 1, 1901. 

van Bemmelen. Die Erblichkeit erworbener Eigenschaften. Biol. Centralbl., x., 
1891. 

Bigelow: Heredity. Reference Handbook of Med. Sciences, 2d ed. 

Bonnet: Die stummelschwänzigen Hunde. Beitr. v. Ziegler, iv., 1888. 

Born: Pfliger’s Arch., xxxii.; Bresl. ärztl. Zeitschr., 1884; Arch. f. mikr. Anat., xxiv. 


1885. 
Boveri: Geschiechtl. erzeugter Organismus ohne mOtterl. Eigenschaften. M. med. 
Woch., 1889. 


Darwin: Das Variiren der Thiere u. Pflanzen, Stuttg., 1873; Die Abstammung des 
Menschen, Stuttgart, 1878; Ges. kl. Schriften v. Ch. Darwin, her. v. Krause, 
Leipzig, 1886. Origin of Species; The Descent of Man. 

Delage: La structure du protoplasma et les théories sur l’heredite, Paris, 1895. 

Eimer: Die Entstehung der Arten, Bd. i., Jena, 1888. 

Emmery: Gedanken zur Descendenz- u. Vererbungstheorie. Biol. Centralbl., xiii., 
1893. 

Galton: Hereditary Genius, London, 1892. 

Hallervorden: Biologische Interferenz u. Erblichkeit. Virch. Arch., 144 Bd., 1896. 

Hartog. Grundzüge d. Vererbungstheorieen. Biol. Cbl., xviii., 1898. 

Hegar: Der Geschlechtstrieb, Stuttgart, 1894. 

Hering: Ueber die individuelle Verschiedenheit des Farbensinns. Prag, 1885. 

Hertwig. O.: Das Problem d. Befruchtung u. d. Isotropie des Eies, eine Vererbungs- 
theorie, Jena, 1884; Exper. Studien am thierischen Ei vor, während u. nach d. 
Befruchtung, Jena, 1890; Entwickelungsgeschichte, Jena, 1898; Präformation 
oder Epigenese? Zeit- u. Streitfragen der Biologie, i., Jena, 1894. 

His: Unsere Körperform, 1874. 

Israel: Angeborene Spalten der Ohrläppchen. Virch. Arch., 119 Bd., 1890. 

Klaatsch: Das Problem d. Vererbung m. Ricks. auf d. Pathol. Münch. med. 
Woch., 1898. 

Kölliker: guedeutung d. Zellkerne f. d. Vorgänge d. Vererbung. Zeit. f. wiss. Zool., 
xlii.. 1885. 

Minot: Vererbung u. Verjüngung. Biol. Centralb., xv., 1895. (See also Original 
Papers in English.) 

v. Nägeli, C.: Mechanisch-physiol. Theorie der Abstammungslehre, München, 1884. 

Ortmann: Ueber Keimvariation. Biol. Cbl., xviii., 1898. 

v. Rath: qpcrerbung von Verletzungen. Biol. Centralbl., xifi., 1883; Telogonie, ib., 
xv., 1895. 

Ribot: Die Vererbung, Leipzig, 189*. 


wg... ‘So Sap: 
1... 


= hin 22-2 2 22.000 


rm. way namen“ m TPS lee pp 


64 THE TRANSMISSION OF INFECTIOUS DISEASES TO THE FCETUS. 


Rohde: Gegenw. Stand d. Frage nach d. Entstehung ‘u. Vererbung individ. 
Eigensch., Jena, 1895. 

Romanes: Die geistige Entwickelung d. Menschen, Leipzig, 1898; Darwinist. Streit- 
fragen, 1895. 

Roux: Der Kampf der Theile im Organismus, Leipzig, 1881; Entwickelungsmechanik 
des Embryo, München, 1885; Die Entwickelungsmechanik der Organismen, Wien. 
1890. 

Sanson: L’heredite normale et pathologique, Paris, 1893. 

Schlatter: Gedanken über die Vererbung. Biol. Centralbl., xvi., 1896. 

Schäffer: Fötale Ohrformen u. Erblichkeit ders. Arch. f. ‘Anthrop., xxi., 1892; Die 
Vererbung, Berlin, 1898. 

Spencer: Unzulinglichkeit d. natürl. Zuchtwahl. Biol. Centralbl., 1893, 1894. 

Spitzer: Beiträge zur Descendenzlehre, Leipzig, 1886. 

Waldeyer: Befruchtung u. Vererbung. Verh. D. Naturforsch., Leipzig, 1897. 

Weismann: Aufsätze über Vererbung, Jena, 1892; Das Keimplasma, Jena, 1892; 
Allmacht der Naturzüchtung, Jena, 1893; Aeussere Einflüsse als Entwickelungs- 
reize, Jena, 1894; Neue Gedanken zur Vererbungsfrage, Jena, 1896; Ueber Ger- 
minalselection, Jena, 1896. 

Wiedersheim: Der Bau des Menschen, Freiburg, 1898. 

Wilkens: Vererbungslehre auf Grund thierzüchterischer Erfahrungen. Zeitschr. f. 
Thiermed., 18 Bd., 1891; Vererbung erworbener Eigenschaften. Biol. Centralbl., 
xiii., 1893. 

Wilser: Die Vererbung der geistigen Eigenschaften, Heidelberg, 1892. 

Ziegler: Können erworbene pathol. Eigenschaften vererbt werden? Beit. v. Ziegler, 

1886; Arb. üb. Vererbung u. ihre Bedeut. f. d. Pathologie, ib., iv., 1888. 
Soe also S$ 16 and 17. 


§ 19. In addition to the pathological conditions already mentioned, 
hereditary transmission appears to occur in the case of a few infectious 
diseases, particularly syphilis, smallpox, varicella, intermittent and re- 
current fever. At all events, cases are observed in which a child, at 
birth or shortly after, shows symptoms of the same disease from which 
the father or mother had been suffering either at the time of procreation 
or during gestation. Such a phenomenon is, however, entirely different 
from that already spoken of as a hereditary transmission. 

The infectious diseases are caused by organisms which multiply in the 
body. The transmission of the disease to the child becomes possible 
only when the micro-organisms causing the disease find their way into the 
sexual germ-cells, and then also into the impregnated egg, or else pene- 
trate from the maternal organism into the tissues of the child during its 
intra-uterine development. The latter can occur as long as the child re- 
mains in the uterus, and we must therefore assume that the infecting 
organisms pass through the decidual membranes and the outer coverings 
of the ovum—in the later stages of pregnancy through the placenta—and 
so are transported from the maternal to the foetal organism. It is also 
possible that when cohabitation is continued after pregnancy, the micro- 
organisms, Which may enter the vagina with the sperm, may penetrate 
into the uterus and thence into the impregnated egg. 

The transmission of infectious diseases to the foetus is beyond all 
doubt a possible occurrence. In the case of syphilis this may take place 
at the moment of impregnation as well as later during the course of 
intra-uterine development, so that syphilis may be transmitted to the 
child by the father as well as by the mother. In the case of smallpox, 
endocarditis, scarlet: fever, many instances of the infection of the foetus 
in utero have been observed; and from recent observations and experi- 
mental investigations there can be no doubt that anthrax-bacilli, pus- 
cocci, and pneumococci, and under certain conditions also typhoid-bacilli 
and tubercle-bacilli can pass through the placenta to the fetus. This 
can only occasionally occur, when the bacteria gain entrance to the 


THE TRANSMISSION OF INEECTIOUS DISEASES TO THE FCETUS. 65 


blood-channels of the placenta and are able to multiply there and to 
penetrate into the foetal vessels, an event which is rendered possible 
chiefly by the damage done to the placental tissue by the multiplying 
bacteria, whereby the latter are able to pass through and also to multi- 
ply within the tissues of the placenta. 

There are, therefore, both germinative and conceptional, also post- 
conceptional, intra-uterine infections, which constitute a pseudo-form 
of inheritance, in which the peculiar characteristics of the individual 
are not transferred to the embryo, but instead an organized poison finds 
its way into the germ or into the already developing foetus, where it in- 
creases and produces the same disease as that affecting the parent. 

Only of the transmission of disease from the mother to the fetus in 
utero do we possess a more exact knowledge. Germinative, paternal, 
and maternal transmission is known to occur only in syphilis, the spe- 
cific poison of which is not yet known tous. If syphilis is due, as is 
supposed, to a schizomycete, the specific organism, in cases of germina- 
tive infection, must at the time of the discharge of the sexual cells have 
been present either in the egg or spermatozoon. In the latter case, coin- 
cidently or immediately following impregnation, the micro-organisms 
gain eutrance into the egg, and remain there in a living state without act- 
ually hindering the further development of the ovum. It must further 
be assumed that the bacteria during the growth of the fotus pass into 
certain tissues and here later give rise to disease- processes. 


Literature. 


( Transmission of Infectious Diseases to the Fetus. ) 


Birch-Hirschfeld: Die Pforten d. placentaren Infection d. Fötus. Beit. v. Ziegler, 
ix., 1891. 

Blumer: Congenital Typhoid. Jour. Amer. Med. Assn., xxxv. 

Charrin et Gley: Rech. sur la transmission hereditaire de l’immunité. Arch. de 
phys., vi., 1894. 

Condorelli: Vaiuolo intrauterino in un feto, Catania, 1890. 

v. Düring: Hereditire Syphilis. Eulenb. encyklop. Jahrb., v., 1895 (Lit.). 

Eberth: Geht der Typhusorganismus auf den Fötus über? Fortschr. d. Med., vii., 


1889. 

Ehrlich: Ueber Immunität durch Vererbung und Säugung. Ztschr. f. Hyg., xii., 
1892. 

Ernst: Intrauterine Typhusinfection einer lebensfähigen Frucht. Beit. v. Ziegler, 
viii., 1890. 

Finger: Die Vererbung der Syphilis, Wien, 1898 (Lit.). 

Fournier: L’hérédité syphilitique, Paris, 1891. 

Kockel u. Lungwitz: Placentartuberkulose beim Kind. Beit. v. Ziegler, xvi., 1894. 

Latis: Uebergang des Milzbrandes von der Mutter auf den Fötus. it. v. Ziegler, 
x., 1891. 

Lubarsch: Ueber die intrauterine Uebertragung pathogener Bakterien. Virch. Arch., 
124 Bd., 1891.. 

Maffucci: Leb. d. Verhalten d. Embryo gegen Infection. Centralbl. f. allg. Path., 
v., 1894. 

Malvoz: Transmission interplacentaire des microorganismes, Ann. de l’Inst. Past., 
1888 and 1889. 

Morse: Fetal and Infantile Typhoid. Arch. of Ped., 1900. 

Weumann: Vererbung der Syphilis. Arch. f. Derm., xxiv., 1892. 

Porak: Du ge des substances a travers du placenta. Arch. de med. exp., 1894. 

Schmorl u. Kockel: Tuberk. der mensch]. Placenta. Beit. v. Ziegler, xvi., 1894. 

Straus et Chamberland: Transmission des maladies virul. de la mére au fetus. 
Arch. de phys., 1883. 

Wolff: Ueber Vererbung von Infectionskrankheiten. Virch. Arch., 112 Bd., 1888. 


5 


CHAPTER II. 


The Spread and Generalization of Disease Through- 
out the Organism. Autointoxications and 
Secondary Diseases. 


Il. Metastasis and Embolism and Their Significance in the Etiology 
of Lymphogenous and Hematogenous Diseases. 


§ 20. The transportation, through the blood or lymph-stream, of a disease- 
producing agent, and the production of disease at the point of deposit of such 
agent, is termed metastasis. This is one of the must common modes of 
the spread of disease throughout the body. Ordinarily the term metas- 
tasis is applied particularly to those cases in which the transportation of 
a given substance is followed by easily recognizable clinical and anatom- 
ical manifestations of disease, especially those of inflammation or tumor- 
formation, so that we are accustomed to speak of metastatic inflammations 
and metastatic tumors. There is, however, no good reason for not inelud- 
ing also under metastasis those cases of transportation of corpuscular 
elements through the lymph or blood stream in which the changes pro- 
duced by the transportation are less striking, and are recognizable only 
through a more careful anatomical or microscopical investigation. 

The term metastasis indicates further that. the substance deposited has 
arisen from some other known place within the body. If the source of 
the transported material is not known, or at least cannot be definitely 
located, we are accustomed to speak of lymphogenous and hematog- 
enous deposits and diseases. The same designation is also applied to 
deposits of known origin. 

The significance of metastasis is in all cases dependent upon the 
properties of the transported body. Insoluble bland foreign bodies of 
small size may have little effect upon the tissue; soluble and chemically 
active substances may, on the other hand, produce important tissue 
changes. Bacteria capable of reproduction may give rise to a disease 
which corresponds in general to that produced at: the primary focus of 
infection. Tumor-cells capable of growth may develop into a secondary 
tumor. The size of the transported body is of essential importance in 
hematogenous metastasis, in that small bodies may pass all the blood- 
vessels, even the capillaries, while larger ones will be carried only 
through those vessels whose lumen is sufficiently large to admit them. 
When the latter have by any means obtained entrance to the arteries of 
the greater or lesser circulation and are carried along by the blood- 
stream, they will become lodged at those divisions of the vessels where 
the vessel-lumen is too small to admit them, and will thereby more or 
less completely obstruct the vessel. This occurrence is designated by the 
special term embolism; the body blocking the vessel is called an em- 
bolus or a vessel-plug (Fig. 2, b,c). The effect of embolism is in gen- 
eral the more or less complete obstruction of the vessel, partly through 

66 


METASTASIS AND EMBOLISM. 67 


the embolus itself, partly through an associated coagulation of the 
blood. Asa result of such obstruction there is an interference with the 
circulation, which may vary greatly in different cases, in that behind the 
point of obstruction there may be established either a complete or partial 
compensatory circulation, or in other 
cases such a compensation may be en- 
tirely wanting. When the compensa- 
tion is incomplete or wholly absent, 
the area of tissue supplied by the ob- 
structed vessel undergoes degeneration 
or dies. 

Both lymphogenous and hemato- 
genous metastasis usually occur in the 
direction of the normal current, but 
under special conditions a transporta- 
tion in the opposite direction may take ria. 2.—Multiple emboli in the branches of 
place—retrograde metastasis. Such Hi? auncie. a, anérial branch: , embolus: 
a change of current in the lymph-vessels c, embolus with secondary thrombouis. j 
oceurs when the normal escape of 
lymph from the region involved is hindered through stoppage of the 
lymphatics, and the lymph is forced to seek other outlets. A similar 
condition may occur in circumscribed areas of the peripheral blood- 
vessels. In this way clots arising in the right heart or in the large 
veins of the body may be transported into the peripheral veins; par- 
ticularly under conditions in which there occur backward waves of 
blood which gradually force the clots back into the smaller veins. 
According to the experimental investigations of Arnold upon dogs, 
foreign bodies (wheaten grits), which were too large to pass the capil- 
laries, when introduced into the jugular or crural veins, as well as into 
the longitudinal sinus of the dura mater, were carried by retrograde 
metastasis not only into the main trunks, but also into the smallest 
branches of the veins of the liver, kidneys, heart, extremities, dura 
mater, pia mater, and orbit, as well as into the posterior bronchial veins. 

In the case of a defect in the septum of the heart, bodies circulating 
in the blood may pass directly from one side of the heart to the other, 
and thereby give rise to a crossed or paradoxical embolism. 

§ 21. The substances which may be transported in the process of 
metastasis may be conveniently divided into six groups, this classifica- 
tion being based partly upon the origin, partly upon the character of the 
transported body, and partly upon the effects of the metastasis. 

In the first group are placed insoluble lifeless substances composed of 
very small particles, which enter the body from without, and which may 
be designated collectively as dust. The majority of these substances 
enter the body in the respired air, and pass from the lungs into other tis- 
sues. A smaller part may enter the tissues directly through accidental 
or intentional wounds (tattoo). Most frequently these substances are 
particles of soot, coal- and stone-dust, more rarely metal, porcelain, 
tobacco, hair, or other kinds of dust. In tattooing of the skin, soot, cin- 
nabar, and other granular pigments are used. 

The behavior of the tissues of the body toward such substances will 
be treated of elsewhere; it is only necessary to mention here that these 
forms of dust, sometimes in a free state, sometimes enclosed within cells, 
are deposited first in the tissues nearest the point of entrance, further in 
the Iymph-vessels and lymphatic glands. In the latter location they 











70 THE SPREAD OF DISEASE THROUGHOUT THE BODY. 


of the body and thence to the heart, the fat-droplets collect especially in 
the capillaries of the lungs (Fig. 3, 6); but they may also pass through 
the lungs into the capillaries of the greater circulation, and are then 
found especially in the intertubular and glomerular capillaries of the 
kidneys (Fig. 4, a, 6), and also to some extent in the capillaries of the 
brain. Capillary fat-embolism causes a noticeable disturbance of the 
circulation only when of extensive occurrence; in this case it: may lead 
to the production of edema. Furthermore, the fat disappears in the 
progress of metabolisın. 

Parenchymatous cells (in so far as the entrance into the circulation 
of small living cells of the character of lymphoid cells is not concerned) 
become lodged in the capillaries or smaller arteries in the case of arterial 
metastasis. The latter is especially true of liver-cells when entering the 
circulation en masse. At the place of lodgment the presence of paren- 
chymatous cells may lead to a heaping-up of blood-plates and a hyaline 
coagulation; this is particularly true of liver-cell emboli. The cells 
themselves do not multiply, but they may remain preserved for a certain 
length of time; according to Lubarsch, as long as three weeks. They 
then gradually die, the protoplasm dissolves, the nuclei swell or shrink, 
and finally lose their chromatin. In the case of multinuclear cells the 
dissolution is preceded by a clumping of the nuclei. 

The point of lodgment of loosened thrombi or fragments of thrombi 
depends upon the path which they take, as well as upon their size. 
Since thrombi may be formed in the systemic veins, right heart, and 
pulmonary arteries, as well as in the pulmonary veins, left heart, and 
systemic arteries (see Chapter IV.), it is possible for embolism to occur 
in any of the arteries of the greater or lesser circulation. Very often 
the emboli fodge at the bifureation of arteries, forming the so-called 
riding or straddling emboli (Fig. 2, c). Through retrograde metastasis 
emboli may be carried from the vene cav:e or larger veins into the 
smaller veins. Defects in the septum of the heart may lead to the pro- 
duction of a paradoxical embolism. 

Small fragments of thrombi, dead red blood-cells or fragments of 
such, endothelial cells undergoing disintegration or fatty degeneration, 
ete., meet the same fate as dust-particles. They may remain free or be 
taken up by cells; they are soon removed from the circulation and col- 
lect: especially in the spleen, liver, and bone-marrow, where they un- 
dergo further ehanges and are destroyed. The products resulting from 
the destruction of red blood-cells may persist for a long time in the or- 
gans named, as colored or colorless deposits. 

The third group of substances producing metastases 1s composed of 
living cells, which, originating from proliferating tissue-foci and hav- 
ing pained entrance to the circulation through direct rupture into the 
blood-vessels, or having entered the lymphatics, are carrried to other or- 
gans. This process may be observed in the case of tumors growing by 
infiltration. The metastasis of living cells from such a tumor leads 
through the proliferation of the transported tumor-cells to the produc- 
tion of metastatic daughter-tumors, which in the case of lymphogenous 
metastasis develop first in the Ivmph-vessels and lymph-glands, but in 
the case of direet rupture into the blood-vessels arise in that part of the 
vascular system to which the tumor-cells are carried by the blood. The 
metastasis usually oeeurs in the normal direction of the blood- and Iymph- 
streams, but retrograde transportation may also oceur, whereby a tumor 
which has broken into one of the systemic veins may give rise to metas- 


METASTASIS AND EMBOLISM. 71 


tases in the region drained by smaller branches of other systemic veins. 
Retrograde metastasis is not infrequently observed in the lymphatic sys- 
tem, when closure of the efferent lymph-channels has produced a change 
in the direction of the lymph-current. 

In the fourth group may be placed all those processes characterized 
by the entrance of vegetable or animal parasites into the circulation. 
If under such circumstances these organisms do not find conditions suit- 
able for their development, they are quickly eliminated from the blood- 
stream and destroyed under the influence of metabolic processes. But 
if they are able to reproduce themselves anywhere, they will give rise to 
the production of metastatic foci of infection, which are located partly 
in the vascular system, but also partly extending thence into the neigh- 
boring tissnes. The secondary foci in the case of bacterial invasion 
have in general the same character as that of the primary. If an em- 
bolus contains organisms capable of producing tissue-necrosis, inflam- 
mation, and putrid decomposition, there will occur, along with the 
embolism and the accompanying disturbances of circulation, suppuration 
and sloughing—that is, there will be a repetition of the same processes 
occurring at the original seat of infection. 

As the fifth group of metastatic processes may be classed together 
those cases in which constituents of the human body having under- 
gone solution are transported in the soluble state and again deposited 
in a solid form ; and also those in which extrinsic substances are 
taken up by the body in a soluble form and are then deposited in the 
tissues in a solid state. Of the first class there occurs most frequently 
the resorption of bile-pigments into the circulation within the liver, so 
that these may permeate through the most varied tissues, and at the 
same time give rise to granular or crystalline deposits of bile-pigment. 
Not infrequently soluble derivatives arising from the destruction of red blood- 
cells in the circulation are deposited in the form of droplets, granules, and 
erystals in the spleen, bone-marrow, liver, and kidneys. Further, soluble — 
derivatives of hemoglobin may be taken up by the lymph and blood from 
hemorrhagic foci, and deposited in different organs. 

When preparations of silver are, for medicinal purposes, introduced 
into the body through the gastro-intestinal tract for long periods of time, 
there may occur a deposit of fine granules of silrer in the connective tis- 
sue of the skin, in the glomeruli, medullary pyramids of the kidneys, 
intima of the large arteries, adventitia of the small arteries, in the neigh- 
borhood of mucous glands, connective tissue of the intestinal villi, in the 
choroid plexus of the cerebral ventricles, aud in the serous membranes. 
Tissues showing such 4 deposit have a grayish-brown color. 

The fact that the epithelial tissues and the brain are not affected 
shows that there is a selective action on the part of the tissues, and that 
this selective action differs essentially from that which is seen in the case 
of a metastatic deposit of corpuscular clements. It may therefore be as- 
sumed that the chemico-physical character and the functional activity of 
the tissues coming into contact with substances in solution exert a deter- 
mining influence upon the separation and precipitation of such sub- 
stances. 

Asa sixth group of metastatic processes may be classed the entrance 
of air into the circulation. If in any manner a large amount of air 
gains entrance to the right heart, an event: which occurs especially 
in case of injury to the large veins lying in the neighborhood of the 
thoracic cavity, or more rarely from the opening of a vein, for example, 


12 THE SPREAD OF DISEASE THROUGHOUT THE BODY. 


of a stomach-vein, through ulcerative processes, the air mingling with 
the blood forms a foamy mass, which the contractions of the heart are 
scarcely able to drive onward. Asa result the left heart receives little 
or no blood, the aortic pressure falls, and the affected individual quickly 
dies. Should the air enter the circulation in small amounts or internit- 
tently, it may be carried by the blood-stream in form of air-bubbles and 
circulate through the entire body. Larger amounts may lodge for a time 
in the vessels of the major or minor circulation, obstruct their lumen, 

and cause disturbances of the circulation, which may give rise to func- 
tional disturbances of the brain and resp) ration. If these conditions do 
not cause death, the air is after a tiie resorbed. 

If the lung-tissue be ruptured through trauma or through violent 
coughing, screaming, or vomiting, ete., air may be forced into the con- 
nective-tissue spaces and lymphatics, and may extend through these 
into all parts of the lungs, pleurs, and the mediastinum, as well as into 
the skin. The conditions thus produced are termed emphysema of the 
skin, of the subcutaneous tissue, of the mediastinum, ete. Under cer- 
tain circumstances the air may spread through a large area of the sub- 
cutaneous lymph-vessels and connective-tissue spaces, whereby the skin 


presents a blown-up appearance and when pressed upon produces a 
crackling sound. 


Arnold, supported by numerous investigations, believes that the lymph-glands 
form a perfect filter for the dust carried to them, and that therefore metastasis of dust 
is possible only through the rupture of a lymph-gland into the blood-stream. In so far 
as the glands do not show too great structural changes, his view appears to me cor- 
rect; but in those cases in which the lymph-glands undergo softening, as a result of 
being overloaded with dust, portions of necrotic tissue containing dust may pass from 
the glands into the efferent lymphatics. 

As will be shown later (sce Inflammation), it is an invariable fact that wherever 
foreign bodies or dead tissue-masses lie in a living tissue, wandering-cells are sure to 
appear; and these, in so far as it is possible, take up into their substance more or less 
of the corpuscular material present. This material is then carried further, especially 
to the lymph-vessels and Iymph-glands. It is very probable that a portion of this 
material—in so far as it may be so utilized—serves as nourishment for proliferating tis- 
sue-cells. 

According to Stebel and Kunkel, granules of cinnabar and indigo injected into the 
blood-stream of a frog are quickly taken up by leucocytes, and after one to two hours 
no more free granules are to be found in the circulating blood. After twenty-four 
hours the leucocytes containing pigment-granules have disappeared from the circula- 
tion, and lie for the greater part clumped together in the capillaries, the greatest num- 
bers being found in the capillaries of the spleen, liver, bone-marrow, and the lungs, 
while they occur in smaller numbers in the capillaries of the kidneys, and in still smaller 
numbers in the capillaries of the heart-muscle. 

Even after two hours free pigment and cells containing granules are found outside 
of the vessels, and after a few days they have almost wholly disappeared from the ves- 
sels. The granules lie then partly in wandering-cells, partly in fixed cells, as well as 
in the free cells of the splenic pulp (Ponfick) and bone-marrow. They may be found 
in these organs for weeks afterward (Zioffmann, Langerhans). In both frogs and dogs 
some of the granule-containing cells find their way into the lumen of the alveoli and 
bronchioles and so pass out of the body. In the liver the pigment-particles for the 
greater part adhere for a short time to the endothelium of the liver-capillaries; another 
part is found in leucocytes, which later wander out from the vessels into the tissues. 
Thence they are for the greater part taken up into the lymphatics of the liver and ulti- 
mately reach the Iymph-glands, A part of the granules finally pass out with the bile, 
but by what course they reach the bile-vessels is not known. In dogs the pigment-- 
granules also collect in the tonsils and are carried to the surface through the epithelium 
by the leucocytes which have taken them up. 

According to the investigations of ron Kupffer, the endothelium of the liver-capil- 
laries (formerly designated as ‘the stellate-cells of Kuptler) possesses phagocytic proper- 
ties, and takes up small particles circulating in the blood-stream., 

According to the observations of Jadussohn (“Pigmentverschleppung aus der 


METASTASIS AND EMBOLISM. 13 


Haut,” Arch. f. Derm., 24 Bd., 1892) and Schmorl (“ Pigmentverschleppung aus der Haut,” 
Central. f. allg. Path., 4 Bd., 1893), both normal and pathological pigment may be 
transported from the skin to the lymph-glands—in other words, a pigment-metastasis 
may take place. 

According to Lewtn (Arch. f exp. Path., 40 Bd., 1897), if the outflow of urine from 
the bladder be hindered, small foreign bodies can pass into the kidney-pelves, and 
thence into the urinary tubules, lymph- -vessels, and veins, and into the general circula- 
tion. 


Literature. 
(Metastasis of Dust.) 


Arnold, J.: Staubinhalation u. Staubmetastasen, Leipzig, 1885; Die Geschicke des 
eingeathmeten Metallstaubes im Körper. Beitr. v. Ziegler, viii., 1890. 
Gaertner: Ucber die Beziehung des schwarzen Pigments in der Leber, Milz und 
Nieren zu den Kohlenstaubablagerungen. Inaug.-Diss., Strassburg, 1885. 
u. Langerhans: Verbleib des in ‘die Circulation eingeführten Zinnobers. 
Virch. Arch., 48 Bd., 1869. 
v. Kupffer: Sternzellen der Leber. Minch. med. Woch., 1899. 
Muscatello: Aufsaugungsvermögen d. Peritoneum. Virch. Arch., 142 Bd., 1895. 
Oekonomides: Ueber die chronischen Bronchialdriisenaffectionen. Inaug. -Diss., Basel, 
1882. 
Ponfick: Ueber die Schicksale körniger Farbstoffe im Organismus. Virch. Arch., 48 
Bd., 1869. 
v. Recklinghausen: Virch. Arch., 28 Bd.; Allgem. Pathol. d. Kreislaufs, Stutt- 
gart, 1883. 
Both: Metastasen von Kalk, Fett Kohlenstaub. Correspbl. f. Schweizer Aerzte, xiv., 
1884. 
Biebel: Ueber das Schicksal von Fremdkorpern in der Blutbahn. Virch. Arch., 104 
1886. . 
Slavjanski: Exper. Beiträge zur Pneumoconiosislehre, ib., 48 Bd., 1869. 
Sticker: Staubkrankheiten. Eulenburg's Realencyklop., xxiii., 1900 (Lit.). 
Sulzer: Durchtritt corpuscul. Gebilde durch d. Zwerchfell. Virch. Arch., 143 Bd., 
1896. 
Weigert: Kohlenstaubmetastase. Fortschr. d. Med., i., 1883. 
Weintraud: Ueber Kohlenstaubmetastase. Inaug. Diss, Strassburg, 1889. 


(Embolism of Fat and of Parenchymatous Cells. ) 


Arnold: Uebertritt v. Knochenmarkzellen ins Blut. Virch. Arch., 140 Bd., 1895. 

Aschoff: Capilläre Embolie von riesenkernhaltigen Zellen. Virch. Arch., 134 Bd., 
1893. 

Beneke: Fettembolie. Beitr. v. Ziegler, xxii., 1897. 

Colley: Fettembolie nach gewaltsamer Gelenkbeugung. Zeitschr. f. Chir.,- 36 Bd., 
1893. 

Ebstein: Lipämie u. Fettembolie bei Diabetes. Virch. Arch., 155 Bd., 1899. 

Flournoy: Contrib. a l’etude de l'embolie graisseuse, Strassburg. 1878. 

Haemig: Fettembolie des Gehirns. Beitr. v. Bruns, 27 Bd., 1900. 

Hamilton: Lipxmia and Fat Embolism. Edinburgh Med. Journal, 1879. 

Hess: Beitr. z. d. Lehre v. d. traumatischen Leberrupturen. Virch. Arch., 121 Bd., 
1890. 

Jürgens: Fettembolie u. Metastase v. Leberzellen. Tagebl. d. Naturf.-Vers. in Ber- 
lin, 1886. 

Klebs: Multiple Leberzellenthrombose. Beiträge v. Ziegler, iii., 1888. 

Leusden: Puerperale Eklampsie. Virch. Arch., 142 Bd., 1805. 

Lubarsch: Parenchymzellenembolic. Fortschr. d. Med., 1893; Zur Lehre von 
den Geschwülsten u. Infectionskrankheiten, Wiesbaden, 1889. 

Maximow: Parenchymzellenembolie. Virch. Arch., 151 Bd., 1898. 

v. Recklinghausen: Aligem. Pathologie d. Kreislaufs, Stuttgart, 1883. 

Ribbert: Fettembolie. Correspbl. f. Schweizer Acrzte, 1894. 

Schmorl: Embol. Verschleppung v. Lebergewebe. Deut. Arch. f. klin. Med., 42 Bd., 
1888, Organbefunde bei Eklampsie. Cent. f. allg. Path., ii.; Unters. tib. Puerpe- 
raleklampsie, Leipzig, 1898. 

Scriba: Fettembolie. Deut. Zeitschr. f. Chir., 1879. 

Turner: Hepatic Cells in the Blood. Trans. of the Path. Soc. of London, 1884. 


14 THE SPREAD OF DISEASE THROUGHOUT THE BODY. 


Virchow: Berl. klin. Woch., 1886, No. 30; Virch. Arch., 5 Bd.; Ges. Abhandlungen, 
1856. 

Warthin: Pulmonary Emboli of Liver-cells and Bone-marrow Giant-cells. Med. 
News, 1900. 

Zenker: Schussverletzung d. Leber mit Verschleppung v. Lebergewebe. Deut. Arch. 
f. klin. Med., 42 Bd., 1888. 


( Metastasis of Lime-Salts. ) 


Chiari: Verkalkung d. Lunge. Wiener med. Wochenschr., 1878. 

Küttner: Ueber Kalkmetastase. Virch. Arch., 55 Bd., 1872. 

Litten: Ueber pathol. Verkalkungen u. Kalkmetastase in den Nieren. Virch. Arch., 
82 Bd., 1881. 

Prévost: Revue med. de la Suisse rom., 1882. 

Roth: Metastat. Herzverkalkung. Correspbl. f. Schweizer Aerzte, 1884. 

Virchow: Kalkmetastasen. Virch. Arch., 8 Bd., 1855. 


(Retrograde and Paradoxical Metastasis. ) 


Arnold: Ueber rückläutigen Transport. Virch. Arch., 124 Bd., 1891. 

Bonome: Trasporto retrogrado degli emboli e embolia crociata. Arch. per le Sc. 
Med., xiii., 1889. 

Cohn: Klinik der embolischen Gefässkrankheiten, Berlin, 1860. 

Cohnheim: Vorlesungen über allgemeine Pathologie, Berlin, 1882. 

Ernst: Itückläuf. Transport in Herz- u. Lebervenen. Virch. Arch., 151 Bd., 1898. 

Hauser: Embol. Verschleppung v. Thromben a. d. r. Herzen in Körperarterien. 
Münch. med. Woch.. 1888. 

Heller: Metastatische Processe in der Leber. Deut. Arch. f. klin. Med.. 7 Bd., 1870. 

Litten: Ueber embolische Muskelveränderungen. Vireh. Arch., 80 Bd., 1880. 

Lui: Due casi di embolia retrograda. Arch. p. le Sc. Med., xviii., 1894. 

v. Recklinghausen: Venöse Embolie u. retrograder Transport. Virch. Arch., 100 
Bd., 1880. 

Ribbert: Retrograder Transport im Venensystem. Cbl. f. allg. Path., 1897. 

Schmorl: Leberruptur mit embol. Verschleppung v. Lebergewebe. Deut. Arch. f. 
klin. Med., 42 Bd., 1888. 

Vierth: Rückläufige Metast. in den Lymphbahnen. Beitr. v. Ziegler, xviii., 1895. 

Vogel: Retrograde Metastase innerh. d. Lymphbahn. Virch. Arch., 125 Bd., 1891. 

Zahn: Paradoxe Embolie. Virch. Arch., 115 Bd., 1889; Geschwulstmetastase, ib., 
117 Bd., 1890. 


(.Lir Embolism. ) 


Couty: Etude exper. sur l'entrée de lair dans les veines. Gaz. méd. de Paris, 1878. 

Damsch: Ueber Unterhautemphysem bei Bronchopneumonie. Deut. med. Woch., 
Fischer: Lufteintritt in die Venen während einer Operation. Deut. Chir., Lief. 18, 
Frantzel: Unterhautemphysem bei Erkrank. dl. Respirationsapparates. Deut. med. 
Hare. Entrance of Air into Veins. Therapeutic Gaz., 1889; Amer. Jour. of Med Se., 


1902. 

Hauer: Erscheinungen im gr. u. kl. Kreislauf bei Luftembolie. Zeit. f. Heilk., xi., 
SOO. 

Heller, Mager, u. v. Schrötter: Arterielle Luftembolie. Zeit. f. klin. Med., 32 Bd.. 
1807, 


Husemann: Luftembolie. Euwlenburg’s Jahrb., viii., 1899. 

Jürgensen: Lufteintritt in d. Venen. Deut. Arch. f. klin. Med., 81 Bd.; Luft im 
Blüte, ib., 41 Bel., 1887. 

Panum: Exper. Beiträge zur Lehre von der Embolie. Virch. Arch., 25 Bd., 1862. 

Passet: Ucher Lufteintritt in die Venen. Arbeiten a. d. path. Institut zu München, 
INS6. 

Senn: Entrance of Air into Veins. Trans. Amer. Surg. Assn., 1885. 


SECONDARY AND GENERAL DISEASES. 15 


il. Secondary Local and General Diseases. Autointoxication. Diseases 
Caused through Disturbances or Cessation of Gland-Functions. 


§ 22. If through the action of any injurious agent a local tissue- 
change is produced, there occurs first a primary local disease or organ- 
disease, which is accompanied by a disturbance of function of the 
affected part. If the injurious agent passes into the body-juices and 
into the blood without causing noticeable changes at the point of en- 
trance, while within the body it gives rise to local changes, the result- 
ing condition may be designated as a solitary or multiple lymphogenous 
or hematogenous local disease or organ-disease. 

Local diseases may during their entire course remain confined to the 
organ originally affected, yet very frequently they lead to further sec- 
ondary diseases of organs or to a general disease. 

The first method by which disease-processes spread through the body is 
through metastasis, already described (§$ 20 and 21), by means of which 
there are very frequently formed, not only solitary, but innumerable foci 
of disease throughout the body. Not infrequently there may occur such 
a generalization of disease by way of the blood and lymph-channels (tuber- 


culosis, suppurations, and carcinomatous growths), that the majority of -— 


the organs will be found to be affected and show correspondingly more 
or less easily recognized functional disturbances. 

A second method of the spread of disease occurs in those diseases in 
which in the primary foci there are formed toxic products which, taken 
up into the lymph and blood, produce such changes in different organs 
that they must be regarded as intorications by poisonous substances arising 
from diseased foci. This intoxication is, as shown in § 12, of very com- 
mon occurrence in the infectious diseases, aud leads not only to secondary 
degenerations of organs, but much more to the picture of a more or less 
severe general disease, as shown by general disturbances of metabolism, 
fever, and disturbances of the central nervous system. 

A third form of the spread of disease-processes throughout the body 
becomes possible by reason of the fact that the integrity and norınal 
fuuctional capacity of many organs are toa great measure dependent 
upon the function of other organs; and, further, upon the fact that the 
organism needs, for the preservation of its normal condition, the perfect 
functional working of its organs, and in the case of many organs cannot 
permanently dispense with their functions. There is, therefore, a large 
group of local and general diseases which arise as the result of the imperfect 
functional activity of this or that organ. 

A fourth mode of origin of secondary diseases is through autointo.rica- 
tion—that is, through a poisoning of the organism by substances which arise 
in the body itself through its own activity (metabolic poisons). The place of 
origin of these substances is in part the intestinal tract (enterogenous 
poisons), and partly the tissues (histogenous poisons). The cause of the 
poisonous action of these products of metabolism lies partly in the fact 
that they are produced in an increased amount or are retained within the 
body as a result of disease of certain glands; partly also that they are 
not transformed to non-poisonous bodies, as is the case under normal 
conditions. In conditions of disturbed metabolism poisons foreign to 
the normal body may be produced. 

Disturbance of the function of different glands may cause, in addition to 
autointocication, other manifestations of disease. 


16 THE SPREAD OF DISEASE THROUGHOUT THE BODY. 


8 23. Secondary diseases which arise as the results of patho- 
logical conditions of individual organs occur with great frequency as 
the result of pathological changes in the blood and circulatory apparatus. 

The circulatory apparatus and the blood therein coutained bear cer- 
tain relations to all the body-tissues, and aceordingly diminution in 
amount and pathological alterations of the blood, as well as changes of the 
blood-vessels, often give rise to diseased conditions of this or that tissue 
or of the entire organism. If the hwemoglobin-content of the blood is 
decreased through a diminution in number of the red blood-cells 
(oligocythemia), or through a pathological condition of the same, or if 
the hemoglobin through the action of carbon monoxide is rendered in- 
capable of taking up the oxygen of the air, the body-tissues will no 
longer receive a hormal amount of oxygen; consequently there will arise, 
in case the amount of oxygenation falls below a certain point, disturb- 
ances of nutrition, as the results of which there occur very frequently 
conditions of fatty degeneration, and under certain circumstances death 
through paralysis of the nervous centres. 

Should an artery become narrowed or closed through thrombosis or em- 
bolism, or thickenings of its walls, as in the case of the arterial disease 
known aswrterioselerosis, there will arise in the region supplied by the 
affected vessel a local deficiency of food-supply and oxygen, local as- 
phyxia, and later degenerative processes, which frequently end in the 
death of the specific parenchymatous elements, at times also of the con- 
nective-tissue framework. — ~ er sr. at 

In the brain and spinal cord the vessel-changes lead to ischemic proc- 
esses of softening, which frequently result in paralysis, and not rarely 
in death. In the heart there results a diffuse fatty degeneration or local 
softening of the heart-musele, giving rise to disturbances of cardiae ac- 
tivity or often even to complete insufficiency. In the kidneys the secret - 
ing glandular parenchyma, together with a portion of the connective 
tissue, undergoes necrosis or atrophy; and the loss of these substances 
gives rise to local or widespread contractions, which, according to their 
origin, are designated as embolic or arterioselerotie atrophies. 

In the stomach ischemia of the mucous membranes gives rise to local 
ulcerations; in the liver and muscles to atrophie conditions. No tissue 
‘an Withstand the harınful effects of a Jong-econtinued ansemia, and con- 
sequently the narrowing and closure of arteries, through the formation 
of clots or through changes in the vessel-walls, play a very important 
röle in pathology; and are not only the causes of anemic necrosis (see 
Chapter V.) and hemorrhagic ‘infarction (see Chapter IV.), but also of 
numerous progressive atrophics of organs. Tn the pathogenesis of the last 
named, arteriosclerosis has an especially important part, since in old 
age it is of very common oceurrence, and gives rise to tissue-degenera- 
tions in organs of the most different structure. As evidences of such 
degenerative processes, the majority of the affeeted organs show later 
areas of sear-tissue, in which the speeifie parenchyma has disappeared 
while the connective tissue has increased. 

The active participation of the vaseular apparatus in all inflamma- 
tory processes (see Chapter VIT.), the disturbance of circulation through 
the alteration of the vessel-walls, the shifting and changes of the vascular 
channels which result from the closure of old vessels by proliferation of en- 
dothelium or through thrombosis, as well as from the formation of new 
ressels, make easily comprehensible the fact that in all chronic inflamma- 
tions the specific cells dependent upon a regulated nutrition undergo 


THE RESULTS OF LOCAL ORGANIC DISEASE. 77 


degeneration and are frequently replaced by connective tissue of a lower 
grade than normal. 

A profuse watery discharge from the intestines may deprive the or- 
ganism of water. If, asa result of stenosis of the wsophagus or pylorus, 
a sufficient amount of food is prevented from entering the intestinal 
tract, or if the stomach and intestine are no longer able to digest the 
food brought to them and to prepare it for assimilation into the body- 
juices, the organism as a whole becomes poorer in albumin and fat. 

If the heart is no longer able to force onward with normal strength 
the blood coming to it, there will arise in various organs changes due to 
venous stasis. If the respiration is hindered or imperfect, the composi- 
tion of the blood suffers changes. Collection of fluid in the thoracic 
cavity causes compression of the lungs; interference with expiration, 
with free inspiration, leads first to distention of the lung and later to 
atrophy. If a part of the lung has been rendered useless by chronic in- 
flammation, the inspiratory enlargement of the thorax affects only that 
portion of the lung which is capable of functionating, and this part be- 
comes over-distended and in consequence finally atrophic. 

Through enlargement of the liver the neighboring crgans are com- 
pressed ; diseases of the parenchyma of the liver give rise to disturbances 
of the circulation of blood through the organ, and stasis throughout the 
portal circulation with resulting ascites. «lv. 7 =; 

Hindrance to the outflow of urine from the ureters renders difficult 
the secretion of the kidneys and leads to their atrophy. The loss of a 
large portion of the parenchyma is followed by increased blood-pressure in 
the aorta, increased action of the heart, and hypertrophy of that organ. 

An increased resistance in the pulmonary circulation due to diseased con- 
ditions of the lungs is often followed by dilatation and hypertrophy of 
the right heart. Obstruction to the flow of blood through the aortic opening 
leads to hypertrophy of the left ventricle. Stenosis and insufficiency of 
the mitral valve cause a stasis of blood backward through the lungs to 
the right heart. This may be compensated for through hypertrophy of 
the right ventricle, or may extend farther back into the veins of the sys- 
temic circulation. 

An oblique position of the pelvis leads to curvature of the spine. Stiff- 
ness and immovability of a joint cause atrophy of the muscles moving the 
joint, the atrophy being due to inactivity. 

Diseases of the nervous system may give rise to functional disturbances 
and anatomical changes in any organ of the body—in glands, muscles, 
skin, bones, lung, heart, intestine, ete. These changes are to be referred 
partly to stimulation, partly to inhibition or arrest of nervous impulses, 
and partly to anesthesia (anesthetic tissues being especially lable to in- 
jury). Destruction of the large ganglion-cells in the anterior horns of the 
spinal cord leads to the atrophy of the corresponding peripheral nerves 
and muscles. Paralyzed extremities become atrophic. Diseased condi- 
tions in the region of the respiratory and vasomotor centres lead to dis- 
turbances of respiration and circulation. After injury to certain por- 
tions of the meduila oblongata, after concussion of the brain and spinal 
cord, through the presence of tumors in the brain, after psychical affec- 
tions, after poisoning of the nervous system, there is caused under certain 
conditions a rapid withdrawal of the glycogen of the liver into the blood- 
stream and the excretion of sugar in the urine. Stimulation of periph- 
eral nerves may produce abnormal reflex sensations and movements as 
well as circulatory disturbances in other parts of the body. Paralysis 


‚. 
ce ran NW 


18 THE SPREAD OF DISEASE THROUGHOUT THE BODY. 


of both vagi or of their branches, the recurrent laryngeal nerves, through 
inflammatory ehanges or through pressure from neighboring lymph- 
glands, ete., may be followed by inflammation of the lungs, in that the 
accompanying paralysis of the laryngeal muscles favors the entrance of 
foreign bodies into the lungs during inspiration. 


The so-called trophoneurotic diseases of the tissues are not mentioned above, for 
the reason that the trophic relations of the nervous system to the individual tissues are 
not yet clear, and the views of different authors as to the dependence of the tissues upcn 
the nervous system vary greatly. Many authors ascribe to the trophic action of the 
nervous system a far-reaching influence upon the conditions of the tissues, and seek the 
nerves forming the connections with the nerve-centres, partly in the motor, secretory, 
sensory, and reflex nerves, as well as in special trophic nerves. Thus, for example, 
muscular atrophy, glandular atrophy, atrophy of the bones and joints (in tabes and 
syringomyelia), different pathological conditions of the skin characterized by thinning, 
exfoliation of the epithelium, loss of hair, inflammations, etc., unilateral tissue- 
atrophies, necroses, also hypertrophic proliferations of muscles, glands, skin, or bones, 
etc., are all referred to affections of the nerves. 

It cannot be doubted that both degenerative and hypertrophic tissue-changes and 
inflammations often occur as sequel to disturbances of innervation, but these most 
probably are not the direct result of the removal or change of nerve-influences affecting 
the tissues, but are rather the results of increased or decreased functional activity of 
the tissue, or of injuries, inflammations, or disturbances of circulation, which have de- 
veloped in connection with the disturbances of innervation—for example, in connection 
with the loss of sensibility. Golz and Fırald, after completely destroying the thoracic 
and lumbar portions of the spinal cord of dogs, were able through great care to pre- 
serve the skin of the animals thus operated upon; they are, therefore, opposed to the 
theory of the existence of trophic centres and nerves. 


Literature. 
( Trophoneurotic Tissue-ckanges. ) 


Baldi: Action trophique du systéme nerveux. Arch. ital. de biol., xii., 1889. 

Charcot: Lecons sur les maladies du systöme nerveux. (Euvres completes, i.-iii. 

Déjerine ct Leloir: Alter. nerv. dans cert. cas de gangréne. Arch. de phys., 1881. 

Durdufi: Exp. Unters. z. Lehre v. d. trophischen Nerven. Cbl. f. allg. Path., v., 
1894. . 

Fränkel: Neurotische Angiosklerose. Wien. klin. Woch., 1896. 

Golz u. Ewald: Hund mit verkürzteın Rückenmark. Pflüger’s Arch., 63 Bd., 1896. 

Harbitz: Om de patologisk-anatom. Forundringer af neurotrofisk oprindelse, Chris- 
tiania, 1900. 

Hochenegg: Ucber symmetrische Gangrän, Wien, 1886. 

Joseph: Neurotische Hautgangrän. Arch. f. Derm., 31 Bd., 1895. 

Kopp: Trophoneurosen der Haut, Wien, 1886. 

Kriege: Vasomot. Störungen d. Haut bei traumat. Neurosen. Arch. f. Phys., 22 Bd., 
1890. 

Leloir: Rech. clin. et anatomo-pathol. sur les affections cutanées d’origine nerveuse, 
Paris, 1882. 

Pitres ct Vaillard: Gungrénes massives d'origine nevrotique. Arch. de phys., v., 
1885. 

v. Recklinghausen: Allg. Pathol. des Kreislaufs und der Ernährung, Stuttgart. 
1883; Multiple Fibrome d. Haut, Berlin, 1882; Akromegalie. Virch. Arch., 119 
Bd., 1890. 

Rosenbaum: Symmetrische Asphyxie. Eulenburg’s Jahrb., ii., 1892. 

Schlesinger: Syringomyelie, Wien, 1895. 

Schwimmer: Die neuropathischen Dermatosen, Leipzig, 18838. 

Springer: Dactylite hypertrophique symétrique. Rev. de méd., vii., 1887. 

Weir Mitchell: Des lésions des nerfs et de leur conséquences, 1874. 

Ziegler: Ursachen d. pathol. Gewebsneubildungen. Internat. Beitr. Festschr. f. Vir- 
chow, ii., Berlin, 1891. 


§ 24. Autointoxications or self-poisonings may take place in a 
variety of ways. In the first place, poisonous products of metabolism of 


AUTOINTOXICATION. 79 


normal character and produced in normal anıounts may fail of proper ex- 
cretion, and, being carried over into the juices of the body, may be 
retained in the same. Secondly, the physiological production of poisonous 
substances may be pathologically increased. Thirdly, it may happen that 
poisonous products of metabolism, which normally are decomposed and 
thereby rendered harmless, may, as a result of a local or general meta- 
bolic disturbance, escape such destruction. Finally, it may also happen 
that, as the result of pathological changes or cessation of the functional 
activity of certain organs, poisonous substances may appear in the blood and 
also in the urine. According to the place of origin poisons may be classed 
as enterogenous, arising in the intestine, and histogenous, arising in 
the tissues. 

If injurious products arising from the decomposition of albumin are 
retained or formed in excessive amounts in the intestinal canal, they may give 
rise to both local changes and a general intoxication. For example, 
through the action of the bacteria present in the intestines, the sul- 
phuretted hydrogen, arising from the sulphur of albuminous bodies, may 
be formed in such amount as to pass into the blood and impart its char- 
acteristic odor to the breath, and to be found also in the urine. Further, 
those to.rins especially which arise from the decomposition of albumin 
through the action of the intestinal bacteria, when taken up into the 
blood are able to produce symptoms of poisoning, vomiting, headache,. 
vertigo, stupor, acceleration and weakening of cardiac activity, ete. 
This action of toxins is especially marked in those cases in which the 
stomach or pancreas produces little or no enzyme, it being known that 
the enzymes have a neutralizing action upon certain toxins (see § 29). 
It is also probable that the tetany occurring rarely in dilatation of the 
stomach may be due to an autointoxication. 

If the function of the kidneys is disturbed to such a degree that the sub- 
stances convertible into urea are excreted in insufficient quantity, symptoms 
of intoxication may manifest themselves as the result of the retention of 
these substances. These symptoms are characterized by a condition of 
coma interrupted by convulsions and by disturbances of respiration—the 
symptoms collectively being designated as ureemia. According to von 
Limbeck, the retained substances have a narcotic action, the first effects 
of the narcosis being a dulling of sensibility and insomnia. According 
to Fleischer, the poison leads, through stimulation of the vasomotor cen- 
tre, to a vascular spasm, as a result of which the brain becomes very 
anemic. It has not yet been determined whether the toxic effects are 
due to a single element or to a mixture of substances. According to 
the investigations of Bohne, it is very probable that the retention of 
chlorides in the organism play the most important part in the production 
of this condition. 

It is very probable that the condition eclampsia, which is associated 
with convulsions, is also to be regarded as a result of changes in the kid- 
neys through which products of metabolism are retained within the or- 
ganism. 

Since many substances are excreted by way of the intestines, it is 
possible that under certain conditions a disturbed function of the intestines 
may render it difficult for the organism to rid itself of poisons and in 
this way lead to an autointoxication. Likewise, an excessive accumula- 
tion of carbonic acid within the blood, through some interference with the 
exchange of gases in the lungs, may cause symptoms of poisoning. 

When the excretion of bile from the liver is hindered or arrested, through 


80 AUTOINTOXICATION. 

some pathological condition in the bile-passages or in the liver itself, 
the elements of the bile are taken up into the blood, and the condition 
known as cholamia is produced. Both the biliary salts and bile- pigment 
enter the blood, and their presence in the circulation gives rise to gen- 
eral lassitude, depression, mental exhaustion, inclination to sleep, slow- 
ing of the pulse-rate, itching of the skin, and abnormal sensations of 
hearing and taste. The effects upon the heart, muscles, and central ner- 
vous system are ascribed to the bile-salts. These also possess a hemo- 
lytic action upon the red blood-cells. According to Bickel, ammonia- 
salts, leucin, and phenol must also be taken into consideration in the 
explanation of the symptoms. 

If the liver has undergone marked pathological changes, not only does 
the production of the bile as well as that of sugar and urea suffer, but 
certain substances brought to the liver from the intestines and normally 
decomposed by this organ may pass through it unchanged. Many be- 
lieve that at least the severe symptoms (conditions of mental excitement, 
delirium, lethargy, coma, and cerebral paralysis) which occur in degen- 
erations of the liver (ieterus gravis) are to be referred in part to the 
presence of such substances in the blood, and base their belief upon the 
fact that under such conditions abnormal substances (ammonium carbo- 
nate) appear in the urine. In degenerations of the pancreas, large 
amounts of dextrose, acetone, and aceto-acetie acid (see § 25) may ap- 
pear in the blood and .urine. The two last-named substances have a 
toxic action, and many are disposed to ascribe such symptoms to a dis- 
turbance of pancreatic function. Finally, after degeneration of the 
thyroid or adrenals (s$ 26 and 27), pathological symptoms arise which 
possibly may be explained in part by the assumption that, as the result 
of the degeneration of these organs, poisonous products of metabolism 
are no longer destroyed. 

In the constitutional disease known as gout, local deposits of meta- 
bolic produets, in the form of urates, give rise to local tissue-degenera- 
tions and inflammations. 


The term autointoxication is not used with the same significance by all writers, 
many of them giving to it a broader meaning than the one given above, and even ap- 
plying the term autointoxication to certain intoxications caused by pathogenic bacteria. 
In justification of such a view it may be said that the poisons in such cases arise for the 
greater part from component elements of the body. At the same time such a widen- 
ing of the significance of the term appears to me inexpedient, in that the cause of the 
decomposition lies not in the body itself, but comes from without, so that the intoxica- 
tion is the result of a preceding infection. It seems to me, therefore, to be more correct 
toapply the term autointoxication only to those forms of poisoning which are produced 
by products of metabolism, either under the influence of the activity of the body-cells 
or through the activity of bacteria constantly present in the intestine. As authoriza- 
tion for including the poisoning by products arising from intestinal decomposition 
among the autointoxications, I draw upon the fact that the intestinal bacilli which 
cause this decomposition are constant inhabitants of the intestine, and, according to the 
investigations of Sehottelius, are indispensable factors in the processes of nutrition of 
man and the higher vertebrates. The enteregenous antotntorications, which are caused 
by these intestinal bacteria and which occur especially in childhood through retention 
of the intestinal contents (ileus) or in acute digestive disturbances (asthma dyspep- 
ticum), are in their severe forms characterized chiefly by disturbance of heart-action, 
small and frequent pulse, evanosis, coldness of the extremities, sunken expression, and 
lowering of the body temperature. They may owe their origin in part to retention of 
intestinal contents in this or that portion of the intestinal tract, and in part to changes 
in the products of decomposition (toxins and toxalbumins) depending either upon the 
especial character of the material taken into the intestines, or upon a change in the 
virulence of the bacteria, or upon a deficient production of enzymes. It is not always 
possible in such cases to decide whether other bacteria, foreign to the intestine, are not 


AUTOINTOXICATION: CONSTITUTIONAL DISEASES. 81 


also concerned in the production of poisons. The appearance of cystin in the urine is 
to be regarded, according to the researches of Baumann and von Udranski, as evidence 
of especial processes of intestinal decomposition resulting in the production of diamins. 

According to the view of Bouchard, autointoxications are caused in particular by 
leucomains—that is, by the earlier products of retrogressive metamorphosis of albu- 
minous bodies, which normally are further decomp in the process of intra-organic 
oxidation until they reach the form of urea and are then excreted. 

Chronic diseases whose chief characteristic appears to lie in a changed condition of 
the entire organism are often grouped together as constitutional diseases. Into 
this category Samuel places the permanent anomalies of the blood, lymph-glands, ner- 


vous tissues (neuropathic predisposition), rachitis, osteomglacia, multiple exostoses, ~ 


feeble muscular development, relaxed articular ligaments, etc. Hoffman (“ Lehrbuch der 
Constitutionskrankheiten,” Stuttgart, 1884) collects under this term the different forms of 
anzmia, hemorrhagic diathesis, hemoglobinemia, rachitis, osteomalacia, chronic rheu- 
matism, progressive myositis ossificans, multiple exostoses, lipomatosis, gout, diabetes 
mellitus, diabetes insipidus, and Addison’s disease. Nothnagel, in his “Handbook of 
Special Pathology,” omits the diseases of the blood from this class, and includes among 
the constitutional diseases only rachitis, osteomalacia, gout, obesity, chronic rheumatism, 
arthritis deformans, diabetes mellitus, and diabetes insipidus. From these examples it 
is clearly evident that the designation constitutional disease is applied to very differ- 
ent conditions. Asa matter of fact, the diseases enumerated are not characterized by 
constitutional anomalies; they represent rather the sequel of anomalies or diseases of 
certain tissues, so that the use of the term “constitutional disease ” finds for the greater 
part no true application. At the most, the designation can still be applied with fitness 
to obesity and gout. 


Literature. 
( Autointoxications. ) 


Albu: Die Autointoxicationen, Berlin, 1895 (Lit.); Jahrb. v. Eulenb., viii., 1898 
(Lit.). 
umann: Die aromatischen Verbindungen im Harn u. d. Darmfäulniss. Zeit. f. 

phys. Chem., x., 1886; Vork. v. Diaminen, sog. Ptomainen im Harn bei Cystinurie, 
ib., xiii., 1889; Alkaptonurie, ib., xv., 1891. 

Bickel: Pathogenese der Cholämie, Wiesbaden, 1900. 

Blum: Autointoxicationen. Münch. med. Woch., 1900. 

Bohne: Bedeutung d. Retention v. Chloriden. Fortschr. d. Med., xv., 1897. 

Bouchard: Lecons sur les autointoxications, Paris, 1887. 

Bubis: Sperminum-Poeh] in chem. u. physiol. Beziehung. St. Petersburger med. 
Woch., 1894. 

Charrin: Poisons de l’organisme, Paris, i.-iii., 1893-1897. 

Chatrin er Cunard: Secret int. du rein (has no internal secretion). Arch. de med. 
exp., 1900. 

Chittenden: Autointoxication. Proc. of the Path. Soc. of Philadelphia, ii., 1899. 

Colosanti: La fonction protectrice du foie. Arch. ital. de biol., xxvi., 1897. 

Ewald: Die Autointoxication. Berl. klin. Woch., 1900. 

Fermi u. Caciani: Autointoxication. Cbl. f. Bakt., xix., 1896. 

Fleischer: Beitr. z. exp. Path. der Niere. Verh. d. VI. med. Congr., Wiesbaden, 
1887. 

Genzmer al Volkmann: Septisches u. aseptisches Wundfieber. Klin. Vortr., No. 
121. 1877. 

Gouget: Insuffisance hépatique et névrite. Rev. de méd., 1897. 

Harz: Die Störungen des Verdauungsapparates als Ursache und Folge anderer 
Erkrankungen, Berlin, 1898. 

Kobert: Lehrb. der Intoxicationen, Stuttgart, 1893. 

v. Limbeck: Zur Lehre v. d. urämischen Intoxicationen. Arch. f. exp. Path., 30 


Bd., 1892. 
Martius: Pathogenese innerer Krankheiten, i. and ii., Leipzig, 1900. 
Minkowski: Die Störungen d. Leberfunctionen. Ergebn. d. path. An., ii. Jahrg., 
Wiesb., 1897. 
u. Brieger: Autointoxicationen intestin. Ursprungs. Verh. d. Congr. f. inn. 
Med., 1898. 


Blesbitt: Res. on Autointoxication. Journ. of Exp. Med., vi., 1899. 
Pfeiffer: Vorkommen u. Aetiologie der Tetanie. Cbl. f. allg. Path., vii. 1896 (Lit.). 
Roger: Les autointoxications. th. gén. publ. p. Bouchard, i., 1895. 

6 


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AP oo, 


/ 


82 DISEASES PRODUCED BY DISTURBANCE OF INTERNAL SECRETIONS. 


Schottelius: Bedeutung der Darmbakterien für die Ernährung. Arch. f. hyg., 34 
Bd., 1898. 

Schwalbe: Vergiftung. Eulenburg’s encyklop. Jahrb., iv., 1894. 

Stadelmann: Der Ikterus, Stuttgart, 1891. 

Uschinsky: Intoxication durch Schwefelwasserstoff. Zeitschr. f. phys. Chem., 17 
Bd., 1892. 

Weintraud: Gastrointestinale Autointoxication. Ergebn. d. allg. Path., iv., 1897. 

Wernigk: Ueber die be! urämischen Anfällen auftret. Veränderungen. Inaug.-Diss., 
Erlangen, 1887. 

Winkler: Zur Lehre v. d. Eklampsie. Virch. Arch., 154 Bd., 1898. 


§ 25. If a gland produces an internal secretion—that is, if it gives 
to the lymph or the blood certain substances which are necessary for the 
normal performance of the functions of other organs or of the organism 
as a whole—an alteration or total failure of this function will cause 
more or less important disturbances of nutrition, as well as of the func- 
tional activity of other organs and of the entire organism. Such an in- 
ternal secretion is ascribed to the liver, pancreas, thyroid, adrenals, 
thymus, and the sexual glands, yet our knowledge of the nature of these 
secretions is very slight and hypothetical. We are able to infer the in- 
fluence exerted by these glands upon metabolism and the life of the 
organism only from the disturbances which arise when the glands in 
question become diseased. Among the most important of the diseases 
belonging in this category are diabetes mellitus, thyreoprival cachezia, 
myxedema, cretinism, Addison's disease, and the functional and anatomical 
changes occurring in the body after castration. In a certain sense it is 
proper to consider in this connection asphyxia, which arises from a fail- 
ure of the lungs to perform properly their function, in that through the 
functional activity of the lungs the requisite amount of oxygen is sup- 
plied to the organism. 

Diabetes mellitus is a disease which is characterized especially by 
the presence of large amounts of grape-sugar in the urine (glycosuria), 
accompanied by a great increase in the total amount of urine secreted 
(polyuria), and often also by a pathological increase of acetone and the 
excretion of aceto-acetic acid and 3-oxybutyric acid in the urine. At 
the same time grape-sugar and these acids are found in the blood and 
often lead to a diminution of its alkalinity. When the acid-content of 
the blood is high, headache, anxiety, delirium, fainting, and finally a 
condition of loss of consciousness (coma diabeticum) develop, and these 
conditions are probably to be ascribed to an acid-intoxication (Stadel- 
mann, Minkowski, Magnus- Levi). 

The entrance of sugar into the urine may be caused by too great an 
ingestion of sugar, so that part passes into the urine unchanged (ali- 
mentary glyeosuria). Giycosuria may also follow an injury to certain 
portions of the medulla oblongata (puncture of Bernard), or as the result 
of disease- processes in the brain (degeneration, epilepsy, mental affec- 
tions, severe psychical disturbances, tumors, parasites), or of certain 
forms of poisoning (carbon monoxide, curare, morphine, strychnine, 
amyl nitrite, nitrobenzole), in which the liver probably gives up its gly- 
cogen into the blood more rapidly than normal, so that a condition of 
hyperglycemia is produced. 

Finally, glveosuria may be due to an inability on the part of the kid- 
neys to hold back the small amounts of glucose found normally in the 
blood, a phenomenon which may be produced experimentally by the 
administration of phloridzin (von Mering) or of caffeine sulphate 
(Jacobj). 


DISTURBANCE OF PANCREATIC FUNCTION. 83 


These alimentary, nervous, and toxic glycosurias are, however, to be 
distinguished from the ordinary form of diabetes, in that in the latter the 
cause of the glycosuria is to be sought, not in an increased conveyance 
of sugar into the blood, or in a pathological excretion of the sugar con- 
tained in the blood, but much rather in the fact that the diabetic patient 
is unable to decompose sufficiently the carbohydrates, and especially 
dextrose, while the sugars which turn polarized light to the left (levu- 
lose and inulin) ordinarily can be oxidized either wholly or at least in 
greater amounts than dextrose. In most cases the power to form fats 
from the carbohydrates is also lessened, yet there are cases in which this 
function is unimpaired and the sugars are stored up in the body in the 
form of fat (diabetogenous obesity). | 

According to the investigations of von Mering and Minkowski, which 
have been confirmed by different authors, this loss of power in the or- 
ganism to oxidize the sugars brought into the body or formed normally 
in the body from albumin, or to store them up as glycogen or fat, is to 
be ascribed to an insufficiency of pancreatic function. This conclusion 
is drawn chiefly from the fact that after total extirpation of the pancreas 
in dogs, a diabetes of severe character, usually fatal within a few weeks, 
is produced, this being characterized, as is diabetes in the human sub- 
ject, by polyuria, polydipsia, hyperglycemia, glycosuria, diminution of 
the glycogen of the tissues, also at times by marked destruction of 
albumin, emaciation, excretion of large amounts of acetone, aceto-acetic 
acid, 3-oxybutyric acid, and ammonia, as well as by the occurrence of a 
comatose condition. In support of the view that there is a definite re- 
lation between disturbances of pancreatic function and diabetes, it has 
been found that in certain cases of this disease in man the pancreas has 
exhibited demonstrable changes, of the nature of atrophy or degenera- 
tion. It should, however, be borne in mind that the anatomical investi- 
gation often fails to reveal a pathological condition of the pancreas; so 
that we are forced to content ourselves with the hypothesis that the 
anatomical changes underlying the functional disturbance of the pan- 
creas are not demonstrable. 

An exact explanation of the causal relations existing between pan- 
creatic disease and diabetes cannot at the present time be given, yet from 
the foregoing experimental researches the hypothesis may be deduced 
that the pancreas produces an internal secretion which is of importance 
in the metabolism of glucose, and that if this function is lost the cap- 
acity for the decomposition of glucose is diminished. Likewise, no ex- 
planation can at present be given for the increased destruction of the 
albumins and the accompanying abundant production of £-oxybutyric 
acid, aceto-acetic acid, and acetone. Since these substances are not al- 
ways found in experimental pancreatic diabetes, their formation probably 
does not stand in direct relation to the excretion of sugar, but is to be 
regarded rather as a complication of diabetes (Minkowski). Their oc- 
currence in diabetes, moreover, is not always constant, and they are 
found in other diseases (intoxications, carcinoma, disturbances of di- 


gestion). 


The occurrence of diabetes after total extirpation of the pancreas is evidence that 
this organ possesses a special function which is of the greatest importance in the nor- 
mal consumption of sugar in the organism. Z,epine is of the opinion that there is in the 
blood a giycolytic ferment, which is formed by the pancreas and passed from this or- 
gan into the blood; and that the cause of the mellituria in diabetic patients and in dogs 

rom which the pancreas has been removed is to be sought in a decrease in the amount 


84 DISEASES PRODUCED BY DISTURBANCE OF INTERNAL SECRETIONS. 


of this ferment. According to Minkowski, the experiments of Lépine do not offer sufti- 
cient support for this theory. At the present time it is impossible to offer a satisfac- 
tory theory of the pathogenesis of pancreatic diabetes. 

If only a portion of the pancreas of a dog be removed, no diabetes occurs, or at 
least the excretion of sugar is much less than after total extirpation (Minkowski). If in 
dogs from which the pancreas has been totally removed a portion of pancreas is trans- 
planted subcutaneously, diabetes does not follow (Minkowski, Hedon), but occurs if the 
transplanted piece be excised. 

According to Minkowski, there is no direct communication between the secretory 
function of the pancreas and that function of the organ concerned in the metabolism of 
sugar, 

Poisoning with phloridzin produces, according to ton Mering and Minkowski. a 
marked glycosuria in most animals and in man, and the same symptoms as those seen 
in diabetes, may be produced by a continuous administration of the poison. Since in 
this case the cause of the pathological excretion of sugar lies in the kidneys and repre- 
sents a flushing-out of sugar from the organism, phloridzin diabetes cannot be identified 
with the ordinary form of diabetes found in man—that is, with pancreatic diabetes. In 
dogs in which diabetes has been produced by the extirpation of the pancreas, phloridzin 
produces an increase in the amount of sugar excreted (Minkoweki). . 


Literature. 
( Diabetes Mellitus. ) 


Arthaud et Butte: Rech. sur la pathogénie du diabéte. Arch. de phys., i., 1888. 

Bernard, Claude: Lecons sur le diabéte, Paris, 1877, and Berlin, 1878. 

Boccardi: Altérations anat. conséc. a exportation du pancreas. Arch. ital. de biol., 
xvi., 1891. 

Dominicis: Pathogénie du diabéte. Arch. de med. exp., v., 1893. 

Ebstein: Die Zuckerharnrulir, Wiesbaden, 1887. 

Frerichs: Ueber den Diabetes, Berlin, 1884. 

Gaglio: Ucber den Diabetes nach Abtragung des Pankreas. . Cbl. f. allg. Path., ii.. 
1891. 

Galeotti: Glykosurie und Acetonurie. Cbl. f. allg. Path., iii., 1892. 

Hansemann: Beziehungen d. Pankreas zum Diabetes. Zeit. f. klin. Med., 26 Bd.. 
1844. 

Hedon: Exstirpation du pancréas. Arch. de méd. exp., iii., 1891, v., 1898; Pathogenie 
du diabéte. Arch. de phys., 1892; Greffe souscutanée da pancréas. Arch. de 
phys., 1892. 

Herter and Wakeman: Adrenalin Glycosuria. Virch. Arch., 1902; Amer. Jour. of 
Med. Sc., Jun., 1903. 

Herzog: Zur Histopathologie des Pankreas beim Diabetes mellitus. Virch. Arch., 
1902. 

Jakobj: Nierendiabetes durch Caffeinsulfosäure. Arch. f. exp. Path., 35 Bd., 1895. 

Kaufmann: Glyc&mie normale et diabéte pancréatique. Arch. de phys., vi., 1895. 

Külz: Beiträge zur Pathologie und Therapie des Diabetes mellitus, Marburg, 1874 and 
1879. 

Lannois ct Lemoine: Le pancréas dans le diabéte. Arch. de med. exper.. iii.. 1891. 

Lepine: Le ferment glycolytique et la pathogenie du diabéte, Paris, 1891; 3. l’exstirpa- 
tion du pancreas. A. de med. exper.. iii. 1891; Pathogenie de la glycosurie, ib.. 

1892; Le diabéte et les lésions du pancréas. Rev. de méd., xii., 1892; 
thogénie du diabete, ib., xiv., 1894. 

Lorenz: Unters. über Acetonurie. Zeitschr. f. klin. Med., 19 Bd.. 1891. 

Lustig: Function des Plexus celiacus. Beitr. v. Ziegler, vii., 1890. 

Magnus-Levi: Die Oxybuttersäure u. d. Coma diabet. Arch. f. exp. Path.. 42 Bd., 
1899. 

v. Mering: Ueber experimentellen Diabetes. Verhandl. d. V. u. VI. Congr. f. inn. 
Med.. Wiesbaden, 1886, 1887; Zeitschr. f. Klin. Med., xiv., 1888, and xvi., 1889. 

v. Mering u. Minkowski: Diabetes mellitus nach Pankreasexstirpation. Arch. f. 
exper, Pathol., 26 Bd., 1890; Zeitschr. f. Biol., 29 Bd., 1892. 

Michael: Diabetes (Cysticercus i im IV. Ventrikel). Deut. Arch. f. klin. Med., 44 Bd., 
1889. 

Minkowski: Diabetes nach Pankreasexstirpation. Arch. f. exp. Path., 31 Bd., 1898 
(Lit.). 

Moritz u. Prausnitz: Phloridzindiabetes. Zeitschr. f. Biol., 27 Bd. 

v. Noorden: Pathologie des Stoffwechsels, Berlin, 1898 (Lit.). 








88 DISEASES PRODUCED BY DISTURBANCE OF INTERNAL SECRETIONS. 


Blum. regards the thyroid as an organ whose function it is to destroy enterotoxins 
arising from the decom position of albumin in the intestine. 

Anatomical investigations have failed to throw any definite light upon the ques- 
tion of the internal secretion of the thyroid. It has been proved that the colloid 
produced by the thyroid cells passes into the Iymph-vessels. It is probable that 
iodothyrin is contained in this colloid substance. According to Bruns, the diminution 
in the size of the goitre after the administration of thyroid-gland-substance or of thy- 
roiodine may be attributed to the fact that in the hypertrophic gland-tissue of the 
goitre which contains numerous follicles—many of which are entirely destitute of col- 
loid, or contain but little of it, or are imperfectly developed—there occurs an increase 
of colloid-secretion in the fully developed follicles, and at the same time d greater 
abundance of colloid is passed into the lymph-stream, while the imperfectly developed 
follicles, on the other hand, atrophy and disappear. After the administration of active 
thyroid substance for a longer time, some of the secreting follicles also undergo 
atrophy. 

According to the investigations of Rogowitsch, Stieda, and Hofmeister, the extir- 
pation of the thyroid in rabbits causes enlargement and peculiar changes in the hy- 
pophysis. 

lt is possible that Basedow's disease, which is characterized by a pulsating and 
highly vascular swelling of the thyroid, ability on of the eyeballs from their orbits, 
acceleration of heart action, and great excitability on the part of the patient, is also de- 
pendent upon a diseased condition of the thyrold—-namely, a hypersecretion (hyperthy- 
reosis). In support of this hy pothesis is the fact that glands so affected are rich in func- 
tionating gland-tissuc; but no positive conclusions can be drawn concerning this point. 


Literature. 
(Cacheria Thyreopriva, Myxedema, Cretinism, and Basedow’s Disease.) 


Askanazy: Z. Kenntn. d. Morbus Basedowii. Deut. Arch. f. klin. Med., 61 Bd., 1898. 

Baumann: Jod im Thierkörper. Zeitschr. f. phys. Chem., 21, 22 Bd., 1895-1896: 
Jodothyrin. Münch. med. Woch., 1896. 

Baumann u. Goldmann: Jodothyrin. Münch, med. Woch., 1896. 

Baumgärtner: Zur Kachexia strumipriva. Arch. f. klin. Chir., 81 Bd., 1884. 

Beadles: The Treatment of Mxyeedema and Cretinism. Journ. of Med. Sc., 1893. 

Blum: Schilddrüse als entgiftendes Organ. Virch. Arch., 158 Bd., 1899. 

Blumreich u. Jacoby: Be ‚deutung der Schilddrüse Arch. f. d. ges. Phys., 64 Bd., 
1806. 

Bozzi: Unters. üb. die Schilddrüse. Beitr. v. Ziegler, xviii., 1895. 

Bruns: Schilddrüsenbehandlung d. Kropfes. Beitr. v. Bruns, xvi., 1896. 

Buschan: Myxödem. Eulenburg’s Realeneyklop., xvi., 1898. 

De Coulon: Thyreoidea u. Ilypophysis der Kretinen. Virch. Arch., 147 Bd., 1897. 

Donath: Wirkung d. Schilddrüse.  Virch. Arch., 144 Bd., Suppl., 1896. 

Drobnick: Folgen d. Exstirp. d. Schilddrüse. Arch. f. exp. Path., 25 Bd., 1888. 

Ehrich: Z. Kenntn. d. Morbus Basedowii. Beiträge v. Bruns, xxviii.. 1900. 

von Eiselsberg: 7. Lehre der Schilddrüse. Virch. Arch., 58 Bd., 1898. 

Ewald: Die Erkrankungen der Schilddrüse, Myxödem und Kretinismus, Wien, 1896 
(Lit.). 

Farner: Morbus Basedowii. Virch. Arch., 143 Bd.. 1896. 

Fuhr: Die Exstirpation der Schilddrüse. Arch. f. exp. Path., 21 Bd., 1886. 

Gauthin: Fonctions du corps thyroide. Rev. de meéd., 1900. 

Gley: Effets de la thyroideetomie. Arch. de phys., iv., 1892; vii.. 1895. 

Grundler: Zur Kachexia strumipriva. Mittheil. a. d. chir. Klinik zu Tübingen, i., 
1584. 

Gull: Cretinoid State Supervening in Adult Life in Women. Trans. of the Clin. Soc., 
London, 1893. 

Hertoghe u. Spiegelberg: Holle d. Schilddrüse bei Ilemmung d. Wachsthums, 
München, 1900. 

Hofmeister: Physiologie d. Schilddrüse. Fortschr. d. Med., 1892; Folgen d. Schild- 
drüsenverlustes. Beitr. v. Bruns, xi., 1894. 

Horsley: Function d. Schilddrüse. Internat. Beitr. Festschr. f. Virchow, i., Berlin, 
IsYL (Lit.). 

Jaquet: Schilddrüse u. Schilddrüsenpräparate. Corrbl. f. Schweizer Aerzte, 1899 

Kocher: Kropfexstirpation u. ihre Folgen. Arch. f. klin. Chir., 2 27 Bd., 1883, Verlhü- 
tung des Kretinismus. Deut. Zeit. f. Chir., 34 Bd., 1892; ; Schilddrüsenfunction. 
Correspbl. f. Schweizer Aerzte, 1895. 


ADDISON’S DISEASE. 89 


Laache: Ueb. Myxödem u. dessen Behandlung mit Gland. thyr. Deut. med. Woch., 
1893. 

Langendorf: Aeltere u. neuere Ansichten über d. Schilddrüse. Biol. Cbl., ix., 1889. 

Langhans: Veränd. d. peripheren Nerven bei Kachexia strumipriva. Virch. Arch., 
128 Bd , 1892. ’ 

Lannois: De la cachexie pachydermique (myxcedéme). Arch. de med. exp., i., 1889. 

Lanz: Zur Schilddrüsenfrage, Leipzig, 1894; Thyreoidismus. Deut. med. Woch., 1895. 

Leichtenstern: Heilung v. operat. Myxödem m. Schilddrüsenfütterung. Deut. med. 
Woch., 1898. 

Leonhard: Bed. d. Schilddrüse f. d. Wachsthum. Virch. Arch., 149 Bd., 1897. 

Meltzer: Leber Myxödem, New York. med. Monatsschr., 1894. 

Notkin: Zur Schilddrüsenphysiologie. Virch. Arch., 144 Bd., Suppl., 1896. 

Ord: On Myxedema. Med.-Chir. Trans., Ixi.; and Brit. Med. Journ., 1877. 

Osler: Sporadic Cretinism in America. Trans. Assn. of Amer. Phys., 1893, vol. viii. 

Oswald: Jodgehalt d. Schilddrüsen. Zeit. f. phys. Chem., xxiii., 1897; Function. 
Münch. med. Woch., 1899. 

Ponfick: Myxödem u. Akromegalie. Cbl. f. allg. Path., ix., 1898; Zeit. f. klin. Med., 
38 Bd., 1899. 

de Quervain: Veränd. d. Centralnervensystems bei Kachexia thyreopriva. Virch. 
Arch., 133 Bd., 1898. 

Reverdin: Note sur vingt-deux opérat. de goltre. Rev. med. de la Suisse rom., 1884. 

Rogowitsch: Veränd. d. Hypophyse uach Entfernung d. Schilddrüse. Beitr. v. 
Ziegler. iv., 1888. 

Roos: Wirkung des Jodothyrins. Zeitschr. f. phys. Chem., xxii., 1896; xxviii., 
1899 


Rouxeau: Thyroldectomie chez le lapin. Arch. de phys., ix., 1897. 
Sanquirico et Canalis: Sur l’exstirpation du corps thyrofde. Arch. ital. de biol., v., 


1884. 

Schmidt: Der Secretionsvorgang in d. Schilddrüse. Arch. f. mikr. Anat., 47 Bd., 
1896. 

Schwerdt: Morbus Basedowii. Münch. med. Woch., 1898. 

Stewart: The Treatment of Myx@dema by Thyroid Feeding. Fortschr. d. Med., 
1894. 

Stieda: Hypophyse d. Kaninchens nach Entfernung d. Schilddrüse Beitr. v. 
Ziegler, vii., 1890. 

Vermehren: Behandlung d. Myxödems und Kretinismus. Deut. med. Woch , 1898. 

Virchow: Kropf. Geschwülste, iii.; Kretinismus. Ges. Abhandl., 1856; Woch., 
1887; Kropfkachexie,. Virch. Arch., 144 Bd., 1896. 

Weiss: Wucherungen in den peripher. Nerven d. Hundes. Virch. Arch., 135 Bd., 
1894. 


§ 27. Addison’s Disease is a peculiar affection, usually fatal after a 
course of about two years on the average, and is very probably to be 
regarded as the result of a functional disturbance of the suprarenals. It is 
characterized chiefly by the appearance of a light-yellow-brown to dark- 
brown, diffuse, and spotted pigmentation of the skin (melasma supra- 
renale), which shows itself first in the portions of the skin normally 
exposed, later in other parts of the body-surface and in the mucous 
membrane of the mouth. Even at the beginning of the disease, or even 
before the pigmentation of the skin, there occur loss of appetite, nausea, 
pain in the epigastrium, diarrhea, constipation, and vomiting—all 
symptoms of a disturbed intestinal and gastric function; later, muscular 


weakness; and finally, nervous symptoms, asthenia, fatigue on slight 4+2- : 


exertion, headache, vertigo, fainting, epileptiform attacks, and coma, 
Occasionally a recognizable increase of the pigment of the skin does not 
occur, and the disease is characterized only by the gastro-intestinal 
symptoms, progressive weakness, and anemia. 

In about eighty per cent of all typical cases of Addison’s disease the 
suprarenals are found to be diseased, in the majority of cases being changed 
into a caseous or fibro-caseous mass. With the exception of these 
changes there are no other lesions so constantly characteristic of Addi- 


( 


} - 


x 


90 DISEASES PRODUCED BY DISTURBANCE OF INTERNAL SECRETIONS. 


son's disease. There can scarcely remain any doubt that the disease of 
the suprarenals bears a causal relation to this disease; it may, therefore, 
be designated as a suprarenal cachexia. In what way the loss or change 
of the function of the suprareual bodies acts injuriously upon the organ- 
ism cannot at present be stated. It Is not improbable that the suprarenal 
bodies, like the thyroid, produce a substance which is necessary for the 
preservation of the organism; or possibly poisonous substances are de- 
stroyed by them. 


The literature of Addison's disease is exceptionally rich, but in spite of the great 
number of clinical and experimental investigations, the pathogenesis of the disease and 
the significance of the adrenals for the human and animal organism have not vet been 
made clear. Nevertheless, it is certain that a normal functional activity of the adrenals 
is necessary to the integrity of the organism. This is based not only upon clinical ob- 
servations and anatomical investigations in man, but also upon animal cx periments. 
For example, the extirpation of the adrenals in dogs, rabbits, cats, and guinea-pigs 
gives rise to a lowering of blood-pressure, muscular weakness, and nervous symptoms, 
paralysis, coma, and, if life be sufficiently prolonged, a loss of strength, and, accord- 
ing to Tézzont, also an abnormal pigmentation of the mucous membranes. The admin- 
istration of adrenal extract Causes in animals an increase of blood-pressure, slowing of 
the pulse-rate, increase in the strength of muscle-contractions after nerve-stimulation, 
and a decrease in respiratory movements. The cause of the increase of blood-pressure 
is regarded by some us the effect of the extract upon the vasomotor centre (Seymono- 
wiez), by others as a direct action upon the arterial walls (Schäfer). The contraction of 
the small vessels has been definitely proved. According to ron Fürth, the active sub- 
stance is hydro-dioxypyridin, which he calls euprarenin. Since the adrenals do not 
show pathological changes in all cases of Addison's disease, the view has been advanced 
by some investigators that the discase is dependent upon other local changes, particu- 
larly upon pathological conditions of the sympathetic and the sympathetic ganglia; vet 
the conditions found thus far are not adequate for such an explanation. That ina 
small minority of cuses the adrenals appear unchanged cannot (even if all these cases 
had been correctly diagnosed, which is surely not probable) be accepted as valid evi- 
dence against the pathogenic significance of the degeneration of the adrenals, inasmuch 
as an apparently normal adrenal may functionate abnormally. 

Inflammatory and degenerative changes in the semilunar ganglia or in other parts 
of the sympathetic, as well as in the intervertebral ganglia have been frequently ob- 
served in Addison's disease, These have been described by a number of investigators, 
and may be explained as an extension of inflammation and degeneration from the adre- 
nals to the parts mentioned. To conclude from this that Addison’s disease is dependent 
upon a disease of the sympathetic and not of the adrenals, is not sufficiently well 
grounded, since the disease of the adrenals actually exists while that of the nerves is 
found only in a minority of cases. 

Manasse found in preparations which, while still retaining the body-heat. were 
placed in solutions of chromic salts and thereby hardened, that the cells of the adrenal 
stand in closest relations to the veins, reaching out free into the lumen of the veins; 
and that in the vessels, particularly in the veins, there is present a peculiar hyaline 
substance, which is colored brown by the chromic salts in the same manner as are the 
neighboring parenchymatous cells. It is therefore possible that the cells furnish to 
the blood some peculiar substance. It should be stated, further, that this substance is 
found also in the arteries. It cannot be demonstrated in alcoholic preparations. 

Asa pathological condition due to the loss of a specific glandular function should 
be classed also those abnormal symptoms in the structure and functions of the body 
resulting from castration—that is. the removal from the body of the sexual glands. 
If the ovaries are removed from a woman after the age of puberty, menstruation usu- 
ally ceases at once, but rarely only after some time, Sexual desire and the erethism 
aecompanying the sexual act are usually diminished in intensity, but may also be un- 
changed, The remaining portions of the genital apparatus undergo atrophy; this is es- 
pecially marked in the case of the uterus. Certain nervous manifestations may follow, 
the most common of which are excitement, with reddening and heat of the skin. cspe- 
cially of the face. often associated with attacks of sweating; these symptoms being of 
most frequent occurrence in the period immediately following the castration. The 
disposition remains unchanged or may become more cheerful, especially in those cases 
in which the woman is by the castration relieved of severe pain. At times depression 
or melancholia may follow. If the ovaries are removed or destroyed during childhood, 
the body comes to resemble in its build the male type: the muscles are more strongly 


EFFECTS OF CASTRATION. 91 


developed, the development of the pelvis is changed, and tlıe breasts do not increase in 
size. 

Castration in an adult male produces no marked change in the build of the body. 
On the other hand, if boys are castrated, the build of the body approaches that of the 
female. There occurs an increased deposit of fat, particularly on the abdomen, while 
the musculature is only feebly developed. The external genitals remain small, the 
prostate is diminished in size, and there is no growth of beard or pubic hair. The 
larynx remains sinall, and the voice is child-like. The mental powers are lacking in 
energy and strength. 

n castrated stags the antlers are not developed; in cocks the combs, wattles, and 
ear-lobes do not reach normal development, while the feathers are developed to a 
greater extent (Sellheim). 

According to White, Kirby, Kümmel, Bruns, and others, castration in fully devel- 
oped animals causes a decrease in the size of the prostate; and it is said that in old men 
suffering from prostatic enlargement, castration may lead to a diminution in size of the 
enlarged prostate. Others (Czerny, Socin) express a less favorable opinion as to the re- 
sults of castration in such cases. 

In what manner the erfirpation of the serual glands affects the entire body has not 
been determined with certainty. By many authors it is assumed that, as a result of 
castration, the trophic influence exerted upon the tissues by the sexual glands, through 
the nervous system, is withdrawn. The cessation of the menses may indeed be re- 
garded as due to the withdrawal of nervous stimuli, and the atrophy of the uterus may 
perhaps be dependent upon the same cause; but in general it is more likely that cer- 
tain chemical substances, which exert a certain influence on the functions, growth, and 
development of the body, are formed in the sexual glands. 

According to the investigations of Loewy and Jtchter, after castration of female 
dogs there occurs a lowering of the oxidation-power of the cells of the body and a de- 
crease in the amount of oxygen used by about twenty per cent. The administration of 
dried ovarian substance or of oöphorin from the ovaries of the cow or hog causes an in- 
crease of the amount of oxygen consumed even greater than the average observed before 
the castration. Preparations of testicles showed no such influence. In male dogs the 
same conditions prevailed; spermin caused only slight increase in the gaseous inter- 
change. odphorin gave a marked increase (as much as forty-four per cent). 

According to the view of Brown-Sequard, all glands produce an especial internal 
secretion, and give to the blood certain substances which are useful to the organism. 
He ascribes to the juice of the generative glands an especial, stimulating, and tonic in- 
fluence upon the organism. According to Poehl, the active substance in the extract of 
the sexual glands is spermin, a base which is found in different glands (thyroid, pan- 
creas, ovaries, spleen), and which through its catalytic action restores the oxidizing 
power of the blood whenever through various causes it may be lowered, and promotes 
tntraorganic oxidation. 

Zoth and Pregel, who have carried out experiments with reference to the effects of 
glycerin extracts of the testicles of animals, report that injections of this extract in- 
crease very markedly the power of muscular contraction. 


Literature. 


(Function of Adrenals and Addison's Disease.) 


Abel: Epinephrin. Zeitschr. f. phys. Chem., 28 Bd., 1899. 

Abelous ct Langlois: Fonction des capsules surrenales. Arch. de phys., iv., 1892. 

Addison: On the Constitutional and Local Effects of Disease of the Suprarenal Cap- 
sules, London, 1855. 

Alexander: Die Nebennieren u. ihre Bezieh. z. Nervensystem. Beitr. v. Ziegler, xi., 
1891. 

Alezais ct Arnaud: Etudes sur la tuberculose des capsules surrénales et ses rapports 
avec la maladie d’Addison. Rev. de méd., xi., 1891. 

Averbeck: Die Addison’sche Krankheit, Erlangen, 1869. 

Babes et Kalindero: Un cas de maladie d’ Addison avec lésions des centres nerveux, 
Paris. 1890. 

Burger: Die Nebennieren und der Morbus Addisonii, Berlin, 1883. 

Chvostek: Störungen d. Nebennierenfunction. Ergebnisse, iii., 1897. 

Dubois: Toxicité des extraits des caps. surr. Arch. de phys., viii., 1896. 

Fleiner: Veränderungen des sympath. u. cerebrospinal. Nervensystems bei der Addi- 
son’schen Krankheit. Cbl. f. allg. Path., ii., 1891; Deut. Zeitschr. f. Nervenheilk., 
ii., 1892. 


92 DISEASES PRODUCED BY DISTURBANCE OF INTERNAL SECRETIONS. 


Fürth: Brenzkatechin u. älınl. Subst. d. Nebennieren. Zeit. f. phys. Chem., 29 Bd., 
1899. 

Gerhardt: Blutdruck steigernde Subst. d. Nebennieren. Arch. f. exp. Path., 44 
Bd., 1900. 

Gottlieb: Wirkung d. Nebennierenextracte. Arch. f. exp. Path., 38 Bd., 1896: 43 
Bd., 1899. 

Guinard et Martin: Suc surrcnal. Journ. de phys., i., 1899. 

v. Kahlden: Ueb. Addison’'sche Krankheit. Beitr. v. Ziegler, xi., 1891; C. f. a. P., 
vii., 1896 (Lit.). 

Lewin: Morbus Addisonii. Charité-Ann., x., 1885; xvii., 1892. 

Manasse: Ueber die Bezieh. der Nebennieren z. d. Venen. Virch. Arch., 87 Bd., 
1804. 

Mosse: Autointoxication bei Morbus Addisonii. Fortschr. d. Med.,'xv., 1897. 

Oliver: On the Therap. Employ. of the Suprarenal Glands. Brit. Med. Journ., ii., 
1895. 

Philips: Addison’s Disease with Simple Atrophy of the Adrenals. Jour. of Exp. 
Med., 1899. 

Rolleston: The Suprarenal Bodies. Brit. Med. Journ., 1895. 

Schäfer: Ueber interne Secretion. Wien. med. BI., 1895. 

Scymonowicz: Function der Nebennieren. Pflüger’s Arch., 64 Bd., 1896. 

Tizzoni: Ueber die Wirkungen der Exstirpation der Nebennieren. Beitr. v. Ziegler, 
vi., 1889. 

Zander: Functionelle u. genet. Bezich. d. Nebenn. zum Gehirn. Beitr. v. Ziegler, 
vii., 1890. 


(Results of Castration ; Internal Secretion of Sexual Glands ; Spermin and 
Organ-extract Therapy.) 


Alterthum: Folgezust. nach Castration. Beitr. v. Hegar, ii., 1899. 

Brown-Séquard: Exper. dem. la puissance dynamogénique chez l’bomme d’un liquide 
extrait de testicules d’animaux. Arch. d. phys., 1889, 1890, and 1891. 

Bruns: Behandlung d. Prostatahypertrophie durch Kastration. Mittheil. a. d. 
Grenzgeb. d. Med. u. Chir., i., 1896 (Lit.). 

Bubis: Sperminum-Poehl. St. Petersburger med. Wochenschr.. 1894. 

Buschan: Brown-Sequard'sche Methode. Eulenburg’s encyklop. Jahrb., iv., 1894; 
Berlin, 1895.—Organsafttherapie, Eulenburg’s Realencyklop., xviii., 1898. 

Curatuto ct Tarulli: [nfl. de Y’ablation des ovaires sur le métabolisme organique. 
Arch. ital. de biol., xxiii., 1895. 

Czerny: Kastration bei Prostatahypertrophie. Deut. med. Woch., 1896. 

Fürbringer: Behandl. v. Erkrankungen m. Gewebsflüssigkeiten. Deut. med. Woch., 
1894. 

Gottschalk: Kastrationsatrophie der Gebärmutter. Arch. f. Gyn., 53 Bd., 1897. 

Hegar: Die Kastration der Frauen. Klin. Vortr. v. Volkmann, 1878; Der Zusammen- 
hang d. Geschlechtskrankheiten mit nervösen Leiden u. die Kastration bei Ner- 
vösen, 1885; Operative Gynäkologie, Wiesbaden, 1897. 

Kümmel: Operative Heilung der Prostatahypertrophie. Berlin. Klinik, 86, 1895 
(Lit.). 

Liesau: Einfluss der Kastration auf den weibl. Organismus. Inaug.-Diss., Freiburg, 
1896 (Liit.). 

Lilienfeld: Anat. Befund am Genitalapparat nach Kastration. Zeit. f. klin. Med., 
XXIX., 1898 (Lit.). 

Loewy u. Richter: Sexualfunction u. Stoffwechsel. Arch. f. Anat., Suppl., 1899. 

Metschnikoff: Spermatoxine et Antispermatoxine. Ann. de l’Inst. Pasteur, 1900. 

Poehl: Die phys. Chemie und Grundlagen der Spermintherapie, St. Petersburg, 1898. 

Sellheim: Secundäre Geschlechtscharaktere. Beitr. v. Hegar, i., 1898. 

Socin: Kastration n. Prostatahypertrophie. Corr. f. Schweizer Aerzte, 1896. 

Zoth u. Pregl: Wirkung orchitischen Extractes. Pflüger’s Arch., 62 Bd., 1895. 


Ill. Fever and Its Significance. 


S28, When a local organic disease takes on the character of a gene 
eral disease, or when a disease at its very inception manifests such a 
character, there is seen very frequently a symplom-complex which is 
designated as fever. Partieularly in the case of those infectious diseases 








FEVER. 95 


In the last-named, afebrile periods (apyrexia) alternate with periods 
of fever, each paroxysm having an initial period, a fastigium, and a 
defervescence. In the infectious disease known as febris recurrens there 
is first a continuous fever, which after a few days falls by crisis; after 
about a week or so a second rise of temperature occurs, which may be 
followed by a second stage of apyrexia, and this by athird period of fever. 

Many diseases—such as typhoid fever, pneumonia, measles, relapsing 
fever, etc.—are characterized by a typical temperature-curve; others— 
as pleuritis, endocarditis, diphtheria, tuberculosis, phlegmon, etc.—have 
no typical course of fever. 

The elevation of the body-temperature in fever is dependent 
primarily on an increase in heat-production through increase of the chemical 
changes occurring in the body. The respiratory interchange of gases—the 
excretion of carbonic acid (Liebermeister, Leyden) and the taking-up of 
oxygen (Zunz, Finkler)—is increased, a proof that the oxidation-proc- 
esses and with these also the heat-production are increased. At the 
same time the excretion of nitrogenous elements in the urine (urea, uric 
acid, creatinin) is increased—on the average about from seventy to one 
hundred per cent, under certain conditions even as much as threefold. 
There is also an increased destruction of the albuminoid substances of the 
body, the albumin of the organs, even in the latent period of the fever 
(Naunyn). 

The increase of heat-production varies in different fevers, but in gen- 
eral does not reach that: degree which can be produced by excessive 
muscle-action and over-feeding with albumin. It is at its highest point. 
at the time of the initial chill, in that the violent muscular contractions. 
thereby produced may increase the production of heat. 

The second cause of the elevation of the body-temperature is deficient 
heat-dispersion. At the height of the fever the patient as a rule gives 
off more heat than the normal individual, but this dispersion is not suffi- 
cient to offset the excessive heat-production. Heat-production is con- 
stantly increased ; heat-dispersion is irregular. 

In the initial stage the cutaneous vessels are contracted as a result of 
‘stimulation of the vasomotors, the skin is pale, the heat-dispersion 
slight, under certain conditions even less than normal. 

Chills occur when, through the contraction of the peripheral arteries, 
the supply of blood, and consequently the heat-supply, to the cutaneous 
nerves is suddenly diminished, while in the interior of the body the tem- 
perature is rising. 

In the second stage of fever the skin is often hot and reddened, and 
in certain diseases sweating occurs; but the increased heat-dispersion 
thereby produced is not sufficient to lower the temperature to the nor- 
mal. The increased excitability of the vasomotors or the deficient irri- 
tability of the vaso-dilators (Heidenhain, Naunyn, Senator) is also 
present during this period, and as a result the skin-temperature, as well 
as the heat-dispersion, varies greatly. The skin is at times pale and 
cold, at other times red and hot, and the hands may be cold while the 
trunk is hot. The centres governing heat-dispersion are therefore act- 
ing faultily. 

In the period of defervescence the relations of heat-dispersion and 
heat- production are changed in favor of the former. The cutaneous ves- 
sels become dilated, the skin gives out a great amount of heat from the 
abundance of blood circulating through it, and when the critical fall of 
the fever occurs there is usually profuse sweating. 


96 EFFECTS OF ORGANIC DISEASES UPON THE ORGANISM AS A WHOLE. 


The cause of fever is not known with certainty, yet this much can be 
said, that fever is most frequently the result of the entrance of a harmful 
agent. into the fluids of the body. Im many cases this harmful agent arises 
demonstrably from a local focus—for example, from erysipelatous and 
phlegmonous inflammations of the skin. Experimentally, fever may be 
produced by very differeut procedures—for example, through the infu- 
sion into the vessels of an animal of blood from one of another species, 
through the injection of animal or vegetable substances that are begin- 
ning to decompose (Billroth, Weber), and through numerous infections. 
In man, the infectious diseases, which are regarded as due to specific 
micro-organisms multiplying in the body, are in particular character- 
ized by fever. 

It is probable that. the parasites multiplying within the body cause an 
increased tissue-destruction, either directly or through the production of 
unformed ferments, and that at the same time substances are produced 
which act as poisons upon the central nervous system. The action of the 
latter may be assumed to be of such a nature that, on one side, the 
activity of the muscles and glands, and consequently the heat- producing 
metabolism, are increased; while, on the other hand, through the dimin- 
ished and disturbed functions of the nerves governing sweating, as well 
as of the vasomotors, the processes of heat-dispersion fall behind those 
of heat-production. Further, though the organism makes an effort to 
regulate the temperature, it is no longer able to maintain it at the nor- 
mal level, because of the disturbances of the regulating apparatus. 
What share in the increase of body-temperature is due to the direct ac- 
tion of bacteria and of the ferments formed by them, or what share is 
due to the increase of metabolism, through the stimulation of the nerves 
as well as by disturbance of heat-dispersion, cannot at present be deter- 
mined. It is, however, certain that the factors vary in different cases. 
That under certain conditions, changes in the nervous system without 
contamination of the tissue-juices are in themselves sufficient to cause a 
feverish increase of temperature, is shown .by the fact that fever may 
occur in epileptic attacks, in the periods of excitation occurring in the 
course of progressive paralysis, after severe frights, after the passage of 
a catheter into the bladder, etc. According to the investigations of 
Richet, Aronsohn, and Sachs, a marked increase in body-temperature 
with increase of the respiratory interchanges of gases and increased ex- 
cretion of nitrogen (Aronsohn and Sachs) may be produced in animals 
by a puncture which passes through the cerebral cortex and strikes the 
corpus striatum. The same phenomenon may be produced also by elec- 
trical stimulation (Aronsohn, Sachs) of the same portion of the brain. 
Nevertheless, fevers dependent upon nervous disturbance are rare, and 
are overshadowed in importance by those caused by infection. 

The rise of temperature in fever is usually accompanied by an in- 
crease in the frequency of the pulse-rate ; but in some cases this effect 
of the elevation of temperature may be so greatly modified through 
stimulation of the vagus—as, for example, in basilar meningitis—that 
the pulse-rate may be lowered. The pulse is at one time full and bound- 
ing, at another time small because of weakened contractions of the heart. 

The impairment of the contractions of the heart-muscle is dependent 
partly upon the constant high temperature, partly upon poisonous sub- 
stances, which are produced by the morbid processes peculiar to the es- 
pecial disease, and which exert a harmful influence upon the muscle- 
substance of the heart or upon the nervous system. 


FEVER. 97 


In diseases accompanied by fever there is usually a marked sensation 
of illness with a heavy feeling in the head. In severe fevers there occur 
clouding of consciousness, symptoms of excitation and depression, hal- 
lucinations, delirium, apathy, involantary evacuations, tremors of the 
hands, convulsions (in children), ete. The muscles of the body become 
weak and not infrequently’ painful. Digestion is decidedly impaired ; 
the appetite for food is slight, but on the contrary there is great thirst ; 
the mouth is dry. There is an increased frequency of respiration; after 
the appearance of muscular weakness the respiratory movements are 
superficial. The excretion of urine is usually diminished; the amount 
of urea in the urine is increased, while that of sodium chloride is dimin- 
ished. 

In prolonged fevers there is marked wasting of the body, in that a 
large portion of the albuminous material and fat of the body is de- 
stroyed. 

To what extent these symptoms in individual cases are dependent 
upon the increase of temperature or to what extent upon the damage to 
the organism caused by the specific morbid process, it is difficult to say, 
but the marked effects upon the nervous system must for the greater 
part be regarded as a result of the infection and intoxication. 

Death results most often from cardiac insufficiency, but it may be 
brought about also by the severity of the infection—that is, by the 
changes in the body-fiuids (through their influence upon the nervous 
system), by the wasting of the strength, as well as by an excessive ele- 
vation of temperature to 43°, 44°, or 45° C. (109.4°, 111.2°, and 113° 
F.). Itshould, however, be remarked that under certain conditions very 
high temperatures may be borne for a length of time without fatal re- 
sults, and that the death following very high temperatures cannot be 
ascribed to the abnormal temperature alone, but is rather to be regarded 
in part or wholly as the result of the infection (see § 3). 


The questions concerning the nature of fever, which Galen designated as Calor 
preter naturam, have been much advanced during the last decades by numerous clin- 
ical and experimental investigations. From these we have learned of the associated 
disturbances of metabolism, the increased consumption of oxygen, the increased excre- 
tion of nitrogen and carbon compounds, as well as of the disturbances of the heat-dis- 
persion. If we, in spite of this knowledge, do not yet possess a full understanding of 
all the morbid processes which in a given case may cause fever, we may attribute this 
to the fact that the causa eficiens of fever is nota single entity, but may be one of 
many different factors, and that the feverish elevation of the body-temperature does 
not always occur in exactly the same manner. The increase of the tissue-changes and 
oxidation-processes within the body is not always brought about in the same way. 
Further, the disturbance of heat-dispersion through radiation from the skin and the 
evaporation of water is not always the same, but changes, not only in the course of one 
febrile disease, but also in different forms of fever. Correspondingly, the röle played 
by the nervous system in the occurrence of the feverish increase of temperature is not 
the same in every case. According to Senator, there is, in fevers, no harmony between 
the regulation of heat and metabolism; and we must therefore assume that heat is de- 
veloped through other processes than those leading to the production of urea and car- 
bonic acid. According to Herz, heat is set free by the changes in the arrangement of 
the molecules of the cell-protoplasm, which occur in many of the cells in fever patients, 
und which lead to the destruction of protoplasm. Further, heat may be liberated by 
processes of swelling and coagulation of the protoplasm, while at the same time the 
diminished activity of the regenerative processes in fever occasions a loss in the stor- 
ing-up of latent heat. On the other hand, KreAl and Marthes are of the opinion that 
oxidation forms the sole source of heat. 


98 EFFECTS OF ORGANIC DISEASES UPON THE ORGANISM AS A WHOLE. 


Literature. 
( Fever.) 


Aronsohn u. Sachs: Beziehungen d. Gehirns zur Körperwärme u. zum Fieber. 
Pflüger’s Arch., 37 Bd., 1885. 

Bouchard: Lecons sur les auto-intoxications dans les maladies, Paris, 1889. 

Cohnheim: Vorlesungen über allgemeine Pathologie, ii., Berlin, 1882. 

Finkler: Pfliger’s Arch., xxvii.; Ueber das Fieber, Bonn, 1882. 

Franke: Die menschliche Zelle, Leipzig. 1898. 

A. Fränkel: Einfluss verminderter Sauersteffzufuhr auf den Eiweisszerfall. Virch. 
Arch., 67 Bd. 

Gangolphe ct Courmont: La fiévre conséc. a l'obliteration vasculaire. Arch. de 
méd. exp., iii., 1891. 

Gerhardt: Oertliche Fieberursachen. Mittheil. a. d. med. Klinik zu Würzburg, Wies- 
baden, 1885. 

Girard: L’infiuence du cerveau sur la chaleur animale. Arch. d. phys., viii., 1886. 

Glax: Ueber die Wasserretention im Fieber, Jena, 1894. 

Guyon: L’hyperthermie centrale, consec. aux les. du cerveau. Arch. de méd. exp. 
1894. 

Hammerchlag: Bezieh. des Fibrinfermentes zum Fieber. Arch. f. exp. Path., 27 
Bd.. 1890. 

Henrijean: Rech. sur la pathogénie de la fidvre. Rev. de méd., ix., 1889. 

Herz: Untersuchungen über Wärme und Fieber, Wien, 1893. 

Hildebrandt: Z. Kenntniss d. phys. Wirkung d. hydrolytischen Fermente. Inaug.- 
Diss., Breslau, 1890. 

Kürgeneen Die Körperwärme des gesunden Menschen, Leipzig, 1878. 

Krehl: Pathologische Physiologie, Leipzig, 1898. 

Krehl u. Matthes: Entstehung der Temperatursteigerung des fiebernden Organismus. 
Arch. f. exp. Path., 38 Bd., 1897 (Lit.); Eiweisszerfall, ib., 40 Bd., 1898. 

Leyden: Respiration im Fieber. Deut. Arch. f. klin. Med., v., vii., 1870. 

Leyden u. Fränkel: Respiratorischer Gasaustausch im Fieber. Virch. Arch., 76 Bd., 
1879. 

Liebermeister: Pathol. u. Ther. d. Fiebers, Leipzig, 1875; Specielle Pathol., Leip- 
zig, 1887. 

Löwit. Die Lehre vom Fieber, Jena, 1897. 

Loewy: Stoffwechseluntersuchungen im Fieber. Virch. Arch., 126 Bd., 1891. 

May: Der Stoffwechsel im Fieber. Zeitschr. f. Biol.. 30 Bd., 1893. 

Mosso: Influence du systéme nerveux sur la température animale. Arch. ital. de 
biol., vii., 1886; Virch. Arch., 106 Bd.: La doctrine de la fiévre et les centres 
theriniques cerébraux. Arch. ital. de biol., xiii., 1890, 

Murri: Sulla teoria della febbre, Fermo, 1874. 

Naunyn: Experimentelles zur Lehre vom Fieber. Arch. f. exp. Pathb., xviii, 
1884 (Lit. ). 

v. Noorden: Pathologie des Stoffwechsels, Berlin, 1893. 

Rabe: Die modernen Fiebertheorieen, Berlin, 1894. 

Rosenthal: Wärmeproduction im Fieber. Biel. Cbl., xi.. 1891. 

Roussy: Rech. exp. sur la pathogénie de la fiévre. Arch. de phys., ii., 1890. 

Sarbö6: Ueber hysterisches Fieber. Arch. f. Psych., 28 Bd., 1891. 

Schultze: Warmehaushalt nach dem Wärmestich. Arch. f. exp. Path., 48 Bd., 1899. 

Senator: Unters. über den fieberh. Process, Berlin, 1873; Arch. f. Anat. u. Phys., 
1872. 

Stern: Wärmeregulation im Fieber. Zeitschr. f. klin. Med., 20 Bd., 1892. 

Ughetti: Das Fieber. Jena, 1895 (Lit.). 

Unverricht: Ueber das Fieber, Leipzig, 1898. 

Volkmann u. Genzmer: Septisches u. asept. Wundfieber. Samml. klin. Vortr., No. 
121, 1877. 

Welch: On the General Pathology of Fever, Philadelphia, 1888. 

Wunderlich: Das Verhalten der Eigenwärme in Krankheiten, Leipzig, 1870. 

Zunz: Ueber den Stoffwechsel fiebernder Thiere. Arch. f. Psych.. 1882. 


CHAPTER III. 


The Protective and Healing Forces of the Human 
Body. The Acquiring of Immunity. 


I. The Natural Protective Contrivances, Protective Forces, and 
Healing Powers of the Human Organism, and their Action. 


§ 29. The human organism is not entirely defenceless against the 
many harmful influences to which men during the course of their lives 
are exposed. It possesses various protective contrivances and pro- 
tective forces, by which it is able in many cases to ward off the injuri- 
ous agent, or at least rapidly to counteract its harmfal influence, so that 
a disease may be either wholly prevented or confined to a slight local 
lesion of much less severity than the disease usually produced by the 
particular injurious agent. As the mode of action of different injurious 
influences varies greatly, so does the manner of defence likewise vary 
greatly. The protective forces may act at very different times—that is, 
sometimes even before the tissues have been damaged, at other times 
after the injurious action has reached a certain stage, and threatens, 
either through direct extension or through metastasis, or through poison- 
ing of the body-fluids, or through disturbance of function, to spread 
further through the body. 

When the environment of the body becomes relatively cold or rela- 
tively warm, those regulating functions are brought into play through 
which the organism can increase or diminish heat-production and heat-dis- 
persion, and in this manner protect itself within certain limits against 
the influence of the external temperature. If these regulating functions 
are imperfectly performed, as in consequence of alcoholic intoxication, 
the individual may more easily die from the effects of cold than when 
under normal conditions. 

We cannot speak of special protecting contrivances against gross 
mechanical influences ; yet it is to be noted that the tissues by virtue of 
their physical properties are fitted to offer resistance to numerous forms 
of traumatism without receiving injury. If small, firm bodies, such as 
dust-particles, reach the mucous membrane of the respiratory or intes- 
tinal tracts, the epithelium forms a protective barrier against their en- 
trance into the tissue-spaces. Further, if ciliated epithelium is present, 
the dust-particles may be carried away by the movements of the cilia, or 
they may become surrounded by the mucus produced by the epithelium 
and mucous glands, and in this way are transported out of the body. 

Not infrequently there appear cells on the surface of the mucous 
membrane which encompass the dust-particles, and, taking these up into 
their substance, are carried away with the secretion of the mucous mem- 
brane. This phenomenon, known as phagocytosis, is observed on the 
mucous membranes of the pharynx and respiratory tract and in the 
alveoli of the lungs. The active agents participating in it are not only 

99 


100 THE PROTECTIVE POWERS OF THE BODY. 


the wandering-cells which pass from the tissues to the surface, and are 
derived chiefly from the blood-vessels and also from the nodes of 
Iymphadenoid tissue in the mucous membrane, but epithelial cells as 
well. The peculiar phenomenon of phagocytosis depends upon the fact 
that the cells can, by movements of their protoplasm, take up little par- 
ticles, which, like insoluble dust, exert no harmful influence upon the 
cell-protoplasm. If these cells laden with dust pass outside of the body, 
the taking-up of the dust by the cells appears to be a useful activity 
which aids in the cleansing of the organs from dust. If the dust-laden 
cells, on the other hand, as happens particularly in the lungs, pass into 
the lymph-channels and are deposited along their walls or are carried to 
the lymph-glands—that is, if a metastasis of the dust-containing cells 
into the internal organs takes place—the tuking-up of dust by these cells 
appears in a less favorable light; and we can regard this act as a useful 
phenomenon only through the consideration that the infiltration of the 
pulmonary connective tissue and lymph-glands with dust is less harmful 
than the deposit of dust on the inner surface of the alveoli. 

When dust-particles, free or enclosed in cells, reach the lymph-glands, 
they are arrested and deposited in the cells of these glands, so that the 
lymph-glands may be regarded as trustworthy filters, which guard the 
blood and the internal organs from the entrance of dust. 

Against the action of poisons the human body is able to protect itself 
in various ways. In the case of corrosive poisons the horny layer of the 
epidermis and the mucus of the mucous membranes offer a certain pro- 
tection; and under certain conditions a marked increase in the produc- 
tion of mucus—in the stomach, for example—may greatly diminish 
the harmful effects of a corrosive fluid. Through a transudation of fluid 
from the blood-vessels on to the surface of the mucous membrane a 
caustic fluid may be so diluted as to modify its action. On the other 
hand, the injurious substance may be thus spread over a greater surface, 
and thereby cause a3 more widespread damage to the tissue. 

On many poisons, abrin, ricin, the toxins of cholera, tetanus, and 
diphtheria, and snake-venom, the digestive juices have such an influence 
that doses invariably fatal when injected under the skin may be borne 
with impunity when taken by the mouth. According to Ransom, 
guinea-pigs are able to withstand, when administered by the mouth, an 
amount of tetanotoxin equivalent to three hundred thousand times the 
minimal fatal dose. According to Nencki and others, this neutralization 
of the poison is produced by the digestive enzymes, at one time chiefly through 
the pepsin, at another time through the trypsin and the mixture of the 
pancreatic juice with the bile. It is probable (Nencki) that the digest- 
ive enzymes cause a slight change in the molecules of the toxin, similar 
to the change of albumin into albumose; and the products arising from 
the toxins may accordingly be termed toxoses or toxoids. 

In the case of those poisons which after their entrance into the body- 
juices act injuriously upon the blood or the nervous system, a favorable 
eounter action on the part of the organism may be given partly by a 
rapid excretion of the poison through the kidneys, liver, and intestine, 
and partly through a chemical change of the poison. This method of pro- 
tection is effective only when it is accomplished before any injury has 
been produced by the poison. 

Of natural immunity against poisons or natural resistance to poisons we 
know but little at present, yet there is no doubt that many poisons are 
poisonous only for certain organisms, and it is probable that man is re- 


THE PROTECTIVE FORCES AGAINST INFECTION. 101 


sistant to many poisons which are injurious to certain animals. The 
same thing holds true especially of the toxic proteids and the organic 
bases, as they are formed by bacteria or by higher animals (snakes) and 
plants. If we consider that many animals are only slightly or not at all 
susceptible to poisons which have marked action upon the human body 
—for example, the hedgehog is immune or resistant to cantharidin and 
the bite of poisonous snakes respectively; birds are immune against 
atropine and opium; goats against lead and nicotine; while dogs, rats, 
or other animals used for experiment show a disproportionately greater 
resistance to bacterial poisons or plant-alkaloids than does man—so it is 
very probable that the reverse is also true. The natural immunity of 
man against many of the infectious diseases of animals must depend 
upon a resistance to the toxalbumins and toxins produced by the par- 
ticular bacteria. According to Ehrlich, this resistance to poisons may 
be explained by the theory that the particular toxin possesses no chemi- 
cal relationship to any one of the bodily elements. 


Literature. | 
(The Action of Digestive Juices upon Torins. ) 


Charrin: Action des sucs digestifs sur les poisons microb. Arch. d. phys., x., 1898. 

Fraser: Remarks on the Antivenomous Properties of the Bile. Brit. Med. Journ., 
1897. 

Nencki, Sieber u. Schoumow: Entgiftung d. Toxine durch Verdauungssäfte. Ctbl. 
f. Bakt., xxiii., 1888. 

Ransom: Das Schicksal des Tetanusgiftes nacn seiner intestinalen Einverleibung. 
Deut. med. Woch., 1898. 


§ 30. Against the infections and intoxications caused by parasites 
the human organism possesses various protective contrivances and 
powers of defence ; and these play a very important röle in the diseases 
caused by bacteria. In the first place, man possesses a natural im- 
munity against many of the micro-organisms pathogenic for animals 
(for example, swine-plague, swine-erysipelas, symptomatic anthrax), so 
that the given micro-organisms are not able to reproduce within the 
body, either because they do not find in human tissues the necessary 
conditions of life, or because the presence of certain chemically active 
substances hinders their increase or kills them directly. For the protec- 
tion of the body against the pathogenic micro-organisms there are avail- 
able certain forces, which, according to their activity, may be divided 
into four groups: the first hindering the entrance of bacteria into the 
tissues; the second hindering the unlimited local spread of those bacteria 
which have gained entrance and have begun to multiply; the third pre- 
venting the entrance of bacteria into the blood and their metastasis; the 
fourth hindering intoxication, or at least weakening it, and reducing it 
to a low degree. 

For the prevention of the entrance of pathogenic bacteria into the 
tissues the same properties of tissues are effective as those hindering the 
entrance of dust; and in such capacity the protective epithelium and the 
mucus play a very important röle. In the respiratory tract the move- 
ments of the ciliated epithelium also furnish protection, and in the stomach 
the poisonous action of the gastric juice upon many pathogenic bacteria is 
an efficient means of defence. There can be no doubt that many patho- 
genic bacteria are not able to penetrate into the tissues, not only through 


102 THE PROTECTIVE FORCES AGAINST INFECTION. 


the uninjured external skin, but also through an unwounded mucous 
membrane, without some assistance favoring colonization and reproduc- 
tion, and that the stomach secretion not infrequently hinders the activity 
of the bacteria (pneumococcus, cholera spirillum), or even kills them. 

It appears also that the mucus secreted by the mucous membranes not 
only can envelop the bacteria, hinder their entrance into the tissue, and 
favor their removal, but that—what is of much greater importance—the 
mucus acts upon the bacteria, causing them to degenerate, either in that 
it contains substances which are injurious to the bacteria or in that it 
offers an unfavorable medium for the growth of the bacteria. In this 
way, according to Sanarelli and Dittrich, pus-cocci, cholera-spirilla, and 
pneumococci gradually lose their virulence and die in the mucus of the 
mouth-cavity, while diphtheria-bacilli apparently are not injured by 
mucus. In the secretion of the vagina and uterus, various kinds of bac- 
teria likewise soon die. 

Not every pathogenic organism, therefore, which gains a foothold 
upon the skin or upon any of the accessible mucous membranes or gains 
entrance to the lungs produces an infection. It has been shown through 
repeated investigations that in normal individuals there not infrequently 
occur in the upper respiratory passages and mouth-cavity not only harm- 
less bacteria—i.e., those which cannot reproduce in human tissues—but 
also those which can undoubtedly produce disease, as, for example, cocci 
which cause suppuration or those which are able to cause croupous in- 
flammation of the lung. It is, therefore, to be assumed that: bacteria 
which are found upon the mucous membranes and have perhaps multi- 
plied there often die and are carried away without having produced in- 
fection. This occurs especially in the case of the cocci above mentioned, 
and tubercle-bacilli, as well as in the case of cholera-spirilla which suffer 
when brought into contact with the acid secretions of the stomach. Fin- 
ally, it may also be assumed that of the pathogenic bacteria entering the 
alveoli of the lnng in the inspired air, many do not reproduce but die. 
Inthe case of a wound, uninjured wound-granulations offer a relatively 
secure protection against infections; in the first place, mechanically, by 
means of the thick layer of cells (Noetzel); and further, from the fact 
that the tissue-juices which escape from the granulations and infiltrate 
the same may weaken the virulence of various bacteria (Afanassieff ). 

When bacteria have succeeded in gaining entrance locally and 
have begun to multiply—no matter whether they have passed through 
the epithelium without the aid of any other influence (typhoid-bacilli, 
cholera-spirilla), or whether they have passed into the connective tissues 
through the medium of small wounds (tetanus-bacilli, pus-cocei, cocci of 
erysipelas, tuberele-bacilli)—if they produce further effects either 
through local destruction of tissue or through the poisoning of the fluids 
of the body, there may be brought into action on the part of the body 
certain counter-influences arhich either hinder the further development of 
the bacteria or weaken or even completely destroy the poisons produced by 
them. The first-named restraining influence must naturally depend upon 
local conditions, either upon vital tissue-processes or upon the effects of 
chemical substances. 

As previously mentioned, the development of bacterial colonies gives 
rise to loeal tissue-degenerations, Inflammation, and tissue-proliferations 
—all of which are processes in which the amount and composition of the 
fluids found in the affected region, as well as the cells themselves, are 
changed. Since in some of these cases a destruction of the bacteria has 


PHAGOCYTOSIS: PROTECTIVE POWERS OF THE BLOOD AND LYMPH. 103 


been observed, and the infection not infrequently comes to an end 
through the complete disappearance of the bacteria, the death of the 
latter must be regarded as dependent upon local conditions, 

Many writers ascribe the prevention of the further spread of the 
infection and the destruction of the bacteria, in local foci of growth, to 
the activity of cells which collect at the seat of infection and take up the 
bacteria into their protoplasm—that is, to phagocytosis is ascribed the 
most important röle in the protection of the body against bacterial in- 
vasion. According to Metschnikoff and others, the amaboid cells of the 
body carry on a fight against the foreign invaders and endeavor to over- 
come them and destroy them. Such a characterization of the phenomena 
of phagocytosis is not supported by the actual facts, and can be regarded 
only as a poetical manner of expression by which consciousness and will- 
power are attributed to the amceboid cells of the body (the leucocytes 
and the proliferating tissue-cells)— which attributes it is evident do not 
exist. Scientifically considered, the gathering of the cells at the infected 
focus and the resulting phagocytosis represent simply an expression of 
certain processes which are natural to the ameeboid cells, and which are 
dependent upon the fact that the cells under the influence of mechanical, 
chemical, and thermal influences perform certain definite movements. 
We know through numerous investigations that the motile cells of the 
body are in part attracted, in part repelled or paralyzed by means of 
chemical substances in certain concentrations of solution (see the Chapter 
on Inflammation); and, further, that contact with hard bodies can stim- 
ulate them to the sending-out of protoplasmic processes. 

Such phenomena are designated as negative and positive chemo- 
tropismus or chemotaxis and as tactile irritability. We must assume 
that the bacteria multiplying within the tissues act upon the ameboid 
cells through the chemical substances which they produce, sometimes re- 
pelling or paralyzing, sometimes attracting, in the latter case affording 
conditions favorable for phagocytosis. This assumption is in harmony 
with the actual behavior of the cells in different local infections, in that 
the bacteria in one case are taken up by the cells, in another they are 
left undisturbed. 

If phagocytosis of the cells, in infections, be regarded as one of the 
vital phenomena of cells, it may be interpreted as a process designed for 
the taking-up of nourishment ; and this interpretation would suffer only 
one exception, whenever microparasites, themselves capable of motion, 
penetrate by reason of their own activity into the cells. 

The result of the taking-up of bacteria into cells depends in a particular 
case partly upon the properties of the devouring cells, partly upon the 
properties of the microparasites, and can result as well in the death and 
dissolution of the parasite, as in the death of the cells; or in a symbiosis 
of the cells with the parasites, the latter living within the cells un- 
changed and giving rise to no disturbance. In the first-named case the 
phagocytosis may be regarded as a curative process which hinders the 
multiplication and spread of the bacteria. In the second and third 
cases, on the contrary, the phenomenon is useless for the prevention of 
the spread of the parasites; indeed, there are cases (leprosy and to some 
extent also tuberculosis) in which the parasites find favorable conditions 
for development inside of the cells, increase within them, and finally 
eause their destruction. If the cells containing bacteria remain pre- 
served for a length of time, they may wander with the enclosed bacteria 
to other parts of the body, in this way effecting a metastasis. 


104 THE PROTECTIVE FORCES AGAINST INFECTION. 


Phagocytosis is therefore only of slight significance us a protective force in 
a certain number of cases ; yet it cannot be doubted that the phagocytes in 
certain infections take up, not only dead or dying, but also living bac- 
teria not yet injured by other agents, and can cause their death. The 
collection of great numbers of cells in the infected tissue may, through 
the close packing of the lymphatics, offer a eertain mechanical hindrance to 
the spread of bacteria, yet the protection so afforded is frequently in- 
sufficient. 

It bacteria, either free or enclosed in cells, pass from the ly miph-ves- 
sels into the lymph-glands, the latter act as filters, as in the dase of 
dust, and retain the bacteria; but the protection which they offer is 
sufficient only when the bacteria so collected in the lymph-glands are 
hindered in their reproduction and are killed by the influence of their 
surroundings. The destruction may be accomplished under the influence 
of phagocytosis, but in many cases phagocytosis is possible only when the bac- 
teria are weakened or have already been killed. Further, the taking-up of 
living bacteria by the cells is not always followed by destruction of the 
bacteria, but there very frequently takes place an intracellular multipli- 
cation of the bacteria. 

More important than phagocytosis for the prevention of the spread 
of bacteria and other microparasites is the influence exerted by certain 
chemical substances in solution in the tissues. Since the saprophy- 
tic, non-pathogenic bacteria, when injected into living tissue, are killed 
within a very short time, we must assume that in the tissues there are 
present chemically active substances which are poisonous for many bacteria and 
can cause their rapid destruction. Further, since many pathogenic bac- 
teria ordinarily increase only loeally (tetanus-bacilli, diphtheria-bacilli, 
cholera-spirilla) and after a certain time perish within the infected area, 
without spreading further through the body, it is very probable that the 
tissues of the body also contain substances which are poisonous for 
many pathogenic bacteria and prevent their spread. The phenomena 
observed in local infections speak also for the fact that such substances 
at times are formed in increased amounts or are aided in their action by 
newly-formed poisonous substances. It is, furthermore, probable that 
the crowding of cells which takes place in the infected tissue or in its 
neighborhood leads also to an increase in the production of these poison- 
ous substances, and may thereby hinder the spread of the bacteria; nev- 
ertheless, attention should be drawn to the fact that in many infections 
the spread of bacteria through the tissues comes to a standstill in places 
where there has been no crowding together of cells. It is also a fact 
that in many infections the spread of bacteria through the body by 
metastasis is either wholly wanting (tetanus, diphtheria) or at least is 
insignificant. in comparison with the local infection, and is usually fol- 
lowed by relatively insignificant local changes. The explanation of this 
fact is to be sought, not so much in the assumption that local tissue- 
changes, through the formation of special chemical substances or through 
the aid of mechanieai substances or through the aid of mechanical hin- 
drances—such as that afforded by a wall of cells—hinder the entrance of 
bacteria into the lymph and blood, but much more in the fact that: there 
are present in the lymph and blood itself certain forces which are able to in- 
jure and weaken the bacteria taken up into these fluids or to destroy 
them. 

The hostile action of the blood oi bacteria has been ascribed to the 
phagocytie action of the leucoevtes; and this theory is supported by the 


PHAGOCYTOSIS: ANTIBACTERIAL PROPERTIES OF THE BLOOD. 105 


fact that such a phagocytosis can be demonstrated very frequently in 
acquired infections or after the artificial introduction of bacteria into the 
blood; and, further, by the fact that the bacteria within the blood, en- 
closed in cells, may often be carried out of the blood-vessels and deposited 
in different organs—for example, the spleen, liver, bone-marrow, and 
the kidneys—and there destroyed or excreted from the body. These 
observations do not warrant the conclusion that phagocytosis forms a 
protection against the spread of bacteria in the lymph and blood; in- 
deed, in those very cases in which a transportation of bacteria through 
the blood does not take place, phagocytosis is also absent; while on the 
contrary, the entrance of bacteria into the blood, and the multiplication 
of the same inside of the blood-vessels, is very often accompanied or fol- 
lowed by phagocytosis. Here, again, phagocytosis is of the nature of a 
secondary phenomenon which occurs when there are present in the blood 
bacteria or protozoa, which like bland dust-particles are not able to pre- 
vent their being taken up into the bodies of the leucocytes—that is, they 
exert a positive attraction on the phagocytes. 

When bacteria are taken up by cells, they either die or continue to 
multiply inside of the cells, according to their properties and their con- 
dition at the time of the phagocytosis. 

The forces which are able to hinder the development of bacteria in 
the blood are believed by the majority of writers to depend upon the 
presence of antibacterial chemical substances, which belong to the 
albuminoid bodies, and are designated as the protective albuminoid 
bodies or alexins (Buchner) or mycosozins (Hankin). 

Emmerich and Buchner assume that the alexins of the blood are 
albuminoid bodies, having an action similar to that of enzymes, and 
therefore class them with the enzymes. This view finds acceptance 
with other authors. On the other hand, Baumgarten and Walz, as well 
as A. Fischer, oppose the view that there are chemically active pro- 
tective substances in the blood; and hold that the natural immunity of 
the tissues and blood against certain bacteria is dependent upon the fact 
that the bacteria do not find the necessary chemical conditions for their 
development and reproduction. 

So far as conclusions can be drawn from the behavior of the human 
and animal organisms in infectious diseases, we may assume that in the 
blood of man there are always present protective chemical substances, that is, 
alexins, particularly so against bacteria which never or only exception- 
ally enter the blood; and that others, on the contrary, are produced only 
during the course of an infection, so that not until a certain stage of the 
infection does an inhibition of the development of the bacteria, through 
the formation of antibacterial substances, occur. In favor of such 
hypothesis speaks the fact that many bacteria (typhoid-bacilh, cholera- 
spirilla, pus-cocei) possess at first their full virulence when distributed 
through the body by the blood, but later suffer a loss of virulence and 
finally die. . 

The protection which the alerins of the blood afford the organism is 
restricted to certain diseases; that is, to those infections in which the 
multiplication of the bacteria is always confined to a limited area, or in 
which at least the transported bacteria suffer a marked decrease of viru- 
lence. Against many infections the peculiar degenerative action of the 
blood upon bacteria is either wholly wanting or, in case it is present, is 
easily overcome, especially so in those infections in which the bacteria 
increase in the blood itself (anthrax), as well as in those in which the 


106 THE PROTECTIVE FORCES AGAINST INFECTION. 


bacteria do not increase in the blood, but suffer no decrease of virulence 
after metastasis (tuberculosis, leprosy, infections with pus-cocci). 

The means of protection which the organism possesses against the 
poisons produced in the tissues by bacteria are to be found, first, in 
the possibility of a rapid excretion of the poisons by the kidneys, or, 
under certain circumstances, also by the stomach, intestine, and skin; 
and this action may in certain cases suffice to prevent a fatal poisoning. 
Further, in certain infections there is evidently an antagonistic action on 
the part of the organism, in the sense that certain poisons are either 
destroyed or neutralized through the action of counter poisons or 
antitoxins; or that the toxins and antitoxins combine to produce 
non-poisonous substances, or that the metabolic products of the tissues 
protect the latter from the action of the toxins. 


The antibacterial properties of the blood and lymph against certain bacteria have been 
demonstrated conclusively by the experimental investigations of various writers. 
These experiments have shown that the bactericidal action of the blood of a given ani- 
mal is exerted only upon certain forms of bacteria and never upon all; and that this 
action is subject to individual variations. 

According to the investigations of Fodor, Petruschky, Nuttal, Ogata, Buchner, Beh- 
ring, Nissen, Pansini, and others, the blood and the serum from dogs, rabbits, and 
white rats are capable of rendering the anthrax-bacillus harmless, and even of killing it; 
but this action is a limited one, so that after the introduction of a large number of the 
bacilli into the blood taken from the vessels, the bacilli after a time begin to multiply. 
Defibrinated blood of dogs and rabbits can destroy the choleza-spirillum and typhoid- 
fever bacillus; but, on the other hand, has no effect upon the different pus-cocci, and 
against proteus; the same is true also with regard to the blood-serum. Human blood 
or blood-serum can kill typhoid-bacilli, diphtheria-bacilli, and the bacilli of glanders. 
If the bactericidal properties be exhausted, these bacteria may grow luxuriantly in the 
blood or serum. Heating of the blood-serum to 55° C. deprives it of its bactericidal 
properties; the enzyme is destroyed (Buchner). 

According to Morter, there are two substances concerned in the bactericidal action 
of the animal fluids; one of which disappears at a temperature of 60° C., while the 
other remains preserved. 

Baumgarten and Walz regard the fact that different bacteria which have been 

assed into the blood or blood-serum do not develop at all, or show but partial or de- 
ayed growth and a great diminution in numbers when cultivated upon plates, as in no 
manner speaking for the presence of bactericidal substances in the blood. According 
to their view, the second transplantation into another culture-medium causes a disturb- 
ance of the processes of assimilation and osmosis. There arise in consequence plasmo- 
lytic changes in the bacteria present in the serum; during the pouring of the plates the 
already injured cells die from disturbances of assimilation. This view is also held, 
supported by experimental investigations, by A. Fischer. On the other hand, it is to 
be noted that A. and JZ. Kossel have demonstrated that certain products of animal 
cells (nucleinic acid, protamine) possess bactericidal properties. 

Hankin, Kanthack, Denys, Hahn, Zöwit, and others assume, on the ground of ex- 
perimental investigations, that the alerins are produced ly the leucocytes. Kossel holds it 
as possible that the nucleinic acid present in the leucocytes in relatively rich amounts 
plays a röle in the destruction of the bacteria. Noesske believes that the eosinophile 
cells of the bone-marrow in particular produce bactericidal substances, It is not possi- 
ble at the present time to draw a definite conclusion as to the part played by the color- 
less cells of the blood in the defence against. infections. 

According to Bitter, the bactericidal substance found tn organs—that derived from 
the Ivmph-glands, spleen, and thymus—is to a certain extent different from that of the 
blood and the blood-serum, and therefore does not originate wholly in the blood. It is 
certain that the bactericidal action of the blood is not the only protective influence 
which can oppose the spread of an infection, or wholly prevent it, and confer im- 
munity, 

According to observations of Czaplersk’, anthrax-bacilli in an infected organism, 
which have been taken up into leucocytes, degenerate as a rule more slowly than those 
Iving free in the blood and tissue-juices. It appears, therefore, as if under certain con- 
ditions the cells afford to the bacteria which they enclose a certain degree of protection 
from the bactericidal substances of the tissue-tluids. 

The antitorins which render the bacterial poisons harmless are usually formed first 


THE PROTECTIVE FORCES AGAINST INFECTION. 107 


during the course of the infection; but, according to the investigations of Wasser- 
mann, Abel, Fischl, von Wunschheim, and others, the serum of healthy men also con- 
tains such substances. Serum which contains the antitoxin against a certain toxin— 
as, for example, that against the diphtheria-toxin—can be a good culture-medium for 
the given bacteria; the antitoxin does not destroy the bacteria. 


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xxii., 1897. 

Arloing: Un mot sur l’immunit& naturelle. Arch. de méd. exp., 1890; Les virus, 
Paris, 1891. 

Arnold: Der Kampf d. menschl. Organismus mit d. Bakterien. Akad. Rede, Heidel- 
berg, 1888. 

Baumgarten: Der gegenwärtige Stand der Bakteriologie. Berl. klin. Woch., 1900; 
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Behring: Infection und Desinfection, Leipzig, 1894; Infectionsschutz u. Immunität. 
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f. Hyg., viii., 1890. 

Pouvoir bactéricide des leucocytes. Ann. de l’Inst. Pasteur, xii., 1898. 

Bitter: Ueb. d. bakterienfeindlichen Stoffe thierischer Organe. Zeit. f. Hyg., xii., 1891. 

Bordet; Rech. sur la phagocytose. Ann. de l’Inst. Pasteur, 1896. 

Brock: Resorptionsvermögen der Haut. Arch. f. Derm., 35 Bd., 1898 (Lit.). 

Buchner: Ueber die bakterientödtende Wirkung des freien Blutserums. Centbl. f. 
Bakt., v., vi., 1889; Ueber die bakterientödtende Wirkungen d. Blutes u. Blut- 
serums. Arch. f. Hyg.. x., 18%, ref. Cbl. f. Bakt., ix.; Hülfskräfte d. Organ- 
ismus gegen Kraukheitserreger. Münch. med. Woch., 1894; Bakteriengifte und 
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Charrin: Les défenses naturelles de l’organisme, Paris, 1898. 

Czaplowsi. Unters. üb. d. Immunität der Tauben gegen Milzbrand. Zeit. f. Hyg., 
xii., 1892. 

Emmerich u. di Mattei: Vernichtung d. Milzbrandbacillen im Organismus. Fortschr. 
d. Med., v.. 1887. 

Emmerich u.Tsuboi: Die Schutz- u. Heilkräfte des Blutes. Verh. d. XI. Kongr. f. 
inn. Med., Wiesbaden, 1892; Mikrobicide Wirkung des Blutserums. Cbl.f. Bakt., 
xiii., 1893. 
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f. Hyg., 35 Bd., 1900. 

Fischl u. v. Wunschheim: Schutzkräfte im Blute d. Neugeborenen. Zeit. f. 
Heilk., 1895 (Lit.). 

v. Fodor: Die Fähigkeit d. Blutes, Bakterien zu vernichten. Cbl. f. Bakt., vii., 1890. 

Friedenthal: Function der weissen Blutkörperchen. Biol. Cbl., xvii., 1897 (Lit.). 

Gabritschewsky: Pathologie der Spirochäteninfection. Cbl. f. Bakt., xxiii., 1898. 

Hankin: Ueber den schützenden Eiweisskörper der Ratte Cbl. f. Bakt., ix., x., 
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Hugenschmidt: Defense de la cavité buccale. Ann. de l’Inst. Pasteur, 1896. 

Jacob: Schutzkraft d. Leukocyten. Zeit. f. klin. Med., 32 Bd., 1897. 

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Kendratieff: Selbstschutz des thier. Organismus. Arch. f. exp. Path., 37 Bd., 1896. 

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108 HEALING POWERS OF THE BODY. 


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v. Ziegler, xii., 1892. 

See also Literature to SS 31 and 32. 


8 31. The healing-powers of the human body are furnished by those 
life-processes which are able to compensate for the disturbances and changes 
caused by disease, and to render harmless or to remove any harmful agent that 
may still be present in the body. If portions of tissue have been destroyed, the 
healing consists essentially in the removal of the changed and dead tissue, and 
its replacement by neie tissue. 

When from any cause the temperature of the body becomes abnor- 
mally low or abnormally high, compensation may be effected in such 
away that through the suitable regulation of the heat-production and 
heat-dispersion the temperature of the body may be brought back 
to the normal. If through trauma a portion of tissue is destroyed, the 
organism may repair the defect either through the local production of 
new tissue (regencration) or by a corresponding inerease in other similar 
tissues (compensatory hypertrophy). 

If poisons enter the body and produce symptoms of intoxication, 
healing can follow only through the rapid ereretion of the poison, or its 
destruction or neutralization within the body: while at the same time the 
damaged. tissues, under the influence of normal nutrition, again return 
to their normal state, existing defects being properly compensated. 


HEALING POWERS OF THE BODY IN INFECTIONS. 109 


In infections the healing processes follow direetly upon the action of 
the protective forces ; indeed, the action of the latter constitutes the first 
stage of healing; the protective and healing processes are in part identical. 
If the alerins are able to hinder the development of bacteria, and if the 
weakened bacteria are dissolved and destroyed in the tissue-fluids, the 
first step in the healing process will have been accomplished, in that the 
causa efficiens has been removed. If the mussing together of cells in the 
infected tissue forms a protecting wall against the spread of bacteria, or 
if the latter are held back in the lymph-glands and there destroyed, such 
phenomens are to be regarded as processes which prepare the way for 
the healing. Phagocytosis may also aid the healing-process. Ina similar 
manner the removal of the poisons or the bacteria which have gained entrance 
to the blood through the excretory organs, kidneys, liver, stomach, and 
intestine, not only acts as a protection against the further localization of 
the disease and against increased intoxication, but also makes possible, 
through the removal of the injurious agents, the restoration of the al- 
ready damaged tissues. __ 

In many infectious diseases the healing influence of protective sub- 
stances already present in the affected body is supplemented by the ap- 
pearance of new substances foreign to the normal organism, which as 
bactericidal substances and as antitoxins antagonize both the infection 
and the intoxication. These counter-poisons are formed either by the 
tissue-cells and the blood, which through the infection have been placed 
under altered conditions of life, or they have been formed by the bae- 
teria themselves; they spread throughout the tissue- juices, and thus hin- 
der the further extension and multiplication of the bacteria. 

The action of these anti-bodies consists either in the inhibition of 
bacterial growth or the destruction of the bacteria, or in the destruction 
and neutralization of the poisons produced by the bacteria, or in their 
combination with the latter to form inert, non-toxic substances. It is 
also possible (see § 32) that in certain infections they render the tissues 
insusceptible to the bacterial poison. 


The cause of the healing of tnfectious diseases is most frequently referable to the fact 
that chemical substances erert an antagonistic action against the intoxication, and that the 
bacteria are prevented from further development and so die out. It has been demon- 
strated, however, that in many cases the bacteria may survive and probably also pro- 
duce poisons, which, however, are harmless because of the presence of the antitoxins. 
In individual cases the theory appears admissible that a lack of proper nutritive mate- 
rial causes the death of the bacteria; as is perhaps the case in localized foci of infection 
(tuberculosis), in which the bacteria, enclosed in dead or slowly degenerating tissue, 
may remain for a long time without being able to escape to new tissues for food mate- 
rial. Further, such changes in the composition of the tissue-juices may be produced 
that the bacteria no longer tind the proper conditions of nutrition. Finally, it is also 
conceivable that bacteria, from intrinsic causes within the bacterial cell itself, may no 
longer multiply. and so die out. . 

According to the investigations of R. Pfeiffer, which have been confirmed by 
Sobernheim, Dunbar, Léfier, and others, the blood-serum of animals rendered immune 
to typhoid-bacilli or cholera-spirilla, or that of human beings ill or convalescing from 
typhoid and cholera, contains, besides antitoxins, also a specific bactericidal substance 
(lysogenous aubstance of C. Fraenkel). This body possesses the power, when the serum 
is added to a virulent bouillon-culture, so to change the culture that the bacteria, when 
injected into the peritoneal cavity of experimental animals, rapidly break up into mi- 
nute globules and are dissolved. 

According to the investigations of Gruber, Durham, Pfeiffer, Kolle, Sobernheim, 
Widal, C. Fraenkel, and others, the blood-serum of individuals ill, convalescing, or en- 
tirely recovered from typhoid or cholera, exerts a damaging influence upon typhoid- 

li or cholera-spirilla respectively ; this influence being of such a nature that in 
bouillon-cultures the bacteria so affected become motionless, clump together, sink to 


110 HEALING POWERS OF THE BODY. 


the bottom of the vessel, and are destroyed. When the serum is added to a hangin 
drop of bouillon-culture, the rapidly-moving vibrios at once become motionless and 
collect in little heaps. Gruber believes that this phenomenon is to be explained by a 
swelling and bursting of the membrane of the bacterial cell, and assumes that this 
change enables the alexins to destroy the bacteria present in the body. He therefore 
designates the active substances in the serum as agglutinins, and believes that to these 
may be attributed the chief agency in the healing of infectious diseases and in the pro- 
duction of immunity against the same. Pfeiffer, on the contrary, denies the occurrence 
of any swelling of the cell-membrane, and explains the phenomenon as due to an in- 
hibition of development, and designates the active substances, the nature of which is 
wholly unknown, as specific paralysins. After Gruber had demonstrated the peculiar 
action of the blood-serum of typhoid-fever patients, Widal (Sem. médicale, Paris, 1896) 
proposed that this action of the blood-serum on cholera-spirilla and typhoid-bacilli be 
utilized as a diagnostic aid during the course of an attack of typhoid. The investiga- 
tions of C. Fraenkel, du Mesnil, and others have demonstrated that it is possible, during 
the course of the attack or for a long time (several months) afterward, that the diag- 
nosis of typhoid may be made from the action of the serum upon cultures of typhoid 
bacilli. 

Metschnikof, Bordet, and others hold that the chief cause of healing from infectious 
diseases and of the acquiring of immunity (see § 82) is to be found in the activity of the 
leucocytes, which, according to their view, supply bactericidal substances to the body- 
juices and destroy the bacteria by taking them up into their cell-bodies. Phagocytosis, 

owever, plays only a subordinate röle, since most of the bacteria are destroyed by 
the cells, only after they have been injured or killed by the bactericidal substances of 
the blood-serum and the tissue-juices. In many infections bacteria are indeed taken u 
by cells, but are not destroyed by them; on the other hand, they may find in the cell- 
protoplasm a soil favorable to their development. 

It has often been assumed that the fever occurring in infectious diseases is a pro- 
tective process favoring the destruction of bacteria; and it is not impossible that in 
indictdual cases it may exert such a favorable influence. Thus, for example, it is con- 
ceivable that a parasitic micro-organism, growing well at a temperature of 37-38° C.. 
will not thrive at a temperature of 40-41° C., so that high fever-temperatures may bin- 
der its power of reproduction. The conclusion should not, however, be drawn from 
this that fever is a useful phenomenon which always favors the counter-balancing of 
pathological disturbances. Even in those cases in which the metabolic processes occur- 
ring during the fever exert an injurious influence upon the bacteria, this is not to be 
taken as proving the usefulness of fever. We can only say that a part of the morbid 
processes occurring during an infectious fever leads to a formation of decomposition- 
products which may possess antibacterial or antitoxic properties. 


Literature. 
(The Healing Powers of the Organism in Infections and Intoxications. ) 


Banti: Sulla distruzzione dei batteri nell’ organismo. Arch. p. le Sc. Med., xiii., 1889. 

Biedl u. Kraus: Ausscheidung d. Mikroorganismen durch Drüsen. Zeit. f. Hyg., 
xxvi., 1897. 

Bitter: Metschnikoff’s Phagocytenlehre. Zeit. f. Hyg., iv., 1888; Bakterienfeindl. 
Stoffe thier. Organe, ib., xii., 1892. 

Bongers: Ausscheidung körperfrender Stoffeim Magen. Arch. f. exp. Path., 35 Bd., 
1895. 

Bordet: Action desserums préventifs. Ann. de l’Inst. Past., 1896; Mécanisme de l’ag- 
glutination, ib., 1899. 

Bouchard: Les microbes pathogénes, Paris, 1892. 

Brieger: Antitoxine und Toxine. Zeit. f. Hyg., xxi., 1896. 

Cavazzani: Ausscheidung der Bakterien durch die Nieren. Chbl. f. Bakt., iv., 1898. 

Denys ct Havel: La part des leucocytes dans le pouvoir bactéricide du sang. La 
Cellule, x., 1893. 

Durham: On a Special Action of the Serum. Journ. of Path., iv., 1896. 

Eichel: Wachsthumsverhältnisse verschied. Bakterien im Fieber. Virch. Arch., 121 
Bd., 1890. 

Foerster: Die Serodiagnostik d. Abdominaltyphus. Fortschr. d. Med., 1897 (Sam- 
melref.). 

Fraenkel, C.: Agglutinine bei Typhus abdom. (Widal’sche Probe). Deut. med. 
\Woch., 1897 (Lit.). 


THE ACQUIRING OF IMMUNITY. 111 


Gamaleia: Destruction des microbes dans les organismes febricitants. Ann. de l’Inst. 
Past., 1883. 

Golgi: Il fagocitismo nell’ infezione malarica. Arch. ital. de biol., xi., 1889. 

Gruber: Immunität geg. Cholera u. Typhus. Wien. med. Woch., 1896; Theorie der 
Immun. (Agglutinine). Münch. med. Woch., 1897; Serumdiagnostik d. Typhus, 
ib.; Theorie der Agglutination, ib., 1899. 

Hahn: Bezieh. d. Leukocyten z. baktericiden Wirkung d. Blutes. Arch. f. IIyg., 25 
Bd., 1895. 

Jetter: Baktericide Eigensch. d. Blutserums. Arb. a. d. path. Inst. zu Tübingen, i., 
1893. 

Loewy u. Richter: Heilkraft des Fiebers. Virch. Arch., 145 Bd., 1896 (Lit.). 

v. Klecki: Ausscheidung d. Bakt. durch d. Nieren. Arch. f. exp. Path., 39 Bd., 1897 
(Lit.). 

Melnikow: Bedeutung der Milz bei Infectionen. Zeit. f. Hyg., xxi., 1896 (Lit.). 

du Mesnil: Gruber-Widal’sche Serumdiagnostik. Münch. med. Woch., 1897. 

Nissen: Bakterienvernichtende Eigenschaften des Blutes. Chbl. f. Bakt., iv., 1889. 

Pawlowsky: Heilung des Milzbrandes durch Bakterien u. das Verhalten der Milz- 
brandbacillen im Organismus. Virch. Arch., 108 Bd., 1887; Bemerk. üb. d. 
Mittheilung v. Emmerich u. di Mattei: Ueber Vernichtung der Milzbrandbacillen 
im Organismus. Fortschr. d. Med., vi.; Infection u. Immunität. Zeit. f. Hyg., 
33 Bd., 1900. 

Pernice u. Scagliosi: Ausscheidung d. Bakt. a. d. Organismus. Deut. med. Woch., 
1392 (Lit.). 

Pfeiffer (Kolle, Vagedes): Ein neues Grundgestz d. Immunität, etc. Deut. med. 
Woch., 1896: Specifische Immunitätsreaction der Typhusbacillen. Zeit. f. Hyg., 
xxi., 1596 (Lit.); Weitere Untersuchungen üb. specifische Immunitätsreaction. 
Chl. f. Bakt., xx., 1896 (Lit.). 

Roger: Elimination des poisons. Path. gén. de Bouchard, i., Paris, 1895. 

Buffer: Destruct. des microbes par les cellules amaboides. Ann. de l’Inst. Past., v., 


1891. 
rrington 5 Exper. on the Escape of Bactcria with the Sccretions. Journ. of Path., 
i., 1893 (Lit.). 

Sirotinin: Entwickelungshemmende Producte der Bakterien. Zeit. f. Hyg., iv., 1888. 

Tsuboi: Die Schutz- und Heilsubstanz des Blutes, Wiesbaden, 1892. 

Wassermann: Pneumokokkenschutzstoffe. Deut. med. Woch., 1899. 

Widal et Sicard: Le sérodiagnostic. Ann. de l’Inst. Past., 1897 (Lit.). 

Ziegler: Die Ursachen d. pathol. Gewebsneubildungen. Internat. Beitr., ii., Festr. f. 
Virchow, Berlin, 1891; Ueb. d. Zweckmässigk. d. pathol. Lebensvorgänge. 
Münch. med. Woch., 1896. 

See also § 30 and $ 32. 


li. The Acquiring of Immunity against Infection and Intoxication. 
Protection through Inoculation. 


§ 32. The acquiring of immunity against a particular infectious 
disease is a phenomenon whose frequent occurrence has long been known 
through clinical observations. This fact has been established chiefly by 
the observation that the great majority of men suffer but one attack of 
such widespread infections as measles, smallpox, whooping-cough, scar- 
let fever, and diphtheria, and that after such attack they are spared by 
the disease, even when they expose themselves under the most varied 
conditions to the danger of infection with its poison. The knowledge of 
this fact is very old, and early in the eighteenth century it had led, in 
the Orient, to attempts to obtain immunity against the natural contagion 
of smallpox by the inoculation of material from smallpox pustules. In 
the latter part of the eighteenth century Jenner discovered that the dis- 
ease known as cowpox—i.e., a milder form of pox, which is either a 
special variety of disease closely allied to human smallpox or a weaker 
form of the latter—afforded protection against the true smallpox. As 
a result of this observation, since the beginning of the year 1796, at first 
by Jenner himself, afterward by the physicians of all civilized countries, 


112 THE PROTECTIVE FORCES AGAINST INFECTION. 


artificial inoculations of cowpox have been carried out upon millions of 
human individuals, with the result that through such inoculation a high 
degree of immunity against the true smallpox has been secured to the 
inoculated; so that at the present time, in all countries where vaccina- 
tion is universally practised, the occurrence of widespread epidemics of 
smallpox, once so frequent, is very rare, and the disease no longer as- 
sumes the character of a dangerous pestilence. 

The investigations of the last decades with regard to the causes and 
origin of infectious diseases, which have covered such an extraordinarily 
broad field, have shown that the acquiring of immunity against a cer- 
tain infectious disease through one attack of the given disease oc- 
curs in different infectious diseases, especially in those running an acute 
course; and represents sometimes a transitory, at other times a per- 
manent peculiarity of the individual concerned, which in pregnant 
. women may be transmitted to the foetus in utero. These observations 
have also shown that the single or repeated inoculation of attenuated 
pathogenic bacteria—that is, of bacteria which on account of their slight 
virulence produce a disease that, in contrast to the natural infection with 
bacteria of full virulence, is relatively insignificant, often localized to a 
limited area—can also confer immunity against the corresponding dis- 
ease. Further, it has been demonstrated that the injection of certain 
chemical substances produced by the bacteria is sufficient to confer 
Immunity against certain infections. 

In explanation of the immunity acquired through an infectious 
disease or through inoculation, we are at the present time limited to 
hypotheses, yet it cannot be doubted that the last few years have brought 
great advance in our knowledge of the forces concerned in the produc- 
tion of such immunity, so that we at least know in what direction 
further researches should be made. 

After Pasteur had, in 1880, proved experimentally that chickens 
could be made immune against chicken-cholera through injections of 
attenuated chicken-cholera poison, and after it had been established by 
the investigations of different authors that similar results could be ob- 
tained in anthrax, symptomatic anthrax, and swine-erysipelas, it: was at 
first believed that the acquiring of immunity could be explained by the 
fact that through the inoculation or the first attack of the given infection 
the food-material in the body had been exhausted (Pasteur, Klebs), so 
that bacteria entering the body later were unable to find food. This 
hypothesis, known as the erhaustion-theory, cannot be brought into har- 
mony with the observed facts, so that it is now generally abandoned. 
Also the view of Metschnikoff, that the mesodermal cells become accus- 
tomed through the preventive inoculations, to the taking-up of the pre- 
viously untouched virulent bacteria, and quickly take them up and 
destroy them after repeated inoculation, can in no wise be regarded as 
an hypothesis based upon scientific foundations. 

According to the facts which have been ascertained by investigations 
eonecerning the natural protective powers of the body against infection, 
and the natural mode of recovery from infections, as well as the experi- 
ments made with regard to protective inoculation and the artificial heal- 
ing of infectious diseases, it is very probable that acquired immunity 
is dependent upon the presence of certain chemical substances which 
are either poisonous for the particular variety of bacteria concerned, or in 
some manner or other counteract the activity of the product formed by these 
bacteria (poison- theory). It is yet an unsettled question whether these 


THE ACQUIRING OF IMMUNITY: THE POISON THEORY. 113 


substances are products of the body-cells; further, whether the loss of 
toxic action of the toxalbuimns and toxins formed by the bacteria is due 
to a destruction of the same, or to the formation of inert combinations 
of these bodies, or to au immunization of the body-cells against these 
poisons. 

Some light with regard to these questions is given by our present 
knowledge concerning the different ways in which, not only in experi- 
mental animals, but also to a certain extent in man, an immunity against 
certain infectious diseases may be obtained. Further light is also ob- 
tained from experiments concerning the artificial healing of infections 
which have already begun to develop. As previously stated, it is possible 
to produce in animals, in harmony with the knowledge obtained through 
Jenner’s cowpox inoculation, an immunity through the inoculation 
of attenuated specific disease-germs; as, for example, in anthrax, 
symptomatic anthrax, chicken-cholera, diphtheria, swine-erysipelas. 

The weakening of the virulence of bacteria may be produced either 
by the action of high temperatures or chemical agents, or by the action 
of the air alone; further, it may also be produced by the inoculation of 
the bacteria into certain animals or through their long-continued culti- 
vation on artificial media. Inoculation is, in general, carried out by in- 
jecting subcutaneously first markedly attenuated, then less attenuated, 
and finally fully virulent bacteria together with their products. 

According to the investigations of numerous authors, immunity in 
animals may also be produced by the injection of sterilized cultures 
in which the bacteria are completely killed—as, for example, against 
American hog-cholera, symptomatic anthrax, diphtheria, the infectious 
disease produced experimentally in rabbits by the injection of the 
Bacillus pyocyaneus, and the infection produced in guinea-pigs by cholera- 
spirilla. It is probable that the immunizing substances are contained 
in the cell-substance of the bacteria (Brieger, Kitasato, Wasserinann). 

A third form of artificial immunization, which Raynaud attempted 
as early as 1877 but was first securely established by Behring in 1890, 
can be produced by the injection into man or an experimental animal of 
blood-serum taken from animals which were previously susceptible, 
but have been rendered immune by means of inoculations. The most 
extensive and at the same time the most successful attempts thus far 
made have been carried out with diphtheria and tetanus ; that is, in dis- 
eases in which intoxication through toxalbumins forms the most striking 
feature. Moreover, successful experiments with the blood-serum of 
immunized animals, in the case of cholcra, swine-erysipelas, anthrax, 
typhoid fever, and plague, have been reported. 

The specific protection which the blood-serum affords may be secured, 
not only by injection before infection occurs, but also after infection 
has already taken place; so that the serum may be designated not only a 
protective serum, but also a healing serum. For both protection 
against and for the cure of a certain infection a definite amount of serum 
is necessary, the precise amount depending, on one hand, upon the se- 
verity of the infection, and On the other, upon the activity of the serum 
itself, which increases with the completeness of the immunization of the 
originally susceptible animal furnishing the serum. If the serum is not 
injected until after infection has occurred, the amount of serum must be 
so much the greater the longer the lapse of time after the beginning of 
the infection. 

In the case of true bacillary diphtheria, the injection of curative 

8 


LANE LIBRARY. v...... . 


ans 


en 


114 THE PROTECTIVE FORCES AGAINST INFECTION. 


diphtheria-serum has now been carried out in thousands of cases, of 
both severe and light forms; and there is without any doubt a beneficial 
influence exerted upon the course of the disease, as shown by a rapid 
improvement of the patient’s general condition (rapid establishment of 


seuphoria, fall of fever, improvement in the pulse), as well as by the 


favorable course pursued by the local disease. In tetanus a definite cur- 
ative action of serum has been demonstrated in the case of experimental 
animals, guinea-pigs, and mice; but the results in man have not yet been 
fully determined. 

The blood-serum of immunized auimals exerts its beneficial action, 
without doubt, through the presence of a ceunter-poison, an antitoxin, 
which neutralizes the poisons produced by the bacteria. In the case of 
the patients treated by a given antituxin, there is produced a poison- 
immunity against the ‘corresponding baect erial poison—as, for example, 
against the poison produced by the diphtheria bacilli, in those patients 
injected with diphtheria- autitoxin—and this immunity is to be ascribed 
to the presence of a definite amount of antitoxin in the blood. 

The chemical nature of the antitoxins, whose oceurrence In numerous 
infections and intoxications (diphtheria, tetanus, pneumonia, snake- 
poison, poisoning with riein, abrin) has been demonstrated, is not 
known. Their mode of action may be explained either by the assump- 
tion that they destroy the specific bacterial poisons ( Behring), or that 
they only render the tissues insusceptible to the action of the latter 
(Buehner, Tizzoni, and others), or finally, that they form in the blood 
and tissue-juices a chemical combination with the toxins whieh is not 
harmful to the cells (Ehrlich). 

Besides the antitoxins, the blood-serum of immunized animals or 
human beings may also contain bactericidal substances, which injure 
or kill the bacteria themselves; and this is said to oceur especially in 
cholera and typhoid infections (R. Pfeiffer, Gruber, Durham) and in in- 
fections with the pneumococcus (Emmerich). Emmerich assumes that 
these substances are of the nature of bacteriolytic enzymes. 

The origin of the immunizing substances in the blood is not vet 
known, and we are at present confined to hypotheses. It is probable 
that the bactericidal substances have not the same genesis as the anti- 
toxic. 

In the case of immunization by means of attenuated cultures or by 
sterilized ehemical bacterial products, the antitoxic substance is pro- 
duced as a new body within the organism, and this process has been 
designated active immunization (Ehrlich); in the case of the injection 
of immunizing serum the antitoxin already formed is introduced from 
without, and this may be spoken of as passive immunization. It is 
probable that in the last case no new-formation of antitoxin occurs after 
the injection. 

lt is most probable that antitorins are formed by the cells of the infected 
in«iridual, according to Khrlich’s view (see below) by those cells which 
are especially influenced by the toxin (in tetanus, for example, by the 
nerve-cells). The antitoxin is probably nothing more than an element 
of the cell-protoplasm, which has an especial relation to the given toxin, 
and, thrown off from the cell and dissolved in the blood, combines with 
the toxin to form a harmless body. The fact that the substance produc. 
ing the immunity is active only against the given infeetion may be ex- 
plained by the assumption that the individual toxins or toxalbumins 
possess the affinity, which is necessary to the production of an intoxica- 


THE ACQUIRING OF IMMUNITY: PROTECTIVE INOCULATION. 115 


tion, only for certain portions of certain cells; and that, therefore, 
following the intoxication, only the immunizing substances for the par- 
ticular poison are produced by the cells and given to the blood. 

By many writers it is believed that the anti-bodies, both bactericidal 
substances and antitoxins, are formed by the bacteria themselves, or that 
the bacterial cells furnish the material for these, in cultures as well as 
within an infected body (Buchner). 


For the foundation researches in regard to inoculation with attenuated cultures of 
bacilli cultivated outside of the body, we are indebted to Pasteur; who, in 1880, demon- 
strated the fact that chickens could be immunized against chicken-cholera through the 
inoculation of cultures of chicken-cholera bacilli, that had been weakened through long 
exposure to the air. 

Since that time numerous ex periments have been carried out with other forms of 
bacteria, especially with attenuated cultures of the bacilli of anthrax and symptomatic 
anthrax. The best results have been obtained from inoculations against the symp- 
tomatic anthrax of cattle. Less favorable are the results in inoculations against an- 
thrax, in that some of the animals die from the effects of the protective inoculation, 
while others are not rendered absolutely immune against a new anthrax infection. 

Sheep and cattle may be made immune against anthrar ; most expediently (Koch) 
by first inoculating them with attenuated cultures of anthrax-bacilli, which will kill 
mice but not guinea-pigs, and then with those which will kill guinea-pigs but not 
strong rabbits. 

As vaccine against symptomatic anthrar, there may be used cultures of the bacillus 
attenuated through heat or such chemical agents as sublimate solutions, thymol, 
eucaly ptol, and silver nitrate; and by such inoculations cattle may be rendered im- 
mune. At the present time heat (J/ess, Kitt) is most commonly used in the preparation 
of the vaccine. The infected muscle of an animal dying with symptomatic anthrax is 
chopped fine, triturated with one-half its weight of water, and pressed through a piece 
of linen cloth. Finally, the fluid is again filtered through a moistened piece of tine 
linen. The virulent material is then spread in thin layers upon glass plates or flat 
dishes, and transferred to a dry chamber at a temperature of 32-35? C. When thor- 
oughly dry the virus is scraped off and removed in the form of powder. When it is 
desired to give inoculations, the virus is triturated with double its weight of water and 
the fluid evaporated in a thermostat. By raising the temperature to 100° C. for six 
hours a weak vaccine is obtained; at a temperature of 85° C. for six hours a stronger 
one. For the immunization of cattle, about 0.5 gm. of the weaker virus in a dilute 
water solution is injected into the subcutaneous tissue of the animal's tail, and after 
eight to twelve days the stronger solution is similarly injected. 

According to observations of Chavreau and others, protective inoculations may also 
be made by the injection of virulent bacteria in very small quantities, or in such a 
manner that the life of the animal shall not be endangered. In the case of sympto- 
matic anthrax this may be accomplished by the injection of very small doses into the 
extremity of the animal’s tail; such injections not causing a fatal illness, but only a 
local disturbance. 

According to Afanassieff, it is possible to render animals immune by inoculating 
the granulating surface of a wound with a virulent culture. 

Cattle may also be immunized against contagious pleuropneumonia (Schatz) by in- 
jecting the tissue-juices from the lung of an animal dying from this disease into the 
tip of the tail. There is produced in this way a circumscribed inflammation, er, at 
least, one which is confined to the tail; after recovery from which the animal is im- 
mune to both natural and artificial infection with this disease. 

Hogs may be rendered immune against inoculation with virulent bacilli of sirine- 
erysipelas (Pusteur), by using, as vaccine, cultures attenuated by successive inocula- 
tions in rabbits. According to Emmerich, rabbits may also be made immune against 
the bacilli of swine-erysipelas through the injection into the car-vein of a small quan- 
tity of a virulent bouillon-culture diluted with fifty times its volume of water. 

Animals susceptibie to diphtheria may be rendered tmmune against this disease, 
according to Behring, by the injection of cultures of diphtheria-bacilli which have been 
weakened in virulence by exposure for sixteen hours to iodine trichloride (1:500). Two 
cubic centimetres of such a culture is injected into the peritoneal cavity; after three 
weeks this injection is repeated with a diphtheria-culture (0.2 c.c.) which has been 
washed four days in bouillon containing iodine trichloride (1:5,500). After this, fully- 
virulent cultures are injected in increasing doses. 

Rabbits may be rendered immune against pneumococci (Zmmertch) by injections 


116 THE PROTECTIVE FORCES AGAINST INFECTION. 


of 0.3 c.c. of a strongly-virulent bouillon-eulture which has been diluted five thousand 
times, followed later by injections of bouillon-cultures of full virulence. 

Protective inoculations against vabies were first carried out in cases resulting from 
bites by rabid animals, particularly in France (Pasteur Institute), Russia, and Italy. 
As inoculation-material, the spinal cord from rabbits which have been infected with 
rabies is used after it has been dried in dry air at a temperature of 33-35 C.; the viru- 
lency of the cord being gradually lost after about fifteen days of the drying-process. 
According to Protopopogf, it is tae temperature, and not the drying (Pasteur), which 
lessens the virulence, According to Mara, the micro-organisms of rabics have already 
been weakened in the body of the rabbit. Small portions of a rabbit's cord thus weak- 
ened in virulence are triturated in sterilized chicken-broth and injected subcutancously 
into the bitten individual; at first pieecs of cord greatly reduced in virulence are used. 
then those of gradually increasing virulence. According to the view held by Pasteur, 
the spinal cord contains both the microbes of the disease and the specific poison formed 
by them; if the latterspreads through the body more rapidly than the microbes, it con- 
fers an immunity against a subsequent spread of the microbes, and affords protection 
to the nervous system in particular. In order to confer immunity it is, therefore, 
necessary to introduce as large a quantity as possible of the chemical poison. Accord- 
ing to the reports of the Institutes in which the Pasteur inoculations against hydro- 
phobia have been carried out, it must be acknowledged that these inoculations have 
been successful in preventing cases of hydrophobia. 

Immunity against cholera may be produced, in both man and animals (Jlafkine, 
Pfeiffer, Holle, Voges, and others), by the injection of sterilized or attenuated cultures 
of cholera-spirilla; this immunity (which is of short duration) depends upon the forma- 
tion of specific bactertcidal anti-bodies in the blood (sce Voges, 1. c.). On the other hand, 
we do not yet possess a specific remedy by which the life of any animal or man in- 
fected with cholera may be saved. 

Immunity against typhoid ferer may be secured in man by the subcutaneous injec- 
tion of sterilized cultures of typhoid-bacilli (Pfeifer, Aolle); and the establishment of 
the immunity may be recognized by the fact that the blood-serum of the individual so 
inoculated is found, after a few days, to contain buclertcidal substances. Attempts at 
immunization in cases already ill with typhoid (Brieger, Wassermann, C. Fraenkel) 
have up to the present time been unsuccessful. 

According to the reports published by Auch (British Medical Journal, 1897; Deut. 
med. Wochen., 1897, No. 16; Centralbatt f. Bukt., xxi., p. 526) of the investigations 
Which were carried out during the winter of 1896-1897 with regard to the cattle-plague 
in Cape Colony, cattle may be immunized against * Rénderpest” by subcutaneous in- 
jections of 10 c.c. of the bile taken from animals dying of the disease; the condition of 
immunity becoming established at the latest by the tenth day. According to the re- 
port of Professor Winkler (* Landwirthschaftl. Bezirks-Verein Giessen,” August, 1900) 
hogs and cattle may be immunized against mouth-and hoof disease through feeding with 
milk of animals which are affected by the disease or have recently recovered from it. 

In the year 1890 Aoeh made the discovery that cultures of tubercle-bacilli contain 
a toxin, “tuberculin,” which, when injected into tuberculous individuals, causes a rise 
of temperature and to some extent local inflammatory changes in the neighborhood of 
tuberculous foci. It was at first hoped that in tuberculin a remedy for tuberculosis had 
been found, but the many trials made with it upon human beings and animals have 
shown that it indecd produces after repeated injections an immunity against. the toxic 
action of tuberculin but does not hinder the multiplication of tubercle-bacilli and the 
consequent spread of the disease. Further, the local inflammation caused by the tuber- 
culin leads to favorable results only under special conditions, but, on the other hand, 
often causes actual harm (through the metastasis of bacilli). Nevertheless, Koch’s dis- 
covery has proved of great importance. In the first place, it is of practical value in 
the diagnosis of tuberculosis, in that tuberculin injections do not excite fever in normal 
individuals. Inoculations for diagnostic purposes are now used very extensively in 
cases of suspected tuberculosis in domestic animals. Moreover, the reports published 
by Aveh gave a great stimulus to further investigations with regard to immunization 
by means of inoculation with bacterial toxins; and these investigations have Jed to the 
discovery of the antitoxins of diphtheria, tetanus, cholera, and typhoid fever. 

Maragliano has recently attempted to obtain a healing-serum against tuberculosis 
by the inoculation of experimental animals (donkey, dog, horse) with the toxins de- 
rived from cultures of tubercle-bacilli. The observations thus far made do not war- 
rant the conclusion that this serum possesses the power to cure tuberculosis in the 
human being. In 1897, Koch (* Ueber neue Tuberculinpräparate,” Deut. med. Woch.. 
1897) succeeded in obtaining from highly virulent cultures of tubercle-bacilli a substance 
which he claims is able to immunize against all of the constituents of the tubercle: 
bacillus. To obtain this substance young cultures of tubercle-bacilli are dried in a 


THE ACQUIRING OF IMMUNITY: EHRLICH’S HYPOTHESIS. 117 


vacuum-exsiccator and then triturated. The product obtained by trituration is mixed 
with distilled water and centrifugated. The active substance is contained in the muddy 
precipitate thus obtained (designated by Auch as T. R.). This is again dried and tritu- 
rated, dissolved in water to which twenty per cent of glycerin is added for the purpose 
of preservation.. (The preparation is manufactured by Meister, Lueius, and Branning, 
‘ ut Höchst-on-the-Main, Germany.) The fluid preparation contains 10 mgm. of solid 
substance in every cubic centimetre, and when it is to be used should be din uted with 
physiological salt solution. Through the use of large doses animals are said to become 
immunized in from two to three weeks. In the treatment of tuberculosis in man the 
dose should begin at „45 ıngm. and gradually be increased up to 20 mgm., the injections 
being given every other day. According to the observations so far published, the T. R. 
preparation does not appear to exert a curative action upon tuberculosis in man. 

Very recently Yabé has reported that there may be obtained from cultures of 
tubercle. bacilli a substance (tuberculo-bactericidin) which has a bactcricidal action; but 
no detinite conclusions can be drawn from the published results of his ex periments. 

The blood-serum treatment of diphtheria, i.e., the enployment of the antitoxins con- 
tained in the blood of an animal immunized against diphtheria as a means of curing 
that disease when it is already contracted, or as a protection against such infection, is 
a discovery which we owe to Behring. The favorable effects of the method discov-- 
ered and proved by him through experimental investigations have been confirmed by 
thousands of observations. In the treatment of diphtheria patients a large quantity of 
the serum (one thousand immunizing units) is usually injected at one time beneath the 
skin of the thigh. 

The term “normal serum ”—i.e., a serum having the value of one immunization 
unit—is used by Behring to designate a serum which, when mixed with a quantity of 
diphtheria poison equal to ten times the minimal fatal dose and then injected in the 
amount of 0.1 c.c. into a guinea-pig of from 200 to 300 gm. weight, will surely protect 
that animal from diphtheria. Sheep and herses are especially adapted for the prepara- 
tion of the serum. It is prepared and sold in doses of from tive hundred to three thou- 
sand immunization units. 

If culture-filtrates of the tetanus-bacillus are weakened by the action of chemical 
agents (iodine trichloride or iodine combined with potassium iodide), it is possible 
through repeated injections of such filtrates of increasing virulence to produce im- 
munity in animals against tetanus (Attasato, Behring, Tizzoni, Buchner). The blood of 
such immunized animals contains an antilurin which affords a sure protection lo expert- 
mental animals against tetanus. The antitoxin treatment of human beings suffering 
from tetanus has not given satisfactory results (see Avhler and Schlesinger, |.c.), not 
even in cases of relatively early injection of the antitoxin, though it appears to be 
effective if administered before the appearance of the tetanus. 

Susceptible animals and human beings may be immunized against bubonteplague 
by means of sterilized cultures of the pest-bacillus ( Yeratn, Haffkine, Aolle); and it ap- 
pears that in the blood-serum of immunized animals (the horse, for example) there are 
present anti-bodies which render the serum utilizable for both protective and curative 
purposes. 

Animals may be made immune against sweake-poisens by means of inoculations of 
very small doses of such poison continued for some length of time (Calmette, Tschisto- 
witach); and the blood-serum of such immunized animals is also found to possess an 
antitoxic action against the given poison, so that it may be used as a healing-serum. 
In Brazil, Mexico, Africa, etc., various methods involving the use of suake-poison 
itself are employed for the immunization of individuals against a snake-bite, or for 
curing them after they have been bitten (drinking of the secretions of the poison- 
glands, rubbing of the diluted poison into small wounds of the skin, ete.) (DBrenning). 

According to the investigations by KArlich, mice may be made immune against 
ricin, to which they are extremely susceptible, by mixing very small doses of ricin 
with their food and then afterward injecting additional small doses subcutaneously. 
The appearance of the immunity occurs on the sixth day after the administration of the 
ricin, so that upon this day the animal can withstand a dose thirteen times as great as 
at the beginning. Through continued systematic inoculations the animal becomes 
immune to a dose eight hundredfold as strong. The immunity is produced by an anti- 
toxic body, antiricin, which neutralizes the poisonous action of ricin. 

Though not giving definite information regarding the processes which lead to the 
acquiring of immunity, the hypotheses of Ehrlich are well qualified to give an explana- 
lion for the observed processes, and possibly correspond to the actual conditions. 

According to Ehrlich’s view, only those substances are poisons which possess a 
chemical relationship with some constituent of the body, and, through combination 
with the same, cause an injurious effect recognizable clinically (toxophorous relation- 
ship). The natural immunity of an individual can, therefore, depend upon the fact 


118 THE PROTECTIVE FORCES AGAINST INFECTION. 


that the poison finds in the immune body no element with which it can effect a chem- 
ical combination, or that the body-element so combined suffers no injury in a clinical 
sense. 

Antitozic immunity can be produced either through the introduction of weak doses 
of toxin or through the injection of a serum containing antitoxin. ‘Phe first is an ae- 
tive immunization, in that the organism itself forms the toxin; the second is a rassire 
tmmunization, in that the antitoxin is injected already prepared, so that immunity is at 
once produced. The active immunity can persist for years; the passive, on the con- 
trary, is usually lost after a few weeks or months at the farthest. 

An antitorin is a cell-product which arises as a result of disease of the organism, 
and is given off into the blood. In passive immunity the body-cells are not active, the 
injected antitoxin is sufficient to neutralize the toxin. Antiricin, when added in a cer- 
tain amount to a ricin-solution, lowers the power of ricin to agglutinate red blood-cells 
in undiluted orin diluted blood. The same mixture also renders ricin harmless for 
animals. 

The torin ia not destroyed by the antilorin. If snake-venom be mixed with the anti- 
toxin (Culmette), so that the mixture is harmless for animals, and if the antitoxin. which 
is the more sensitive to heat, be destroyed by warming the mixture to 68° C., this again 
becomes poisonous, A similar fact has been demonstrated in the case of the toxin and 
antitoxin of the Bacillus pyocyanena ( Wassermann). 

The torin becomes harintess through tts union with the antilorin to form a harmles 
chemical combination. 

The antitoxin produced in the body in cases of active immunization does not arise 
from the toxin. The poisons forming antitoxins show, in contrast to other poisons, 
certain peculiarities, which consist essentially in that they possess chemical affinities 
for certain elements of the cells, the “side-chains.” The complicated protoplasmic 
bodies possess (as does the benzol ring), besides the “governing nucleus” or “central 
group,” a great variety of such “atde-chains.” It ınay be assumed that certain sub- 
stances intluence certain side-chains, enter into chemical combination with the same, 
and through the medium of these side-chains affect the central chain and thereby dam- 
age the vital capacity of the cells. If thereby the life of the cell and with this its 
capacity for compensation are not damaged, if there occurs only a functional disturb- 
ance but no definite injury to the central group, the cells may restore the side-chains, 
even build up new ones in excess, which may be thrown off and given to the blood, 
the side-chains thua given off constituting the antitorin. The antitoxin is therefore no 
new subsfance, but one occurring normally, which under certain conditions ia pro- 
duced in an increased amount, giren orer to the blood, and in the ctreulation combines the 
toxins entering the blood into harmless bodies, and thus prevents the action of the 
toxins upon the cells. As expressed in the words of Behrtng: “The same substance in 
the living body, which lying in the cells is the hypothetical essential to an intoxica- 
tion, becomes the cause of healing when it is found in the blood.” 

Ehriich’s hypothesis is without doubt well adapted to explain the phenomena of 
antitoxic immunity. It has been supported by recent observations of different authors. 

Wassermann has found that the substance of the central nervous system which is espe- 
cially affected in tetanus is able to combine the tetanus poison after the manner of an 
antitoxin and to render it harmless. Tetanus-poison, when mixed with the triturated 
brain-substance of a healthy guinea-pig, becomes so weakened that guinea-pigs can 
bear without harm a dose equal to ten times the fatal dose. 

Ransom and Marie obtained the same results. The former also showed that the 
poison of tetanus, wnen injected in fatal doses into doves, could be demonstrated in all 
organs with the exception of the central nervous system, in which it had entered into 
combination with chemical elements. 

Ehrlich’s hypothesis has been attacked especially by Rour, Borrel, Metschnikoff, 
and Auorr; but their observations may be brought into harmony with the hypothesis 
(see Weigert, 1.c.). 

Baeterieidal immunity depends chiefly upon the presence of newly-formed immune- 
bodies, which are able to withstand heating to 56-60° C., and. wholly specific in their 
action, are directed against the variety of bacteria corresponding to the immunization 
(Fe. Pfeiffer and others). 

These immune bodies exert their influence under certain conditions; according to 
the view held by Bordet, Ehrlich and Morge:roth, ron Dungern, and Wassermann, their 
activity is dependent upon the addition of a thermolabile ferment-like substance, which 
is found even in normal blood-serum (according to Dordet, the alerin of Buchner, the 
a ldiment or complement of Ehrlich). 

Of exactly the same composition as the bactericidal are also the corresponding 
globulicidal üommune-sera (specific hermolysins\, which are produced by the introduction 
of blood into the body of an animal of a different species (Bordet, von Dungern, Land- 


THEORY OF SPECIFIC IMMUNE-SERA. 119 


steiner); in this case also the action of the immune-serum depends upon the presence of 
two substances—the tmmune-body produced through the immunization, and the comple- 
ment already present in normal blood-serum. Ehrlich and Morgenroth have further 
explained the mechanism of these processes by means of experiments at combining 
these substances. The immune-body shows great specific aflinity for the correspond- 
ing erythrocytes; it combines with these even at 0° C., and, thus separated from the 
complement remaining. in the serum, is neveriheless not able to dissolve the blood- 
corpuscles by itself. The complement will not be combined by the blood-cells without 
the immune-body. If the latter is present at the same time, the complement is taken 
at higher temperatures out of the serum by the erythrocytes, whereby the solution of 
the red cells takes place. 

Ehrlich and Morgenroth explain this by the assumption that the complement, which 
represents the active substance proper, ts carried ocer to the erythrocytes by means of the 
éamune-body. This conclusion accords very well with the side-chain theory. The tm- 
mune-body is a side-chain, which, produced in excess, is thrown off into the blood. To 
the production of the immune-body a certain molecule-group of the erythrocytes gives 
occasion, and this group is indced the same which in hemolysis enters into combination 
with the immune-body (ron Dungern). The immune-bodies are distinguished from the 
analogous antitoxins only in that they are more complex; they possess, besides the 
haptophorous complex which has a chemical affinity for the corresponding complex of 
the proper erythrocytes, yet another haptophorous group, which is able to combine the 
complement. Corresponding complementophile side-chains may also be demonstrated 
in the organs; the most varied kinds of tissuc-cells are able to take out the complement 
from the blood-serum (con Dungern). 

In the reaction of immunity the immune-bodies are produced exclusively ; the com- 
plement is not increased beyond the amount required (ron Dungern). 

The property of many normal sera to dissolve foreign blood-cells is dependent, ac- 
cording to the investigations of Ehrlich and Morgenroth, exactly as in the case of the 
immune-sera, upon the joint action of two substances. Many times there can also be 
demonstrated, besides the complement, an “intermediary body ” corresponding to the 
immune-body (the complement is therefore not wholly to be identified as Buchner's 
alexin, which embraces both substances). 

In an analogous manner to that produced against bacteria and red blood-cells, a re- 
action of immunity may occur against other cells when introduced into a strange 
organism—for example, against ciliated epithelial cells (con Dungern), against sperma- 
tozoa (Landsteiner, Metschnikoff, Moxter), against leucocytes (Metschnikoff and others). 
The immune-sera obtained in this manner act, in so far as they have been studied (ron 
Dungern, Morter), according to the same mechanism as the hemolytic and bactericidal. 

The reaction of the animal organism, which hinders or makes tuposstble the life of cells 
foreign to tt, is mantfested not only upon bacteria but upon all possible forms of life Joreign 
to tt. According to the investigations of Ehrlich and Morgenroth, the same reaction 
may occur even against blood-cells of the same species. After intraperitoneal injection 
of laked blood of the same species, the blood-serum of a given species acquires the _ 
power to dissolve the red blood-cells of another individual of the same species (isolysin). 
An autolysin has, on the other hand, not yet been observed. The latter could indeed 
not exist in the blood; it would be combined with the corresponding side-chains of the 
cells (receptors) and occasion the production of an antiautolysin. 

The acquired specific immunity against the causes of infection is, therefore, to be 
referred to the general law of the formation of anti-bodies. 


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120 THE PROTECTIVE FORCES AGAINST INFECTION. 


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Wasserman: Immunität. Eulenburg’s Jahr., iv., 1894; Zeit. f. Hyg., xxii., 1896; 
Serumtherapie. Deut. med. Woch., 1897; Künstl. Immunität. Berl. klin. Woch., 
1898; Seitenkettenimmunität. Ib., 1898; Neue Versuche auf dem Gebiete der 
Serumtherapie. Deut. med. Woch., 1900. 

Weigert: Arbeiten zur Theorie der Antitoxinimmunität. Ergebn. d. allg. Path., iv., 
1899. 

Welch: The Huxley Lecture. Bull. of the Johns Hopkins Hosp., 1902. 

Yabe: Etude sur l’immunité de la tuberculose, Paris, 1900. 

Yersin: La te bubonique. Ann. de |'Inst. Past., 1897. 

See also SS 80 and 81. 


122 HZEMOLYSINS; IMMUNE-SERA. 


(Hemolysins ; Immune-sera against Cells.) 


Bordet: Les serums hémolytiques. Ann. de l’Inst. Past., xiv., 1900. 

Bruére: On the Hwmolytic Potency of Certain Sapotoxins Dissolved in Blood-Serum. 
Jour. of Med. Res., 1902. 

Bulloch: On the Nature of Hemolysis. Trans. Lon. Path. Soc., 1901. 

v. Dungern: Globulicide Wirkungen des thier. Organismus. Münch. med. Woch., 
1009: Immunserum gegen Epithel. Ib., 1899; Beiträge zur Immunitätslehre. 
b., 1900. 

Ehrlich u. Morgenroth: Ueber Hämolysine. Berl. klin. Woch., 1900. 

Flexner: The Pathology of Lymphotoxic and Myelotoxic Intoxication. Univ. of 
Penn. Med. Bull., 1902, 

Flexner and Noguchi: Snake-Venom in Relation to Hemolysis, Bacteriolysis, and 
Toxicity. Univ. of Penn. Med. Bull., 1902. 

Halban: Agglutinationsversuche mit Mütterlichem u. Kindlichem Blute. Wien. klin. 
Wochensch., 1900. 

Kyes: Ueber die Wirkungsweise des Cobragiftes. Berl. klin. Woch., 1902. 

Landsteiner: Spec. auf Blutkörperchen wirkende Sera. Cbl. f. Bakt., xxv., 1899. 

Levin: The Influence of the Spleen on Natural or Acquired Hemolytic Properties of 
Blood-Serum. Jour. of Med. Research, 1902. 

Metschnikoff: Sur les cytotoxines. Ann. de l’Inst. Past., 1900. 

Moxter: Immunserum gegen Spermatozoén. Deut. med. Woch., 1900. 

Noguchi: The Interaction of the Blood of Cold-blooded Animals, with Reference to 
ILemolysis, Agglutination, and Precipitation. Univ. of Penn. Med. Bull., 1902; 
A Study of Immunization, Hemolysins, Agglutinins, Precipitins, and Coagutins in 
Cold-blooded Animals. Ibid.; The Anti-hemolytic Action of Blood-Sera, Milk, and 
Cholesterin upon Agaricin, Saponin, and Tetanolysin, etc. Ib. 

Stewart: The Mode of Action of Various Laking Agents on the Blood-Corpuscles. 
Jour. of Med. Res., 1902. 

Sweet: A Study of a Hemolytic Complement found in the Serum of the Rabbit. Univ. 
of Penn. Med. Bull., 1902. 


CHAPTER IV. 


Disturbances in the Circulation of the Blood and of 
the Lymph. 


I. General Disturbances of the Circulation Dependent upon Changes 
in the Function of the Heart, Changes in the General Vascular 
Resistance and Changes in the [lass of the Blood. 


§ 33. The mass of blood is kept constantly in motion by means of the 
rhythmical contractions of the auricles and ventricles of the heart. The 
blood, as it is driven into the elastic tube of the aorta toward the periph- 
ery of the body, meets a signiticant. degree of resistance, which is caused 
by the friction in the innumerable divisions and subdivisions of the 
arterial system. This resistance occasions a relatively high pressure 
throughout the entire arterial system, which in the human femoral artery 
equals that of about 120 mm. of mercury. After passing through the 
capillaries the blood arrives in the veins with very little velocity, and 
stands in the veins under a very slight pressure, which varies according 
to the location of the vein, and is greatest where a high column of 
blood rests upon the lumen of the vein. In the great venous trunks in 
the neighborhood of the thorax the pressure is usually negative, espe- 
cially during inspiration, as the thorax during this stage of respiration 
aspirates the blood from the veins lying outside of the chest. Only dur- 
ing forced expiration does the positive pressure in the veins rise some- 
what higher. 

Assuming the mass of the blood to be constant, the degree of pressure 
within the aorta, at any given moment, is dependent upon the work of the 
heart and the resistance in the arterial system. The latter in turn is 
dependent upon the variations in the total diameter of the combined 
cross-sections of the blood-vessels, due to the elasticity and contractility 
of the arteries. In the major circulation the arterial tone is very pro- 
nounced; in the lesser circulation it is slight, the blood-pressure in the 
pulmonary artery being only from one-third to two-fifths that in the 
aorta. Both the heart and the arteries are under the influence of the 
nervous system, which regulates their activity. 

The activity of the heart consists in rhythmical contractions of its 
musculature; and its normal efficiency presupposes that the heart-mus- 
cle, and also the cardiac ganglia, are sound. Every disease of the heart, 
therefore, in so far as it diminishes the contractile capacity of the heart- 
muscle and lessens the activity of the ganglion-cells, and in so far asa 
lessened functional activity of certain parts of the cardiac muscle is not 
compensated by an increased activity of other parts, will diminish the 
functional capacity of the heart. 

In many cases in which the functional capacity of the heart-muscle 
is impaired, certain anatomical changes, such as fatty degeneration and 
necrosis of its cells, can be demonstrated; in other cases no anatomical 

123 


124 DISTURBANCES OF THE CIRCULATION. 


changes can be made out, especially in those cases in which the diminu- 
tion of working-capacity follows the exhaustion caused by excessive 
overexertion. This may occur when the heart is forced to work for 
some time only slightly above the normal, but under unfavorable condi- 
tions, as, for example, in eases of elevation of the body-temperature; as 
weil as in cases when for a short period it is overworked to an excessive 
degree. Under certain conditions disturbances of nutrition and intoxi- 
‘ations, such as occur in the infectious fevers, as well as a sudden 
diminution in blood-supply from the obstruction of a coronary artery, 
may cause an insufficiency of the heart within so short a time that the 
heart-muscle presents no recognizable anatomical lesion. The work of 
the heart may also be made difficult at times through the formation of 
wdhesions between the epicardium and pericardium, and between the lat- 
ter and the contiguous pleura, in consequence of which the contractions 
of the heart are hindered. 

Through the collection of fluid in the pericardial sac in the course 
of certain diseases, further, through marked deformities of the thorax 
causing an abnormal smallness of the thoracic cavity, and through a high 
position of the diaphragm, the diastolic dilatation of the heart and the 
free afflux of blood from the veins may be hindered to such an extent 
that the ventricles receive too little blood. If, following pathological 
processes in the heart-valves, there result rents or distortions of the flaps 
or adhesions between them, or if in case of dilatations of the heart and 
the valvular orifices the valve-flaps beeome relatively too short, there 
inay arise those conditions of the auricular and ventricular orifices known 
as insufficiency and stenosis. The former condition is characterized by 
a failure of a valve to close completely during the diastole of the auricle 
or ventricle Iving behind the given valve; the second condition, by the 
fact that during the contraetion of the auricle or ventricle the valvular 
orifice does not suffice for the passage of the blood through the opening. 
The effect. of a stenosis is that of opposing additional obstacles to the out- 
flow of the blood during systole. In aortic and pulmonary insufficiency 
the blood regurgitates, during the ventricular diastole, back from the 
great vessels into the ventricles; in mitral and tricuspid insufficiency the 
systole of the ventricle causes a regurgitation into the corresponding 
auricle. 

Finally, there are not infrequently formed in the heart masses of 
coagula, which under certain conditions—in case they lie near the orifices 
—may on the one hand interfere with the proper closing of the valves, 
or on the other cause a narrowing of the ostium. 

As the result of all the above-mentioned pathological conditions, the 
efficiency of the heart’s function is impaired, so that in a given time 
too little blood passes into the arterial system, the aortic pressure conse- 
quently falls, and the velocity of the blood-eurrent is diminished; while 
in the venous system the blood collects more and more, and the venous 
pressnre rises. There is consequently an inadequate filling of the arteries 
throughout the entire body, varving, indeed, according to the degree of 
contraction maintained in individual arterial systems, while both veins 
and capillaries are, on the other hand, overfilled with blood. There 
develops, therefore, a condition of general venous hyperemia, which 
in some parts may become so marked that the tissue, because of the en- 
rorgement of the capillaries with venous blood, arquires a blue-red, eya- 
notic appearance, When the difference in pressure between the arterial 
and venous systems becomes redneed to a certain minimum, the circula- 


IMPAIRMENT OF CARDIAU FUNCTION. 125 


tion comes to a standstill, while the right. side of the heart becomes 
greatly distended with blood. 

Should the contractions of the heart from any cause become weak and 
imperfect, the pulse-wave also becomes small. If the rate of the heart- 
beat becomes diminished in frequency, the arterial system empties itself 
to a greater extent than norınally during the pause between the systoles. 

If the impairment of cardiac efficiency involves the left heart esseı- 
tiall;;, as is the case, for instance, in valvular disease of the left side, the 
disturbance of circulation is manifest first in the systemic arteries, as 
‘ well as in the pulinonary vessels. 

In stenosis of the aortic valves, the arteries, if the heart’s action re- 
main unchanged, fill but slowly and incompletely (pulsus tardus). In 
aortic insufficiency a normal or even an increased amount of blood is 
thrown into the arteries during systole (pulsus celer), but a part of this 
flows back again during diastole. In both cases the left ventricle be- 
comes more and more distended, the emptying of the left auricle is hin- 
dered, its cavity also becomes dilated, and finally the blood is backed up 
in the pulmonary veins. Owing, however, to the low pressure in the 
pulmonary circulation, the blood is readily dammed back upon the right 
ventricle, and the blood stasis may finally extend beyond this into the 
right auricle and into the systemic veins. 

Valvular lesions at the mitral orifice produce similar effects upon 
those portions of the circulatory apparatus lying behind the left auricle, 
as in such eases there is produced also a condition of pulmonary stasis, 
with a rise of pressure in the pulmonary arteries and veins; while the 
left ventricle either receives too little blood (stenosis) or during its con- 
traction drives a portion back into the auricle (insufficiency ). 

In valvular lesions of the orifices of the right heart the damming back 
of the blood is limited to the veins of the systemic circulation, while in 
the pulmonary circulation both pressure and velocity are diminished. 
Further, the pressure in the aorta also falls, since the left side of the 
heart receives too little blood. 

The damming back of the blood in the great systemic veins may 
manifest itself by venous pulsations in the neighborhood of the thorax, in- 
asmuch as retrograde waves of pressure proceeding from the heart may 
pass through the veins toward the capillaries, distending the veins to 
such an extent that the venous valves, particularly those of the jugular 
bulb, are rendered inadequate. The essential condition of the transmis- 
sion of the venous pulsation is the insufficiency of the venous valves. 
In the ease of imperfect function of the valve in the jugular bulb, a 
slight pulsation may be observed even during normal action of the heart; 
but when the veins are distended, and particularly in the case of tricus- 
pid insufficiency, the pulsation becomes much stronger and extends 
further toward the periphery. If the tricuspid is adequate the venous 
pulsation (presystolic) is only the expression of the rhythmical occur- 
rence of a hindrance to the outflow of blood from the veins (negative or 
normal venous pulse). In tricuspid insufficiency the contraction of the 
right ventricle forces blood back through the tricuspid opening into the 
right auricle and into the veins beyond, giving rise to a systolic venous 
pulsation (positive venous pulse). 

If in a heart affected with a valvular lesion the chambers lying be- 
hind the Jesion become distended with blood, the muscular walls of these 
chambers, in case they are otherwise normal, may by an increased ac- 
tivity compensate for the valvular lesion within certain limits. In the 


126 DISTURBANCES OF THE CIRCULATION. 


course of time there results an increase in the volume of the heart-mus- 
cle, a hypertrophy of the heart-muscle, which enables the heart to carry 
on its increased work for an indefinite period. Such compensation fre- 
quently becomes inadequate, with the result that the aortic pressure is 
permanently lowered, while the venous pressure, on the other hand, is 
abnormally high. There is, at the same time, the danger that the heart- 
muscle may in time become exhausted, or that a very slight illness may 
render the heart insuflieient. Thus, for example, a prolonged quickeu- 
ing of the heart’s rate, by shortening the diastolic periods, of rest, may 
cause cardiae exhaustion and insufticiency. Arrest of the heart's action 
finally follows, with great accumulation of blood in the heart, since the 
heart is no longer able to drive onward the mass of blood entering it. 

An increase of the heart’s action—that is, an increase in the fre- 
quency of the heart’s contractions, these at the same time remaining 
strong and complete—eauses an Increase in arterial pressure and an in- 
creased velocity of the blood-current. When increased demands are fre- 
quently made upon the left side of the heart—as frequently happens in 
heavy bodily labor, conditions of luxurious living, abnormal irritability 
of the cardiac nerves, ete.—the left ventricle may become hypertrophic 
and act permanently with greater foree. Inasmuch as the quickening of 
the blood-stream causes the right heart to receive a greater amount of 
blood during diastole, a hypertropny of the right ventricle is usually 
found in connection with the hypertrophy of the left ventricle. 

lessening of the mass of blood or general anzemia from the loss of 
blood leads temporarily to a fall of pressure in the aorta; but if the loss 
of blood was not excessive, the blood-pressure rises again, as the vessels 
adapt themselves to the changed conditions, and, as the result of the 
stimulation of the vasomotor centre through local ansmia, show a 
greater degree of contraction. Under normal conditions the mass of blood 
is quickly inereased through the absorption of fluids, and later by a re- 
generation of the blood. Similarly, in anhydremia—i.e., a diminution 
of the water of the blood—the arterial pressure is lowered and the blood- 
current slowed. After severe hemorrhages the arterial pressure is low- 
ered for a greater length of time, the circulation is slowed, and the pulse, 
because of the lessened stimulation of the vagus-centre (Cohnheiın), is 
frequent and small. 

In the case of lasting diminution of the blood-mass—i.e., the condi- 
tion known as chronic anemia, which occurs under varying conditions 
—the vascular system is imperfectly filled, the blood-pressure lowered, 
and the blood-current slowed. Both heart. and blood-vessels adapt them- 
selves to the new conditions and become diminished in volume. In the 
case of a marked deficiency of haemoglobin, degenerations of the heart- 
muscle, particularly fatty degeneration, frequently oceur. 

Increase in the mass of the blood, through the injection of blood or 
salt-solution into the blood-vessels, is followed in animals by only a tem- 
porary increase in pressure and in the velocity of the blood-current. A 
return to the normal is brought about, partly by the dilatation of a part 
of the vaseular system, particularly in the abdomen, and partly through 
the elimination of the surplus from the vessels. If the mass of blood, as 
the result of some especial predisposition or of high living, comes to 
stand in an abnormally high porportion to the body-weight, if there 
exists a permanent plethora, the pressure in the aorta becomes perma- 
nently raised, the work of the heart is permanently increased, and there 
develops a corresponding hypertrophy of the heart, 





CHANGES IN BLOOD PRESSURE. 127 


§ 34. Increase of the general vascular resistance may occur in 
either the greater or the lesser circulation, and results in an increased 
pressure behind the point of increased resistance, and a diminished press- 
ure beyond it. 

In the systemic circulation the hindrance may lie either in the main 
vessel, the aorta, or in the arterial branches, whose degree of contraction 
maintains and governs the normal pressure in the aorta. Vascular con- 
traction involving a great number of arteries and their branches, and 
sufficiently well marked to increase the blood-pressure, is generally a 
temporary phenomenon, passing off with the relaxation of the arterial 
tension. Nevertheless, a permanent increase in the aortic pressure with 
consequent hypertrophy of the left ventricle does occur; and this cannot 
be explained otherwise than as the result of the contraction of the lumen 
of the smaller arteries. Transitory arterial contraction and increase of 
pressure occur particularly through an increase of the amount of car- 
bonie acid contained in the blood. A permanent increase of aortic 
pressure is, on the other hand, a result of chronic diseases of the kidney, 
in which the secreting parenchyma is destroyed. Inasmuch as the por- 
tion of the vascular system which is thus cut off is much too small to 
cause such an increase of pressure throughout the whole aortic system, 
since the vessels leading to other organs might become correspondingly 
dilated, it must be assumed that in the case of contracted kidney some 
other hindrance to the circulation occurs throughout more extensive 
vascular areas. This hindrance would most naturally be sought in the 
apparatus which normally serves to keep the aortic pressure at its proper 
height, namely, in the smaller arteries of the body. Whether the condi- 
tion is caused by nervous stimuli arising in the kidney, or by the action 
of retained urinary substances upon the vasomotor centres or directly 
upon the vessel-walls, or whether the heart is excited by nervous stimuli 
to increased action, we are not at present able to say. 

Increase of resistance in the aorta may result from stenosis of this 
vessel, as occurs in rare cases at the isthmus, or from congenital narrow- 
ings of the whole aorta, large aortic thrombi, or from extensive disease of 
the vessel-wall, in consequence of which the intima is rough and nodu- 
lar, the entire vessel rigid, inelastic, and unyielding; or, finally, from a 
general dilatation of the vessel, whereby eddies are formed in the blood- 
stream. 

Lowering of the total resistance in the systemic circulation is pos- 
sible through the relaxation of the tone of a large part of the arteries, 
and this event may happen when the vasomotor centre is paralyzed, or 
when the cervical cord is divided or partly destroyed through any otner 
process. Since the blood, in this case, flows abnormally quickly from 
the arteries into the veins, the difference in blood-pressure between the 
arteries and veins is lessened, the current becomes slower, the heart re- 
ceives too little blood during diastole, and, finally, the circulation may 
come to a standstill. 

Increase of the resistance in the pulmonary circulation occurs most. 
frequently as the result of disease of the lungs and pleura. Adhesions 
of the pleura, as well as spinal curvatures, which hinder the expansion 
of the langs and their change of volume during inspiration, thereby de- 
priving the circulation of an efficient aid, may cause such increase of 
pulmonary resistance. Of great influence, moreover, are such affections 
of the lung as idiopathic emphysema, retractions and indurations of the 
lung, and destruction of lung-tissue—all of which lead to the oblitera- 


128 DISTURBANCES OF THE CIRCULATION. 


tion of a portion of the pulmonary eapillaries; further, compression of 
the lung through pleural exudate; and, finally, compression of the pul- 
monary arteries by aortic aneurism or by tumors. 

If the hindrance is only slight, the blood may make for itself a new 
passage to the left heart without any increase of pressure; the rate of the 
current in the blood-vessels which are unobstructed alone being increased. 
Greater obstacles cause an increase of pressure in the pulmonary artery 
and the right heart, and if the condition persists for some time the right 
ventricle through increased exertion may become hypertrophic. This 
can occur, however, only when the heart-muscle is adequately nourished 
and when the mass of the blood is not: diminished to correspond to the 
diminution of the area of the pulmonary vessels. If the right heart is 
not able to overcome the obstacles in the pulmonary circulation, the 
blood is dammed back upon the right heart, and eventually upon the 
systemic veins. 

An increase of the pressure in the right side of the thorax hinders the en- 
trance of the venous blood into the right heart, and causes an accumula- 
tion of blood in the systemic veins. A sudden increase of pressure may 
cause a retrograde flow of blood into the neighboring veins. 


According to the investigations of Pomberg, Pässler, Bruhns, and Müller, pneumo- 
cocci, diphtheria-bacilli, and the Bacillus pyocyaneus injure the circulatory apparatus 
of the rabbit, in that they cause paralysis of the vasomotor centres in the medulla. 
This paralysis leads to a diminution of the arterial blood-pressure and to a change in 
the distribution of the blood. The splanchnic vessels become overfilled, the vessels of 
the brain, skin, and the muscles become empty. The heart is not concerned in this 
disturbance of the circulation. In general, it is affected secondarily as a result of the 
deficient flow of blood due to the vasomotor paralysis. A central paralysis of the vaso- 
motors is also responsible for the circulatory disturbances occurring in the acute tnfee- 
tions ; and is the chief cause of the failure of the circulation. 

The observation that hypertrophy of the heart follows different diseases of the 
kidneys has been interpreted in various ways. Some writers seek the cause in an in- 
crease of the volume of the blood (Traube, Bamberger), others (Senator, Ewald) believe 
it to be due to the changed character of the blood, while others (Gull and Sutton) 
ascribe it to a widespread change in the walls of the small arteries. Budd holds that it 
is due to the over-nourishment of the heart. According to the investigations made up 
to the present time, there can be no doubt that the hypertrophy of the heart in diseases 
of the kidney is dependent upon an increase of the aortic pressure. This increase is 
best explained by an increase of the resistance in the small arteries of the entire body, 
duc to the contraction of the small arteries. This contraction must be brought about 
either through the direct action of the urinary substances contained in the blood or by 
some reflex stimulus from the kidneys, or finally by some influence exerted upon the 
vasomotor centre. It is possible that the heart also may be excited to increased 
activity. 


Literature. 


( Disturbances of the Circulation. ) 


Bamberger: Ueber Morbus Brightii. Samml. Klin. Vortr., No. 178, 1879. 

v. Basch: Allgem. Physiologie u. Pathologie des Kreislaufs, Wien, 1892. 

Cohnheim: Vorlesungen über allgem. Pathologie, Berlin, 1882. 

Gull and Sutton: Med.-chir. Transact., Iv., 1852. 

Janowski: Jiagnost. Bedeutung der Pulsuntersuchung. Klin. Vortr., Nos. 192 
193, Leipzig, 1897. 

Jürgensen: Erkrankung d. Kreislauforgane, Insufficienz des Herzens, Wien, 1899. 

Krehl: Pathologische Physiologie, Leipzig, 1898. 

Löwit: Ueber die Entstehung des Lungenddems. Beitr. v. Ziegler, xiv., 1898. 

Lukjanow: Allgemeine Pathologie des Gefässsystems, Leipzig, 1894. 

Mackenzie: The Venous and Liver Pulses. Journ. of Path., 1i., 1898. 

Romberg, Pässler, Bruhns u. Müller: Kreislaufstörung bei acuten Infections- 
krankheiten. Deut. Arch. f. klin. Med., 64 Bd., 1899. 


LOCAL HYPERZMIA,;, LOCAL ANAEMIA. 129 


Rosenbach: Herzkrankheiten. Eulenburg’s Realencyklop.; Einfluss der Raumbe- 
schränkung in der Pleurahöhle auf den Kreislauf. Virch. Arch., 105 Bd., 1886. 

Thoma: Patholog. Anatomie, i., Stuttgart, 1894. 

Traube: Ges. Abhandlungen, Berlin, 1874-78. 


ll. Local Hyperzmia and Local Anemia. 


$ 35. To the blood is assigned the function of supplying all the or- 
gans and tissues of the body with nourishment. The cells and cellular 
structures of which the various tissues are composed are able to maintain 
their existence without the advent of fresh nutritive material only for a 
short time; and for this reason the majority of the tissues are supplied 
with blood-vessels, and those not possessing vessels of their own are 
placed in the most intimate connection with vascular structures. 

The demands of the different tissues for blood are not always the 
same, and there is consequently in the various tissues a corresponding 
increase or decrease in the afflux of blood and in the amount of blood 
contained within an organ or tissue at any given moment. An organ 
rich in blood is designated as hypersemic; one poor in blood as ansemic. 

The regulation of the amount of blood which an organ receives under 
physiological conditions is brought about by a change of the resistance 
in the afferent arteries; and this change is effected entirely through a 
variation in the calibre of the arteries. Since the total mass of the 
blood in the body is not sufficient to fill all the vessels at the same time, 
an extra supply of blood to one organ is possible only by supplying a 
less amount of blood to other parts. The change in the calibre of an 
artery is determined, aside from the blood-pressure, by the elasticity of 
the artery-wall and the degree of contraction of its smooth muscle-fibres. 
These fibres are the regulating element; their activity is dependent 
partly upon influences affecting them directly, and partly upon ner- 
vous influences from the intravascular plexuses and from the vasomotor 
centres in the medulla oblongata and in the spinal cord, some of these 
stimulating, others inhibiting the muscular action. 

When the departures from the average blood-supply of any part of 
the body overstep the physiological limits, or if such variations arise 
without physiological causes, or are unduly prolonged, the condition is 
spoken of as pathological hyperemia and pathological anemia. These 
conditions are in part brought about by the same regulating mechanism 
which governs the normal blood-supply of an organ. 

X 36. Hyperzmia of an organ is caused under pathological con- 
ditions either by an increase in the arterial supply or through an ob- 
struction and damming-back of the venous outflow; and there are dis- 
tinguished, accordingly, two forms, an active or congestive (arterial) 
hyperemia and a passive or stagnation (venous) hyperemia. Active hy- 
perzmia arises through an increase of the afflux of blood (congestion), and 
may be either idiopathic or collateral. The first of these plays the more 
important role. It depends upon a relaxation of the muscular tunies of 
the artery, which may be brought about either by paralysis of the vaso- 
constrictors (neuroparalytic congestion), or through a stimulation of the vaso- 
dilators (neurotic congestion), or through direct weakening and paralysis of 
the muscles (a8, for instance, by heat, bruising, action of atropine, brief 
interruptions of the blood-current.), or, finally, through a diminution of 
the erternal pressure exerted upon the vessels. Collateral hyperemia is 
merely the result of a diminished flow of blood to other parts. It oc- 

9 


130 DISTURBANCES OF THE CIRCULATION. 


curs first in the immediate neighborhood of the parts whose blood- 
supply is lessened; later, the blood may be driven also to such other 
more distant organs as may require it. 

Active hyperemia is characterized by a more or less marked redness and 
swelling of the part, which are very striking in tissues rich in blood-ves- 
sels. The blood flows through the widened channels with increased 
velocity, and lends to the tissue the color of arterial blood. Superficial 
tissues which are exposed to cooling become as a result of the increased 
blood-supply warmer than the neighboring tissues which are less richly 
supplied. 

Passive Hyperemia arises through the retardation or obstruction of 
the flow of blood from the veins. A general passive congestion of the systemic 
reing occurs in those cases in which, through weakness of the heart’s ac- 
tion, valvular insufficiency or stenosis, or obstructions to the pulmonary 
circulation, the emptying of the large veins into the right heart is hin- 
dered. In the pulmonary circulation stagnation of the blood-stream 
may be brought about by any cause hindering the outflow of blood from 
the lungs, particularly valvular lesions of the left heart, weakness of the 
left side of the heart, and, more rarely, obstructions in the systemic 
arteries. Not infrequently such a stasis of the pulmonary circulation 
may reach such a degree that the blood is dammed back into the right 
heart, and into the veins of the systemic circulation (see §§ 33 and 34). 

Local passive congestion may arise directly from the fact that the 
progress of blood through the veins is not adequately supported by the 
activity of the muscles and the aspiration of the blood from the veins dur- 
ing the inspiratory enlargement of the thorax. The absence of the first 
factor is most apparent in the case of the branches of the inferior vena 
cava; as, for example, in individuals who pass a large part of their time 
sitting or standing without active bodily exercise, so that the emptying 
of the deep-seated venous branches into the vena cava is dependent al- 
most wholly upon the activity of the vein-walls, which by virtue of their 
elasticity and contractility work against the pressure of the column of 
blood resting upon them. The absence of the inspiratory aspiration of 
the venous blood may, on the other hand, make itself felt in disturbance 
of inspiration through inflammation or other disease-processes of the 
lungs or pleura. 

A further cause of local passive hyperemia consists in the narrowing 
or closing of individual veins, as in the case of compression, ligation, 
formation of thrombi ($ 38), and the invasion of the veins by new- 
growths. Forexample, the pregnant uterus or a pelvic tumor may com- 
press the pelvic veins, a thrombus may obstruct the cerebral sinuses or 
the femoral or portal veins, or a sarcoma of the pelvis may grow into 
the large pelvic veins. 

When, through the above-mentioned processes or through ligation, 
single veins become occluded, the effect of the occlusion is often very 
insignificant, inasmuch as the veins concerned may possess free commu- 
nication with other veins, so that but slight obstruction is offered to the 
outflow of the blood. If, on the other hand, the oceluded vein possesses. 
no collateral communications, or very small ones which are inadequate 
for the passage of the blood—as, for instance, is the case with the main 
divisions of the portal vein, the sinus of the dura mater, the femoral and 
the renal veins—there results a more or less marked passive congestion 
in the area supplving the given vein. 

The effect of an obstacle to the outflow of blood shows itself first in. 


ACTIVE AND PASSIVE HYPERAEMIA; HYPOSTASIS. 131 


that portion of the vein lying between the obstruction and the periph- 
ery, the blood-current becoming slowed or checked entirely, while at the 
same time there follows a progressive filling and dilatation of the veins 
through the continued afllux of blood from the capillaries. If through 
the counteractive effect of the increasing tension of the elastic and con- 
tractile vein-walls the obstacle is overcome, the circulation is main- 
tained, and the blood flows toward the heart through the channels which 
it still finds open. Not infrequently the small veins thus called upon to 
perform this increased labor become gradually much dilated, and are 
converted into larger veins. When the obstacle cannot be overcome and 
communicating vessels capable of dilatation are not present, the circula- 
tion comes to a standstill, and a condition of stasis ($ 41) or thrombosis 
(§ 38) is produced in the obstructed vessel and its tributaries. 

If the congestion within a venous area extends to the capillaries, so 
that they become overfilled with blood, the affected tissue becomes blue- 
red or cyanotic, exhibiting at the same time a certain degree of swelling. 

Both active and passive hyperemia, observed during life, may, after 
death, show a very different appearance, and not infrequently disappear 
entirely. This is especially the case in the active hyperemias of the 
skin, in part also in those of the mucous membranes. This is dependent 
upon the fact that the tissues, put upon the stretch by the dilatation of 
the capillaries, contract upon the latter, after the stoppage of the cir- 
culation, and by their counter-pressure drive the blood from the capil- 
laries into the veins. In this way a tissue which was red during life 
may become pale after death. On the other hand, tissues which during 
life were pale or at least showed no especial redness, may after death 
take on a blue-red color. This takes place particularly upon the sides 
and back of the trunk (in those parts not pressed upon by the body- 
weight), on the neck, and the posterior aspects of the extremities of 
cadavers lying upon their backs; and is to be explained by the fact that. 
after death the blood sinks to the most dependent parts of the body, and 
fills not only the veins, but finally also the capillaries. This phenome- 
non is known as post-mortem hypostasis, and the areas of discoloration 
as ‘‘death-spots”’ or livores. They appear within about three hours 
after death, and are the more pronounced the greater the amount of 
blood contained in the skin and subcutaneous tissues at the time of death. 

In the internal organs post-mortem hypostasis is particularly notice- 
able in the pia mater, the dependent veins being usually more markedly 
distended with blood than those situated higher. In the lungs the set- 
tling of the blood causes an engorgement not only of the veins, but also 
of the capillaries. 

If the general circulation during life, as a result of cardiac insuffi- 
ciency, is imperfect, and there results a general passive congestion, the 
blood may also collect in the dependent portions of the body, partly be- 
cause it is not driven out of them, and partly because it sinks into these 
parts from those situated on a higher level. This phenomenon is also 
known as hypostasis, and occurs particularly in the lungs (hypostatic 
congestion). 


For the observation of the circulation and its disturbances during life the tongue 
or the web of the curarized frog, properly spread upon a glass plate, may be used 
(Cohnheim, Virch. Arch.. Bd. 40). This may be done in a very simple manner by draw- 
ing the frog’s tongue over a cork ring, which is cemented to a glass plate, and fasten- 
ing it to the sides of the ring with pins The pulsating arterial current and the con- 
tinuvus venous stream possess a cles zone of blood plasma, in both the normal and 


133 DISTURBANCES OF THE CIRCULATION. 


the quickened circulation. If, through the ligation of the efferent veins of the tongue. 
passive congestion is produced and the current slowed, the plasma-zone in the veins is 
lost, and both veins and capillaries become greatly distended with accumulated red 
cells. After a certain time the tongue swells as the result of an infiltration with trans- 
uded fluid. 

According to the investigations of ton Landerer (* Die Gewebsspannung,” Leipzig. 
1884), the wall of a capillary vessel embedded in tissue supports only from one-third 
to one-half of the blood-pressure. The remaining portion is borne by the tissues, which 
afford an elastic resistance, and thereby maintain the tension which is necessary to keep 
the blood in motion. In both active and passive hyperemia both the tissue-pressure 
and the tissue-tension are increased ; in anemia they are diminished. 


§ 37. Local anemia or ischemia, the lack of proper blood-supply 
to a tissue, is always the result of a diminution in the afflux of blood. 
If the total mass of the blood is normal, the cause of the anzmia is 
purely local; if there is a general poverty of blood, the local ansemia, in 
part at least, is secondary. 

The pathological diminution in the blood-supply to an organ is at 
times merely the result of an abnormal increase of the arterial resistance, 
due to the contraction of the muscular coats. In other cases pathological 
obstructions—such as compression of the arteries, narrowing of the 
arterial lumen through pathological changes In the vessel-walls, deposits 
on the inner surfaces of the arteries, occlusion of the vessels by emboli 
(compare § 20), ete.— may act as hindrances to the blood-stream. 

The immediate result of the narrowing of an artery is always a slow- 
ing and diminution of the blood-stream beyond the point of constriction. 
Complete occlusion of an artery brings the circulation beyond the obstruc- 
tion to an immediate standstill. If back of the point of constriction or 
occlusion the artery is provided with large arterial communicating 
branches—the so-called arterial collaterals—the disturbance of the circu- 
lation may be compensated by an increased afflux of blood through the 
collateral arteries; and this compensation is the more complete the larger 
and the more distensible are the collaterals. If the narrowed or occluded 
artery possesses no collateral branches in its area of distribution—if it is 
a so-called terminal artery—the slowing or cessation of the circulation be- 
yond the point. of obstruction or occlusion cannot immediately be done 
away with, and the affected vascular area becomes partly or wholly emp- 
tied of blood, in that, through the contraction of the arteries and the 
pressure of the tissue on the capillaries and veins, the blood is almost 
wholly driven out of the area supplied by the obstructed artery. Fre- 
quently there occurs after a time an afflux of blood from the neighboring 
capillaries. 

When the current and the pressure beyond a constricted point have 
sunk to a certain minimum, the driving force gradually becomes unable 
to propel the mass of blood. The red corpuscles, in particular, cease to 
move, and collect in the veins and capillaries, so that the area supplied 
by the artery in question becomes again filled with blood ; only not with cir- 
culating, but with stagnant blood. The same thing occurs when, after com. 
plete occlusion of a terminal artery, the blood slowly and under low press- 
ure enters the vessels of the affected area from small arteries incapable 
of adequate enlargement, or merely through anastomosing capillaries. 
Finally, an accumulation of blood within the angsemic area may also oc- 
cur by a reflux from the veins. This takes place when the intravascu- 
lar pressure within this area has sunk to nothing in the arteries and 
capillaries, while in the veins a positive pressure exists. A condition of 
passive congestion in the veins favors such a reflux. 


THE SEQUEL OF ISCHAEMIA. 133 


A further cause of anemia of one organ may be found in the abnor- 
mal congestion of other orgaus,»as in that case the total mass of the 
blood is not sufficient to supply adequately the remaining organs. Such 
an anemia is designated collateral anemia. 

All anemic tissues are characterized by paleness. At the same time 
they are flabby, not turgesgent, and show their individual color more 
distinctly. Are dle 

The significance of ischemia lies especially in the fact that, on ac- 
count of the need of the tissues for a continuous supply of oxygen and 
food-material, the persistence for a certain length of time of the condi- 
tion of imperfect blood-supply brings about tissue-degenerations (compare 
§ 1). Total arrest of the blood-supply leads in a short time to the death 
of the tissue involved. If the blood comes to flow anew into the degen- 
erating and dying tissues in the area of distribution of an obstructed ves- 
sel, and there stagnates, an extravasation of blood into the tissue may 
tuke place, leading to the formation of a hemorrhagic infarct (compare 


§ 45). 

The rapidity and completeness of the derelopment of a collateral circulation after the 
occlusion of an artery depends upon the size and distensibility of those vessels which 
are in communication with those of the anemic area. If these are numerous and dis- 
tensible, the anemic area is soon again supplied with an approximately normal volume 
of blood. If this is not the case the disturbance of the circulation is more slowly com- 
pensated; and the stasis and increased pressure are found to extend farther back from 
the point of obstruction toward the heart, so that a collateral hy peremia occurs in ves- 
sels situated farther back toward the heart. In the further course of the process of 
re-establishing the circulation the resulting increase of volume and velocity remains 
confined to such vessels as communicate with the area of the obstructed artery, that is, 
confined to the capillary and arterial anastomoses, where the increase of volume and 
velocity become permanent. This leads further to a lasting dilatation of the vessels 
concerned, and at the same time to an increase in the vessel-walls, not only in thickness, 
but also in length, as is evident from the increased tortuosity of the vessels. Accord- 
ing to Nothnagel, the phenomenon of the increase in thickness of the walls of the anas- 
tomosing arteries may be demonstrated in the case of rabbits in about six days after 
the ligation of an artery; and after the ligation of large vessels in their continuity, the 
smal] arteries which carry on the collateral circulation become changed in the course 
of a few weeks, into quite capacious, thick-walled arteries. 


Literature. 


(Local Disturbances of Circulation.) 


Baldwin: Multiple Anwmic Infarction of the Liver. Jour. of Med. Research, 1902 

( ult. ). 

Bier: Entstehung d. Collateralkreislaufs. Virch. Arch., 147, 158 Bd., 1897, 1898 (Lit.). 

Cavazzani: Sur la genese de la circulation collatérale. Arch. ital. de biol., xvi., 1892. 

Cohn: Klinik der embolischen Gefässkrankheiten, Berlin, 1860. 

Cohnheim: Vorles. über allgemeine Pathologie, Berlin, 1882. 

Hektoen: Embolism of the Coronary Arteries. Med. News, 1892. 

Krauss: Der Verschluss der Vena Cava sup. u. d. Vena Cava inf. Inaug.-Diss., Tü- 
bingen 1894 (Lit.). 

Löwit: Rückläufige Blutströmung. Centralbl. f. allg. Path., viii., 1897. 

Lukjanow: Allgemeine Pathologie des Gefüsssystems, Leipzig, 1894. 

Marchand: Gehirnembolie. Berl. klin. Wochenschr., 1894. 

Mögling: Zur Kenntn. des hämorrhagischen Infarktes. Beitr. v. Ziegler, i.. 1886. 

Nothnagel: Die Entstehung des Collateralkreislaufs. Zeitschr. f. klin. Med., xv., 
1888. 

v. Recklinghausen: Pathologie des Kreisiaufs u. der Ernährung, Stuttgart, 1883. 

Reimar: Embolie der Art. centralis Retine. Arch. f. Augenheilk., 38 Bd., 1899. 

Saveliew: Gehirnarterienembolie. Virch. Arch., 135 Bd.. 1894. 

Talma: Ueber collaterale Circulation. Pflüger’s Arch., 23 Bd., 1880 

Thoma: Pathologische Anatomie, i., Stuttgart, 1894. 

Virchow: Ocrtliche Störungen des Kreislaufs. Handb. d. spec. Path., i., Erlangen, 
354. 


COAGULATION OF THE BLOOD. 135 


guished as red, colorless or white (that is, yellow or grayish-white), and 
mized thrombi. 

The coagulation of the blood is a peculiar process, difficult of exact 
interpretation. Histologically, it is characterized, both in extravascular 
clotting (Fig. 12, d, d,) and in intravascular as well (Fig. 13), by the 
formation of little rods and threads between the red cells, at one time ar- 
ranged in 3 meshwork, at other times in stellate or fascicular groups 
around centres. These little rods and fibres are known as fibrin; and 
are in part smooth and shining, in part covered by little grannles, or 
partly interrupted by granules, or are composed entirely of such collected 
together. Besides the threads there occur also free granules, granular 
masses, and blood-plates of varying size and form; and not infrequently 
such formations lie in the centre of the fibrin-stars. At times the stellate 
and fascicular forms of fibrin are found arranged about leucocytes or at- 
tached to endothelial cells of the intima of the vessel. 

In the red blood-cells there occur here and there degenerative appear- 
ances, in the form of plasmolysis, plasmorrhexis, and plasmoschisis. In 
plasmolysis or erythrocytolysis there occurs a passage of soluble substances 
from the red cells into the blood plasma, so that the red cells become 
smaller, and the so-called microcytes and red blood-cell ‘shadows ” are 
produced. At the same time individual cells may become swollen. 

In plasmorrhexis or erythrocytorrhcxis and in plasmosthisis or erythro- 
cytoschisis, bright, shining globules arise from the red cells, or the latter 
become covered with little prickle-like projections, or come to resemble 
mulberries, or send out protoplasmic processes. Through the snaring- 
off of these prominences round, disc-like, angular, or thread-like bodies 
are formed, which are partly homogeneous and partly finely granular, 
and not infrequently enclose larger shining bodies. Finally, the red cells 
may break up into disc-like or globular pieces, and finally into granules. 
The formations known as blood-plates ave nothing more than peculiarly 
formed products of plasmorrhexis and plasmoschisis of the red cells ; and it is 
possible to distinguish among them those which are colorless, those con- 
taining hemoglobin, and homogeneous and granular forms. 

In fresh coagula, changes. cannot usually be demonstrated in the col- 
orless corpuscles of the blood ; but in the later course of the process degen- 
erative appearances are found in these also. 

Between the destruction of the red blood-cells and the coagulation of the 
blood, both extra- and intravascular, there exist undoubtedly close relations ; 
that is, coagulation is set into action through the occurrence of changes 
in the red cells as above described. According to our present knowledge, 
it must be assumed that many red cells, probably the oldest ones, very 
easily suffer such changes, so that, for example, adherence to a diseased 
portion of the vessel-wall, which is prevented by the normal condition of 
the intima, is sufficient to cause a disintegration of certain red cells, with 
formation of blood-plates, and later coagulation and thrombus-forma- 
tion. The origin of coagulation has also been regarded as due to plas- 
molysis and plasmorrhexis of the leucocytes; further, similar degenera- 
tions of the endothelium may also induce coagulation. The possibility 
that the endothelial cells play a certain part in the origin of coagulation 
cannot be excluded, but it must be emphasized that the degenerative 
changes ordinarily preceding coagulation cannot be demonstrated in these 
cells. The facts brought forth, particularly by Hauser and Zenker, that 
the fibrin-threads not infrequently are attached to endothelial cells, or 
leucocytes, or to the remains of such cells, do not prove that these are 


136 DISTURBANCES OF THE CIRCULATION. 


the erciters of coagulation, or that they offer material for the formation 
of fibriu; inasmuch as the deposit of the fibrin upon these cells may 
be due to purely mechanical 
causes. 

The chemical processes 
concerned in coagulation can- 
not at present be explained. 
It is assumed that for its oc- 
currence the presence of a 
fibrinogenie substance, a fer- 
ment (thrombin), and certain 
salts, particularly calcium salts, 
is necessary; and that the 
fibrinogenic substance is an 
albuminoid body belonging to 
the globulins, which is present 
in the blood-plasma, while 
the ferment is produced by 

Fin. 13.—Rundles and starshaped clusters of Abrin the cells. According to A. 
BE RESTE Ep ED tm Schmidt, thrombin is derived 
x 500. “ from a parent-substance, pro- 

thrombin. By means of the 
thrombin there is formed, in an as yet unknown manner, from the globu- 
lins pre-existing in the alkaline solution, a greatly swollen albuminoid 
body, which is precipitated by the calcium salts contained in the plasma. 
In the process of coagulation we must, therefore, recognize two stages, 
namely, the stage of the production of the fibrin-ferment, and the stage 
of the action of the ferment or coagulation proper. 

According to Pekelharing, on the other hand, thrombin is a calcium 
compound of prothrombin, which 
arises from the cellular elements 
of the blood; and coagulation 
consists essentially in the fact 
that thrombin carries calcium 
over to the fibrinogen, whereby 
the insoluble caleium-compound, 
fibrin, is formed. Hammarsten, 
on the contrary, is of the opin- 
ion that calcium is carried down 
with the fibrinogen only as a 
contamination, and has no sig- 
nificance in the change of fibri- 
nogen to fibrin, in the presence 
of thrombin, According to his 
theory, the calcium salts are a 
necessary factor only for the 
change of prothrombin into 
thrombin. 

The red thrombus is formed 
under such conditions as the com- 
plete stoppage of the circulation or 
a marked slowing of the same, and 
s the total mass of the red cells (Fig. 14). The precipitated 
rms granules (Fig. 14, b) and threads (a). In fresh clots in 














fibrin fi 





THROMBOSIS. 137 


small vessels, it is not infrequently possible to demonstrate after death, 
by means of special methods, the presence of bundles aud star-shaped 
clusters of fibrin-rods (Fig. 13), which radiate from centres of coagula- 
tion. In such cases, however, it is often impossible to distinguish with 
certainty to what extent the coagulation is intravital or to what extent 
post-mortem. Such form of coagulation is most frequently observed in 
inflamed tissues, and the conclusion is warranted that changes in the 
blood occurring in such inflammatory areas are the cause of this variety 
of fibrin-formation, 

Immediately after its formation the red thrombus is soft and rich in 
the fluids of the blood; later it becomes tougher, denser, and more dry, 
as the fibrin contracts and squeezes out a portion of the fluid. At the 
same time it becomes paler, brownish-red or of a rust-color, inasmuch as 
the blood-pigment undergoes changes similar to those occurring in ex- 
travasations. 

The cause of the ante-mortem intravascular coagulation is to be 
found either in an increase in the production of fibrin.ferment or fibrinogenic 





Fra. 15.—Section from a mixed thrombus rich in _F1G. 16.—Section from a white thrombus contain- 
calla" (Müiler's Quid. Dermatoxsiln.) 0. Red blood- ng bat few cells. (Mülter's Guid; hemnafozyiin.) 
Tassen; c, Yeticular fibrin con Abrogranular Ahrin form- 


Sinine many leucocytes; d, threads of übrin in fiat net lkerekeriim: €, Obrin-threads in 
parallel arrangement. X 200. arrangement. x 20. 


substances or in a diminution of the power possessed by the normal vessel-wall 
of inhibiting coagulation. Under certain conditions the more marked ad- 
hesion of the blood to a degenerated area in the vessel-wall may in itself 
be sufficient to induce coagulation. This occurs accordingly in ligated 
vessels, when the endothelium at the point of ligation is injured. It 
takes place, furthermore, when, as the result of the disintegration of 
great numbers of red cells, fibrin-ferment is set free in large amounts 
into the blood-stream—a condition which can be brought about by the 
injection of laked blocd, in which the red cells are for the greater part 
destroyed. 

White, mixed, and often distinctly laminated thrombi arise in the 
flowing blood, and consist of masses of yellowish color, or of various 
shades of red, or of alternating layers of red and white. The micro- 
scopical examination shows them to consist of granular and thread-like 
masses (Figs. 15 and 16), leucocytes, and red cells, which in varying pro- 


138 DISTURBANCES OF THE CIRCULATION. 


portion and arrangement make up their structure. White thrombi may 
consist almost eutirely of granular masses (Fig. 16, a) and fibro-granu- 
lar fibrin, which in some cases is arranged in a meshwork (b), in others 
in fibres running nearly parallel (¢) which enclose few leucocytes. In 
other cases the number of cells may be much greater. In mixed thrombi 
(Fig. 15), granular fibrin (b), more rarely hyaline masses, thready 
fibrin (ec, d,), aud red blood-cells (a), in varying proportion and in alter- 
nating stratification, constitute the thrombus-mass, and all of these ele- 
ments enclose more or less numerous, often many leucocytes. 

The jibrogranular masses which form part of the structure of the 
thrombus are composed of precipitated fibrin. The granular and hyaline 
masses, on the other hand, 
probably arise directly from 
the products of the plasm- 
oschisis and plasmorrhexis 
of the red blood-cells, in 
particular from the blood- 
plates. In large thrombi 
they often show a coral-like 
arrangement. 

The causes of the forma- 
tion of white and mixed 
thrombi are especially: 
changes in the intima of the 
heart and the vessels and dis- 
eases of the vascular appara- 
tus, which lead to a general 
or local slowing or irregularity 
of the blood-stream. The for- 
mation of thrombi may be 
A studied directly, in suitable 

Fra. 0. subjects, under the micro- 

IE.-Rapkip orig blentatream, a. Axia steam: Scope, both in the case of 
ne eb Isola leurocstes, a tater Eierth cold. blooded and warm- 
Moderately slow bloodstream. a, Axtal stream;  Dlooded animals; and the ob- 
| zone with numerous leucocytes, d. (After Servations made in this line, 
ee “mn . u especially by Bizzozero, 
In welth bibonieplatenz €. x Tiwod-plates; Eberth, Schimmelbusch, and 
leucorytes, (After Eberth and Schinmelbusch.) Léwit, have led to very im- 

portant results. 

When the blood flows with normal velocity through a blood-vessel, 
there may be seen under the microscope a broad, homogeneous red stream 
of the blood-vessel (Fig. 17, a), while at the sides there lies a 
zone (b) free from red cells, This may be observed in the 
. s, and large capillaries, but is best seen in the veins, while 
in the small capillaries, which are just large enough to permit the pas- 
sage of the red cells, this difference between the axial stream and plasma- 
zone is not present. 

In the axial stream the different constituents of the blood-stream are 
not recognizable; in the plasma-zone there appear, from time to time, 
white blood-corpuscles (Fig. 17, @) which roll slowly on along the vessel- 
wall. 

If the hlood-stream becomes retarded to about the degree that the red 
cells of the axial stream are indistinctly recognizable (Fig. 18, a), the 


































THROMBOSIS. 139 


number of white corpuscles, which roll slowly along in the plasma-zone, 
at times adhering to the vessel-wall, becomes constantly increased (Fig. 
18, d), so that they finally come to lie in great numbers in this zone. 

If the current is still further retarded so that the red cells become 
plainly recognizable (Fig. 19, a), there appear in the peripheral plasma- 
zone, in addition to the colorless blood-corpuscles (d), also blood-plates 
(6), which increase more and more in number with the progressive retar- 
dation of the current, while the leucocytes again become diminished in 
numbers. When total arrest of the blood-current finally occurs, there 
follows a distinct separation of the corpuscular elements in the lumen of 
the vessel. 

If, in a vessel in which the circulation is retarded, the intima is in- 
jured at acertain point by compression or crushing, or by means of 
chemical agents, as corrosive sublimate, nitrate of silver, or sodium 
chloride, and if the lesion of the wall does not lead to a complete stop- 
page of the circulation, blood-plates may be seen adhering to the injured 
portion of the wall; and in a short time the injured spot is covered with 
many layers of the same (Fig. 19, c). Often, more or less numerous 
leucocytes (d,) become embedded in this mass, and their number is the 
greater the more numerous these are in the plasma-zone. Under certain 
conditions they may be very numerous and partly cover up the blood- 
plates. In case of great irregularity of the circulation or more severe 
changes in the vessel-wall, red cells may also drop out of the circulation 
and become adherent to the vessel-wall or the colorless deposit already 
formed. Not infrequently portions of the thrombus-mass are again torn 
loose, in which case a new deposit of blood-plates occurs. The vessel 
may finally be closed as the result of a long-continued deposit of the 
blood-elements. 

When at any point blood-plates in large numbers have become ad- 
herent to the vessel-wall, they become after a time coarsely granular at 
their centre, and finely granular or homogeneous at their periphery, and 
become fused together into one compact mass, The final result of this 
process is the formation of a colorless blood-plate thrombus, within which 
more or less numerous leucocytes may be imprisoned. Eberth designates 
the sticking together of the blood-plates as conglutination, their fusion 
into a coherent thrombus-mass as viscous metamorphosis. 

If we compare the observations made upon warm-blooded animals, 
by Bizzozero, Eberth, and Schimmelbusch, and more recently by Lowit, 
with the histological findings in thrombi occurring in the human subject, 
we are warranted in drawing the conclusion that the formation of thrombi 
in the circulating blood of man occurs in part in the same way as that 
observed in the lower animals. Thrombosis is, therefore, directly depend- 
ent upon two causes: namely, disturbances of the circulation, particu- 
larly retardation of the current and the formation of eddies which drive the 
blood-plates against the vessel-wall ; and local changes in the vessel-walls. 
It is also probable that thrombosis is favored by pathological changes in 
the blood. From the variety of conditions under which thrombosis in 
man occurs, we must assume that at one time one cause, at another time 
another, plays the chief part in the formation of the thrombus, or that 
all three may take an equal part in the process. 

If a blood-plate thrombus or a conglutination-thrombus has formed 
at any point, coagulation may subsequently occur, yielding fibrin-threads 
which enclose a greater or less number—often large numbers—of the 
cellular elements of the blood. Conglutination and coagulation may occur 


140 DISTURBANCES OF THE CIRCULATION. 


in combination ; and the frequency with which this comes to pass, judging 
from the composition of the thrombi occurring in man (Figs. 15 and 16), 
seems to denote the fact that fibrin-ferment is produced during the for- 
mation of the blood-plate thrombus, and that consequently, in the neigh- 
borhood of the conglutinated blood-plates, processes of coagulation 
occur in the adjacent plasma-zone of the blood-stream. If white corpus- 
cles alone are circulating in this zone, the mass of coagulum is white 
(Fig. 16) and encloses a greater or less number of red cells; if red cor- 
puscles also circulate in the peripheral zone, or if the coagulation extends 
into the red axial stream, mixed thrombi will be formed (Fig. 15). 

If in marasmic individuals, as not infrequently happens, or in those 
who have been subjected to some traumatism, extensive thrombosis oc- 
curs, this occurrence is probably connected with a ferment-intoxication 
(Kohler, von During); and the local disturbances of circulation only 
decide the location of the coagulation. Vaquez is of the opinion that 
infectious play a very prominent röle in the origin of cachectic thrombi. 


According to Naunyn, Franken, Köhler, Plosz, Gyorgyat, Hanau, and others, a 
more or less extensive thrombosis may be produced by the injection into the blood- 
vessels of laked blood, solutions of hemoglobin, salts of cholic acid, ether and other 
substances; yet the results of this experiment are not constant (Schiffer, Ilögyes, Lan- 
dois, Eberth), and coagulation may not occur. The probability of effecting coagulation 
is proportionate to the degree of disturbance produced in the blood by the substance 
injected. 

According to Arthus and Pages, the blood flowing from the veins becomes inca- 
pable of coagulating spontaneously, if sodium oxalate, sodium fluoride, or soaps’ are 
added to it in such quantities that the mixture contains 0.07-0.1 per cent of the oxalate, 
or about 0.2 per cent of the fluoride, or 0.5 per cent of soap. These salts all act by 
precipitating the calcium salts. If to blood, kept fluid by treatment with oxalic acid, 
one-tenth of its volume of a one-per-cent solution of calcium chloride is added. coagu- 
lation occurs in six to eight minutes, and the calcium salts pass into the combination of 
the fibrin-molecule. The fibrin-ferment can act upon the fibrinogen only in the pres- 
ence of calcium salts. Under the influence of the fibrin-ferment, and the presence of 
calcium salts, the fibrinogen undergoes a chemical change which results in the forma- 
tion of a caleium-compound, fibrin. Zlammarsten, who holds that the presence of cal- 
cium is not necessary for the change of fibrinogen into fibrin, attempts to explain the 
observation of Artius and Pages, through the assumption that the calcium salts are 
necessary factors for the conversion of prothrumbin into thrombin. 

If blood be allowed to tlow beneath a layer of oil, into a vessel coated with a film 
of vaseline, it will not coagulate (Freund); and from this it may be assumed that the 
cause of the coagulation is to be found in the adhesion of the blood to a foreign body. 

Bizzozero, in the year 1882, described us a new element of the blood. small, fiat, 
homogencous structures, Which he designated as blood-plates, and regarded as identical 
with the hwematoblasts described by Hayem. Supported by thorough experimental 
investigations, he assumed that it was these bodies, which in breaking up. induced 
coagulation; and, therefore, denied this to be a property of the leucocytes. Ruuschen- 
buch, Heyl, Weiyert, Lait, Eberth, Schimmelbusch, lara, Groth, and others, have op- 
posed the teaching of Bizzozero, in that they in part oppose the causal relation of the 
blood-plates to coagulation, and in part (Neigert, Hlaca, Halla, and Zöwit) regard the 
blood-plates not as constant formed elements of the blood, but as degeneration-products 
of the colorless blood-corpuscles, or as a product of a precipitation of globulin (Zéuwit). 
From their contributions we may also gather that the disintegration of leucocytes in 
fluids containing fibrinogen may give rise to coagulation, so that the blood-plates are 
not the only tibrin-formers. According to Groth, the injection of large numbers of 
leucocytes into the blood-vessels leads to thrombosis. According to Rauschenbach, the 
dissolution of leucocytes is constantly occurring in the blood; but through the inhibi- 
tory powers of the organisin, the fibrin- ferment is rendered inactive. 

“thn, in 1805, was the first to differentiate strictly between red, white, and mixed 
thrombi. Ife regarded the colorless substance of the white and mixed thrombi as for- 
mations, arising from colorless corpuseles, which become separated from the axial 
stream, attach themselves to rough places of the vessel-wall, and fuse together to form 
homogencous or granular masses. Up toa few years ago most authors have accepted 
this view; but there can be no doubt, according to the investigations of Bizzozero, 


THE ORIGIN OF THE BLOOD-PLATES. 141 


Lubnitzky, Eberth, Schimmelbusch, and Lowit, that there is also a blood-plate thrombus 
in the production of which the leucocytes play only a subordinate röle, and that 
the tbready fibrin of thrombi also may often contain but very few leucocytes (Fig. 16). 

According to Léwit, the blood-plates are not found in the normal blood, but appear 
only under certain conditions; and represent nothing more than globulin precipitated 
in the form of platelets. For their formation very slight changes in the circulation 
and composition of the blood are sufficient; and it is therefore difficult to make observa- 
tions of the circulating blood without producing them. It is possible, however, by 
observing the greatest precaution, to demonstrate that the blood circulating in the 
mesentery of the mouse contains no formed elements except the red corpuscies and the 
leucocytes. Changes in the vessel-wall and slowing of the current lead to the precipi- 
tation and deposit of blood-plates upon the vessel-wall; and the blood-plates thus pre- 
cipitated are quickly changed into a substance closely related to fibrin, whereby they 
become soluble with difficulty, swell somewhat, and in part present a granular appear- 
ance. The blood-plate fibrin is in its staining-reactions closely related to thready 
fibrin, so that the production of a blood-plate thrombus is, in fact, a form of coagula- 
tion. In cold-blooded animals, under the same conditions as those leading to the for- 
mation of blood- plates in warm-blooded animals, the globulin is precipitated in a gran- 
ular form, but not in the shape of blood-plates. The small spindle-shaped elements 
found in the blood of cold-blooded animals and in birds, and which have been regarded 
by Bizzozero, Eberth, and Schimmelbusch as equivalents to the blood-plates, are nothing 
more than young colorless cells, which in part become transformed into ordinary leu- 
cocy tes, and in part into red blood-cells. They possess nuclei, and can assume a round 
form, while the blood-plates are non-nucleated, and cunnot actively change their form. 
Changes in the vessel-walls and slowing of the current lead in the case of cold-blooded 
animals to the formation of thrombi consisting essentially of leucocytes, which may 
be converted into granular masses. At the beginning of cell-deposition the spindle- 
shaped leucocytes are often deposited in great numbers. 

The view of Zörit as to the genesis of the blood-plates I cannot accept; I hold 
rather that the blood-plates are products of red blood-cells which are either thrown 
off from degenerating red cells, or are formed by the disintegration of the same. | 
base my opinion upon the investigations which Wlassow, at my suggestion, carried out 
in my laboratory in 1893. Wlassow studied both the early stages of thrombosis, and 
the behavior of the blood-corpuscles when treated with different fluids. His observa- 
tions would indicate that, on the one hand, in the beginning of thrombosis, in circulat- 
ing blood, the red corpuscles become adherent, undergo changes and are converted into 
a granular mass; that on the other hand, a portion of the red cells (most probably those 
which are the oldest and are approaching their disintegration) are very unstable cells, 
from which there may be easily formed structures which correspond to the blood- 
plates, in so far as their properties are concerned. Whether such structures develop 
under normal conditions, or whether in the normal disintegration of the red cells the 
colorless elements of their cell-bodies pass immediately into solution, cannot be decided; 
this much only can be demonstrated. : that the most diverse influences may cause a 
plasmoschisis of the red cells with formation of the so-called blood-plates. Arnold has 
recently published observations upon the products of the red cells resulting froma 
process of constriction and setting free of portions of the cell; and these confirm and 
extend the observations made by Wlussow and myself. 

A, Schmidt, in his work on the blood, published in 1892, in which he collects the 
results of many years of study on the coagulation of the blood, regards the fibrin- 
ferment or thromitn as a cell-derivative, which arises from an inactive antecedent sub- 
stance, prothrombin, under the influence of certain zymoplastic substances which are also 
cell-derivatives. He likewise regards the fibrinogenic substance or metaglobulin, as a 
product of the disintegration of cellular protoplasm. Therefore, the substances caus- 
Ing coagulation as well as those producing thrombosis must all be regarded as cell- 
derivatives, and the red blood-cells in particular are the source of the materials of coag- 
ulation, 

According to Corin, coagulation occurs in the blood of the cadater only achen the fer- 
ment was present tn the blood during life ; and the extent of the coagulation is dependent 
directly upon the amount of ferment contained in the blood during life. A further 
formation of ferment does not take place after death: on the other hand, it is probable 
that there is formed by the vessel-walls a body inhibiting coagulation. Between the 
blood of those dying suddenly (strangulation), and that of individuals dying slowly. 
there is only a relative difference, depending upon the amount of ferment present. A 
fluid condition of the blood of the cadaver can, therefore, be of no significance in so far 
as the diagnosis of the manner of death is concerned. 


142 DISTURBANCES OF THE CIRCULATION. 


Literature. 
(.Blood-plates, Coagulation of the Blood, and Thrombosis. ) 


Arnold: Freie Kugelthromben. Beitr. v. Ziegler, viii., 1890; Biologie der Blutkdrper, 
Virch. Arch., 145 Bd., 1896; Die Herkunft der Blutplättchen. Cbl. f. allg. Path., 
viii., No. 8, 1897; Morphologie der extravasculären Gerinnung. Virch. Arch., 150 
Bd., 1897; Morphologie der intravasc. Gerinnung. Ib., 155 Bd., 1899; Gerin- 
nungscentren. Cbl. f. allg. Path., 1899. 

Arthus: La coagulation du sang, Paris, 1899. 

Arthus ct Pages: Nouvelle theorie chimique de la coagulation du sang. Arch. de 
phys., ii., 1890. 

Aschoff: Ueber den Aufbau der menschl. Thromben. Virch. Arch., 180 Bd., 1892. 

Baumgarten: Zur Lehre von rothen Thrombus. Cbl. f. die med. Wiss., 1877; Ueber 
die neuen Standpunkte in der Lehre von der Thrombose. Berl. klin. Woch., 1886. 

Bizzozero: Blutplättchen u. Blutgerinnung. Cbl. f. d. med. Wiss., 1882, 1883; 
Virch. Arch., 90 Bd. ; Arch. per le Sc. Med., 1888; Arch. ital. de biol., i., ii., iii., iv. 
and xvi.; Festschr. f. Virchow. Internat. Beitr., i., 1891. 

Böttcher: Verhalten d. Blutes in doppelt unterbund. Gefässen. Beitr. v. Ziegler, ii., 
1888. 

Brücke: Ucber die Ursache der Gerinnung des Blutes. Virch. Arch., 12 Bd., 1857. 

Büchlers: Autochthone Hirnsinusthrombose. Arch. f. Psych., 15 Bd., 1898. 

Castellino: Nature du zymogene du fibrino-ferment. Arch. ital. de biol., xxiv., 1895. 

Corin: Ueber die Ursachen des Flüssigbleibens des Blutes bei der Erstickung u. and. 
Todesarten. Vierteljahrsschr. f. ger. Med., v., 1893. 

v. During: Fermentintoxication u. ihre Bezieh. z. Thrombose. Deut. Zeit. f. Chir., 
xxii., 1885. 

Eberth u. Schimmelbusch: Die Thrombose nach Versuchen u. Leichenbefunden, 
Stuttg., 1888; Dyskrasie u. Thrombose. Fortschr. d. Med., vi., 1888. 

Eisen: Blood-Plates. Journ. of Morph., xv., 1899. 

Feldbausch: Bed. d. roth. Blutkörp. f. d. Gerinnung. Virch. Arch., 155 Bd., 1899. 

Freund: Blutgerinnung. Limbeck’s Pathologie des Blutes, Jena, 1896. 

Halliburton: The Coagulation of the Blood. British Med. Journ., 1898. 

Hammarsten: Lehrb. d. phys. Chemie, Wiesbaden, 1899. 

Hauser: Beitr. zur Lehre von der Fibringerinnung. Deut. Arch. f. klin. Med., 50 
Bd., 1892: Gerinnungscentren. Virch. Arch., 154 Bd., 1898; Cbl. f. allg. Path., 
x., 1899. 

Hayem: Du sang et de ses alterations anatomiques, Paris, 1889. 

Hlava: Bezieh.«. Blutplättchen zur Gerinnung u. Thrombose. Arch. f. exp. Path., 
xvi., 1883. 

Lilienfeld: Blutgerinnung. Zeitschr. f. phys. Chem., xx., 1894. 

v. Limbeck: Klin. Pathologie des Blutes, Jena, 1896. 

Löwit: Blut gerinnung. Sitzber. d. K. Akad. d. Wiss. in Wien, 89, 90 Bd.. 1884; 
Blutplättchen u. Blutgerinnung. Fortschr. d. Med., iii., 1885; Die Beobachtung 
der Circulation am Warmblüter. Arch. f. exp. Path., xxiii., 1887; Blutplättchen 
u. Thrombose. Ib., xxiv., 1888; Blutplättchen u. Thrombose. Fortschr. d. Med., 
vi., 1888; Beziehung der weissen Blutkörperchen zur Blutgerinnung. Beitr. v. 
Ziegler, v., 1889; Präexistenz der Blutplättchen. Virch. Arch., 117 Bd., 1889: 
Coli. f. allg. Path., ii., 1891; Studien zur Physiologie u. Pathologie des Blutes, 
Jena, 1892. 

Müller: Die morphol. Veränderung der r. Blutkörperchen. Beitr. v. Ziegler, xxiii., 
189. 

Pekelharing: Bedeutung d. Kalksalze für die Gerinnung. Festschr. f. Virchow, 
Berlin, 1891; Unters. üb. das Fibrinferment, Amsterdam, 1892; Gerinnung. Deut. 
med. Woch., 1892. 

Petrone: Nulla coagulazione del sangue, Morgagni, 1897. 

Sacerdotti: Piastrine del sangue. Arch. per le Sc. Med., xiii., 1898; Anat. Anz., xvii, 


1900, 

Salvioli: Comparticipaz. dei leucociti nella coagulazione. Arch. per le Sc. Med., xix., 
1895. 

Scherer: Zooid- u. Ockoidbildung i. d. rothen Blutkörp. Zeitschr. f. Heilk., xvii., 
TRO. 


Schmidt, A.: Die Lehre v. d. fermentativen Gerinnungserscheinungen, Dorpat, 1877; 
Zur Blutlehre, Leipzig, 1892: Weitere Beiträge z. Blutlehre, Wiesbaden, 1895. 
Schmiedeberg: Elementarformen einiger Eiweisskörper (Fibrin). Arch. f. exp. Path., 

39 Bd., 1897. 





144 DISTURBANCES OF THE CIRCULATION. 


ete. Perforating wounds of the vessels, crushing of the vessel-wall, and 
laceration of the intima lead likewise to the formation of thrombi; and 
thrombotic precipitates are formed also upon foreign bodies lying in the 
vessels, According to the cause of the injury to the vessel-wall there 
may be distinguished: traumatic, infectious, and thermic thrombi, as well 
as those produced by degenerative changes in the wall, foreign bodies, and 
tumor proliferation. Thrombi occurring in enfeebled individuals with 
poor circulation (cardiac weakness) are usually designated as marasmic 
or cachectic. 

Thrombi may be classed also according to their relation to the vessel- 
lumen. Thns thrombi attached to the wall of the heart (Fig. 20, ¢) or 
blood-vessel are known as parietal 
thrombi, those situated upon the valves 
of the heart or veins (Fig. 21, d) are 
terned valvular thrombi. In both 
cases the thrombi may consist only of 
delicate, translucent, membranous, hy- 
aline deposits; but are often thicker 
and firmer and project into the lumen 
of the heart or blood-vessels. Their 
surface often shows ribbed elevations 
which are paler than the other portions. 
A thrombus completely closing the lumen 
of the vessel is called an obturating 
thrombus (Fig. 21, a, b). The coagula 
first formed are designated as primary 
or autochthonous, those subsequently 
deposited upon these as induced throm- 
bi. Through growth by accretion a pa- 
rietal thrombus may become changed to 
an obturating one. In this way it not 
infrequently happens that upon au orig- 
inally white or mixed thrombus a red 
one (Fig. 21, c) is formed; the throm- 
bosis at the beginning occurring in cir- 
culating blood, while later, after the clos- 
ing off of the vessel, the blood stands 
still and clots en masse. The reverse 
may occur—that is, upon a thrombus 
originally red there may be deposited 
white or mixed coagula—when a red 
thrombus obturating a vessel becomes 
smaller by contraction, and thus opens up 
a channel for the free passage of blood. 

Thrombi may occur in any part of the vascular system. In the heart 
they are formed chiefly in the auricular appendages and in the intertra- 
beeular spaces, as well as upon any diseased spot (Fig. 20, 6) in the 
all. They begin usually in the deep recesses between the tra- 
but through continual accretions they form larger masses of 
which project: above the surface in the form of polypoid masses 
1, which are called heart-polypi. They are sometimes more or 

ali ape, with a broad base; at other times they are more 
often ribbed. In rare cases large spherical 
or knobby thrombi may become loosened; and, in case they cannot pass 





of femoral and 


red thrombus 






















148 DISTURBANCES OF THE CIRCULATION. 


mation of the thrombus, the process of organization is brought about by 
formative cells which wander in from the outer layers of the vessel-wall. 
The thrombus itself takes no part in the organization; it is a dead mass 
which excites inflammation in the surrounding tissues. In the course of 
time the dead thrombus-mass is replaced by vascularized connective tissue 
(Fig. 23, b, c, d). 

The cicatricial tissue formed in the place of the thrombus contracts 
more or less in the course of time. The cicatrices formed after ligation 
may thus become very small. Such a cicatrix in the continuity of a ves- 
sel may later appear simply as a thickening of the vessel-wall, or there 
may remain only threads and trabeculae (Fig. 22, b, c, d), which cross 
the lumen of the thrombosed vessel, so that the blood-stream can once 
more pass the affected spot. Not infrequently the connective-tissue 
strands crossing the vessel cause a marked narrowing of the lumen; or 
the vessel may become completely obliterated (Fig. 22, a), so that the 
vessel for a greater or less distance becomes converted into a solid fibrous 
cord. 

The pieces broken loose from a thrombus and carried into an artery 
and there lodged—that is, emboli—generally induce new deposits of 
fibrin upon their surface. Later they undergo the same changes as 
thrombi, and may either soften, or contract (Fig. 24, a), or become calei- 
fied. If the emboli are non-infective they usually become replaced by 
vascular connective tissue (Fig. 23, b, c). 

In many cases the new-formation of connective tissue leads to the ob- 
literation of the artery (Fig. 23). In other cases in the place of the em- 
bolus there is developed only a ridge of connective tissue or a nodular or 
flat thickening of the intima. In still other cases the lumen of the vessel 
is traversed by strands of connective tissue (Fig. 24, 6), which either run 
separately or, interlacing, form a fine- or coarse-meshed network. 

If pyogenic organisms are present in the emboli, as is very likely to 
be the case when the emboli arise from a thrombus lying in a suppurat- 
ing focus, there is produced a purulent. process (Fig. 25, #) at the site of 
the embolus (Fig. 25, g), and occasionally ulceration also. 





Literature. 
(Thrombosis. ) 


Apollonio: Organisation des Unterbindungsthrombus. Beitr. v. Ziegler, iii., 1888. 

Arnold: Die Geschicke d. Leukocyten bei der Fremdkörperenbolie. Virch. Arch., 
133 Bd., 1898. 

Baumgarten: Die sog. Organisation des Thrombus, Leipzig. 1877. 

Bubnoff: Ueber die Organisation des Thrombus. Virch. Arch., 44 Bd., 1868. 

Büchlers: Autochthone Hirnsinusthrombose. Arch. f. Phys., 25 Bd., 1898. 

Flexner: Agylutination Thrombi. Jour. of Med. Research. 1902. 

Herz: Ueber ältere Thromben im Herzen. Deut. Arch. f. klin. Med., 87 Bd., 1885. 

Heuking u. Thoma: Susbtitut. d. marant. Thrombus durch Bindegewebe. Virch. 
Arch., 109 Bd., 1887. 

Justi: Hvaline Capillarthrombose. Inaug.-Diss., Marburg, 1894. 

Lubnitzky: Die Zusammensetzung des Thrombus in Arterienwunden. Inaug.-Diss., 
Bonn, 1885. 

Osler: Trans. of Assn. Amer. Phys., 1887. 

Pernice: Sulla fusione purulenta del trombo. Sicilia Med., i., Palermo, 1889. 

Pick: Hyaline Thrombose. Vireh. Arch., 138 Bd., 1894. 

Raab: Anat. Vorgänge nach Unterbindung der Blutgefässe. Virch. Arch., 75 Bd.. 
1879. 

v. Recklinghausen: Freie Kugelthromben. Deut. Arch. f. klin. Med., 87 Bd., 1885. 





150 DISTURBANCES OF THE CIRCULATION. 


more distended and the pressure within these rises to the height of that 
at the point of divergence of the nearest permeable artery. In this way 
a large portion of the fluids of the blood are pressed out of the capillaries 
and veins, and as a result of this the red blood-cells become so closely 
packed together that their contours are no longer distinguishable, and 
the total contents of the vessel form a homogeneous, scarlet-red column 
(Fig. 26). The red blood-cells, however, are not fused together; as soon 
as the hindrance to the outflow is removed and the circulation restored, 
the individual corpuscles become once more separated from one another. 

Stasis may be caused by many injurious influences which affect the 
vessel-wall and the blood itself. Thus, for example, heat and cold, irri- 
tation with acids and alkalies, action of concentrated solutions of sugar and salt, 
action of chloroform, alcohol, etc., cause not only contraction or dilatation 
of the vessels and disturbances of circulation, but also under certain 
conditions produce stasis. These injurious agents act in the first place 
by abstracting water from the blood and vessel-walls, and further by 
producing essential changes in the composition of the blood-corpuscles, 
blood-plasma, and vessel-walls; so that the red cells become less mobile 
and the vessel-walls come to offer increased frictional resistance to the 
blood-stream, and at the saıne time to permit the fluid portions of the 
blood to pass through them the more readily. Stasis may also be pro- 
duced by loss of water and drying of the tissues, an event which may oc- 
cur, for example, in injuries which lay bare tissues lying within the body 
(intestine). 


Literature. 


(Stasis. ) 


Cohnheim: Vorlesungen über allgemeine Pathologie, Berlin, 1882. 
v. Recklinghausen: Allgem. Pathologie d. Kreislaufs u. d. Ernährung, Stuttgart, 
1883. 


IV. CEdema. 


§ 41. The free fluid which permeates the tissues is essentially a tran- 
sudate from the blood, though under certain conditious a portion of the 
tissue-fluids contained in the cells and fibres may also pass over into the 
free lymph. The passage of fluid from the vessels is not a simple proc- 
ess of filtration, but is rather to be regarded as of the nature of a secre- 
tion, accomplished by means of a specific function of the capillary walls. 
The fluid secreted by the capillaries mingles with the products of metabo- 
lism in the tissues, and is taken up from the tissue-spaces by means of 
the lymph-vessels, and through the thoracic duct is again returned to the 
venous blood. 

Every increase in the transudation of the fluids of the blood causes 
first a more marked saturation of the tissues, which may be compensated 
for by an increased absorption through the lymph-vessels. This com- 
pensation has, however, its limits; with increased transudation from the 
blood-vessels there is produced a more or less permanent over-saturation 
of the tissues with the transuded fluids. 

The condition which is produced by this collection of fluids in the tis- 
sues is known as dropsy, cedema, or hydrops. According to the extent 
of the condition there may be distinguished a general and a localized hy- 
drops. An oedema extending over the superficial portions of the body is 
known as anasarca or hyposarca. 


(EDEMA. 151 


The transudate from the blood which constitutes the edema or the hydrops is 
always much poorer in albumin than the blood-plasma. The fluid collects at 
first in the tissue-spaces as free tissue-fluid, but may also soak into the 
tissue-elements themselves and cause a swelling of the cells and fibres, and, 
under certain conditions, the formation of vacuoles (Fig. 27), due to the 
collection of drops of fluid in the cells or their derivatives. 

This may be most frequently demonstrated in the epithelium of the 
body-surfaces and of glands, but becomes at times distinctly evident 
in other tissue-elements—for example, in connective-tissue cells and 
muscle-fibres (Fig. 27), whose fibrille become pushed apart by drops of 
fluid. Moreover, it often happens in edematous tissues that cells be- 
come loosened from their basement-membrane, particularly in the lungs 
and serous membranes, where the epithelial cells in large number may 
be mixed with the fluid. 

Tissues which are the seat of cedema appear swollen, though the de- 
gree of swelling depends essentially upon the structure of the affected 
tissue. The skin and the subcutaneous tissue are able to take up into 
their lymph-spaces large quantities of fluid, so that an extremity may 
become enormously swollen through edema. In this condition it is pale, 
possesses a doughy consistence, and 
pits on pressure. On incision an 
abundance of clear fluid escapes, 
revealing the tissues thoroughly 
saturated with fluid. 

The lung behaves in a similar 
way. Owing to its limited room S 
it cannot become greatly distended, mus9, 87.-Longitudinal section of oedematous 
but it contains great numbers of Chronic rr re saletion 
cavities filled with air, which, in nl) Scag. u“ ("emmings scion 
the advent of edema, become filled 
with fluid, which on pressure escapes from the cut surface, generally 
mingled with air-bubbles. 

(Edematous swellings of the kidney, which may become very marked, 
are caused especially by the retention in the dilated urinary tubules of 
the water of the urine secreted by the glomeruli. In the connective tissue 
between the tubules large amounts of fluid collect but rarely. 

The amount of blood contained in oedematous tissues is variable, and 
their color varies accordingly. 

Body-cavities which are the seat of a dropsical effusion contain at one 
time a large, at another time only a small amount of a clear, usually 
light-yellow, rarely quite colorless, alkaline fluid, which at times con- 
tains a few fibrin flakes (see the chapter on Inflammation). Compressi- 
ble organs are compressed by the effusion, the body-cavities are dilated. 

A collection of fluid in the abdominal cavity is known as ascites. 

The albumin-content of pure transudates is not the same in all the 
body-cavities and (issues, but differs in a pronounced degree. Accord- 
ing to Reuss, the albumin-content of transudations of the pleura is 22.5 
pro mille ; that of the pericardium, 18.3; of the peritoneum, 11.1; of the 
subcutaneous connective-tissue, 5.8; of the cavities of the brain and 
spinal cord, 1.4. These facts may be taken as a proof of the different 
constitution of the vessel-walls in the various tissues of the body. 





The water of the organs and tissues, according to Heidenhain (* Versuche und Fra- 
gen zur Lehre von der Lymphbildung,” Arch. f. d. ges. Phys. 49 Bd., 1891, and Verh. 
10 


t ANT yinnan 





152 DISTURBANCES OF THE CIRCULATION. 


des X. internat. med. Cong.., ii., Berlin, 1891) consists of three parts—the water of the 
blood present, the lymph of the organ under consideration, and the water contained in the 
cells and fibres—the tissue-water. Under certain conditions the last-mentioned may 
undergo considerable variation, and can increase at the expense of the free water of the 
blood or lymph, or diminish in their favor. 

If the proportion of crystalloid substances (urea, sugar, salts) in the blood be in- 
creased, both the blood and lymph become at the same time richer in water; and this 
is possible only in that the substances injected into the blood pass into the lymphatics, 
and, by their affinity for the tissue-water, excite a passage of water from the tissue- 
elements. The rapid passage of the crystalloid substances from the blood into the 
lymph is accomplished with the aid of a force inherent in the capillary cells, and is not 
a simple diffusion-phenomenon. This is evident by the fact that the content of the 
lymph in sugar or salts is often greater than that of the blood. 


§ 42. According to their etiology we may distinguish four varieties 
of edema: cedema from stagnation of the blood; eedema caused by a hin- 
drance to the outflow of the lymph ; edema caused by disturbance of the capil- 
lary secretion due to changes in the capillary walls; and edema ex vacuo. 
The third one of these varieties is designated by the practising physician 
as inflammatory, hydremic or cachectic, or neuropathic @dema, accord- 
ing to the clinical features of the case. 

(Edema due to stagnation of the blood arises when, as a result of 
the marked hindrance to the outflow of blood from the capillaries, the 
pressure in the capillaries rises and the fluid portion of the blood seeks a 
lateral outlet, so that an increased amount of fluid escapes from the ves- 
sels. The amount of the escaped fluid is the larger the greater the de- 
gree of discrepancy between inflow and outflow; it is therefore increased 
through a coincident increase of the blood inflow. 

The escaping fluid is always poor in albumin, but with increased 
pressure in the veins the albumin-content is increased (Senator); the 
fluid may contain also a greater or smaller number of red blood-cells, the 
number being increased in proportion to the degree of stagnation. 

The immediate result of an increased transudation from the blood- 

vessels is an increase in the lymph-flow, and this may be sufficient. to 
carry off all the fluid. If it does not so suffice, the fluid collects in the 
tissue-spaces and there results the condition of stagnation-cedema or 
dropsy. According to Landerer, this occurrence is favored especially by 
the fact that the elasticity of the tissues becomes diminished as the result 
of the long-continued increase of the pressure to which they are sub- 
jected. 
’ Obstruction to the outflow of lymph, as experiments in this direc- 
tion have shown, is not ordinarily followed by cedema. The lymph- 
vessels in the different. regions of the body possess such extensive anas- 
tomoses that an obstruction to the outflow of lymph does not readily occur. 
Even when all of the lymph-channels of an extremity are obstructed, if 
the amount of lymph formed is normal there results no edema, inasmuch 
as the blood-vessels are able to take up the lymph again. Only the 
occlusion of the thoracic duct is likely to lead to a stagnation of the lymph 
and the production of cedema, particularly of ascites, but it must be ob- 
served that even in this case collateral channels may be opened up and 
suffice to carry off the lymph. 

Although lymphatic obstruction is not ordinarily sufficient in itself to 
produce cedema, yet: it does increase an cedema caused by an increased 
transudation from the blood-vessels. 

Pathological changes in the walls of the capillaries and veins of 
such a nature as to cause an increase in the vascular secretion, and 
thereby give rise to an cedema, may occur as the result of a long-contin- 


CEDEMA. 153 


ued passive congestion and the consequent imperfect renewal of the blood. 
Such changes occur, however, much more frequently as the result of 
prolonged ischemia, lack of oxygen, action of high or low temperatures, 
traumatic injury, infection, and intoxication. It is also probable that either 
trritation or paralysis of the vasomotor nerves may lead to an increase of the 
vascular secretion. Just what changes the vessels suffer under these 
conditions we are not able to state precisely, but it may be assumed that 
some alteration of the endothelial cells and of the cement-substance plays 
the chief réle. The cedemas produced by the influences above-mentioned 
may be classed according to their cause as toxic, infectious, thermal, 
traumatic, ischemic, neuropathic, etc.; and such a classification has 
much to commend it. Hitherto the forms of cedema here under consid- 
eration have been classed ordinarily into two groups—namely, inflam- 
matory and cachectic cedema. 

Inflammatory cedema is without doubt to be referred to an altera- 
tion of the vessel-wall, and occurs both as an independent affection, in 
the form of circumscribed or more diffuse swellings and hydropic effu- 
sions, and also as a coincident phenomenon in the neighborhood of severe 
inflammatory processes. In the latter case it is frequently designated 
collateral edema. Inflammatory edema is distinguished from stagnation- 
cedema by the fact that the transuded fluid is markedly richer in albumin 
and in the number of white blood-corpuscles present, and, further, in the fact 
that larger masses of coagula occur in it (see chapter on Inflammation). 
Its cause is to be sought sometimes in infectious and toxic, sometimes in 
thermal and traumatic influences, at other times in a temporary isch®gmia. 

As to hydremic or cachectic cedema, it was formerly believed that 
hydr#mia—that is, the diminution of the solid elements of the blood— 
as well as hydremic plethora—that is, a retention of water in the blood 
—could directly cause an increased transudation from the blood-vessels. 
It was supposed that the vessel-walls behaved as dead animal mem- 
branes, and allowed a fluid poor in albumin to filter through more easily 
than one richer in albumin. The vessel-wall is not, however, a lifeless 
animal membrane, but must be regarded as a living organ. An hy- 
drzmia experimentally produced does not, according to Cohnheim, give 
rise to an edema. Even when an hydremic plethora is produced by the 
over-filling of the blood-vessels with a watered blood, and there results 
an increased transudation from the vessels, eventually leading to cedema, 
the cedema so produced occurs only when the proportion of water in the 
blood becomes very high, and does not develop in the same regions where 
the so-called hydremic cedema in man appears. We must therefore as- 
sume that the cedema of cachectic individuals, as well as that occurring 
in individuals suffering from nephritis with impairment of renal func- 
tion, depends essentially upon an alteration of the vessel-wall, which is 
caused either by the hydremic character of the blood or by a poison cir- 
culating in the blood. Probably other lesions of the tissue through 
which the elasticity of the tissue is diminished are also concerned (Lan- 
derer). Hydremia therefore favors the occurrence of edema, but is not the 
sole cause thereof, and, in particular, does not determine its localization. 

Hydremic @dema is distinguished from inflammatory by the fact 
that the fluid is less rich in albumin and contains but few corpuscular ele- 
ments. . 

(Edema ex vacuo occurs chiefly in the cranial cavity and in the spinal 
cord, and arises in all cases in which a portion of the brain or spinal cord 
is lost and not replaced by some other tissue. In atrophy of the brain 


154 DISTURBANCES OF THE CIRCULATION. 


and spinal cord the subaraclınoidal spaces in particular become enlarged, 
occasionally the ventricles also. Local defects become filled either by a 
dilatation of the nearest subarachnoidal spaces or of the adjacent por- 
tions of the ventricles, or through a collection of fluid at the site of the 
defect itself. 


According to Cohnheim and Lichtheim, injections of aqueous solutions of salt into 
the vascular system of dogs (Vireh. Arch., 69 Bd.) show that hydreemia does not pro- 
duce adema. If the mass of the fluids of the blood be increased. there results an in- 
crease of almost all the secretions (saliva, intestinal juices, bile, urine, etc.), and also of 
the flow of the lymph; the latter, however, not universally, in particular not in the 
extremities. In a high degree of hydremic plethora the abdominal organs become 
dropsical, but never the extremities. Control-experiments recently carried out by 
Francotte contirm the observation that hydnemic plethora artificially produced in ani- 
mals causes in the first place a dropsy of the abdominal organs; but this observer was 
able to produce also an wdema of the skin and subcutaneous tissues. 

The view that the so-called hydramic awdema is merely the result of an increase in 
the absolute amount of water in the blood, is championed especially by ton Reckling- 
hausen and by Psenti. The distribution of the dropsy is, according to ron Reckling- 
hausen, essentially dependent upon bodily position, external pressure, impeded circula- 
tion, difference in the innervation of different vascular areas, and the consequent 
difference in the fulness of their vessels. 

I can subscribe to these opinions only in so far as they apply to the influence of 
the above-mentioned modifying factors upon the distribution of the wdema, but not 
as regards the main point. or the other side speak not only the experiments 
of Cohnheim and Lichtheim above mentioned, but also the fact that in nephritic and 
cachectic individuals wdema not infrequently appears at a time when no hydremic 
plethora is present; and, further, in cases of hydrwmic plethora no edema may occur. 
I therefore look upon the increase in the amount of water as only one factor which is 
favorable to the occurrence of @dema. 

According to the investigations of Pickhurdt, pathological transudates constantly 
contain uric acid: the fluid of ascites about 0.0086 per cent; the fluid of @dema, 0.0075 
per cent; and pleuritic exudates about 0.0015 per cent. Sugar is also constantly pres- 
ent, usually as dextrose. 

Effusions into the large serous cacities of the body occasionally present a milky appear- 
ance, or a certain degree of opalescence. This phenomenon is most often due to the 
presence of chyle (hydrops chylosus), or of fat (hydrops adiposus or chyliformis), or of 
both. Moreover, the presence of different albuminoid bodies, mucoid substances 
(Hammarsten), casein-like bodies (Zion), lecithin (Mitchell, Mattiroli, Gross), may pro- 
duce cloudiness of the transudate. In so far as chyle is not the cause, the substances 
producing the cloudiness arise for the greater part from disintegrating cells. 

According to Jleidenhain, the specific function of the capillary walls plays a con- 
trolling part in the formation of the lymph. Consequently, the lymph-production can 
be influenced by various substances present in the blood. The crystalloid substances 
are quickly climinated from the capillaries, and cause a discharge of tissue-fluid into 
the lymph, as has already been mentioned in 841. Jlcidenhain has, however, found 
substances which, when injected, cause an increase in the transudation of water from 
the blood into the lymph. This may be accomplished, for example, with decoctions of 
the muscles of crabs and of fresh-water mussels, or of the heads and bodies of leeches, 
or through injections of peptone and egg-albumen. By these means the amount of 
lymph flowing from the thoracic duct may be increased five-, six-, and fifteenfold. At 
the same time the amount of organic constituents in the lymph is increased. The 
active substances must therefore stimulate the specific function of the cells of the 
vessel-walls which secrete the lymph. According to these observations, it is probable 
that many of the affections of the skin described as neuropathic, and which are charac- 
terized by hyperemia associated with edematous swelling—as, for example, urticaria, 
erythema nodosum, herpes zoster—are to be regarded as symptoms of intoxications 
coupled with nervous affections and with disturbance of the secretory activity of the 
capillaries. It is also possible that the secretion of the capillaries may be directly af- 
fected by nervous influences. 

Asher and Barbera hold the view that the regulation of the transudation-process 
takes place not through the capillary walls, but through the vital activity of the tissue- 
cells. 

Magnus, on the other hand, on the ground of experimental investigation (infusions 
of physiological salt-solutions in normal animals, irrigation of dead animals after poi- 
soning with arsenic, chloroform, chloral hydrate, and ether, and after the removal of 


CEDEMA. 155 


the kidneysand ligation of the ureters), arrives at the following conclusions: The capil- 
lary walls during life offer a resistauce to the passage of fluids; after death this resist- 
ance disappears. An injury to the capillary wall, and a diminution of its resistance, 
favor the occurrence of edema. There are poisons which are able to injure the capil- 
lary-wall in such a manner that it becomes abnormally permeable. 


Literature. 
(Gdema; Effusions into the Body- Cavities. ) 


Asher u. Barbera: Eigensch. u. Entstehung d. Lymphe. Zeit. f. Biol., 1897. 
Bargebuhr: Chyldse Ergüsse in der Pleura. Deut. Arch. f. klin. Med., 54 Bd., 1895 


Bernheim: Beitr. z. Chemie der Exsudate u. Transsudate. Virch. Arch., 131 Bd., 
1893. 

Boddaert: Developp. de l’ad&me. Ann. de la Soc. de med. de Gand, 1893; (Edeme 
lymphatique. Acad. Roy. de med. de Belgique. 1895. 

Citron: Eiweissgehalt u. spec. Gewicht pathol. Flüssigkeiten. Deut. Arch. f. kl. 
Med., 46 Bd., 1890. ‘ 

Cohnheim: Allgem. Pathologie, 1882; Untersuch. üb. d. embolischen Processe, Ber- 
lin, 1872. 

Cohnheim u. Lichtheim: Ueber Hydrämie u. hydrämisches (Edem. Virch. Arch., 
69 Bd., 1877. 

Cohnstein: Transsudation u. Lymphbildung. Virch. Arch.,: 185 Bd.; Pflüger’s 
Arch., 59 Bd., 1894; C(Edem u. Hydrops. Ergebn. d. allg. Path., iii., Wiesbaden, 
1897 (Lit.). 

Emminghaus: Abhängigkeit d. Lymphabsonderungen v. Blutstrom. Arb. d. phys. 
Anst. zu Leipzig. viii., 1874. 

Francotte: De l’wd&me hydrémique. Bull. de l’Acad. Roy. de med. Belgique, ii., 
Bruxelles, 1888. 

Gross: Pseudochylöse Ergüsse. Arch. f. exp. Path., 44 Bd., 1900. 

Grossmann: Muscarinlungenödem. Zeitschr. f. klin. Med., xii., 1887. 

Halliburton: Chemische Physiologie u. Pathologie, Heidelberg, 1893. 

Hamburger: Hydirops von mikrobiellem Ursprung. Beitr. v. Ziegler, xiv., 1893. 

Hammarsten: Mucoidsubstanzen in Ascitestlüssigkeit. Zeit. f. phys. Chem., xv., 
1891. 

Heidenhain: Zur Lehre von der Lymphbildung. Verhandl. d. X. internat. med. 
Congr., ii., Berlin, 1891; Arch. f. d. ges. Phys., 49 Bd., 1891. 

Klebs, A.: (Edem d. Hornhautepithels. Beitr. v. Ziegler, xvii., 1895. 

Landerer: Die Gewebsspannung, Leipzig, 1884. 

Lassar: Ueber CEdem u. Lymphstrom bei der Entzündung. Virch. Arch., 69 Bd., 
1877. 

Lazarus: The Pathol. of CEdema. Brit. Med. Journ., i., 1895. 

Leydhecker: Carcinom d. Duct. thoracicus mit chylésem Ascites. Virch. Arch., 184 
Bd., 1893. 

Lion: Ascite laiteuse non chyleuse. Arch. d. med. exp.. xv., 1893. 

Löwit: Entstehung d. Lungenödems. Beitr. v. Ziegler, xiv., 1893; Lungenödem, 
Cent. f. a. Path., 1895. 

Lukjanow: Allgem. Pathologie des Gefässystenis, Leipzig, 1894. 

Magnus: Entstehung d. Hautödeme bei hydr. Plethora. Arch. f. exp. Patlı., 42 Bd., 
1899. 

Munk: Transsudate. Eulenburg’s Realencyklop., xxiv., 1900. 

Pickardt: Zur Chemie patholog. Ergüsse. Berl. klin. Woch., 1897. 

Pisenti: Beitrag zur Lehre von den Transsudaten. Cbl. f. allg. Path., ii., 1891. 

Quincke: Hydrops chylosus u. adiposus. Deut. Arch. f. klin. Med., 6 Bd.; Ascites. 
Ib., 30 Bd. 

v. Recklinghausen: Handb. d. allg. Path. d. Kreislaufs u. der Ernährung, Stutt- 
gart, 1883. 

Reuss: Verhältn. d. spec. Gew. z. Eiweissgehalt in serösen Flüssigkeiten. Deut. 
Arch. f. klin. Med., 28 Bd.; Beurtheiluny von Exsudaten und Transsudaten. 
Ib., 24 Bd. 

Senator: Ueber Transsudation und Ober den Einfluss des Blutdrucks, auf die Beschaf- 
fenheit der Transsudate. Virch. Arch.. 111 Bd., 1888: Ascites cliylosus u. Chylo- 
thorax bei Carcinom d. Ductus thor. Cbl. f. inn. Med., 1896. 

Starling: On Absorption from and Secretion into the Serous Cavities. Journ. of 





H/EMORRHAGE. 157 


A collection of blood in the uterine cavity is designated as hemato- 
metra, in the pleural cavity as hemothoraz, in the tunics of the testicle as 
hematocele, in the pericardium as hemopericardium. 

Hemorrhages of the skin not caused by trauma are usually termed 
purpura (Fig. 28). Collections of blood and fluid beneath the epidermis 
in the place of the loosened deeper epithelial layers give rise to hemor- 
rhagic blebs. 

Recent extravasations show the characteristic color of either arterial 
or venous blood. Later the extravasate shows various alterations which 
are characterized particularly by color-changes. Suggillations of the 
skin become first brown, then blue, and green, and finally yellow. In 
the course of time the extravasate is absorbed (see Chapter V.), and dur- 
ing this absorption tissue-proliferation often occurs. Large collections 
of blood may become partly organized into connective tissue or may 
become encapsulated (see Chapter VII). 

A hemorrhage may occur, in the first place, from rupture of the 
heart or the vessel-wall—that is, per rhexin or per diabrosin. This is 
the only form of cardiac and arterial heiınorrhage. From the capillaries 
and veins hemorrhage may occur also per diapedesin—that is, by a proc- 
ess In which the red cells escape through the vessel-wall without the oc- 
currence of a tear in the same. Very often such hemorrhages are small 
and of slight extent; in other cases the process continues for a longer 
time, and the infiltration of the tissues with red cells reaches a significant 
degree. Hzmorrhages by diapedesis are therefore not always small, 
hemorrhages by rhexis not always large. The rupture of a capillary 
or small vein does not give rise to a large hemorrhage; on the other 
hand, a hemorrhage through diapedesis can reach an important size. In 
a given case it 1s not always easy, and often impossible, to decide whether 
the hemorrhage has arisen through rhexis or diapedesis. 


The phenomenon of diapedesis may be observed under the microscope in the frog’s 
mesentery or in the web of its foot. If before the examination the efferent veins are 
ligated, the capillaries and veins are seen to be engorged with blood. After a certain 
time the red cells pass from the capillaries and veins (sec Cohnhetm, “ Allgem. Pathol. ,” 
i., and Virch. Arch., 41 Bd.). Hering (Sitzungber. d. Wiener Akademie, 1868, Bd. 57) 
regards the phenomenon as a filtration-process. As a result of the obstruction to the 
outtlow the blood seeks to escape laterally, and is forced through the vessel-wall. 

Exhaustive investigations in regard to diapedesis of the red corpuscles, as well as 
in regard to the escape of other elements of the body which have been introduced into 
the blood-vessels, we owe to Arnold (Virch. Arch., 58, 62, 64 Bd.). Arnold believes 
that we must assume the presence of openings in the endothelial tube at the poiut of 
exit of the corpuscular elements; these openings he designated as stigmata and stomata. 
Later he recognized the supposed openings to be local accumulations of the cement- 
substance between the endothelial cells. Under pathological conditions the cement- 
substance becomes softened and permits the passage of the red cells. 


§ 44. The causes of interruption of continuity of the heart-wall 
and vessel-walis are in part traumatic injuries, in part increase of intra- 
vascular pressure, and in part diseased condition of the heart and vessel-wall. 
Increase of the blood-pressure in the capillaries and smallest veins can 
lead to rupture without the aid of vascular changes, particularly in the 
case of marked passive congestion. The heart, normal arteries, and nor- 
mal veins of large size cannot be ruptured through increase of pressure 
alone, but abnormally thin-walled or diseased areas in either the heart, 
arteries, or veins may be so ruptured. Newly formed vessels are easily 
torn. 

Diapedesis may be caused by an increase of pressure in the capillaries 


ra 


158 DISTURBANCES OF THE CIRCULATION, 


and veins, as well as by an increased permeability of the vessel-wall. If the 
outflow of the venous blood in a given vascular area be totally ob- 
structed, diapedesis of red cells from the capillaries and veins takes place; 
and this is to be regarded as a result of the increased pressure in the ves- 
sels. Diapedesis as a result of changes in the vessel-wall occurs partieu- 
larly after mechanical, chemical, and thermal lesions of the vessel; and 
it may be assumed that certain poisons produce especially marked changes 
in the vessel-walls. Further, an abnormal permeability of the vessel- 
walls is also observed when for a long period the vessels have not been 
traversed by the blood-stream, and have suffered in their nutrition in 
consequence. 

When an ‚individual shows a special tendency to hemorrhage, thie 
condition is designated as hemorrhagic diathesis. Two forms may be 
distinguished—a congenital and an acquired. 

The congenital hemorrhagic diathesis or congenital hemophilia, 
which, as already mentioned in $S 16 and 17, belongs to the diseases 
which may be inherited, depends most probably upon an abnormal con- 
stitution of the vessel-walls. The composition of the blood may also be 
pathological, so that a hemorrhage once started is not arrested, as usual, 
by the coagulation of the blood. 

An acquired hemorrhagic diathesis occurs, in the first place, in 
those diseases which are known as scurvy, morbus maculosus Werlhofii, 
purpura simplex, purpura (peliosis) rheumatica, purpura hemorrhagica, 
hemophilia, and meleena neonatorum, and Moller’s or Barlow’s disease ; 
and, further, in many infections and intoxications—namely, septiczemia, 
endocarditis, anthrax, typhus fever, cholera, smallpox, plague, acute 
yellow atrophy of the liver, yellow fever, nephritis, phosphorus poison- 
ing, after snake-bites, etc. ; and, finally, also in pernicious anemia, leu- 
kemia, and pseudoleukemia. In the first group of diseases named—all 
of which are characterized by hemorrhages in the skin, mucous mem- 
branes, and parenchyma of other organs and tissues (in Barlow’s disease, 
which often occurs in children of from one and one-half to two years old 
in association with rickets, the haemorrhages are subperiosteal)—the cause 
has been generally supposed to lie in disturbances of nutrition and of the 
circulation ; but recent observations make it very probable that these 
affections, at least in a great part, belong to the infectious diseases. W. 
Koch is of the opinion that seurvy is an infectious disease, and that the 
different forms of purpura, erythema nodosum, and the hemorrhages oc- 
eurring in the new-born represent. varieties of this infection. In the last 
few vears bacteria have been repeatedly found in these conditions— 
namely, purpura hemorrhagiea and the hemophilia of the new-born. In 
this connection should be mentioned especially the investigations of Kolb, 
Babes, Gartner, Tizzoni, and Giovannini, who have found in these dis- 
eases certain bacilli which were pathogenic for animals, and which, when 
inoculated into the latter, produced a disease characterized by hemor- 
rhages. These diseases are also associated with other infections charac- 
terized by hemorrhages, and it may be assumed that the hemorrhages are 
in part caused by local changes of the vessel-wall which are due to local de- 
velopment of bacteria, and in part to the injurious influence of thc toxic sub- 
stances nroduce di by the bacteria themselves. 

The hiemorrh: wes oceurring in anemic conditions are to be regarded 
as the result of anemie degeneration of the vessel-wall, though partly also 
as a result of efreulatory disturbances, 

A number of apparently spontaneous hemorrhages are connected with 


HZEMORRHAGE. 159 


irritation or paralysis of the vasomotor nerves, arising either from the cen- 
tral nervous system or by reflex action, or through lesions of the con- 
ducting nerve-fibres. In this category belong the hemorrhage of men- 
struation, many forms of hemorrhage from the nose, intestine, and 
urinary bladder, also hemorrhages from the conjunctiva, skin (stigmati- 
zation), from the normal kidney, mammary glands, from hemorrhoids, 
wounds, etc. Further, certain hemorrhages from the lungs following 
severe cerebral lesions are also to be considered in this connection, 
though in a given case it is not always possible to judge with certainty, 
since disturbances of respiration, as well as the aspiration of irritating 
substances into the lungs, may likewise lead to hyperemia and to hemor- 
rhages in the lung. Finally, in cerebral disease, particularly in disease 
of the crura cerebri, there occur hemorrhages from the stomach and in- 
testines, which are dependent upon the cerebral lesion. According to 
von Preuschen, the condition known as melzena neonatorum, which is 
characterized by the occurrence of gastric and intestinal hemorrhages 
during the first days of extra-uterine life, belongs also in this category, 
inasmuch as during labor hemorrhages and effusions into the brain and 
its membranes not infrequently occur, as a result of which the intestinal 
hemorrhages follow. By others (Gartner) melzna neonatorum is re- 
garded as an infectious disease. 

Hemorrhages per rhexin cease when the extravascular pressure comes 
to equal the pressure within the bleeding vessel, or when the narrowing 
of the vessel and the processes of coagulation and thrombosis close the 
rent. Hemorrhage by diapedesis ceases through a cessation of blood-sup- 
ply to the bleeding vessel, or when the abnormal intravascular pressure 
is lowered and the vessel-wall is restored to its normal state. 


Literature. 
(Congenital Hemophilia. ) 


Coates: North Amer. Med. and Surg. Jour., 1828. 

Dunn: Amer. Jour. of Med. Sc., 1893. 

Fischer: Zur Kenntniss der Hämophilie, München, 1889. 

Grandidier: Die Hämophilie, 1877. 

Hoffmann: Lehrb. d. Constitutionskrankheiten, Stuttgart, 1893. 

Hössli: Geschichte u. Stammbaum der Bluter von Tenna. Inaug.-Diss., Basel, 1885. 
Koch: Die Bluterkrankheit, Stuttgart, 1889. 

Legg: Treatise on Hemophilia, London, 1872. 

Lossen: Bluterfamilie. eut. Zeitschr. f. Chir., vii. 

Otto: Medical Repository, N. Y., 1808. 


(Hemorrhage due to Various Causes.) 


Afanasiew FR Mikroorganism. a. d. Gruppe d. Septikemia hemorrhag. Cent. f. Bakt., 
xiii., 1888. 

Babes: Bacillen d. hamorrh. Infection. Cbl. f. Bakt., ix., 1891: Bacille produis. les 
hemorrhagies dans le scorbut. Arch. de med. exp., v., 1893; Infect. hémorrhag. 
Ann. de l’Inst. de Path. de Bucarest, iv., 1894. 

Claisse: Purpura A pneumocoque. Arch. de méd. exp., iii., 1891. 

Dennig: Ueber septische Erkrankungen, Leipzig. 1891. 

v. Dungern: Hämorrhag. Sepsis bei Neugeborenen. Chl. f. Bakt., xiv., 1893. 

Fujinami: Entsteh. d. hämorrhag. Lungeninfarkts. “Virch. Arch., 152 Bd., 1898. 

Geertner: Bakterienbefund bei Melsena (Bacillen). Arch. f. Gyn.. 45 Bd., 1894. 

Hamill: Hemorrhage into the Suprarenal Capsule in Still-born Children and Infants. 
Arch. of Ped., 1901. 

Härle: Die Purpura u. ihr Verhältniss zum Skorbut. Inaug.-Diss., Heidelberg, 1897. 


160 DISTURBANCES OF THE CIRCULATION. 


Klein: Neuere Arbeiten über Barlow’sche Krankheit. Cbl. f. allg. Path., 1897 (Lit.). 

Koch: Die Bluterkrankheit u. ihre Varianten, Stuttgart, 1889. 

Kolb: Aetivlogie d. idiopath. Blutfleckenkrankheit. Arb. a.d.K. G.-A., vii., Berlin, 
1891. 

Kratter: Diagnose d. Erstickung. Vierteljahrsschr. f. ger. Med., 1895 (Blutungen 
finden sich namentlich im retromediastinalen Gewebe) (Lit.). 

Neumann: Melaena neonatorum. Arch. f. Kinderheilk., xii., 1890. 

Beimar: Retinitis hemorrhagica in Folge Endarteritis proliferans. Ann. f. Augen- 
heilk., 38 Bd., 1899. 

Runge: Die Krankheit der ersten Lebenstage, Stuttgart, 1893. 

Schoedel u. Nauwerck: Unters. üb. d. Möller-Barlow’sche Krankheit, Jena, 1900 
(Lit). 

Tavel u. De Quervain: Hämorrhag. Bakteriämie d. Neugeborenen. Cent. f. Bakt., 
xii., 1892. 

Tizzoni u. Giovannini: Entstehung d. hämorrhag. Infection. Beitr. v. Ziegler, vi. 
1889. 

Voges: Hamorrhag. Septikämie. Zeitschr. f. Hyg., 23 Bd., 1896. 


(Neuropathic Hamorrhages. ) 


Charcot: Lecons sur les maladies du systéme nerveux. (Euvr. compl., i. 

Ebstein: Blutextravasate in der Magenschleimhaut. Arch. f. exp. Path., ii., 1874. 
Flatten: Lungenaffectionen nach Kopfverletzungen. Eulenburg’s Vierteljahrsschr., 
53 Bd., 1890. H 
Hitler: In den Lungen nach Verletzungen d. Gehirns auftret. Blutungen. Oesterr. 

med. Jahrb, 1875. 
Jehn: Blutaustritte in d. Lungengewebe bei Hirnleiden. Cbl. f. d. med. Wiss., 1874. 
Klemperer: Nierenblutungen b. gesunden Nieren. Deut. med. Woch., 1877. 
Nau: Contrib. a l’etude de la congestion et de l’apoplexie unilatérale dans les cas de 
ramollissement du cerveau, Paris, 1887. 
Nothnagel: Hirnverletzungen u. Lungenhämorrhagie. Cb. f. d. med. Wiss., 1874. 
Ollivier: De l’apoplexie pulmonaire unilatérale dans ses rapports avec !’hemorrhagie 
eerebrale. Arch. gen. de med., 1873. 
Pisenti: Emorragie da causa nervosa. Lav. dell’ Instit. Anat. Patol. di Perugia, 1890. 
v. Preuschen: Verletzungen des Kindes als Ursache der Melaena neonatorum, Wien, 
1894. 
v. Recklinghausen: Allg. Pathol. des Kreislaufs u. der Ernährung, Stuttgart, 1883. 
Vulpian: Lecons sur V’appareil vasomoteur, 1875. 


x 45. The sudden closure of an artery by thrombosis, or embolism, 
or by ligation, or by any other means, leads, as has already been stated 
(8 37), to a stoppage of the circulation beyond the point of obstruction, 
after the vessel has more or less completely emptied itself by the con- 
traction of its walls. At the same time there is an increase of pressure 
in the vessel from the point of obstruction back to the point of divergence 
of the nearest arterial branch. If the branches of the artery beyond the 
point of obstruction have free arterial communication with some other 
unobstructed artery, the latter by becoming dilated may be able to sup- 
ply a sufficient amount of blood to the affected area and the circulation 
is thus restored. 

If the area of the obstructed artery has no collateral connections 
through which it may draw its blood-supply, the portion of tissue de- 
prived of blood remains amemic and dies, thus giving rise to an anzmic 
infarct. Parenehymatous organs—as, for example, the spleen and the 
kidneys—present in such infarcted areas a cloudy, opaque, yellowish- 
white, often clay-colored appearance. The microscopical examination 
shows that the tissues are dead, the nuclei no longer staining (Fig. 29, ce, 
d, e, f, 9). 

When the area of distribution of the obstructed vessel possesses no 
collateral anastomoses, as in the case of a terminal artery, but if, on the 
other hand, there is a scanty influx of blood from neighboring capillaries 








HASMORRHAGIC INFARCTION: LYMPHORRHAGIA. 163 


Von Recklinghausen considers the principal factor in the formation of a hwmor- 
rhagic infarct to be a hyaline thrombosis of the capillaries of the obstructed area. If 
blood subsequently enters from neighboring vessels into the still pervious vessels of 
the area, it encounters resistance, becomes stagnant, and then escapes from the vessels. 
According to Klebs (Schweizer Arch. f. Thierheilk., 28 Bd., 1886). emboli introduced into 
the circulation of animals lead to the formation of infarcts, only when blood rich in 
ferment is injected after the embolus, or whren substances exciting coagulation are 
mixed with the obstructing plug. . 

Embolic hemorrhagic infarcts of the lung occur in man, especially in passive 
congestion of the lungs; the introduction of emboli into the pulmonary arteries of 
animals with normal pulmonary circulation is not followed by infarction. The essen- 
tial cause of the escape of blood in the case of hemorrhagic infarction lies in the stag- 
nation of the blood in the affected area, and in the degeneration or death of the tissue and 
the blood-vessel walis. The latter change may be recognized with certainty through 
the disappearance of the nuclei (Fig. 30, «). Secondary thrombosis in the vessels of the 
obstructed area (Fig. 30, c) is of frequent occurrence, and increases the stagnation and 
hemorrhage, but thrombi are not always present at the time of the hemorrhage, and, 
therefore, cannot be regarded as the essential factor in the production of the latter. 

According to investigations by Orth, haemorrhagic infarcts may be produced in dogs 
through the introduction of chemically irritating emboli into the pulmonary arteries. 

In the lungs, in conditions of passive congestion and inflammation, there not infre- 
quently occur extensive hemorrhages, which, in case they are restricted to a circum- 
scribed area, closely resemble infarcts. They are usually less sharply outlined and less 
firm, so that in the majority of cases they are casily distinguished from the embolic 
infarcts. 


Literature. 


(Hemorrhagic Infarction.) 


Cohn: Klinik der embolischen Gefässkrankheiten, Berlin, 1860. 

Cohnheim: Untersuch. üb. d. embol. Processe, Berlin, 1872; Allgem. Pathol., Berlin, 
1882. 

Faber: Die Embolie der Art. mesenterica sup. Deut. Arch. f. klin. Med., 1875. 

Fischer: Ueber die Embolie der Art. centralis retin®, Leipzig, 1890. 

Grawitz: Die hämorrhag. Infarkte d. Lungen. Festschr. d. Assist. f. Virchow, Ber- 
lin, 1891. 

Kaufmann: Verschluss d. Art. mesenterica sup. durch Embolie. Virch. Arch., 116 
Bd., 1889. 

Krebs: Hyaline Thromben in hämorrhagischen Infarkten. Beitr. v. Ziegler, ii., 1888, 

472 


p. 472. 

Litten: Ueber die Folgen des Verschlusses d. A. mesent. superior. Virch. Arch., 63 
Bd., 1875; Untersuchungen über den hämorrhagischen Infarkt, Berlin, 1879. 

Lukjanow: Allgem. Pathologie des Gefässystems, Leipzig, 1895. 

Mögling: Zur Kenntniss des hämorrhag. Infarktes. Beitr. v. Ziegler, i., Jena, 1886. 

Obermüller: Hyaline Thrombusbildung u. hämorrhag. Lungeninfarkte. Inaug.-Diss., 
Strassburg, 1886. 

Orth: Erzeugung des hämorrhag. Infarktes. Chl. f. allg. Path., 1897, p. 859. 

v. Becklinghausen: Handb. d. allg. Patlı. d. Kreislaufs u. d. Ernährung, Stuttgart, 
1883. 

Bibbert: Niereninfarkte. Virch. Arch., 155 Bd., 1899. 

Schäffer: Ueber das sog. IIyalin in Lungeninfarkten. Fortsch. d. Med., vi., 1888. 

Virchow: Handb. d. spec. Pathol, i., 1854: Ges. Abhandl., Frankfurt, 1856. 

Welch: Hemorrhagic Infarction. Trans. Assn. Amer. Phys., 1887. 

Willgerodt: Hämorrhag. Infarkte d. Lunge. Arb. a. d. path. Inst. zu Göttingen, 
Berlin, 1893. . 

Woolley: Thrombosis of the Central Vein of the Right Adrenal with Engorgement 
and Necrosis (Infarction). Jour. of Med. Research, 1902. 


VI. Lymphorrhagia. 


§ 46. Lymphorrhagia occurs when the continuity of a lymph-vessel 
is interrupted at any point and the lymph is poured out into the neigh- 
boring tissue. Since the pressure in the lymph-vessels is very low—that 
is, not greater than in the surrounding tissues—an outflow of lymph 


164 DISTURBANCES OF THE CIRCULATION. 


from a lymph-vessel can occur only when the injured vessel lies on the 
external surtace, or when a natural cavity is at hand into which the 
lymph can flow, or when, through the same cause producing the rupture, 
an open space is formed at the same time in the tissues. So, for exam- 
ple, an escape of lymph together with the blood may take place from 
wounds, but the outflow is stopped by very slight counterpressure. If, 
after the wounding of a lymphatic, the opening persists, so that there is 
a permanent outflow of lymph, escaping externally (as in ulcers) or into 
one of the body-cavities, there is formed a Iymph-fistula, through which 
considerable quantities of lymph may be lost. Most important and also 
most dangerous is the rupture of the thoracic duct, which occurs sometimes 
as the result of traumatism, and occasionally as a result of an obstruc- 
tion to the Iymph-flow at some point in the lumen of the duct. (after in- 
flammation or in the course of the growth of tumors). The lymph is 
poured out into the thoracic or abdominal cavity, giving rise to a chylous 
hydrothoraz or a chylous ascites, or in very rare cases to a chylopericardium. 


In very rare cases it happens that the urine, as it comes from the bladder, has the 
appearance of a milk-white, or a yellowish, or, through the admixture of blood, a red- 
dish emulsion; and contains besides albumin a large quantity of finely-divided fat- 
droplets. This phenomenon is known as Chyluria. It occurs as an endemic disease 
in certain tropical regions (Brazil, India, the Antilles, Zanzibar, Egypt) where it is 
caused by a parasite, the Filarta Bancrofti, which inhabits the lymph-vessels of the 
abdominal cavity and there produces its embryos (/ilarta sangutnia); these, during the 
repose of the patient in a horizontal position, swarm in great numbers in the blood, 
and are also found in the chylous urine. The connection between the chyluria and the 
invasion of the lymph-vesscels has not yet been satisfactorily demonstrated by anatomi- 
cal investigations; but it is probable that the chyle-like fluid does not come from the 
blood and through the kidneys; but, as a result of the obstruction in the lymph-circu- 
lation, chyle escapes from ruptured lymphatics of the bladder and mingles with the 
urine (Scheube, Grimm). Tn corroboration of this view is the fact that, at autopsy, the 
abdominal lymphatics exhibit marked dilatation (/facelburg), while the Kidneys are but 
little changed; and further, according to an observation made by Harelburg, the urine 
obtained from the ureter showed no admixture of chyle, though chyluria was present 
at the same time. 


Literature. 
(Chylous Effusions in the Body-cavities ; Chyluria.) 


Bargebuhr: Ascites chylosus. Deut. Arch. f. klin. Med., 51 Bd., 1893; Chylöse Er- 
güsse im Pleuraraum, ib., 54 Bd., 1895 (Lit.). 

Busey: Amer. Jour. of Med. Sciences, 1889. 

Edwards: Chylous and Adipose Ascites. Ref. Handb. of Med. Sciences, 1901. 

Goetze: Die Chylurie, Jena, 1887. 

Grimm: Ueber einen Fall von Chylurie. Virch. Arch., 111 Bd., 1888. 

Henry: Case of Indigenous Parasitic Chyluria. Med. News, 1896. 

Heydecker: Chyléser Ascites. Virch. Arch., 184 Bd., 1898. 

Letulle: Epanchements chvliformes du péritoine. Rev. de méd., 1884. 

Lothrop and Pratt: Amer. Jour. of Med. Sciences. 1900. 

Reichenbach: Chyléser Ascites. Virch. Arch., 123 Bd., 1891. 

Scheube: Filariakraukheit. Sammi. klin. Vortr. No. 232, 1883; Parasitäre Hamo- 
chylurie. Beitr. z. path. Anat. u. z. klin. Med.; Festschr. f. Wagner, Leipzig. 
1887, 

Senator: Chylurie. Eulenburg’s Realencyklop., iv. 

Zune: Urines chyleuses et hématochyleuses, Bruxelles, 1898. 

See also § 42. 


CHAPTER V. 


Retrograde Disturbances of Nutrition and Infiltra- 
tions of the Tissues. 


I. General Considerations Concerning the Retrograde Disturbances 
of Nutrition and the Tissue-Infiltrations. 


§ 47. The retrograde disturbances of nutrition are characterized in 
general by degeneration of the affected tissue, often also by diminution in 
size and disappearance of the individual tissue-elements, the functional capac- 
ity of the tissue being, at the same time, lowered. 

The tissue-infiitrations are characterized essentially by the deposit in 
the tissue of pathological substances which have either been formed within 
the body or introduced into it from without. The functional capacity of 
the part affected is likewise usually diminished. The infiltration is often 
only a result of preceding degenerative changes, or may itself constitute the 
chief feature of the degeneration. 

Retrograde disturbances of nutrition may affect the body in its fully 
developed state, or during its period of development and growth; and in 
either case may lead to an abnormal smallness of the affected organ or 
tissue. In the former case the diminution in size is due to a disappear- 
ance of the individual elements of the affected tissue, and is designated 
atrophy. In the latter case, on the other hand, it is due to a defective 
development of the affected organ, as shown by a more or less rudimen- 
tary condition of its elements. If in this way an organ or a part of an 
organ wholly fails of development, so that it is totally absent or at least 
is represented only by its rudimentary anlage, the condition is designated 
agenesia or aplasia. But if the development of the affected part is of a 
certain degree, yet not reaching the normal, the condition is known as 
hypoplasia. 

The causes of agenesia and hypoplasia are partly intrinsic, and 
partly extrinsic—that is, the stunting and imperfect development of an 
organ may depend as well upon a pathological condition of its anlage, 
as upon external injurious influences which may affect the developing 
part. The disturbance of development may further affect either the 
whole body or only a part of the same. In the first case there results a 
dwarf; in the second, a stunting of individual parts or organs. 

The causes of the tissue-degenerations and the associated atrophy 
are for the greater part to be found in extrinsic harmful influences to 
which the tissues are exposed during life; but they may also depend 
upon intrinsic conditions. This latter is particularly the case when the 
tissues in old age reach their physiological limit and gradually become 
incapable of properly nourishing and preserving themselves. In many 
tissues a similar retrograde change, due to intrinsic causes, occurs earlier 
in life, as, for example, physiologically in the ovary and thymus. 

As extrinsic harmful influences which may lead to degenerations 

165 


166 THE RETROGRADE CHANGES. 


should be considered all those agencies mentioned in Chapter I. Dis- 
turbances of circulation, lack of oxygen and food supply, and intoxica- 
tions play a very important réle. In the majority of cases degenerations 
are localized, so that we may speak of degenerations of special tissues 
or of special organs. Not infrequently the disturbances of nutrition 
are more general, so that the entire organism suffers. Thus the picture 
of a general disease may be produced by a degenerative or atrophic con- 
dition of the blood—that is, a diminution in the number of red blood- 
cells (oligocythamia), at times also a deficiency of hemoglobin (chloro- 
sis), so that a permanent condition of insufficient blood-supply or a 
general anemia is produced, the nutrition of the body being corre- 
spondingly impaired. 

As the result of a diminished ingestion of food, or of disturbed me- 
tabolism, and of an increased waste of the proteids and fats of the body, 
there may result a condition of general emaciation and weakness, often 
associated with anıemia, a wasting of the entire body, which is designated 
cachexia or marasmus. If under such circumstances it appears likely 
that certain substances are formed in the body, which, when taken up 
into the blood and tissue juices, cause a contamination or alteration of 
these, the condition may be spoken of as a dyscrasia. 


Literature. 
(Disturbances of Nutrition.) 


Charcot: Maladies des vieillards. (Euvr. compl., vii., 1890. 

Demange: Et. clin. et anatomo-pathol. sur la vieillesse, Paris, 1886. 

Le Gendre: Troubles et maladies de la nutrition. Traité de med., i., Paris, 1891. 
Halliburton: Chemische Physiologie und Pathologie, Heidelberg, 1893. 
Hoffmann: Lehrbuch der Constitutionskrankheiten, Stuttgart, 1802. 

Krehl: Pathologische Physiologie, Leipzig, 1898. 

Neumeister: Lehrbuch der physiologischen Chemie, i.. Jena, 1898. 

v. Noorden: Pathologie des Stoffwechsels, Berlin, 1898. 

v. Recklinghausen: Pathologie des Kreislaufs u. der Ernihrung, Stuttgart, 1888. 
Verworn: Allgemeine Physiologie, Jena, 1897. 


Il. Death of the Organism. 


$ 48. All life comes sooner or later to an end—to death. When this 
occurs at an advanced age, without preceding well-defined symptoms of 
disease, it may be regarded as a normal termination of life. This occur- 
rence may be attributed, at least in part, to the fact that the functions of 
certain organs necessary to the maintenance of life, become discontinued 
as the result of intrinsic causes; although in most cases it is impossible 
to exelude the influence of extrinsic influences in helping to bring about 
the cessation of function of the organs in question. 

When death occurs prematurely—that is, at an age earlier than the 
average age of death in man—and when preceded by symptoms of dis- 
ease, it must be regarded as a pathological phenomenon. Its occurrence 
under these circumstances is for the most part referable to demonstrable 
extrinsic influences, but at times may be dependent also upon intrinsic 
inherited causes. It is obviously impossible to draw any sharp line of 
separation between physiological and pathological] death. 

The causes of premature—that is, pathological—death are to be found 
in those influences, which have been discussed in Chapters I. and II. as 
the causes of disease. 


DEATH. 167 


An individual is to be regarded as dead when all of his functions 
have forever ceased. Death is inevitable at that instant in which one or 
more of the functions imperatively necessary to life has ceased, though 
it is not necessary that at that moment all the functions should have 
ceased. Indeed, it often happens, that after life is irretrievably lost, 
many organs are still capable of performing their function, and it is 
only after a certain time that all the organs die. The life of the organism 
passes gradually, by progressive cessation of the functions of its different or- 
gans, into the state of death. 

Cessation of the functions of the heart, lungs, and nervous system 
results in an immediate death of the entire organism. Cessation of the 
functions of the intestines, liver, or kidneys leads inevitably to death 
after a certain length of time, often measured by days. Destruction of 
the sexual glands does not endanger the life or health of the affected indi- 
vidual, and likewise man may also spare one or more of his organs of 
special sense. 

The occurrence of death is usually determined by the last recogniz- 
able efforts at respiration and by the stoppage of the heart. With the 
cessation of respiration it is impossible for any organ to remain alive 
after a certain short period. The stoppage of the heart likewise makes 
impossible any further nourishment of the tissues, in consequence of 
which the central nervous system very quickly becomes unable to con- 
tinue its functions. 

After death the body may present a variety of appearances. The 
aspect of the external visible portions is largely dependent upon the dis- 
tribution of the blood at the time of death. An abundant supply of 
blood in the skin gives it a blue-red color, anzmia gives it a pale color. 
Further, the preceding disease may alter the external appearance of the 
body in different ways. 

Within a certain time after death various changes occur in the tis- 
sues of the body, which in part may be regarded as the absolute signs 
of death. In the first place the temperature of the body falls, sometimes 
rapidly, at other times slowly, until it reaches the temperature of the 
surrounding air. It must be borne in mind, however, that the temper- 
ature at times does not begin to sink immediately after death, but first 
rises somewhat. The rate of cooling of the body depends partly upon 
the character of the body itself, and partly upon the nature of its sur- 
roundings. The time required may vary from one to twenty-four hours. 

The coldness of the dead body is termed algor mortis. 

At the time of death the skin for the greater part becomes pale; but 
after six to twelve hours, sometimes earlier, bluish-red spots appear on 
the skin over the dependent parts of the body. These are known as the 
death-spots or livores mortis (post-mortem hypostasis), and are due to the 
local accumulation of blood in the veins and capillaries of the more de- 
pendent portions. They are not found in those parts of the body sub- 
jected to the pressure of the weight of the body. Their number and size 
depend upon the amount of blood in the skin at the time of death. 
Parts which have been cyanotic during life may retain this appearance 
after death, especially the head, fingers, and toes. The color of post- 
mortem hypostasis is usually blue-red; the intensity of the color varies; 
in cases of poisoning with carbon monoxide it is a bright red. 

The weight of the body causes flattening of those muscular parts upon 
which it rests. 

Sooner or later there occurs a stiffening and contraction of the mus- 

11 


168 THE RETROGRADE CHANGES. 


cles, due to the coagulation of the contractile substance (Bruecke, 
Kühne). This is known as the cadaveric stiffening or rigor mortis. It 
usually comes on about four to twelve hours after death, but may occur 
almost immediately, or as Jate as twelve to twenty-four hours. It begins 
usually in the muscles of the jaw, throat, and neck, and extends from 
them to the trunk and extremities. After twenty-four to forty-eight 
hours it usually vanishes, but under certain conditions may persist for 
several days. ’ 

Rigor mortis affects also the smooth muscle fibres; and the contrac- 
tion of these in the skin gives rise to the so-called goose flesh of the 
cadaver. 

The decomposition of the cadaver begins with the disappearance of the 
rigor mortis. Its occurrence is shown partly by the odor of putrefaction, 
partly by changes of color in the skin and mucous membranes, and through 
changes in the consistency of the tissues. The commencement and prog- 
ress of putrefaction depend partly upon the condition of the bedy-nutri- 
tion and the nature of the disease preceding death, partly upon the 
conditions of the surroundings, especially the temperature. Not infre- 
quently putrefaction may occur in local dead areas of the body, even 
before death of the body as a whole. When putrefactive bacteria are 
present in the body, decomposition of the cadaver may begin immedi- 
ately after death. 

AS an early sign of decomposition there is usually present a greenish 
discoloration of the skin, appearing first over the abdomen. With the 
progress of putrefaction the unpleasant odor and discoloration increase; 
and gases are formed in the intestine, later in the blood and in the tis- 
sues, which at the same time become soft and friable. 

Shortly after death the cornea becomes lustreless and cloudy, the eyeball 
loses its prominence, and dark spots appear in the sclera, which, gradually 
increasing in size, become confluent. These changes are due to evapor- 
ation and decomposition. If the eyelids are not closed, the uncovered 
portions of the eyeball show the results of drying. Whenever the skin has 
lost its epidermis the exposed tissues undergo desiccation. 


If all of the phenomena of life be reduced to a minimum, there may result a condi- 
tion of apparent death which may be mistaken for real death. Though post-mortem 
hy postasis, rigor mortis, and putrefaction are unmistakable evidences of death, these 
changes may not take place until some time after death, so that an interval is left dur- 
ing which it may under certain conditions be doubtful as to whether death has actually 
occurred. To ascertain the true condition under such circumstances it must be de- 
termined by appropriate examination whether the heart still beats, whether respiration 
still takes place, whether the blood still circulates, and whether the nerves and muscles 
retain their irritability. 

Conditions which are designated as apparent death occur under a variety of cir- 
cumstances, as, for example, in individuals suffering from cholera, in cases of cata- 
lepsy, hysteria, after excessive bodily exertion, violent concussion of the central ner- 
vous system, after severe hemorrhage, suspension of respiration through hanging. 
strangulation, or drowning, in certain cases of poisoning, after lightning-stroke, after 
prolonged exposure to cold, etc. The duration of this condition is usually only short, 
but may occasionally be extended over several hours or even days. 

According to the investigations of Fuchs (“Ueber Todtenstarre,” Zeitschr. f. Heil- 
kunde, 1900), the heart is the first muscle to show rigor mortis, this organ being affected 
at a time (in animals, after three to five hours) in which rigor mortis cannot be demon- 
strated in any of the skeletal muscles. 


NECROSIS. 169 


Ill. Necrosis. 


§ 49. The condition of local death, or death of individual cells or 
groups of cells, is known as necrosis. As the result of necrosis the 
functions of the affected tissue are forever lost. 

The necrosis of a cell-group or of an entire organ is only under cer- 
tain conditions immediately associated with recognizable changes of 
structure. The slight histological changes which the cells undergo dur- 
ing their death do not always permit us to determine with certainty the 
exact moment of cessation of life; nor does the macroscopic appearance 
of the visible portions of the body always inform us when a portion 
thereof becomes necrotic. 

Necrosis is therefore evident upon anatomical investigation only when 
certain changes in structure have occurred, either coincidently with the 
death or subsequently thereto. Necrosis is shown immediately by histo- 
logical changes only in the case of the action of a limited number of in- 
jurious agencies; in all other cases the necrosis is followed by such 
changes after a longer or shorter interval. According to the nature of 
the subsequent tissue-changes it is possible to distinguish different varie- 
ties of necrosis. 

Histologically the necrosis of a cell is shown in the first place by the 
disintegration and disappearance of the nucleus, whereby the chromatin of 
the cell—that part taking nuclear stains—forms small clumps and gran- 
ules which at times pass out from the nucleus into the cell-protoplasm, 
where they become dissolved and disappear (karyorrheris).. At other 
times the nucleus before its disappearance shows signs of shrinking, and 
in this condition takes the nuclear stain more deeply than under normal 
conditions (pyknosis). In other cases the nucleus retains its form but loses 
its staining power with nuclear stains, and then dissolves and disappears 
(Fig. 31, c, d), so that in well-fixed and stained preparations no trace 
whatever of the nucleus can be found (karyolysis). Thus, for example, 
in an anemic infarct of the spleen or kidney caused by arterial embolism 
the nuclei of the spleen and kidney cells are lost very soon after the 
death of the tissue (Fig. 29, c, d, f, g). At the same time the affected 
area becomes strikingly pale, cloudy, yellowish-white, or cream-colored ; 
so that the occurrence of the necrosis may be recognized by the naked 
eye. 

The protoplasm of the dying cells sooner or later also undergoes 
changes, which, according to the mode of death, may in some cases begin 
before the cells die, or in others may take place only after the cells are 
dead. The kind of change is dependent upon three factors: the nature 
of the cells themselves, the character of the destructive influence, and 
the amount and character of the fluids surrounding and infiltrating the 
cells. Ameeboid cells usually assume a globular form after death. Deli- 
eate and only slightly modified cell-bodies, rich in protoplasm, often 
become, before or after death, markedly granular, less frequently homo- 
geneous and lumpy. Through the taking-up of fluid the protoplasm or 
even the nucleus may become swollen and show drops of fluid (vacuoles) ; 
and this may lead to breaks in the continuity of the protoplasm (plasmos- 
chisis). Not infrequently as a result of plasmoschisis portions of the cell 
may be extruded or cut off by constriction. The ultimate end of all these 
changes is the disintegration of the protoplasm and the nucleus into granular 
masses, this process being often accompanied by a formation of fat. 


NECROSIS. 171 


it is spoken of as direct necrosis. When it occurs slowly and is pre- 
ceded by different tissue-degenerations it is designated indirect necrosis 
or necrobiosis. 

Mechanical, chemical, thermal, and infectious sources of injury, as 
well as anemia, may act coincidently, or separately, one after the 
other. When the tissue is damaged by any one of the first-named 
group of injurious influences, the blood itself very often suffers a 
change, which leads to stasis and coagulation in the capillaries, as well 
as in the veins and arteries, and in this way the circulation may be 
arrested. 

Whether or not a given injury will cause necrosis of the tissue de- 
pends, not only upon its nature and severity, but also chiefly upon the 
condition of the tissue at the time of the injury. A tissue whose vital- 
ity has already been lowered as the result of long-continued disturbances 
of circulation, general marasmus, hydremia, changes in the composition 
of the blood, etc., dies more easily than when in a normal condition. In 
severe cases of typhoid fever relatively slight pressure on the trochanters, 
elbows, sacrum or heels, etc., may suffice to bring about a gangrenous 
necrosis of the skin and subcutaneous tissues. Such forms of necrosis 
are known as marasmic necrosis or marasmic gangrene, and as decu- 
bitus or decubital necrosis. 

The course of necrosis—that is, the tissue-changes resulting from the 
death of cells—is dependent upon the character of the affected tissue, its 
location, the manner of its death, and the cause of the necrosis. Further, 
the amount of lymph and blood in the tissue, and the opportunity afforded 
for the access of air and putrefactive organisms, also exert a very im- 
portant influence. Tissue-changes which preceded the necrosis, such as 
fatty degeneration, inflammation, hemorrhage, etc., are also of signifi- 
cance in determining the character of the necrosis. 

As the result of the necrosis of a certain tissue-area, there always 
develops an inflammation of greater or less intensity in the surrounding tissues 
(Fig. 29, f and Fig. 30, e). This reactive inflammation is most marked 
when the necrotic area becomes gangrenous. Through the formation of 
an inflammatory zone the necrotic area becomes marked off from the 
surrounding tissue, and is isolated or sequestrated; this process is spoken 
of as a sequestrating or limiting inflammation, and the dead area thus shut 
off is called a sequestrum. A more detailed description of these inflam- 
matory processes will be found in Chapter VII. 

Excluding the more especial complications of necrosis, such as the 
development of specific irritating substances, five chief sequelz of ne- 
crosis may be distinguished: 1. The dead tissue may be removed by 
absorption, or may be cast off from the surface, and its pluce taken by nor- 
mal tissue (regeneration). 2. The dead tissue is similarly removed, but 
instead of the normal tissue being restored, the defect: is filled wholly or 
in part by the formation of connective tissue, the so-called cicatricial 
tissue. 3. The necrotic tissue is cast off or liquefied (as in the formation 
of a gastric ulcer through the digestion of the dead part), the defect is 
not filled in, and there remains an ulcer. 4. The necrotic tissue is partly 
absorbed, but a portion remains as a sequestrated necrotic mass which 
not infrequently later becomes calcified and surrounded by a connective-tis- 
. ue capsule. 5. The area becomes encapsulated by connective tissue, the 
dead tissue becomes absorbed or liquefied, and the space becomes filled 
with fluid, forming a cyst. This sequela of necrosis occurs most. fre- 
quently in the brain. 


172 THE RETROGRADE CHANGES. 


The time required to kill tissue by the shutting-off of the circulation varies with 
the different tissues. Ganglion-cells, kidney epithelium, and liver-cells die in two 
hours, while ekin, bone, and connective tissue may live for twelve hours or longer. 
Epidermis under certain conditions may remain alive for a number of days, and still 
retain its power of proliferation (see Transplantation). 

The cause of the above-mentioned nuclenr changes and of the disappearance of the 
nucleus is to be found in the infiltration of the necrotic tissue with lymph. These 
changes do not occur in those tissues to which, after necrosis, the lymph no lon; 
obtains access. In putrefaction the nuclei disintegrate and disappear very rapidly. 
According to Fr. Krana, tissue preserved under aseptic precautions, and protected from 
bacteria in moist chambers at the body-temperature, also loves its nuclei. Liver-tissue 
(Geidmann) shows this change most rapidly and completely, the tissues of the spleen 
and kidney more slowly and less completely, so that all nuclei may not have dien 
peared after cight to fourteen days. The disappearance of the nucleus occurs only 
the presence of a relatively abundant supply of fluid (Goldmann), and may be pre- 
vented by desiccation of the tissue. 





§ 50. According to the various conditions in which the tissues may 
be found after they have died, four chief forms of necrosis may be distin- 
guished: coagulation-necrosis, caseation, liquefaction-necrosis, and gangrene. 

Coagulation-necrosis (Weigert, Cohnheim) is characterized by the 
occurrence of coagulation, either extracellular, in the fluids about the 
cells; or intracellular, in the latter 
case leading to peculiar changes with- 
in the cells. 

As coagulation-necrosis with extra- 
cellular coagulation may in the first 
place be regarded both the intravas- 
cular (Figs. 13-16) and the extravas- 
cular (Fig. 30, d) coagulation of the 
blood, inasmuch as this phenomenon 
may be regarded as the death of the 
blood; and in fact a destruction of 
cells does occur. Further, there may 
of Rx Oragullonnernei in te ener he considered as belonging to this 
from a cue of typhold fever. (Alcohol, doin class the various forms of coagulation 
stain.) Network of fibrin between the necrotle R FA . 
cells. X BUN. which occur in inflammations, partly 

on the surface and partly in the in- 
terior of the tissues (see Chapter VIL.); and which are characterized by 
the forınation, in some cases, of stringy fibrin (Fig. 32), in other cases 
by the formation of granular or hyaline masses of cı 

Intracellular coagulation oceurs when dead cells or cell-products are 




















infiltrated with a fibriuogen-containing lymph. The cells lose their nu- 
clei, present either a granular (Fig. 29, e, d, e, and Fig. 31, ¢, d) or a 





hy umpy appearance. They remain in this condition for a certain 
time and then break down into granules and become dissolved. 

This phenomenon is most frequently observed in anemic, toxic, and 
thermal tissue-neeroses, as for example, in anemic infarcts of the kidney 
(Fig. 29) and of the spleen, also in many inflammations which are asso- 
ciated with marked infiltration of the tissues (Fig. 32) due to exudation 
from the blood-vessels. In the necrosis of striped muscle, which is of 
very frequent occurrence in typhoid fever, the contractile substance 
acquires a hyali ppearance and breaks up into hyaline lumps 
(Fig. 38, 0). 

The necrotic 
cream-colored. Mi 
line coagulation are 



























issue of anwmic infarcts looks pale yellowish-white, or 
‘les containing many dead fibres in a state of hya- 
ale red, and of a dull lustre, resembling fish-flesh. 






COAGULATION-NECROSIS : 


Inflamed tissues undergoing coagulation 
opaque, and grayish-white; but the color 


CASEATION. 173 


necrosis are likewise cloudy, 
may undergo marked changes 


through the admixture of blood or the 
imbibition of bile, as in the intestine, for 
example. 

The structure of a tissue which is the 
seat of a coagulation-necrosis, may still 
be clearly recognized if only the more del- 
icate parts have been destroyed. When 
all parts have been changed, the entire 
tissue may be converted into a structure- 
less, hyaline, or granular mass, containing 
no nuclei or but few. This change takes 
place very often in the necrosis of in- 
flamed tissues which are infiltrated with 
exudate. Through the proper treatment 
of preparations there may be frequently 
demonstrated in these necrotic areas an 
intercellular stringy fibrin; this is seen 
occasionally in anemic infarcts, but more 





often in inflammatory tissue - necroses degeneration of muscle, Tom & a case of 
(Fig. 32). {yphold fever, 9, Normal 4 


Caseation is a form of necrosis closely 
related to coagulation-necrosis, and is 
characterized by either a hard or a soft 
cheesy appearance of the necrotic area. In the first case the dead tissue 
is like firm, yellowish-white, hard cheese, or similar to raw potato; in 
the second case it is white, soft, sometimes dry, sometimes moist, and 
not infrequently resembling thick cream. 

Typical caseation occurs most frequently in tubercles and represents 
the characteristic end of the retrogressive changes in this condition. It 
also occurs in syphilitic granulomata and in very cellular tumors; in- 
flammatory exudates may also become 
changed into cheesy masses. 

The process of caseation of cellular 
tissues, which is a characteristic of tu- 
berculous granulations, takes place grad- 
ually, and is therefore to be regarded as 
a form of necrobiosis. The cells are 
changed successively into non-nucleated, 
homogeneous, lumpy masses, which later 
disintegrate and break up into a gran- 
ular mass (Fig. 34, a, a). At the same 
time with these changes there often ap- 
pears between the cells a hyaline sub- 
stance, sometimes forming a framework 





in the 
Sntitrated with cells. „x 250. 





Fic. 34. - Tissue from a partly caseated 


tuberculous focus, containing bacilli. (Al- 
ook, furtsit. aniiine blue.) a, Granular: 


Brocelinlar tw: c. pariy necrotte giant, d the cell: t other times more 
2] o 
A z AA nt aroun ie cells or at er times n 


lumpy or granular, and fibrin-like—the 
so-called “ fibrinoid substance.” Typical 
firillated fibrin (Fig. 35, a) staining deep 
blue with Weigert’s fibrin stain is often also present. It may therefore 
be assumed that both substances represent coagulation-products of a 
fluid which has escaped from the blood-vessels. 

Through progressive cleavage and disintegration of the dead cells, 


In the cellular tissue; ¢, bacilli In neerotie 
Ye: J, bacilll enclosed within cel 








176 THE RETROGRADE CHANGES. 


condition is designated dry gangrene (gungrena sicca) or mummifica- 
tion. When the dead part remains moist, the terms moist gangrene 
(gangreena humida) or sphacelus may be applied. If through the agency 
of bacteria there occurs a foul-smelling putrefaction, the condition is known 
as a putrid gangrene (gangrena fetida). Development of gas-bubbles 
asa result of the putrefactive changes leads to emphysematous gan- 
grene (gangrena emphysematosa), 

Moist gangrene and putrid gangrene are in general identical, since 
bacteria can develop only in moist tissues. Nevertheless a dry gangrene 
is not infrequently a putrid gangrene, since bacteria may develop in the 
tissue before drying takes place. Dry gangrene may also develop from 
a moist gangrene, or through the absorption of water become changed 
into the latter. 

When the dead tissue, in either mummification or moist gangrene, 
contains a large amount of blood, it appears black, dark brown, or 
greenish-black in color, and is then called black gangrene. If, on the 
other hand, the dead tissues are anemic, the condition is sometimes 
spoken of as white gangrene, although there is more or less discolor- 
ation of the dead part, so that the expression is often inappropriate. 

In the case of gangrene of superficial parts of the body, there may be 
distinguished, according to the temperature of the dead part, a cold and. 





Fra, 37.—Dry gangrene of the toes, due to narrowing and closure of the arteries through arteriosclerosis. 


a warm or hot gangrene, the latter designation being used when the gan- 
grenous area is kept warm by the blood flowing through the neighboring 
tissues. 

Gangrene may be caused by external injuries, heat, cold, corrosives, 
crushing, pressure, infection, ete., as well as by disturbances of the cir- 
ation. 

Gangrene due to disturbance or arrest of the circulation occurs not 
infrequently in old people (senile gangrene), involving the extremities, 
particularly the toes, feet, and le; It is usually of the dry variety, 
and is dependent upon general disturbances of the circulation and nar- 
rowing of the arteries of the iti i i 
arterial wall ( The 
mming-back of the blood. General disturbances of the circulation, 
in heart-disease and embolism of the arteries may cause similar 
nyges, 

Gangrene from cold affects chiefly the tips of the extremities, nose, 
and ears, and is characterized by changes similar to those described above. 

Gangrene from heat is confined to the area directly affected by the 
heat. 





e 




















GANGRENE. 177 


Pressure-gangrene or decubitus (bedsore) occurs in marasmic indi- 
viduals, most frequently upon the sacrum and the heels, both of which 
regions are exposed to pressure when the individual lies upon his back. 
The bedsore begins with the formation of bluish-red spots, within whose 
area the tissue dies, and through the agency of bacteria undergoes de- 
composition and finally disintegrates. The gangrenous area may be of 
large extent, especially when over the sacrum; the bone mav be laid bare 
over a large area through the destruction of the overlying soft parts. 

Toxic gangrene occurs chiefly in ergot poisoning as a result of the 
contraction of the small vessels and formation of thrombi. The tips of 
the extremities are usually affected. 

Infectious gangrene occurs particularly in different infections of the 
skin and subcutaneous tissue, and may be associated with gas-formation. 
In the form known as foudroyant gangrene different varieties of bacteria 
have been found; the bacillus of malignant cedema, an anaérobic bacil- 
lus (Welch, E. Frankel, Hitschmann and Lindenthal), proteus (Hauser), 
and bacterium coli. Infections associated with putrid gangrene may 
occur in the internal organs, but affect chiefly the lungs and intestines. 

A so-called neuropathic gangrene occurs when a tissue affected with 
either sensory or motor paralysis is wounded or subjected to continued 
pressure. It is dependent partly upon circulatory disturbances and 
partly upon infection. Gangrene resulting from the withdrawal of the 
influence of trophic nerves has not yet been demonstrated. Symmet- 
rical gangrene, which affects corresponding parts of the extremities 
and has been regarded by many as a neuropathic disease, is dependent 
upon changes in the blood-vessels; likewise, the perforating ulcer of the 
foot (mal perforant du pied), which begins as a callesity following me- 
chanical influences, and is characterized by an accompanying gangrene 
which rapidly penetrates into the deeper tissues, is dependent upon the 
closure of an artery of the foot. 

In moist gangrene the tissues break down with a varying degree of 
rapidity, the fascis resisting for the longest time. As crystalline prod- 
ucts of the chemical changes there may be found needles of fat and 
tyrosin, spherules of leucin, coffin-lid crystals of triple phosphate, and 
crystals of hematoidin. If the gangrene comes to a standstill, the gan- 
grenous tissue becomes sequestrated through the formation of a zone 
of demarcation—that is, becomes separated from the living tissue, and 
under favorable conditions may be thrown off from the body. In the 
ease of necrotic portions of bone a very long time is required for seques- 
tration. Extension of gangrene (through infection or continued circu- 
latory disturbance) leads sooner or later to death, especially if toxic sub- 
stances or bacteria are taken up into the blood or lymph. 


Literature. 
( Necrosis and Gangrene. ) 


Albrecht: Neuc Fragestellung z. Pathol. d. Zelle. Münch. med. Woch., 1899. 

Arnheim: Coagulationsnekrose d. Kernschwund. Vireh. Arch., 120 Bd., 1890. 

Balser: Ueber Fettnekrose. Virch. Arch., 90 Bd., 1832. 

Chiari: Ueber die sog. Fettnekrose. Prager med. Woch., 1893. 

Condorelli: Istio-patologia del nucleo nelle contusioni, Catania, 1891. 

Dejerine et Leloir: Alter. nerv. dans cert. cas de gangrene. Arch. de phys., 1881. 
e: Ueber die Veränderungen der Gewebe bei Brand, Frankfurt, 1857. 

Ellis: (X-Ray Necrosis) Lit. Amer. Jour. of Med. Sc., 1903. 


- 


178 THE RETROGRADE CHANGES. 


Falta: Gangraena senilis. Zeitschr. f. Heilk., xx., 1899. 

Flexner: Fut Necrosis. Jour. of Exp. Med., 1897; Focal Necrosis. Johns Hopkins 
Hosp. Rep., 1897. 

Frangois: Essai sur les gangrénes spontanées, Paris, 1832. 

Frankel: Ueber die Gasphlegmone, Hamburg, 1893; and Münch. med. Woch., 1899. 

Goldschmidt: Gangréne symetrique (endarterite oblitérante). Revue de méd., vii., 
1887. 

Goldmann: Veränderungen aseptisch aufbewahrter Gewebssticke. Fortschr. d. 
Med., vi., 1888; Reiskörperchenhaltiges Hygrom der Sehnenscheiden. Beitr. v. 
Ziegler, vii., 1890. 

Haga: Spontane Gangrän. Virch. Arch., 152 Bd., 1898. 

Hartmann: Exp. Unters. über Chromsäurenephritis. Inaug.-Diss., Freiburg, 1891. 

Hitschmann u. Lindenthal: Gangrene foudroyante. Sitzb. d. Ak. d. Wiss., Wien, 
1899. 

Hochenegg: Ucber symmetrische Gangrän u. locale Asphyxie, Wien, 1886. 

Israel: Anim. Nekrose d. Nierenepithelien. Virch. Arch., 128 Bd., 1891; Biolog. 
Studien, ib., 141 Bd., 1895; 147 Bd., 1897; Tod d. Zelle. Berl. klin. Woch., 
1897. 

Kaufmann: Die Sublimatintoxication, Breslau, 1888. Virch. Arch., 117 Bd.,” 1889. 

Kraus: Im abgestorb. Gewebe auftretende Veränderungen. Arch. f.exp. Path., xxii., 
1886 


Langerhans: Ueber multiple Fettgewebsnekrose. Virch. Arch., 122 Bd., 1891. 

Le Count: Focal Necrosis. Jour. of Exp. Med., 1897. 

Lesser: Anat. Veränderungen d. Verdauungskanales durch Aetzgifte. Virch. Arch., 
83 Bd., 1880. 

Lévai: Mal perforant du pied. Zeit. f. Chir., 49 Bd., 1899. 

Mallory: Focal Necrosis. Jour. of Exp. Med., 1898; Necroses of the Liver. Jour. 
of Med. Research, 1901. 

Manz: Ueber die Bildung der Reiskörperchen. Inaug.-Diss., Freiburg, 1892. 

Neuberger: Wirkung des Sublimates auf die Nieren. Beitr. v. Ziegler, vi., 1889. 

Obolonsky u. Ziegler: Wirkung d. Phosphors auf Leber u. Nieren. Beitr. v. Ziegler, 
ii., 1887. 

Oertel: Die Pathogenese der epidemischen Diphtherie, Leipzig. 1887. 

Peiper: Eiterige Schmelzung der Gewebe. Virch. Arch., 118 Bd., 1889. 

Pfitzner: Zur pathologischen Anatomie des Zellkerns. Virch. Arch., 103 Bd., 1886. 

Rath: Bakteriologie der Gangrän. Cbl. f. Bakt., xxv., 1899. 

Raynaud: De l’asphyxie locale et de la gangréne symétrique des extrémités, Paris, 
1862. 

Reed: Focal Necrosis. Amer. Jour, of Med. Sc., 1895. 

Rischpler: Histol. Veränderungen nach der Erfrierung. Beitr. v. Ziegler, xxviii., 
1900. 

Schmaus: Zelltod. Ergebn. d. allg. Path., iii., Wiesbaden, 1897. 

Schmaus u. Albrecht: Ucber Karyorrhexis. Virch. Arch., 188 Bd., 1895 (Lit.); Die 
käsige Nekrose, ib., 144 Bd., Supplh., 1896; Coagulationsnekrose. Deut. med. 
Woch., 1889. 

Seitz: Blutung, Entzündung u. brandiges Absterben des Pankreas, Berlin. 1892. 

Sternberg: Endarteritis u. spontane Gangrän. Virch. Arch., 161 Bd.. 1900. 

Stroebe: C'elluläre Vorgänge u. Erscheinungen in Geschwülsten. Beitr. v. Ziegler, 
x., 1891. 

Tesdorpf: Symmetrische Gangrän. Arch. f. Psych., 88 Bd., 1900. 

Verworn: Allgem. Physiologic, Jena, 1897; Der körnige Zerfall. Pflüg. Arch., 63 
Bd., 1896. 

Weigert: Pathologische Gerinnungsvorgänge. Virch. Arch., 79 Bd.; Coagulations- 
nekrose mit besonderer Berücksichtigung der Hyalinbildung und der Umprägung 
reronnencr Massen. Deut. med. Woch., 1885; Weisse Thromben. Fortschr. d. 
Med., v., 1887; Coagulationsnekrose oder Inspissation. Cbl. f. allg. Path., ii., 1891. 

Weiss: Venenspasmus. Wien. med. Presse, 1882; Syumetr. Gangrän. Wien. med. 
Klin., 1882. 

Wells: Experimental Fat Necrosis. Jour. of Med. Research, 1908. 


IV. Hypoplasia, Agenesia, and Atrophy. 


$ 52. Hypoplasia, or the defective development of anlage, may affect 
either the body as a whole, or only single organs or parts of organs, and 
may oecur either during the period of intra-uterine development or later 
during the period of post-embryonal development. 


HYPOPLASIA. 179 


When either the entire skeleton or at least the greater part of it is 
under-developed, and especially if the bones do not attain their normal 
length, the affected individual is abnormally low in stature, and is called 
a dwarf (Figs. 38 and 39). The individual parts may be fairly well pro- 
portioned (Fig. 38), or they may be unsymmetrieally developed (Fig. 





Fa, 98.—Skoleton of a female eretin, thirtyone foars of age, 118 cm. in beight, with klloncepballe 
skull. The cartilage sutures of the the long bones and pelvic bones still show 


frontal putur The Imdirkdual parts za cl tbe skeleton ‘ae, on the whole, in the proper proportion, the Upper 
extremities alone being 

Fig. 2.-Skeleton oat men dwart of fifty-eight years UIT em, {m height, with very short 
gatremiiin and long trunk. "Tho caruiage suturos aro sül BET prensat: the Articular eos of the binenare 
thiek. 


39). For example, the trunk may be of normal size, while the extrem- 
ities are abnormally short (Fig. 39); or both the trunk and the extrem- 
ities may be abnormally small, while the head is of normal size, and 
consequently appears relatively too large for the small body. When the 
lack of development affects individual parts of the skeleton exclusively, 
or if it is more marked in certain parts than elsewhere, there results a 
stunting of individual portions of the body. 

For example, defective development of the cranium gives rise to 





1S2 THE RETROGRADE CHANGES. 


The tissue composing hypoplastic organs or parts of organs, though 
of less bulk than normal, may present no abnormalities of structure. In 
other cases there may be associated with the smallness of size a disturb- 
ance of internal organization, so that often the more highly specialized 
elements of the organ fail of development, the hypoplasia being at the same 
time associated with an agenesia of individual parts. Thus, for example, in 
hypoplasia of the ovary (Fig. 45, e) the development of the ova and the 
ripening of the follicles may fail in part; in hypoplasia of the brain 
there may oceur at the same time a defective development of the gan- 





Fic. 45.—Cruss sections of ovaries at different periods of life. (Hsematoxylin and eosin.) a, b,c, d, 
Normal ovaries; a, girl of five years; bh, twenty-three years; c, twenty-nine years: and d, twenty-one 
years: e, hypoplastic ovary of girl of twenty-seven years; f, g, senile ovaries from women of eighty and 
eighty-three vears of age. (Natural size.) 


glion-cells and nerve-fibres, and at times portions of the brain may con- 
sist only of membranous masses (Fig. 42, d) in which no ganglion-cells 
are present. In hypoplasia of the lung there may be under certain con- 
ditions a complete failure of development of the alveoli, so that the 
lung-tissue consists merely of a very vascular connective tissue through- 
out which lie the bronchi, the latter in the course of time usually be- 
coming dilated. 


Literature. 
(Hypoplasia and Agenesia. ) 


Forster: Die Missbildungen des Menschen, Jena, 1865. 

Hertz: Ueber Hemiatrophia facialis progressiva. Arch. f. Kinderheil., vii., 1887. 

Hektoen: Anatomical Study of a Short-limbed Dwarf. Amer. Jour. of Med. Sc., 1908. 

Mehnert: Die individuelle Variation d. Embryo. Morph. Arb. v. Schwalbe, v., 1896. 

Paltauf, A.: Ueber den Zwergwuchs, Wien, 1891. 

Rählmann: Mikrophthalmus u. Hemimikrosoma, Stuttgart, 1897. 

Vierordt: Anatomische, physiologische u. physikalische Daten u. Tabellen, Jena, 1888. 
See also Chapter IX. 


§ 53. Atrophy is a diminution in the size of an organ due either to a 
diminution in size or disappearance of its individual elements. It may 
oceur at any period of life, and is a very common result of many path- 
ological processes. Within certain limits it may be regarded as a physi- 
vlogical phenomenon, in that in old age there constantly occurs a certain 
degree of retrograde change in all the organs, associated with a diminu- 
tion in their size. Certain organs undergo such an atrophy with partial 
or total loss of their functional power, even before old age, as, for exam- 
ple, the thymus, which atrophies completely even before the end of the 
period of growth; and the ovary (Fig. 45, f, 9), a part of whose ova are 
discharged during the period of sexual activity, the remainder being 





184 . THE RETROGRADE CHANGES, 


In atrophy of the kidney the epithelial cells of the urinary tubules 
(Fig. 50, f) become smaller and may finally wholly vanish so that the 
tubules collapse. Likewise, the epithelium of the glomeruli (d) is lost, 
while the capillaries become obliterated, 

The same thing occurs in simple atrophy of the liver, in that all the 
liver-cells of a lobule may disappear without any perceptible decrease of 
the supporting reticulum, Likewise the ganglion cells of the brain and 
spinal cord may atrophy without the neuroglia being diminished. Not 
infrequently the latter may become increased, 

In atrophy of the bones the true bone-tissue becomes diminished, 
while the bone-marrow in excentrie atrophy and osteoporosis beeomes 
increased. Moreover the 
fat in the cells of the mar- 
row may also vanish, so that 
free spaces are formed which 
become filed with fluid. 

In atrophy of the lymph- 
glands and of the spleen the 
free cells in particular dis- 
appear and in parts are com- 
pletely absent. 

The changes leading to 
atrophy may take place with- 
out the occurrence of any 
apparent change of structure 
in the individual tissue-ele- 
ments (Fig. 49), so that the 
condition of atrophy is 
reached essentially through 
a loss of volume of the in- 
dividual parts. Both the 
cell-body and the nucleus 
may become smaller; and 
the latter change may be ob- 
served particularly in the 
liver in cases of starvation- 
atrophy (Lukjanow). This 
form of atrophy is known 
as simple atrophy, and is 
to be distinguished from the 
degenerative atrophies, in 
which the fissue-elements 
Ti. pr up omg oe lew a ee 

structure, and frequently 
contain pathological substances. Thus a cell may become granular, 
and undergo fragmentation, or may swell up and liquefy, or there 
may be formed within the cell drops of fat or mucus; all of these 
changes signifying degenerative conditions of the cell-protoplasm. 
These processes are classed as special forms of degeneration and will be 
discussed in the paragraphs of the following seetion. Degenerative 
changes can occur at the same time in the nuclei, as shown by fragmen- 
tation, distorted shape, clumping of the chromatin, diffusion of ehro- 
matin into the cell-protoplasm, swelling and liquefaction of the nucleas. 

















188 THE RETROGRADE CHANGES. 


Literature. 


(Atrophy. ) 
Borel. Contribution a l’etude des asymétrics du visage. Thése de Berne, Genéve, 


Charcot: Maladies des vieillards. (CEuvres compl., vii. 
Coén ign tt inanizione acuta. Bull. delle Scienze Med. di Bologna, ser. vii., vol. i, 
Demange: Ftude clinique et anatomo-pa:hologique sur la vieillesse, Paris, 1886. 
Demme: Hemiatrophia facialis. xxii. Ber. üb. d. Thätigkeit d. Kinderspitals, Bern, 
5. 
Flemming: Richtungsfigur im Ei bei Untergang d. Follikel. Arch. f. Anat., 1885. 
Herz: Hemiatroph. fac. progressiva. Arch. f. Kinderheilk., viii., 1887. 
Homen: Zur Kenntniss der Hemiatrophia facialis. Neurol. Cbl., 1890; Festskrift 
fran Pathologisk-Anatomiska Institutet, Helsingfors, 1890. 
Jarotzky: Veränd. d. Pankreaszellen bei Inanition. Virch. Arch., 156 Bd., 1899. 
Joseph: Trophische Nerven (Haarausfall nach Nervenexcision). Virch. Arch., 107 
., 1887. 
Levin: Halbscitige Gesichtsatrophie (Zusammenstellung der publ. Fälle). Charité- 
Annalen, ix. 
Lukjanow: L’inanition du noyau cellulaire. Rev. scientif. Paris, 1897. 

Merkel: Die Gewebe beim Altern. Verh. d. X. internat. med. Congr., ii., Berlin, 1891. 
Morpurgo: De la nature des atrophies par inanition. Arch. ital. de. biol. xii., 1889; 
Karyometrische Untersuchungen bei Iuanition. Virch. Arch., 152 Bd., 1898. 

Möbius: Der umschriebene Gesichtsschwund, Wien, 1895. 

Mühlmann: Die Veränderungen im Greisenalter. Cbl. f. allg. Path., xi., 1900 (Lit.). 

Nötzel: Rückbildung der Gewebe im Froschlarvenschwanz. Arch. f. mikr. Anat., 45 
Bd., 1895. 

Penzoldt: Hemiatrophia facialis. Münch. med. Woch., 1886. 

Pfitzner : Zur path. Anat. d. Zellkerns. Virch. Arch., 108 Bd., 1886. 

v. Recklinghausen: Handb. d. allg. Path. d. Kreislaufs u. d. Ernährung, Stuttgart, 
1893. 

Salvioli: Sulla pretesa influenza trofica di nervi. Arch. per le Sc. Med., 1896. 

Seeligmüller: Gesichtsatrophie. Eulenburg’s Realencyklop., 1895. 

Stier: Verhalten d. Musk. u. Nerven nach Läs. d. Nervensyst. Arch. f. Psych., 29 
Bd., 1897 (Lit.). 

Voit: Handb. d. Physiol. v. Hermann, vi., Leipzig, 1881. 
See also § 28. 


V. Cloudy Swelling and Hydropic Degeneration. 


§ 54. The term cloudy swelling or parenchymatous degeneration or 
granular degeneration is applied to that form of cell-degeneration which is 
characterized histologically by a swelling and enlargement of the cells 
due to the formation within the cell-protoplasm of 
free granules, which according to their microchemi- 
cal properties (solubility in acetic acid, insolubility 
in alkalies and ether) are to be regarded as albumin- 
ous bodies. The epithelial cells of the kidney and 
liver (Fig. 54), and the cells of heart-muscle frequent - 

Fic. 54.—Cloudy awe. LY Show this degeneration, thereby acquiring a cloudy 
ing of liver-cells (scraping appearance, as if covered with dust, while at the same 
u oor aan icing time their normal structure and form are lost. Thus, 
oT septicemia, examaed for example, in cloudy swelling of the kidney-epi- 
x BH thelium the rod-like markings of the protoplasm are 

lost (Fig. 55, a), as are also the cell-processes pro- 
jeeting into the lumen of the tubules. The swollen cells (6, c, d) are 
larger, more plump, and contain dark granules. This change is to be 
regarded as a disorganization of the protoplasm following an absorption 














192 THE RETROGRADE CHANGES. 


Among the conditions of life which lead to a pathological accumulation of 
Jat are: first, a luxurious mode of living ; further, wasting of bodily strength, 
and marasmus, such as is observed especially in chronic tuberculosis. In 





Fi. €0.—Lipomatosts of the calf muscles, associated with atrophy. (Miller's uid, carmine.) a, Trans- 
verse section of normal fibre; a}, of atrophic fibre; ay, transverse section of sarcolemma tabe containing 
disintegrated contractile substance ; b, connective tissue; ¢, fattimsue. x 60. 


the first case the deposit of fat is a generalone. In the last, the accumu- 
lation of fat is usually confined to the liver (Fig. 59), the liver-tissue at: 
the seat of deposit becoming clear yellowish-gray to a straw-yellow in 
color. In the first case the cause of the fat-deposit is the excess of nutri- 









lar atrophy with lpomatosis, in ascending atrophy of the anterior uorns of the 
Bismarck brown.) Section from the calf muscle. a, Transverse section of 
x; b. perimysium; ¢, fat-Ussue; d, artery; ¢ veln. X 6), 


spinal 
Atrophie mus 





tive material ingested; in the last case it is the inability of the organism 
to use up in sufficient measure the fat taken in or elaborated within the 
body. 


PATHOLOGY OF ADIPOSE TISSUE. 193 


Under certain conditions a more marked local fat-deposit may occur as 
@ sequela to tissue atrophy, as, for example, in the neighborhood of con- 
tracted kidneys, and in muscles (Fig. 61, c), which suffer a progressive 
atrophy (a), as the result of diseases of the spinal cord. 

If through a diminution in the amount of nourishment taken into the 
body, or through a deficient formation of fat within the body, or through 
an increased metabolism, the normal amount of body-fat is lost, the con- 
dition is known as atrophy of the fat-tissue. In the process of absorp- 
tion and decomposition of the fat, the latter becomes broken up into 
small droplets, and the fat-cells are finally converted into small connec- 
tive-tissue cells. If, after the disappearance of the fat the spaces be- 
tween the shrunken fat-cells become filled with a serous fluid, the fat- 
tissue acquires a translucent appearance similar to that of myxomatous 
tissue; and this condition, which occurs especially often in the pannicu- 
lus of the heart, is designated serous atrophy of the fat-tissue. Occasionally 
pigment may be deposited in the atrophic fat-cells, so that the tissue 
acquires a yellow or yellowish-brown color. This condition is designated 
yellow atrophy of fat-tissue. 


The fat deposited in the body may, in the first place, arise from that ingested, so 
that in dogs fed with mutton-fat there occurs a deposit of mutton-fat (Hosenfeld), and 
the feeding of iodized fat leads also to a deposit of iodized fat in the fat-depöts ( Win- 
ternitz). fe is ordinarily assumed, particularly with reference to the fat-droplets in the 
chyle, that such fat, finely emulsified, is taken up through openings in the cuticular 
margin of the epithelium of the intestinal mucosa. Against this view is opposed the 
fact that such an absorption of fat by the intestinal epithelium cannot be followed step 
by step. Flemming, therefore, assumes that, in the case of the absorption of fat from 
the intestine, as well as its entrance into the fat-cells, the elements of the fat are tuken 
up by the cells tn the form of soluble combinations, and are converted in the cells by the 
chernical activity of their protoplasm again into fat; and that, further, in atrophy of 
fat-tissue, the fat ts chemically split up into soluble combinations and ao passed out of the 
cells. According to Connstein, the absorbable fats in the stomach and intestine are for 
the greater part split up; and, through the combination of the fatty acids with the 
alkalies present in the intestine, are converted into soluble soaps which are absorbed by 
the epithelium. These soaps are changed in the intestinal epithelium (in the same way 
that the absorbed peptone is again changed to an albuminate) back again to globules of 
neutral fat. The glycerin necessary for this process is absorbed directly from the in- 
testine where it is present in the free state, having been split off from the neutral fats. 

Besides that formed from fat and fatty acids, the organism can also form and store 
up fats from carbohydrates and albumin. The formation of fat from albumin is denied 
by various authors (Pflüger), but has been established beyond any doubt by different 
observations (see Lindemann, l.c.). 

According to Voit, the immediate factor in metabolism is not the action of oxygen, 
but lies in the organization of the cells, the protoplasm of which possesses the power, 
in proportion to the external conditions, to break down complex chemical combinations 
into simpler ones. The albumin brought to the cell in a soluble form, and after this the 
carbohydrates are the most easily decomposed by the cells, fat with greater difficulty, 
either that taken in with the food or formed within the body from albumin or carbo- 
hydrates. When fat is supplied in excess, or when the activity of the cells is exhausted 
before the fat split off from albumin is further decomposed, there will occur a deposit 
of fat. The same thing will happen when fat and carbohydrates or albumin are sup- 
plied at the same time, if the cells after decomposing the latter are incapable of further 
activity. Increase of food-supply, muscular action, and elevation of body-temperature 
calıse an increase in the metabolic activity of the cells, while alcohol, morphine, and 
quinine weaken it. Obesity depends upon a greater assimilation of food than can be 
used by the body. The metabolism in this condition may either be normal, or may be 
diminished through weakness of the cells or diminution of their number. The cause 
of the increased deposit of fat in ansemic conditions may be explained by the diminution 
of the cell-mass of the body and the consequent weakening of metabolism. The de- 
posit of fat in the cells of the intermuscular connective tissue of atrophic muscle may 
be regarded as due to diminished metabolism in the muscle. 

According to Gautier, the decomposition of albumin in the cells is the result of 
their functional activity, and occurs in two phases, In the first, the phase of ferment- 


194 THE RETROGRADE CHANGES. 


action without oxidation, or hydrolytic splitting, there are formed from the protoplasm 
urea or analogous combinations (salts of uric acid, kreatin-bodies), and at the same 
time the carbohydrates form the fat-bodies. Tn the second, the phase of oxidation, the 
sugar and fat disappear, both that formed from albumin and that derived from the in- 
gested food. The carbohydrates are in part oxidized; but the greater part, especially 
during muscular inactivity, are changed into fat through a simple process of_ferment- 
action, by which a large amount of carbonic acid is set free. Finally, the fat-bodies 
are also oxidized and disappear. 


Literature. 


(The Pathology of Adipose Tissue.) 


Connstein: Resorption u. Assimilation der Fette. Med. Woche, 1900. 

Dercum: Adiposis Dolorosa. Ref. Hdb. of the Med. Be., 1900; with McCarthy: 

. Jour, of Med. Se., 1902. 

Ebstein: Die Fettleibigkeit und ihre Behandlung, Wiesbaden, 1892; Über Wasserent- 
ziehung und anstrengende Muskelbewegungen bel Fettsucht, etc., Wiesbaden, 
1885. 











in muscularis progressiva, Leipzig, 1801. 
dung u. Rückbildung d. Fettzelle im Bindegewebe. Arch. f. mikr. 
vi Bd., 1871; Hypothesen über Fettresorption. 


Gaule: Das Auftreten von Feit in den Zellen. Arch f. Anat., 180. 
Gautier: Die Ernährung der Zelle. Biol, Cbl., xiv., 1894. 

Kaufmann: L’origine de la grai rch, de phys., viii., 

Kisch. Die Fettleibigkeit, Stuttgart, 1888: ‘Bulcaburg’s Realeneyklop., Art. Fettsucht, 

1895. 

Lee: L'obesité, Paris, 1886. 

Lindemann: Ücher puthologische Fettbildung: Bei 
Munk, J.: Virch. , and 101 Bd.; Biol. 








. v. Ziegler, xxv., 1899 (Lit.). 
bl. 1886; Art. Fette in 


Nasse: Fettzersetzung u, Fettanhäufung im thierischen Körper. Biol. Cbl., vi., 1888. 
v. Noorden: Pathologie des Stoffwechsels, Berlin, 1893; Di 'ettsucht, Wien, 1900. 
itisch-physiol. Besprechung d. Ebstein’schen Bebandl, d. Fettleibigkeit, 
ix. 1885. 
auung u. Resorption der Fette. Pfiüger’s Arch., 82 Bd., 1900. 
y phic der Muskel: Arch. f. Psych., xx., 1889. 
Giebt es eine fettige Degeneration? Verh. d. Congr. f. inn, Med., 1897 


logie des allg. Stoffweehsels. Hermann's -Handb. d. Physiol., vi., 1881; 

der Fettablagerung im Körper, 1884; Biol. Cbl., vi. 

Winternitz: Verhalten von Jodfetten im Organismus. Zeit. f. phys. Chem., 24 Bıl., 
1897. 

Zawarykin: Fettaufnahme im Dünndarm durch Wanderzellen. Arch. f. d. ges. 
Physiol. 
























$ 57. Fatty degeneration is that form of cell-degeneration in which 
fat is formed from the albumin of the cell-body—that is, from the albu- 
min of the organism—and appears within the cell in the form of gran- 
ules, droplets, ordrops. Cells 
which are in the condition 
of fatty degeneration present 
within their  cell-substance 
amall or larger droplets, which 
are clear, and highly refrac- 
tive (Fig. 62, ¢, d,e, f, and 
Fig. 63), insoluble in acetic 
acid, and soluble in aleohol 
and ether. With osmic acid 
they become black (Fig. 64, 
b and Fig. 65, A, B, C); in 


Fic, a 
cells.” und 
ef fatty de 





FATTY DEGENERATION. 197 


degeneration, for the reason that in these cell-masses there is an insuffi- 
cient supply of nutrition. 


In the majority of cases fatty degeneration is the only histological 
change which can be demonstrated in the cells, but it is at times asso- 
ciated with other degenerative changes. The most frequent combination is 
that of cloudy swelling and granular disintegration with fatty degeneration ; 
but Aydropic degeneration with vacuole formation (Fig. 66, c) may also occur 
at the same time with fatty degeneration. Both of these combinations occpr 
especially in cases of poisoning and in inflammations. Moreover, fatty 
degeneration of the cells accompanies many degenerations of the ground- 
substance, as, for example, amyloid degeneration of the connective tissue 
(see § 63, Fig. 81). 


The question whether the fat found in the cells is a degeneration or a deposit is in 
many cases very difficult and uncertain of answer; and it often cannot be determined 
in a given case whether there is a true fatty degeneration present, in the sense that the 
fat is formed in the cell out of the cell-albumin. In general, fatty degeneration is as- 
sumed to be present when fat fs found in cells which ordinarily contain no fat, and 
when clinically there is apparent a diminution of functional activity, and anatomically 
a degeneration of cell-structure. It must be noted, however, that careful investiga- 
tions (Unna, Sata) have shown, that many cells even under normal conditions contain 
fat more frequently and regularly than has been generally supposed (for example, the 
epithelium of the sweat-glands and lachrymal gland, and of the epidermis, and also car- 
tilage cells). Moreover, both in fetal tissues and in proliferating cells (not degenerat- 
ing) with cell-division figures, fat is often present. Under conditions, in which the 
assumption of a weakening and degeneration of the organ concerned is well founded, 
nothing further may be recognized by which it is possible to say whether the fat pres- 
ent has arisen from the albumin of the affected cells, or whether it has been produced 
from carbohydrates or from the lecithin of the cells, or out of substances brought to 
the cells from without. For this reason we should not go so far as to deny the occur- 
rence of a true fatty degeneration, that is, a formation of fat out of the cell-substance 
(Rosenfeld); but in the diagnosis of cells showing fatty degeneration we must at times 
bear in mind the different possibilities of the origin of the fat. 

Requiring a special consideration are certain round cells of different size, which 
are entirely filled with fat droplets, and are therefore known as fat-granule globules or 
fat-granule cells (Fig. 67, a). They occur especially in degenerative processes in the 
brain and spinal cord; and have been repeatedly regarded as tissue-cells which have 
undergone fatty degeneration, in the brain as ganglion-cells and glia-cells presentin g this 
degeneration. The true fat-granule globules or cells are, however, not the fixed tissue- 
cells which have become fatty, but are amaboid leucocytes and tissue-cells arising through 
proliferation, which through phagocytic action have taken up into their substance the fatty 
detritus arising from the disintegration of tissue. According to Arnold, the fat-granules 
also arise through the conversion of plasmosomes into fat. 

According to the investigations of Lindemann, the fat arising through degeneration 
of the heart-muscle differs essentially from the fat deposited in the heart or in the subcu- 
taneous tissue. The degeneration-fat is able to take up 108.55 per cent of iodine, nor- 
mal heart-fat only 61.1 per cent, the content in free fatty acid amounting to 18.35 as 
against 7.8 in normal heart-fat. 


Literature. 
(Fatty Degeneration. ) 


Arnold: Fettkörnchenzellen- und’Granulalehre. Anat. Anz., xviii., 1900. 

Aschoff: Fettgehalt fötaler Gewebe. Cbl. f. allg. Path., viii., 1897. 

Beneke: Fettembolie. Beitr. v. Ziegler, xxii., 1897. 

Binz u. Sehulz: Kohlenoxydgasvergiftung. Arch. f. exp. Path., xiv., 1881. 

Ehrlich: Das Sauersto ürfniss des Organismus, Berlin, 1885. 

Elbe: Hist. Unters. über Jodoform u. Arsenintoxication. Inaug.-Diss., Rostock, 1899. 

Frankel: Einfluss d. verminderten Sauerstoffzufuhr auf den Eiweisszerfall. Virch. 
Arch., 67 Bd., 1876. 

Handwerck. Verh. d. Fettkörper zu Osmiumsäure u. Sudan. Zeit. f. wiss. Mikr., 
xv., 1898. 


198 THE RETROGRADE CHANGES. 


v. Kahlden: Actiologie und Genese der Nephritis. Beitr. v. Ziegler, xi., 1892. 

Krehl: Fettige Degeneration des Herzens. Deut. Arch. f. klin. Med., 51 Bd., 1898. 

Leo: Fettbildung u. Fetttrausport bei Phosphorvergiftung. Zeitschr. f. phys. Chem.. 
ix., 1885. 

Leyden u. Munk: Die acute Phosphorvergiftung, Berlin, 1865. 

Lindemann: Ueber pathologische Fettbildung. Beitr. v. Ziegler, xxv., 1899 (Lit.): 
Wirkung des Oleum Pulegii. Arch. f. exp. Path., 32 Bd., 1896; Zeit. f. Biol., 39 
Bad., 1900; Das Fett des normalen u. des fettig entarteten Herzmuskels. Zeit. f. 
Biol.. 38 Bd., 1899. 

Lubarsch: Fettdegencration u. Fettinfiltration. Ergebn. d. allg. Patlı., iii.. 1N97. 

Lukjanow: Vorles. über die allgem. Path. der Zelle, Leipzig, 1893. 

Lummert: Thicrische Fette. Pfliger’s Arch., 71 Bd., 1898. 

Michaelis: Milchseeretion. Arch. f. mikr. Anat., 51 Bd., 1898. 

Runge: Die Krankheiten der ersten Lebenstage (acute Fettdegeneration), Stuttgart, 
1893. 

Sacerdotti: Knorpelfett. Virch. Arch., 159 Bd.. 1900. 

Sata: Fetthildung durch verschiedene Bakterien. Chl. f. allg. Path., xi., 1900; Ueber 
das Vork. von Fett in der Haut u. in einigen Drüsen. Beitr. v. Ziegler, xxvii. ; 
Fett in patholog. Geweben, ib., xxviii., 1900. 

Schmaus: Vork. d. osmirten Fettes in d. Leber bei Phosphorverg. Münch. med. 
Woch., 1897. 

Schulzen u. Riess: Stoffumsatz bei Phosphorvergiftung. Ann. d. Charité-Kranken- 
hauses, XV. 

Starke: Ueber Fettgranula. Arch. f. Anat. u. Phys., 1895. 

Steinhaus: Morphologie der Milchabsonderung. Arch. f. Anat., 1892. 

Taylor: Lipogenesis. Amer. Journ. of Med. Sc., 1899; Journ. of Exp. Med., 1899; 
On Fatty Degeneration. Journ. of Med. Res., 1908. 

Unna: Nachweis d. Fettes in der Haut. Monatsh. f. prakt. Derm., 1898. 

Weber, H.: Fettige Entartung des Herzens. Virch. Arch., 12 Bd., 1857. 

Wentscher: Eireuleben menschl. Epidermiszellen. Beitr. v. Ziegler, xxiv., 1898. 

Werhowsky: Wirkung erhöhter Eigenwärme. Beitr. v. Ziegler, xviii., 1895 (Lit.). 

Weyl u. Apt: Fettgehalt pathologischer Organe. Virch. Arch., 95 Bd., 1884. 

Ziegler u. Obolonsky: Arsenikvergiftung u. Phosphorvergiftung. Beitr. v. Ziegler, 
ii., 1888. 


x 58. The fats which occur in the human body consist almost entirely 
of a mixture of the glycerin-esters of oleic, palmitic, and stearic acids 
which are designated olein, palmitin, and stearin. The first is fluid at 
ordinary temperatures, the second melts at 46°, the third at 53° C. 
Since the body-fats contain varying proportions of olein, palmitin, and 
stearin, they vary in consistency and melting-point. As fat is not solu- 
ble in water or watery fluids, the fat in the body, either free or enclosed 
within cells, is not dissolved in the tissue-fluids. At most, only traces 
of it are dissolved in the blood, lymph, chyle, and bile, which contain 
small amounts of soaps. If after death the fat-containing tissues of the 
body are cooled below the melting-point of the contained fat, the stearin 
and palmitin may separate and form fine stellate or feathery needles 
(Fig. 68, b, e, d), which are commonly called margarin needles, and 
which, according to the conditions, are found sometimes in fat-cells, at 
other times free in the tissue-fluids. 

Cholesterin oecurs in the form of delicate rhombic plates (Fig. 68, 
a), the edges and corners of which are often notched. These may be 
found wherever there are formed masses of detritus containing fat, aris- 
ing from degenerating cells or extravasations of blood, as in the diseased 
tunica vaginalis of the testis, in a dilated sebaceous duct or gland, or in 
a softened area of degeneration in the wall of a diseased aorta. When 
the substance in which the cholesterin plates are formed is fluid, these 
may often be visible to the naked eve as little glistening scales. 

Cholesterin is a constant constituent of the bile, and is furnished by 
the mucous membrane of the gall-bladder and bile-ducts, and held in 
solution by the bile salts and soaps. It is found also in the medulla of 


CHOLESTERIN, GLYCOGEN. 199 


the nerve-fibres, and in small amounts in the blood, where it is held in 
solution by fats and soaps. According to Burchard traces of cholesterin 
are found in all the organs. 

Cholesterin is insoluble in water, dilute acids, caustic alkalies, and 
cold alcohol; it is soluble in boiling alcohol, ether, chloroform, and 
benzol. 

When treated with a mixture of five parts of concentrated sulphuric 
acid and one part of water the edges of cholesterin erystals take on a 
carmine-red color, which gradually passes into violet. Sulphuric acid 





Fic. 68.—a, Cholesterin plates; b, free cluster of margarin needles; c, needles enclosed within fat-cells ; 
d, grass-like bunch of margarin needles. X 300. 


and water mixed in the proportions of three to one give a violet color to 
the edges of the crystals. Concentrated sulphuric acid containing a trace 
of iodine colors the crystals violet, blue, green, and red. 

. The origin of cholesterin is not known with certainty. It is probable 
that it is an intermediate product in the decomposition of albumin. Cor- 
responding to this view, it is found under those pathological conditions 
in which albuminous substances break down with the formation of fat. 


Literature. 


(Cholesterin. ) 


Hoppe-Seyler. Handb. d. physiol. u. path.-chem. Analyse, v. Aufl. 
Munk: Art. Cholesterin. Eulenburg’s Realencyklop. u. Eulenburg’s Jahrbuch, i., 
1891. 


Vil. The Deposit of Glycogen. 


£59. Glycogen is a carbohydrate which is readily convertible into 
sugar; and in the body is formed chiefly from the carbohydrates of the 
food, but may also be formed from albumin and gelatin. 

In the tissues of the body glycogen is found as a hyaline substance, 
most often within the cells, but occasionally in the tissue-spaces. It 
usually occurs in the form of spherules of different sizes. In the cells 
these spherules are most frequently found in the neighborhood of the 
nucleus. 

Glycogen is soluble in water, but the solubility of that found in dif- 
ferent tissues varies (Langhans); that found in the liver, kidneys, mus- 

13 


200 THE RETROGRADE CHANGES. 


cles, and pus-corpuscles is more easily soluble than that of cartilage 
cells and surface epithelium. Fixation of the tissue in alcohol renders 
the glycogen less soluble in water. After death the glycogen of the 
liver is quickly converted into sugar through the action of a diastatic 
ferment. 

Glycogen becomes brownish-red when treated with iodine. In order to 
avoid the solution in water of the glycogen contained in fresh prepara- 
tions, a syrupy mixture of gum and iodine (Ehrlich), or glycerin to 
which iodine has been added (Barfurth) may be used when it is desired 
to test for this reaction. Sections of tissues fixed in alcohol give best re- 
sults (Langhans) when treated with dilute tineture of iodine (one part 
tincture of iodine, four parts absolute alcohol), and cleared with oil of 
origanum, In which the reaction remains preserved for a long time. 

Glycogen is present in almost all the tissues of the embryo, also in 
the fietal membranes at an early period of development; and in the 
adult body in the liver-cells, muscles, heart-musele, cartilage cells, epi- 
thelium of the body of the uterus, portio vaginalis and vagina (Lang- 
hans), in the leueocytes, and in the blood-serum (Gabritschewski). 
During starvation the glyeogen of the liver is diminished, and under 
pathological eonditions may wholly disappear. 

In diabetes the epithelial cells of the kidneys show a very rich de- 
posit of glycogen, particularly those of the loops of Henle. In the isth- 
mus of the latter the cells are almost wholly filled with glycogen. If 
this be dissolved out with water, the cells appear as clear vacuoles. In 
the blood of diabetic individuals the glycogen, both the intracellular and 
extracellular, is increased. 

In fresh intlammatory exudates glycogen is present in the pus-cor- 
puscles. According to the investigations by Brault all tumors, careino- 
miata and sarcomata, exhibiting rapid growth contain large amounts of 
glyeogen in their cells, so that these contain large vacuoles. In slowly- 
growing tumors or in those whose growth is at a standstill, or in those 
showing beginning degeneration (fatty), glycogen is not present. The 
tumor-cells form the glycogen, and its presence is not to be regarded as 
an evidence of degeneration, but rather as a sign of good nutrition and 
luxuriant cell-growth. 


Literature. 
(Glycogen, ) 


Barfurth: Histochem. Untersuch. über das Glykogen. Arch. f. mikr. Anat., 25 Bd.., 
INS. 

Brault: Glycogenése dans les tumeurs. Arch. des sc. méd., 1896; La production du 
elycogéene dans les tissus qui avoisinent. Arch. gen. de med., 1899; Le pronostie 
des tumeurs.  L’ceuvre med.-chir.. 1899. 

Butte: La fonction glyeogenique du foie dans quelques maladies. Arch. de phys., 
1891. 

Czerny: Zur Kenntn. d. glykogenen u. amyloiden Entartung. Arch. f. exp. Path., 
35 Bal., 1818. 

Driessen: Unters. über glykogenreiche Endotheiiome. Beitr. v. Ziegler, xii., 1892. 

Ehrlich: Glykogen im diabetischen u. im norm. Organismus. Zeit. f. klin. Med., vi., 
18833, 

Gabritschewski: Glykovenreaction im Blute. Arch. f. exp. Path., 28 Bd., 1891. 

Külz: Glykoren. Festschr. d. med. Fac. Marburg f. C. Ludwig, Marburg, 1891. 

Langhans: (@lvkogen in pathol. Neulfildungen u. Eihäuten. Virch. Arch., 120 Bd. 
IN. 

Marchand: (reschwulst aus quergestr. Muskelfusern mit Glykogen. Virch. Arch., 
100 Bad, 1885. 





202 THE RETROGRADE CHANGES, 


thereby acquire a gelatinous, transparent appearance, may be mentioned 
fibrous connective tissue, also cartilage, bone, adipose tissue, bone-mar- 
row, and sarcomatous tissue. In these tissues it is chiefly the ground- 
substance (Fig. 71, 6) which undergoes mucous change aud is converted 
into a homogeneous, structureless mass. The cells may remain un- 
changed, or may become fatty, or also undergo mucous degeneration. 
In the last event the entire tissue ultimately forms a hyaline mass, in 








Fie. 70. Fig. 71. 
Tro, 70.- Epithelial cells which have undergone mucous degeneration. from a oystadenoma of the ovarı. 
4, Cells showing slight change; b, cells showing marked degree of mucous change. X 400. 


Tia, 71.—Mnoous degeneration of the connective timsue of the sortie valves (osmio acid. giyverin). a. 
us tissue; }, myxomatous tissue. X B60. 


which only scattered fibres of connective tissue, or single cells or groups 
of cells are left to suggest the original tissue. 

The stringy, or gelatinous material, which results from mucous de- 
generation, does not represent a single chemical substance; in it there 
may be found different varieties of mucins as well as of pseudomucins. 

The mucins (submaxillary, intestinal, and tendon mucin) are nitro- 
genous substances somewhat resembling albumin. They dissolve or 
swell up in water forming a stringy, mucous fluid, from which they may 
be precipitated in a stringy form by means of alcohol or acetic acid; but 
differ from the true albumins in the fact that the precipitate is not redis- 
solved in an excess of the acid. The precipitated mucins are soluble in 
neutral salt-solutions, caustic alkalies, and alkaline carbonates; and are 
gradually converted into alkali-albuminates in case of solution by the 
last named. 

All mucins contain nitrogen and sulphur; their content in carbon, 
oxygen, nitrogen, and sulphur varies in the different forms. By proper 
treatment a carbohydrate, ealled animal gum (Landwehr, Hammarsten), 
may be split off from the mueins. For this reason mucin may be called 
a glycoproteid (Pfannenstiel). 

Pseudomucin also dissolves in water, forming @ gelatinous fluid, 
from which it may be precipitated in stringy masses by alcohol. The 
recipitate redissolves in water. Solutions of pseudomucin are not pre- 
tipitated by acetic acid. Boiling with dilute mineral acids leads to the 
splitting-off of a carbohydrate (as is the case with mucin), which reduces 
copper sulphate in alkaline solution (P’fannenstiel). 

Psendomu found particularly in ovarian cystomata, and is the 
cause of the tinons character of the cyst-contenta. It is produced 
by the epithelium of these tumors (Fig. 70); and in its formation the 
same changes take place in the cells, as in the formation of mucin from 
epithelium. In all probability the mucous substance present in gelat- 
inous carcinomata is a body closely related to pseudomucin or metalbu- 
min—that is, there are different varieties of pseadomucin (Pfannenstiel), 
of which the two mentioned are examples. 





























206 THE RETROGRADE CHANGES. 


lium which do not possess the characteristics of mucin. I have, therefore, also classified 
as colloid those epithelial concretions which on account of their reaction with iodine 
(brown or blue color when treated with dilute iodine solutions) have hitherto been re- 
garded as amyloid bodies. If objection is made to the classification of these formations 
as colloid, they may be placed under the heading of epithelial hyalln. 

As epithelial hyalin (keratohyalin’) may be classed also the hyaline granules and 
spherules described by Ruxsel, Klein, and others, and which are found especially in can- 
cer cells. They stain intensely with fuchsin, and also with Gram’s method or with 
Weigert’s fibrin stain. It should be noted further that similar bodies of varying size 
and form have been observed in the epithelium during the development of a vaccination 
pustule (/Zückel), and have been by many regarded as parasites. 


Literature. 
(Colloid. ) 


Biondi: Beitr. z. Structur u. Function d. Schilddrüse. Berl. klin. Woch., 1888. 

Bozzi: Untersuch. über die Schilddrüse. Beitr. v. Ziegler, x viii., 1895. 

Bubnow: Chemische Bestandtheile der Schilddrüse. Zeitschr. f. phys. Chem., viii., 
1883. 

Ernst: Ueber Hyalin u. seine Bezieh. z. Kolloid. Virch. Arch., 180 Bd., 1892. 

Hückel: Die Vaccinekörperchen. Beitr. v. Ziegler, Supplh., 1898. 

Hürthle: Secretionsvorgänge in d. Schilddrüse. Pflüg. Arch. f. d. ges. Phys., 56 Bd., 
1894. 

Klein: Russel-sche Fuchsiukörperchen. Beitr. v. Ziegler, xi., 1892. 

Langendorf: Beitr. z. Kenntn. d. Schilddrüse. Arch. f. An., Supplh., 1889. 

Marchand: Kolloidentartung. Eulenburg’s Realencyklop., 1895. 

Pianese: Histol. u. Aetiol. d. Carcinoms. Beitr. v. Ziegler, Supplh., 1896. 

Podbelsky: Kolloid in den Lymphgef. d. Schilddrüse. Prager med. Woch., 1892. 

Pratt: Goitre. Ref. Handb. of Med. Sc., 1902. 

v. Recklinghausen: Ally. Pathol. des Kreislaufs u. der Ernährung, Stuttgart, 1288. 

Reinbach: Bildung des Kolloids in Strumen. Beitr. v. Ziegler, xvi., 1894. 

Russel: Characteristic Organism of Cancer. Brit. Med. Journ., ii., 1890. 

Virchow: Die krankh. Geschwülste, iii. Bd.. und Ueber d. eigenthüml. Verhalten al- 
buminöser Flüssigkeiten bei Zusatz von Salzen. Vi. Arch., 6 Bd., 1854. 

Wölfler: Der Bau des Kropfes, Berlin, 1883. 





X. The Pathological Cornification of Epithelium. 


$ 62. The cornification of the surface epithelium over the entire 
skin is a physiological process, characterized essentially by the fact that 
the cells in the outer strata of the prickle layer of the stratum germina- — 
tirum undergo a horny change. This cornifieation takes place first at —~—® - 
the periphery of the cells and in the processes binding the cells together, nd 
while at the same time the inner portions of the cell and the nucleus —== ! 
shrink, so that the cells become changed into thin, flat, horny scaies. 
This horny substance or keratin is a very resistant modified albuminoid 
body of homoge neous composition, and is capable of resisting digestion 
by the gastrie or pancreatic juices. 

As accompanying phenomena of cornifieation there appear in the cells = * 
of the prickle layer “peculiar hyaline granules and spherules resembling Ss 
colloid, which stain intensely with nuclear stains and are known as kera- a 
tohyalin (Waldever). In those areas of the skin possessing a thick horny — 
laver, there is formed a.sharply limited layer of such keratohyalin-con- 
taining cells; this layer is known as the stratum granulosum. In those= = 
places where the horny layer is thin, the stratum granulosum is imper- 
fectly developed and exhibits breaks of continuity. 

Pathological cornification may oceur, in the first place, as a wide- 
spread or localized increase of the horny layer, resulting in a conditiom 
of hypertrophy of the horny layer of the epidermis (see Chapter VI., § 77), 








— th 





CORNIFICATION. 207 


or hyperkeratosis. This phenomenon may be primary—that is, due to 
intrinsic causes inherent in the anlage of the skin (ichthyosis, lichen 
pilaris)—or may be acquired as the result of external intluences, mechani- 
cal lesions, infections and inflammations (callosities, corns). Further, 
there may occur disturbances in the process of cornification of the skin, 
so that certain pathological manifestations recognizable by the naked 
eye may make their appearance, such as desquamation of theskin. Such 
changes are included under the term parakeratoses. They occur especially 
as sequel® or concomitant phenomena of infections of the epidermis, and 
of inflammations of the corium and papillary body, sometimes without 
any recognizable cause; and in these cases either the process of cornifica- 
tion or of the formation of keratohyalin, or both, is disturbed. 

Finally, pathological cornification often occurs in regions where normally 
it either does not occur at all or but to a slight extent. In the skin the cor- 
nification may extend to the ducts of the sebaceous glands and to the 
hair-follicles (ichthyosis) or to the sweat-glands (porokeratosis). Fur- 
ther, pathological cornification occurs not infrequently in the mucous 
membrane of the mouth, giving rise to white thickenings of the epithe- 
lium or to hair-like formations (hairy tongue). Horny change may be 
observed also in the mucous membrane of the middle ear, in the mastoid 
cells, in the descending urinary passages (formation of cholesteatomata), 
and in these places it may lead to the formation of shining white scales. 

Cornification of cancer cells is not infrequently seen, particularly in 
cancers of the skin, in whieh the horny scales are found usually in the 
form of round masses resembling onions or pearls. Similar horny prod- 
ucts are also found in cholesteatomata of the pia and brain. 

The pathological formation of horny substance in the mucous mem- 
branes or in tumors takes place either simply through cornification of the 
cell-membranes with contraction of the cell, or it may be combined with 
the formation of keratohyalin as in the case of typical cornification. 
The formation of keratohyalin and the cornification of epithelial cells 
often occur irregularly distributed, particularly in cancers. 


According to the view of Mertsching and Ernst, the granules of keratohyalin are 
derived from the nucleus, and represent chromatin which has escaped from the nucleus. 
In favor of this view is the fact that the nuclei lose their chromatin simultaneously with 
the appearance of the keratohyalin. 


Literature. 


Cornification. 


West: Verhornung des Bindehautepithels. Beitr. v. Deutschmann, 34 H., 1898. 

Wostriém: Piale Epidermoide. Cbl. f. allg. Path., viii., 1897. 

Wrosin: Die schwarze Haarzunge, Leipzig, 1888. 

Wenoir: De la langue noire, Paris, 1878. 

Winkler: Schwarze Haarzunge. Virch. Arch., 118 Bd., 1888. 

“Ernst: Bezieh. d. Keratohyalins zum Hyalin. Virch. Arch., 180 Bd., 1892 (Lit.); 
Normale Verhornung. Arch. f. mikr. Anat., 47 Bd., 1896; Pathol. Verhornung. 
Beitr. v. Ziegler, xxi., 1897 (Lit.). 

aug: Das Cholesteatom d. Mittelohrräume. Cbl. f. allg. Path., vi., 1895. 

3 h: Porokeratosis. Arch. f. Derm., 39 Bd., 1897. 

eloir: Leukoplakie buccale. Arch. de phys., x., 1887. 

Mertsching: Keratohyalin u. Pigment. Virch. Arch., 116 Bd., 1889. 

Wehrkorn: Meningeale Perlgeschwulst. Beitr. v. Ziegler, xxi., 1897. 

Posner: Schleimhautverhornung. Virch. Arch., 118 Bd., 1889. 

Unna: Handb. d Hautkrankheiten, Leipzig, 1883; Die Histopathologie der Haut- 
krankheiten, Berlin, 1894; Wesen der Verhornung. Münch. med. Woch., 1896. 
Wassmuth: Hyperkeratosis diffusa. Beitr. v. Ziegler, xxvi., 1899. 














212 THE RETROGRADE CHANGES. 


it is but rarely observed. In rare cases the degeneration occurs without 
being associated with any of the above-mentioned diseases. 

According to investigations by Czerny, Krawkow, Lubarsch, David- 
sohn, Maximow, Nowak, Petrone, and Schepilewsky amyloid may be 
produced experimentally in the spleen, liver, kidneys, and intestines of 
various animals, rabbits, chickens, doves, mice, and dogs, through the 
production of suppurations lasting several weeks, Suppurative processes 
caused by staphylococci and oil of turpentine appear in particular to 
favor the formation of amyloid. In a number of cases amyloid was also 
successfully produced through injections of decomposed bouillon, dead 
cultures of staphylococci, rennet-ferment, and pancreatin (Schepilew- 
sky), when the inflammation produced by these agencies ran a somewhat 








Section of an umylold kidney. (Müller's Auld. osmic arid, methyl violet.) a, Normal vasra- 

oops: D.amylold vascular loops, ,{aity glomerular eplibellum : ey. fatty capentar epltheilum: d, fat- 

rope Iring again he outer surface Of the caplary wall: e. ftiy oplinellum en elle; J desqianiat 
fatty epith 2, byaline coagula (cast); I, transvense section of & 

amyloid artery ingot eapiiary #1 eelutar taitradon of un copnective tissue’ me round cele Within 

the tubules. £ 









chronic course. Krawkow observed the beginning of amyloid formation 
after three days, Nowak after eight days. 

The origin of the amyloid substance has not yet been definitely deter- 
mined. The results of experimental investigation vary greatly, the de- 
generation being often absent in cases of chronic suppuration (particu- 
larly in dogs It is probable that the blood brings to the tissues some 








substance which is changed into amyloid at the site of deposit. It has 
been many times shown that as the antecedent of amyloid there is found 
a hyaline substance in the. ti 


sues, which does not give the amyloid reac- 
have been oceasionaily made in mau. The 
rom whieh amyloid arises is fermed, perhaps, by disintegrating 
s or tissue-cells at the seat of the primary disease. 













According to Arwrkor, there are found normally in the artery-wall of the horse, in 
the ligamentum nucixe of cattle, in the stroma of the spleen of calves, and in the mu- 


LOCAL AMYLOID INFILTRATIONS AND CONCRETIONS. 213 


cous membrane of the stomach, combinations of chondroitin-sulphuric acid which are 
closely related to amyloid. 


Literature. 

( Amyloid.) 
Abraham: Ueber eigenthümliche Formen amyloider Entartung. Inaug.-Diss., Frei- 
Burchardt: Amyloidfärbung (Gentianaviolett, Salzsäure). Virch. Arch., 117 Bd., 


Czerny: Zur Kenntn. d. glykogenen u. amyloiden Entartung. Arch. f. exp. Path., 
31 Bd., 1898. 

Davidshon: Exper. Erzeugung von Amyloid. Virch. Arch., 150 Bd., 1897; Erken- 
nung zweier Stadien der Amyloidentartung, ibid., 155 Bd., 1899. 

Eberth: Die amyloide Entartung. Virch. Arch., 80 Bd., 1880. 

Friedreich u. Kekulé: Zur Amyloidfrage. Virch. Arch., 16 Bd., 1859. 

Grandis et Carbonne: Reaction de la substance aınyloYde. Arch. ital. de biol., xiv., 
1891. 

Grigorieff: Resorptionsfähigkeit d. Amyloids. Beitr. v. Ziegler, xviii., 1895. 

Hennings: Zur Statistik u. Aetiologie der amyloiden Entartung. Inaug.-Diss., Ber- 
lin, 1880. 

Hjelman: Studier öfver Amyloidin jurens. Inaug.-Diss., Helsingfors, ref. Cbl. f. 
allg. Path., ii., 1891. 
Jürgens: Eine neue Reaction auf Amyloidkörper. Virch. Arch., 65 Bd., 1875. 
Krawkow: Exper. Erzeug. v. Amyloid. Cbl. f. allg. Path., 1895: Arch. de med. 
exp., 1896: Chemie der Amyloidsubstanz. Arch. f. exp. Path., 40 Bd., 1897. 
Kühne u. Rudnew: Zur Chemie der amyloiden Entartung. Virch. Arch., 33 Bd., 
1865. 

Kyber: Die amyloide Degeneration, Dorpat, 1871; Virch. Arch., 81 Bd., 1880. 

Levene: (Chondroidin-sulphuric Acid), Med. Rec., 1900. 

Lindemann: Jodschwefelsäurereaction u. Amyloid (Krystalle). Cbl. f. allg. Path., 
1897. 

Lubarsch: Exper. Erzeugung von Amyloid. Virch. Arch., 150 Bd., 1897; Hyaliue 
u. amyloide Degen. Ergebn. d. allg. Path., iv., Wiesbaden, 1899. 

Maximow: Experimentell hervorger. Amyloidentartung. Virch. Arch., 153 Bd., 


1898. 

Neumann. Ueber Amyloiddegeneration des Fettgewebes. Centralbl. f. allg. Path., 
i., 1800. 

Nowak: Aetiologie der Amyloidosis. Virch. Arch., 152 Bd., 1898. ’ 


Petrone: Degen. amyloide expérimentale. Arch. de méd. exp., 1898. 

Babe: Amyloidentartung bei Thieren. Jahresber. d. K. Thierarzneischule z. Han- 
nover, 1883-84. 

Schepilewsky: Exper. Erzeugung amy loider Degeneration. Cbl. f. Bakt., xxv., 1899. 

Tschermak: Stellung d. amyloid. Subst. Zeitschr. f. phys. Chem., xx., 1875. 

Virchow: Ueber eine im Gehirn und Rückenmark des Menschen aufgefundene Sub- 
stanz mit der chemischen Reaction der Cellulose. Vir. Arch., 6 Bd., 1854. 

Wichmann: Die Amyloidentartung. Beitr. v. Ziegler, xiii., 1893. 

Ziegler: Amyloide Tumorbildung in der Zunge und im Kehlkopf. Virch. Arch., 65 
Bd., 1875. 


§ 64. The form of amyloid degeneration just considered is a disease, 
which usually appears as a multiple affection of several organs, or, if 
confined toa single organ, appears as a diffuse change extending through- 
out the whole organ. There is, however, a localized form of amyloid 
deposit, appearing either as a local amyloid infiltration of the tissues or in the 
form of free concretions. 

The local amyloid infiltrations occur in part in very cellular granu- 
lations (conjunctiva) and in tissues showing chronic inflammatory proc- 
esses; and in part in sears and in hyperplastic proliferations of connec- 
tive tissue. They are also found occasionally in tumors in which other 
retrograde changes have begun. In certain cases only small deposits are 
found in the affected tissues, usually in the vessel-walls. In other cases 


214 THE RETROGRADE CHANGES. 


larger nodules consisting almost wholly of amyloid may be formed, and 
these may acquire a wooden hardness, 

Here also the amyloid substance is deposited in the ground-substance of the 
tissue; but it has been claimed by some authors (Rählmann) that the 
cells of the tissue may acquire a hyaline appearance and give the amy- 
loid reactions. 

Such local formations of amyloid have been found in the inflamed 
conjunctiva, in syphilitic scars of the liver, tongue, and laryusx, in in- 
flamed lymph-glands, ulcers of bone, and in tumors of the larynx and 
stomach. Tumor- nodules of amyloid also occur in the conjunctiva, 
tongue, larynx, and trachea under conditions in which it is impossible 
to establish any relationship between them and inflammatory processes, 
and where besides the hyaline masses there is but: little normal connec- 
tive tissue present. According to Manasse such tumors may arise also 
from sarcoma-like proliferations. 

Free amyloid concretions or corpora amylacea occur most frequently 
in the tis f the central nervous system, especially in the substance 
cord, and in the ependyma of the ventricle. They are 
found also in the prostate. In the 
nervous system they appear as 
small (Fig. 82, ec), dull-shining, 
mostly homogeneous bodies, more 
rarely consisting of a nucleus and 
an outer shell (Redlich); in the 
prostate they form larger (Fig. 82, 
«) bodies which usually show a dis- 
tinct stratification. Corpora amy- 
lacea have also-been found in car- 

cinomata (Wagner, Langhans), and 
©, have been repeatedly observed in 
© @ he lung (Friedreich, Zahn, Zieg- 
® ler), where they occur in intlam- 
@ ce matory areas, hemorrhagic extra- 
vasations (b), and in emphysema. 
; The local deposits of amyloid and 
ee AOL, Corpus amsincenn {NE free amyloid concretions cannot be 
hoetorriagie encarta toe ung sit regarded as being wholly of the same 
Corpora ainylucea from the spinal card, > 400, nature as the progressive amyloid de- 
generation of connective tissue. Some 
of them indeed give characteristic amyloid reactions, and the corpora 
amylacea of the nervous system, in particular, become blue when treated 
with iodine and sulphuric acid. But, in the case of these bodies, we 
have to do with formations which are dependent essentially upon local 
conditions for their origin; and which are derived in part from epithe- 
lium, and in part from connective-tissue cells. They are, therefore, to 
be regarded partly as modified epithelial hyalin (3 61), and partly as 
modified connect issue hyalin ($ 66). The prostatic concretions are 
formed through the fusion of 1 »s of degenerating epithelial cells or 
of fragments of the same (epithelial colloid, § 61); and the simiiar bodies 
found in the Jungs and in tumors are composed essentially of the pro- 
ducts of disintegrated cells, though in part also of albumin derived from 
the blood. Redlich considers the corpora amylacea of the nervous sys- 
tem, which stain deeply with hematoxylin, to be derived from the nuclei 
of the neuroglia-cells, and to represent a senile retrograde change of 
































































HYALIN. 215 


the tissue. On the other hand, according to Stroebe, they are formed 
from fragments of swollen axis-cylinders, while by Siegert they are be- 
lieved to be of cellular origin. 


Literature. 
(Zocal Formation of Amyloid and Amyloid Concretions.) 


Burow: (Larynxtumoren.) v. Langenbeck’s Archiv, xviii., 1867. 

Ceci: Corpusculi amilacei dell’ encefalo e midollo spinale. Atti de Lincei, ix., 1881. 

Eiger: Zur Aınyloidfrage. Chi. f. allg. Path., xi., 1900. 

Friedreich: Corpora amylacea in den Lungen. Virch. Arch., 9, 10 Bd., 1856. 

Fumagalli c Krach: Degen. amiloide della congiuntiva. Arch. per le Sc. Med., xix., 
18495. 

Glockner: Tumorförmiges Amyloid d. Larynx. Virch. Arch., 160 Bd., 1900. 

Grawitz: (Nase und Luftréhre des Pferdes.) Virch. Arch., 94 Bd., 1883. 

Hildebrand: Corpora aınylacea in einem endostalen Sarkom. Virch. Arch., 140 Bd., 
1895. 

Hippel: (Augenlid.) Arch. f. Ophthalm., 25 Bd. 

‚Kraus: (Zunge, Augenlid, Trachea, Leber.) Zeitschr. f. Heilk., vi., 1885; vii., 1886. 

Langhans: Corpora amylacea der Lunge. Virch. Arch., 38 Bd., 1867. 

Leber: (Augenlid). Arch. f. Ophthalm., xix. and xxv. 

Manasse: Tumorförmiges Amyloid des Larynx. Virch. Arch., 159 Bd., 1900. 

Posner: Ueber Prostataconcretionen. Zeitsch. f. klin. Med., 16 Bd., 1889. 

Rahlmann: (Augenlid.) Arch. f. Augenheilk., x.; Virch. Arch., 87 Bd., 1882. 

Redlich: Die Amyloidkörperchen des Nervensystems. Jahrb. f. Psych., x., 1891. 

Rumschewitsch: Hyaline u. amyloide Entartung d. Bindehaut. Arch. f. Augenh., 
25 Bd., 1892. 

Schmidt: Amyloidtumoren d. Zunge. Virch. Arch., 143 Bd., 1896. 

Siegert: Unters. üb. d. Corp. amylacea. Virch. Arch., 129 Bd., 1892. 

Stilling: Entstehung von Concrementen der Prostata. Virch. Arch., 98 Bd., 1884. | 

Stratz;: Amyl. Degen. e. Uteruspolypen. Zeitschr. f. Gebh., xvi., 1889. 

Stroebe: Iteparat. Vorgänge bei Heilung von Rückenmarkswunden. Beitr. v. Zieg- 
ler, xv., 1894. 

Vossius: Amyloide Degeneration der Conjunctiva. Beitr. v. Ziegler, iv., 1889. 

Zahn - Corpora anıyloidea der Lung: Virch. Arch., 72 Bd., 1878. 

Ziegler: Amyloide Tumoren der Zunge und des Kehlkopfs. Virch. Arch., 65 Bd., 
1875. 


XII. Hyaline Degeneration of Connective Tissue and the: Hyaline 
Products of Connective-tissue Cells. 


§ 65. Under the head of hyaline degeneration of connective tissue 
may be grouped those changes in which the fibrous ground-substance of the 
connective tissue of the blood- vessels acquires a hyaline character without giving 
the specific reactions of amyloid (Fig. 83). The change may involve nor- 
mal connective tissue (Fig. 83), or that altered by inflammation, as well 
as the newly formed connective tissue of inflammatory new-growths and 
of tumors. It is dependent partly upon local and partly upon general 
disturbances of circulation. Hyaline degeneration is found most often 
in the connective tissue of the thyroid (Fig. 83, 6); the valvular endo- 
cardium; intima of the arteries; the entire wall of the smaller vessels, 
particularly of the brain and spinal cord; the lymph-glands (Fig. 85, a, 
b); glomeruli of the kidney; the connective tissue and blood-vessels of 
connective tissue tumors of the dura mater (psammoma), parotid, and 
submaxillary glands (angiosarcoma); the connective tissue of corneal 
sears; the peripheral portions of tuberculous nodules; the connective 
tissue of tuberculous tendon-sheaths and bursz mucose (Fig. 84, b). 

Hyaline degeneration of connective tissue possesses no specific staining 





HYALINE DEGENERATION OF CONNECTIVE TISSUE. 217 


part. It may therefore be assumed that there is a form of hyaline de- 
generation of the connective tissue, which is closely related to amyloid, 
and may become changed into the latter (see § 63); and that it arises 





Fig. &. Fra. 86. 
Fig. &,—Hyaline degeneration of the blood-vessels of ic axillary Iymph-gland. (Alcobol, 
Carmine) te Hyaline vowel with open Lumen; I ohllermed vamcl. x 


Fra, 88.-Hyaline degeneration of the connective tissue of the myocardium: (Alcohol, beematoxylin, 
carmine.) a, Normal connective thwue; 2, hyaline connective tissue; c, hyaline masses; d, transve 
section of normal muscle-cells, of atruphic (e). X 250. 


through the deposit of a hyaline insuluble albuminous body which is 
probably derived from the blood. 


The preparation shown in Fig. 86 was taken from the heart of a woman of fifty- 
five years of age, the greater part of the heart-wall presenting a hyaline degeneration, 
In both endo- and pericardium there were numerous hyaline nodules and flattened 
masses. The muscle tissue was in part degenerated, as shown in the figure. Associ- 
ated with this condition there was extensive degeneration of the blood-vessels, par- 
ticularly of the intestines, tongue, lungs, heart, and urinary bladder. The peritoneum 
was also thickly covered with hyaline nodules. The fact that the small areas and the 
periphery of tle larger ones gave no iodine-reaction, while the central portions of the 
larger areas did so, appears to point conclusively to. close relationship between hyaline 
degeneration and amyloid. This is further supported by the fact that amyloid organs 
occasionally contain areas of hyaline degeneration which give no iodine reaction. 














Literature. 
(Hyaline Degeneration of Connective Tissue.) 


Alsheimer: 3, Kolloidentartung des Gehirns. Arch. f. Psych., xxx., 1898. 

Arndt: ung der Hirngefässe. Virch. Arch.. 41 Bd.. 1867. 

Best: even ato mnAlirungsstdrungen (hyaline Concretionen) bei bandförmi- 
ger Hornhauttrübung, Hamburg, 1900. 

Billroth: Beitrage zur pathol. Histologic, 1858. 

‘Birch: Hirschfeld: Degenerat. Processe in Hornhautnarben. Gracfe's Arch., 48 Bd., 


Bringen; livatine Entartung d. Hirngefässe. Vierteljahrsschr. f. prakt. Heilk., 
875. 
Ernst: fi alin u. seine Beziehungen zum Kolloid. Virch. Arch., 180 Bd., 1892. 
Grawite: Amyl. u. hyal. Neubildung in d. Nasenschleimh. e. Pferdes. Virch. Arch., 
Holschewnikoff: Hyal. Degen. der Hirngefässe. Virch. Arch, 
Lubarsch: Albuminöse Degenenitionen. Ergebn. d. allg, Patl 
Lubimoff: Kolloiddegeneration dl. Hirngefüsse. Arch. 
Oeller: Hyal. Gefssdeg, im Auge (Bleivergiftung). . 
Bählmann: Iiyaline u. amyloide Deg. d. Conjunet. Virch. Arch., 87 Bil. 1882. 
v Becklinghausen Patholo; Kreislaufs u. der Ernährung, Stuttgart, 1883. 
Bumschewitsch: Amy]. u. hyaline Degen. d. Bindehaut, Arch. f. Augenhk., 25 
1. 1802. 














112 Ba. 
1895. 











218 THE RETROGRADE CHANGES. 


Stilling: Amyloide u. hyaline Degen. d. Milz. Virch. Arch., 103 Bd., 1886. 
Vossius: Hyaline Degeneration d. Conjunctiva. Beitr. v. Ziegler, v., 1889. 
Wieger: Hyaline Entartung der Lymphdrisen. Virch. Arch., 78 Bd., 1879. 

v. Wild: Amyloide u. hyal. Degen. d. Bindegewebes. Beitr. v. Ziegler, i., 1886. 
Ziegler: Ursachen d. Nierenschrumpfung. Deut. Arch. f. klin. Med., 25 Bd., 1878. 


8 66. Hyaline products of connective-tissue cells arise in the first 
place from spherical masses of flat connective-tissue cells arranged in con- 
centric layers, which, in a manner similar to the cornification of epi- 
thelial cells, become changed into a hyaline substance containing no nuclei. 
These formations occur most frequently in the meninges, the chorvid 
plexus, and the pineal gland, and in the new-growths arising in these re- 
gions. Through subsequent calcification they lead to the formation of 
laminated concretions of calcium salts (see § 67, Fig. 92). . 

Another kind of hyaline formation probably owes its origin to asecre- 
tory activity of the connective-tissue cells. This may be designated 
secretory connective-tissue hyalin, but it must be noted that under this term 
there is included a variety of different formations, and that, as in the 
production of colloid, the cells as a whole may be converted into hyaline 
products. In this category may be placed first the so-called granules 
(granula)—that is, the small granules which are found in the proto- 
plasm of certain leucocytes, and also in many connective-tissue cells in 
both normal and inflamed, or otherwise altered, or proliferating tissues. 
Some of these granules are oxyphile, and stain especially with eosin, so 
that they have been designated eosinophile cells. Others stain intensely 
with basic stains, and are usually designated as mast-cells (Ehrlich). In 
both forms of cells the granules may be so numerous as to convert the 
cells into granule-spheres. 

Further belong here certain granules and spherules of hyaline ap- 
pearance which stain especially intensely with fuchsin, though staining 
also with methyl violet, gentian violet, etc.; and which are known as 
fuchsinophile bodies. They are also often called Russel’s bodies from the 
fact that they were described closely by Russel, who regarded them as 
parasitic fission-fungi. In the sand-tumors of the meninges the ante- 
cedents of the caleareous granules may be represented by intracellular 
hyaline spherules. 

Fuchsinophile bodies are found both in normal and in slightly altered 
tissues (adrenals, various mucous membranes—as that of the stomach 
in the brain, spleen, and lymphadenoid tissues), also in inflamed tissues 
(particularly the mucous membranes, for example, of the stomach), in- 
flammatory new-growths (polypi of the stomach), and in connective- 
tissue tumors. They are partly intracellular, sometimes in great num- 
bers, and partly extracellular. They are to be regarded as cell-products, 
probably of the nature of a cell-secretion, or formed as the result of the 
disintegration of the cells. Of their genesis and their composition noth- 
ing definitely is known; it is possible that they have a close relationship 
with the mast-cells. Those oceurring iu the brain and spinal cord are 
generally classed with the corpora amylacea (§ 64), even when they give 
no specific jodine reaction. 

Finally, there should be considered in this connection the larger hya- 
line spherules and casts of tubes (changed blood-vessels) resembling epithe- 
lial colloid, which are not infrequently seen in sarcomata (see Endothe- 
lioma and Angiosarcoma), inasmuch as these formations are also to be 
regarded as products either of a seeretory or of a degenerative process on 
the part. of cells. 





HYALINE PRODUCTS: CELL-GRANULES. 219 


The significance of the granules of eosinophile and mast-cells, as well as the neu- 
trophile granules of the leucocytes (which stain with a neutrak dye obtained through a 
mixture of acid fuchsin and basic methyl green), cannot be positively stated at the 
present time. Ehrlich, Heidenhain, and Zöwit regard the granules of the leucocytes 
as secretory products of a specific metabolism of the cells in which they are found, so 
that these cells may be looked upon as unicellular glands. By some writers (Broreiez, 
Baudnitz) the so-called mast-cells are regarded as degeneruting-cells, others (Neumann) 
Jook upon them as representing a stage in the development of proliferating cells, while 
others still (Zhrlich, Rosenheim, Korybutt-Daszkiewicz) believe that they are simply cells 
which have received an excess of nutriment. 

Arnold regards the cell-granules which may be demonstrated by means of especial 
stains in leucocytes, pus-corpuscles, bone-marrow cells, and also in other cells, not as 
granules of secretion, but as representing changed structural elements of the cells aris- 
ing out of a metamorphosis of the plasmosomes—that is, the microsomes of the cell- 
cytoplasm (see 881). Acidophile cells may be transformed into basophile, or the reverse 
may occur; these phenomena ure to be regarded as the expression of different stages 
of development with changes in the physico-chemical properties. 


The formations described in &§ 65 and 66 as connective-tissue hyalin are undoubtedly 
pathological products, which differ from each other in so far as their mode of origin and 
their chemical composition are concerned. Since we do not yet know the nature of the 
processes leading to these hyaline formations, there is nothing to do but to group them 
according to definite points of view. 

Von Recklinghausen gives to the term hyalin a much more comprehensive meanin 
than Ido. He includes under the head of hyaline degeneration different pathologica 
changes which I have placed under other heads. He defines hyalin as an albuminous 
body which stains intensely with eosin, carmine, picrocarmine, and acid fuchsin; is 
homogeneous and strongly refractive; is but slightly changed by acids; and in its re- 
sistance to alcohol, water, ammonia, and acids resembles amyloid, but does not give the 
iodine reaction. As hyalin he includes epithelial colloid and the hyaline products of 
connective tissue cells, as well as hyaline degeneration of the ground substance of the 
connective tissue, also hyaline thrombi, and the hyaline coagula of inflammatory exu- 
dates, and hyaline tissue-necroses. According to this author, all these formations result 
from the fusion of the elements of neighboring cells. From their external appearance, 
all these products may be properly designated Ayalin ; but the following varieties must 
be recognized: epithelial hyalin (colloid, keratoliyalin), connectire-tissue hyalin (hyaline 
degeneration of the ground-substance of connective tissue, hyaline products of cells, and 
cells which have become hyaline), blood-hyalin (hyaline thrombi), erudatice hyalin (hya- 
line coagula of exudates on mucous membranes, serous surfaces, inflamed conuective 
tissue, in the urinary tubules, tubercles, etc.), and hyaline tissue-necroser. In the case 
of connective-tissue hyalin a distiuction must be made between the hyalin formed as a 
secretion in the cells (closely related to epithelial colloid, in its mode of origin), and 
hyaline degencration of the ground-substance of connective tissue. 


Literature. 


(Hyaline Products of Connective-tissue Cells and Leucocytes ; Cell-granules. ) 


Altmann: Die Elementarorganismen u. ihre Beziehungen zu den Zellen, Leipzig, 1890. 

Arnold: Ueber Granulafärbung lebender Leukocyten und Gewebe. Virch. Arch., 157 
Bd., 1899; 159 Bd., 1900; Farbenwechsel der Zellgranula. Cbi. f. allg. Path., 
x., 1899; Vitale Granulafärbung in Knorpelzellen, Muskelfasern, und Ganglienzel- 
len. Arch. f. mikr. Anat., 55 Bd., 1900. 

Ballowitz i Ehrlich’sche granulirte Zellen bei winterschlafenden Thieren. An. Anz., 
vi., 1891. 

Browicz: Sur les celles granuliféres d’Ehrlich. Bull. de l’Acad. des sciences de 
Cracovie, 1890. 

Ehrlich: Physiol. u. Pathol. d. versch. Formen d. Leukocyten. Zeitschr. f. klin. Med., 
i., 1880; Granulirte Bindegewebszellen u. cosinophile Leukocyten. Arch. f. 
Anat., Phys. Abth., 1879; Untersuch. z. Histologie d. Blutes. Gesch. Mittheil., i., 
1891. 

Galeotti: Die Granulationen in d. Zellen. Monatsschr. f. Anat., xii., 1895. 

Goldmann: Malignes Lymphom. Cbl. f. allg. Path., ini., 1892. 

Hansemann: Hyaline Zellen in Magenpolypen. Virch. Arch., 148 Bd., 1897. 


14 


220 THE RETROGRADE CHANGES. 


Heidenhain: Histol. u. Physiol. d. Dünndarmschleimhaut. Pfliger’s Arch., 23 Bd., 
Suppl., 1888. 
Elien: Russel’sche Fuchsinkdrperchen u. Altmann’sche Granula. Beitr. v. Ziegler, 





xi., 1892, 

Löwit: Neubildung u. Beschaffenheit d. weissen Blutkörperchen. Beitr. v. Zi 
x.. 1891. 

Lubarach: Fuchsinkörper u. Corp. amylacen. Ergebn. d. allg, Path. 1995, 

Marwedel: Verind, d. Knocheumarks bei eiterig. Entzünd. ‘Beitr. v. Ziegier, xxiii, 
1897. 

Neumann: Mastzellen bei path, Veränd. im Gehirn. Virch. Arch., 122 Bd., 1890. 

Prus: Fuchsinophile Degeneration. Cbl. f. allg. Path., vi., 1886. 

Ranvier: Traite technique d’histologie, Paris, 1875-1888. 

Rosenheim: Mastzellen im ystem. Arch. f. Paych., 17 

Russel: Characteristic Organi Brit. Med. Journ., ii., 1890. 

Baltikow: Iyaline Körper in Magenpolypen u. and. Gew. Virch. Arch., 153 Bd., 
















1808. 

Sanfelice: Experim. Erzeugung d. Russel’schen Körperchen. Cbl. f. Bukt., xxiii., 
1898. 

Tettenhammer: Entstehung d. acidophilen Leukocytengranula. Anat. Anz., viii., 
1893. 


Thorel; Hyaline Körper in Magen- u. Darmschleimhaut. Virch. Arch., 151 Bd., 1898. 
Touton: Russel'sche Fuchsinkörp. u. Goldmann’sche Kugelzellen. Virch. Arch., 132 


Ba., 1883. 
‘Wolff: Bedeutung der cosinophilen Zellen. Beitr. v. Ziegler, xxviii., 1900 (Lit.). 
See also $ 65. 


+ XIII. Petrifaction of the Tissues and the Formation of Concretions 
and Calculi. 


§ 67. It is, on the whole, of rather frequent occurrence for firm erys- 
talline, or amorphous, granular masses to be deposited in various parts 
of the body-tissues; and when such deposits are of such extent as to 
cause hardening of the 
affected tissue, the result- 
ing condition is known 
as petrifaction, or when 
the deposit consists of 
lime-salts (particularly 
phosphates) as calcifica- 
tion. . 

The deposit may 
occur, in the first place, 
in a tissue which forms 
an integral element of 
an organ, and which 
bears its normal relation 
to the surrounding ti: 
sues. In other cases it 
takes place in portions 
of tissue which have 
been loosened from their 

« f surroundings; or insol- 

‚a, 87.-Scleronis and calcification of a uterine artery. (Forms. ble substances which 

Un, biematorylin, and eosin.) a, Selerotiefntinia b..caleiloain: p> % Hocome chan) ged in. 

to a firm state; or, final- 

ly, in foreign bodies which have entered the body from without, and 
form the centres of a process of inerustation. 

In the first case there a petrifactions of the tissues; in the sec- 
ond, free concretions and calculi. It is to be noted, however, that un- 














222 THE RETROGRADE CHANGES. 


In rare cases there may occur a deposit of lime-salts in organs which 
show but slight changes—for example, in the lungs. Since in part of 
such cases there is found at the same time a more rapid absorption of 
the skeleton ( atrophy of the bones, destruction of the bones by 
tumors), this deposit is regarded as metastatic in nature, due to the over- 
loading of the blood with lime-salts Even under these cireumstances 
the immediate cause of the calcification is local, and is dependent upon 
retrogressive changes—in the lung tissue (senile atrophy, obliteration of 
vessels, venous congestion); and the increased absorption of the skeleton 
is but a favoring factor. According to investigations by Kockel the 
elastic lamellw of the small and medium-sized vessels in particular be- 
come calcified, but the elastic fibres and capillaries of the alveolar septa 
are also involved. 

The lime-salts are first deposited in the tissue in the form of small 
granules ( 88); and preparations may occasionally be obtained in 
which the separate calcareous granules are yet distinctly visible. 

Through the confluence of such granules larger clumps and spherules 
are formed (Fig. 89). More frequently, however, there results a more 











Fic, 91. Fro. 9, 
Fig. 91.—Calcareous concretions. a, Concretions from an inflamed omentum: b. calvarewus man 
froura tuberculous Iymphgiand which had undergone caseation. x 200. 


Fra, 9. -Sertion from m psammoma of the dura mater, with coneretions. (Alcohol, plerie acd. 
haematoxylin, ein.) a, Hyaline nucleated spherule with enclosed calcareous 

eretion with hyaline non-nucleated capsule. embedded In Abrous connective 
tion surrounded by hyaline connective tite; d, calcareous spleule in connective tissue: ¢, calcareous 
splcule containing three separate concretions, embedded in the connective tissue. X 175, 





homogeneous deposit, in which it is impossible longer to distinguish the 
individual granules. 

The calcification may affect. both the cells (Fig. 90, d, e) and inter- 
cellular substance (Figs. 87, 88, and 89). During the process of caleifi- 
cation the degenerated tissue shows different reactions toward certain 
stains from that exhibited by unchanged intercellular substance or liv- 
ing cell-protoplasm, in that the area of calcification stains a dark bluish 
violet with hematoxylin (Fig. 87, d, c, d; Fig. 90, d, e), and red with 
picrocarmine. This applies, however, only to deposits of carbonates and 
phosphates of lime, but not to those of calcium oxalate. According to 
von Kossa, the presence of calcification may be also demonstrated by 
means of dilute solutions of silver nitrate, a black color being produced 
during the formation of silver phosphate from the organic constituents 
remaining in the granules of calcium phosphate. 

Calcification may affect small or large areas of tissue, causing in the 














CALCIFICATION: FORMATION OF CONCRETIONS. 223 


latter case a hardening and whitish coloration of the tissue. At times 
the areas of calcification may appear as sharply circumscribed spherical 
or nodular masses (Fig. 91 and Fig. 92, a, b, c), or long spicules (Fig. 
92, d) or cactus-like formations. In this manner there are produced 
concretions lying in the tissues, and these not infrequently may be 
recognized by the naked eye. Under physiological conditions such con- 
cretions in the forin of laminated calcareous spherules occur particularly 
in the pineal gland and the choroid plexus (the so-called brain-sand, acer- 
vulus cerebri). AS pathological formations they are found in different 
parts of the pia and dura mater, in many tumors of the same (psammoma 
or sand-tumors, Fig. 92), also in areas of caseation (Fig. 91, 5), or in 
thickened connective tissue (Fig. 91, a). The origin of these formations 
may be studied to the best advantage in the psammomata. In general 
they arise through the conversion of tissue-cells (Fig. 92, a, 6, c) or 
fibrous connective tissue (d) into hyaline masses, at first containing nu- 
clei (a) but later showing none (8, e), these masses then taking up lime- 
salts. Spherical concretions arise in particular from hyaline masses of 
cellular origin (a, 6, c); the spicules (d) from hyaline connective tissue, 
though spherical concretions may be formed also in hyaline connective 
tissue (e). The connective tissue which undergoes hyaline degeneration 
and calcification is for the chief part ordinary fibrous tissue, but the spi- 
cules of lime-salts and round concretions may be formed also in the vessel 
walls. 


Literature. 
( Calcification of Tissues, and Formation of Concretions in the Tissues. ) 


Arnold: Bau und Entwickelung der Psammome. Virch. Arch., 52 Bd., 1871. 
Diemer: Kalkablagerung in d. Serosa des Herzens. Zeit. f. Heilk., xx., 1899. 
Ernst: Ueber Psammome. Beitr. v. Ziegler, xi., 1892. 

Friedländer: Verkalkung der Ganglienzellen. Virch. Arch., 88 Bd., 1882. 

Golgi: Bau und Entwickelung der Psammome. Virch. Arch., 51 Bd., 1870. 

Gottschalk: Ueber die Einwirkung des Aloinsauf die Nieren. Inaug.-Diss., Leipzig, 
1882. 

Kaufmann: Die Sublimatintoxication, Berlin, 1888; Virch. Arch., 117 Bd.. 1889. 

Kockel: Kalkincrustation d. Lungengewebes. Deut. Arch. f. klin. Med., 64 Bd., 
1899. 

v. Kossa: Künstlich erzeugbare Verkalkungen. Beitr. v. Ziegler, xxix., 1901. 

Küttner: Ein Fall von Kalkmetastase. Virch. Arch., 55 Bd., 1872. 

Leber: Conjunctivitis petrificans. v. Graefe’s Arch., li., 1900. 

Leutert: Die Sublimatiutoxication. Fortschr. d. Med., xiii., 1895. 

Levi: Untersuchungen über den Bau und die Entstehung der Concretionen in Psam- 
momen der Dura mater u. der Kalkplättchen in der Arachnoidea spinalis. Inaug.- 
Diss., Freiburg, 1890. 

Litten: Der hämorrhag. Infarkt, 1879; Verkalkungen in d. Nieren. Virch. Arch., 
83 Bd., 1881. 

Mallory: Calcareous Concretions in the Brain. Journ. of Path., ii., 1894. 

Meyer: Structur und Entstehung der Sandkörper. Virch. Arch., 143 Bd., 1896. 
Neuberger: Ueber die Wirkung des Sublimates auf die Niere. Beitr. v. Ziegler, vi., 
1889; Ueber Kalkablagerung in den Nieren. Arch. f. exp. Path., 27 Bd., 1890. 

Paltauf: Ueber Phosphorvergiftung. Wien. klin. Woch., 1888. 

Bey: Ausscheidung u. Resorption des Kalks. Arch. f. exp. Path., 35 Bd., 1895. 

Ricker: Verkalkung und Steinbildung. Ergebn. d. allg. Path., iii., 1897. 

Both: Verkalkung der Purkinje’schen Zellen. Virch. Arch., 53 Bd., 1879. 

Saikowsky: Veränderungen im Organismus durch Quecksilber. Virch. Arch., 87 
Bd., 1866. 

Schujeninoff: Muskelverkalkung. Zeit. f. Heilk.. xviii., 1897. 

Steu : Zur Kenntniss der Sandgeschwülste. Virch. Arch., 50 Bd., 1870. 

Virchow: Kalkmetastasen. Virch. Arch., 8u. 9 Bd.; Die krankhaften Geschwülste, 
ii., Berlin, 1865; Verkalkung abgestorbener Gehirnzellen. Virch. Arch., 50 Bd., 
1870; Cyanquecksilbervergiftung. Münch. med. Woch., 1888. 


224 THE RETROGRADE CHANGES. 
Werra: Folgen d. vorübergeb. u. dauernd. Verschlusses d. Nierenarterie. Virch. 
Arch., 88 Bd., 1882. 


Zanda 
5 






‘clung der Osteome der Arachn. spinalis. Beitr. v. Ziegler, v.. 1889. 





also § 


§ 68. The more common petrifactions consist of deposits of phosphate 
of lime, sometimes of carbonate; with these some magnesium salts may 
be mixed. Under especial conditions there occur also deposits of uric- 





Fra. $8.—Depostts of urates In the knew-Jolnt, in a case of gout. a. Condyles of the femur; b, urate 
iepralts on the cartlage. “Two tas palatal aise 


acid salts; particularly in the disease known as gout, which is a chronic 
disturbance of the general nutrition characterized by a uric-acid Miathesia 
leading to a deposit of uric acid in the tissues. nn 
Gout is usually inherited, and but rarely acq it Occurs most 
frequently in certain re; as, for example, in England and in North 
Germany ; and is v re in other countries, as inSouth Germany. Of 
the ultimate cause of the disease we have as yet no positive knowledge. 
It is characterized chiefly by the deposit in the body of uric-acid salts, 
chiefly sodium urate, with which small quantities of carbonate and phos- 
phate of lime are sometimes associated (Fig. 93, b). The deposit of 
these salts takes place usually during acute, typical paroxysms charac- 
terized by pain and inflammation, but very great departures from a 
typical course may occur. The deposits are found in the kidneys, skin, 
snbeutaneous tissue, tendon 
sheaths, tendons, ligaments, 
burse, and articular cartilages 
(Fig. 93), but may finally be 
present in almost all the organs. 
The metatarsophalangeal joint. 
of the great toe is a favorite site 
of deposit, and often the first 
part affected. The deposits con- 
sist essentially of clusters of fine 
yrig in ne arial vonder "rater tanercan) Slender needles (Fig. 94), in 
x 1m whose neighborhood the tissues 
are degenerated or necrotic; and 
from this it may be assumed that the urates entering the'tissues in solu- 
tion give rise to the necrotie changes in the latter. 

















cour. 295 


The areas of necrosis and incrustation are at first of small size, but 
occasion inflammation and tissue-proliferations in their neighborhood. 
Later, with the occurrence of 
other paroxysms the deposits 
become larger, so that large 
nodules (the so-called tophi) 
are formed. These consist of 
white, plaster-like masses, aud 
under certain conditions may 
form marked nodular thick- 
enings in the joints and ten- 
dons (Fig. 

In the joints the articular 
cartilages at first appear as 
if sprinkled over with plaster- 
of-Paris (Fig. 93, 5), but later 
the white masses penetrate 
deeper and may permeate the 
entire articular cartilage. In 
the kidneys the tissue-necrosis 
caused by the uric acid, and 
the resulting inflammation 
may lead to contraction and 
induration of the organ. The 
deposit affects chiefly the 
medullary pyramids, but is 
found also in the cortex. 

According to Garrod and 
Ebstein the acute paroxysms 
in gout depend upon an ex- 
cessive accumulation of uric 
acid, either as the result of 
deficient excretion by the kid- 
neys (Garrod) or of local 
changes (Ebstein). Accord- 
ing to Pfeiffer the gouty pre- 
disposition is due essentially 
to the fact that the uric acid Fra. 9.—Gouty nodes of the hand. (After Lancereaux.) 
in the body-fluids is produced 
in a form which is soluble with difficulty, and tends to be deposited in 
the tissues where it may collect in such quantity as to cause a localized 
necrosis. The symptoms of the gouty paroxysm are supposed to depend 
upon an increased alkalinity of the body-fluids caused by especial con- 
ditions, as a result of which there follows a partial solution of the de- 
posited uric acid, in the course of which process attacks of pain and 
symptoms of inflammation are produced. On the other hand, von 
Noorden regards the formation and deposit of uric acid as a secondary 
process, due to the local action of a special ferment, and quite inde- 
pendent of the amount and condition of the uric acid in other parts of 
the body. 





226 THE RETROGRADE CHANGES. 


Literature. 


(Gout and Gouty Deposits.) 


er. Harnsäureablagerungen. Verh. d. pathol. Gesell. ii, Berlin, 1900. 
of the Gouty Paroxysm. Brit. Med. Journ., i., 1885. 

Gentani; Specielle Pathol, u, Ther. der Stoffwechselkrankheiten, ii., Berlin. 1880. 

Charcot: Mulndies des vieillands, goute et rheumatismes, (Euwres compl., vit. 
Paris, 

Duckworth: Truité de la goutte, Paris, 1893; Die Gicht, Leipzig, 1894. 

Ebstein: Die Natur u. Behandlung d. Gicht, Wiesbaden, 1882: Verhandl. d. VIII. 
Congr. f. inn. Med., Wiesbaden, 1889; Beitr. z. Lehre v. d. harnsauren Diathese, 
Wiesbaden, 1881. 

Ebstein u. Sprague: Beitr. z. Analyse gichtischer Tophi. Virch. Arch., 125 Bd.. 
1881. 

Freudweiler: Exp. Unters, über das Wesen d. Gicht. Deut. Arch. f. klin. Med., 68 

Garrod: Die Natur und die Behandlung der Gicht, Würzburg, 1861. 

His: Wirkung des sauren barns. Natrons. Deut. Arch. f. klin. Med., 67 Bd., 1900. 

Kolisch: Wesen und Behandlung der uratischen Diathese, Stuttgart, 1885. 

Kionka: Vogelgicht. Arch. f. exp. Path., 44 Bd., 1900. 

Levison: Die harnsaure Diathese, Berlin, 1893. 

Likhatscheff: Uratablagerung nach Urcterunterbindung. Beitr, v. Ziegler, xx. 1890. 

Minkowski: Phys. u. Pathol. d. Harnsfure. Arch. f. exp. Path., 41 Bd., 1898. 

Mordhorst: Entstehung der Umtablagerungen, Virch. Arch., 143 Bd., 1897. 

vy. Noorden: Pathologie des Stoffwechsels, Berlin, 1898. 

Pfeiffer: Das Wesen der Gicht, Wiesbaden, 1891. 

Riess: Gicht. Eulenburg’s Realencyklop., 1895. . 








$ 69. Free concretions are formed in the first place in the various 
ducts and cavities of the body which are lined by epithelium, as in the 
intestines, in the ducts of the glands pouring their secretions into the in- 
testine, in the gall-bladder, urinary passages, and respiratory tract. In 
& certain sense the concretions formed in the blood-vessels and serous 
cavities might also be included in 
this group, although they are for 
the greater part firmly united to 
the surrounding tissues. 

All free concretions possess an 
organic base or nucleus. Thus en- 
teroliths which form in the intes- 
tines have a nucleus of inspissated 
feces, or foreign bodies which 
have been swallowed, such as hairs 
(bezour stones or egagropile), or 
indigestible portions of vegetable 

food, ete., in and about which 
FIG, Buena Ara (ne gulkladder. nhosnhates (ammonium - magne- 

sium phosphate and calcium ph: 
phate), and carbonates are deposited in varying proportions according 
to the nature of the food ingested. In the mouth-cavity incrustations of 
the teeth, known as dental caleuli or tartar, are formed by the deposit of 
i i ting of mucus, cell-detritus, and bacteria. In 
re formed in the ducts of the salivary glands and pan- 
creas oval or spherical faceted, or irregularly nodular, glandiform concre- 
tions, through the caleareous impregnation of a substance derived from 
the epithelium of the gland, 

Bronchial ealeuli ave formed by the calcification of thickened bronchial 













THE FORMATION OF CONCRETIONS. 227 


secretion; the stones found in veins and arteries (phleboliths and arterio- 
liths) from the caleification of thrombi; prostatic calculi through the cal- 
cifieation of the so-called amyloid concretions; navel stones through the 
retention and inerustation 
of desquamated epithelium, 
hairs, and other substances 
which may enter the navel- 
depression. 

The biliary calculi and 
gall-stones found in the bile 
passages and gall-bladder are 
in part small granules, and 
partly larger spherical, oval, 
faceted stones (Fig. 96), 
which on fracture appear 
to consist purely of erystal- 
line masses. By the em- 
ployment of proper methods 
it may be shown that these 
stones also possess & Mitro- jig, g7—sectio through « small cholesterin stone after 
genous ground-substance. removal of the cholesterin. x 13, 

According to their essen- 
tial composition gall-stones may be classed as cholesterin, cholesterin- 
pigment, bilirubin, biliverdin-calcium, and calcium carbonate stones. 
The first. two varieties are the most common; they present a rayed, crys- 
talline, often laminated fracture ; and vary in color and in their mottling 
according to the amount of bile-pigment present. When no pigment is 
present they may be color- 
less and translucent. 

If the cholesterin be dis- 
solved out of a cholesterin 
stone by some suitable 
method, it will be found 
that the form of the stone 
is preserved, and a delicate, 
for the greater part yellow- 
ish, mass remains. This, 
when carefully embedded 
and cut into sections, is 
found under the microscope 
to consist of a delicate, ho- 
mogeneous substance (Fig. 
97) which shows concentric 
stratification and radiating 
clefts or spaces which were 

Fic. 98. Uric-achd infarct of the new-born. (Alcobol, hema- formerly occupied by the 
warlin. Prawn from 4 apreparation that had ieee wasted en crystalline masses. Asim- 
a. Transverse section of unchanged collecting tubule from the ilar ground-substance may 
papilla: b. dilated collecting tubule Alled with urle-eld con- 


Fretkons; remains of coneretions after washing with water. DE demonstrated in other 
7 me. ealeuli after solution of 


‚aleium salts, 

There can, therefore, be no doubt that gall-stones are also the result 
of the inerustation of an organic substratum, which is in all probability 
derived from the mucous membrane of the biliary passages aud the gall- 




















228 THE RETROGRADE CHANGES. 


bladder. Gall-stones occur especially in advanced years; stagnation of 
the bile favors their formation. Intlammations of the mucous membranes 
of the bile-passages (angiocholitis) lead to desquamation and destruction 
of the epithelium (eventually also to escape of leucocytes), and in the 
products derived from these pathological changes bilirubin and choles- 
terin are deposited. When once a concretion is formed it increases in 
size through the deposit of new products of cell-disintegration which be- 
come encrusted with cholesterin, pigment, and calcium, According to 
Naunyn the originally soft nucleus of the concretion undergoes a change. 
in that it separates into firm, granular masses of pigment-caleium and 








crystals of cholesterin which are deposited upon the outer crust, and into 
A. 





fluid, so that the stones may at times contain a cavity filled with flu 
In the course of time this y may again be filled with cholesterin; 
and aiso the pigment and calcium in the remaining portions of the stone 





av 





Fic. W. . Fic. 100. 


Fic, 99. Coralatnp stone frum the bladder, composed of ealctum oxalnte and phomhate. 
sine, 





tural 


Fig. 100. ‘Transverse section of two 
sodium urate und 





es from the bladder, elogely Atted together, and consisting of 
onium-mugneslun phosphate. Natural size. 





may be gradually replaced by cholesterin. Further, ealeium carbonate 
may also be deposited. 

The cholesterin masses from which the concretions are formed are 
derived chi from the disintegration of epithelial cells; -likewise, the 
lime-salts combining with bilirubin are also furnished by the mucous 
membrane. 

As Ebstein has shown, the wrinary ealeuli, gravel, and stones are also 
composed of an orga ground-substance, an albuminous stroma, in 
which the veri of the urine may become deposited. Ac- 
cording to loc inguish caleuli of the kidney and those of 
the descending uri In the kidneys the deposits may form 
only smail granules Iying in the tissue itself, or in part also free in the 
lumen of the urinary tubules, in the latter place lying in the products 
derived from the disintegrati tic epithelial cells, This is true 
in the t place of the ¢ tions which, as mentioned above, occur in 
the vecrosed renal epithe after poisoning with corrosive sublimate, 
bismuth, aloin, copper-salts, iodine, phosphorus, potassium chromate, 
and oxa The same thing is true of some of the gouty deposits. 
Finally, belongs here the so-called wrie-acid infaret of the new-born, a con- 











































THE FORMATION OF CONCRETIONS. 229 


dition characterized by the appearance of yellowish-red stripes in the 
medullary pyramids. The condition is not infrequently seen in children 
dying during the first five weeks after birth. The epithelium of the 
tubules is usually well preserved, but in places desquamation and disin- 
tegration of single cells may be found. The lumina of the tubules are 
filled with very small, colorless or yellow granules of urates or uri«: acid, 
which at times show fine radiating lines (Fig. 98, b). On solution of 
these granules a delicate stroma remains (ce). If as the result. of the 
presence of the infarct further changes in the epithelium of the tubules 
are produced, leading to the formation of albumi- 
nous material in the tubules, single granules may 
under certain conditions develop through accretion 
into large stones, but this occurrence is rare. 

In the pelvis of the kidney, ureters, urinary 
bladder, urethra, and under the prepuce concre- 
tions may be formed, either as sand, gravel, or 
stones, The last-named are oval or spherical, and 
may be smooth or ‘rough and nodular, not: infre- 
quently resembling a mulberry or mass of coral 
+ Figs. 99and 100). When several stones lie close- 
ly together, their surfaces may become faceted 
(Fig. 100). Those found in the kidney pelvis 
may form casts of the cavity and of the calyces. 

When examined in section, urinary calculi are 
sometimes homogeneous, at other times distinctly 
stratified (Fig. 100) or show radiating lines. Not. 
infrequently there may be seen a nucleus and 
several zones of different appearances. The erys- 
talline masses lie partly in the spaces of the 
stroma, and partly in the latter itself; and it may, 
therefore, be assumed that the stroma is a product 
of the mucosa of the urinary passages, and that 
its formation follows catarrhal inflammations or 
toxie necroses of epithelium when these lead to the 
collection of mucus or cell-detritus in the tubules. 

What substances are deposited in a given case 
in the products of the mucous membrane depends 
upon the existing conditions. When the condi- 
tions favoring stone-formation are associated with 
a uric-acid diathesis, or if the excretion of uric- 
acid salts by causing tissue-neerosis has at the 
same time produced the conditions favoring the _ Fre. 101.—Ierusted tead- 
development of concretions, the deposits in the  penell,Jze%n, lng, taken from 
organic ground-substance will consist chiefly of Reduced A. 
urates. Decomposition of the urine with forma- 
tion of ammonium-magnesium phosphates leads to the production of 
caleuli consisting chiefly of this substance. Cystin ealeuli may be 
formed when cystin is excreted by the kidneys, as the result of pe- 
euliar metamorphoses of albumin in the intestine, due to the action of 
bacteria (Baumann, von Udransky, Brieger). When once a stone is 
formed, the irritation which it ses upon that portion of the mucous 
membrane with which it comes in contact, as well as the decomposition 
of the retained urine, favors its further growth by accretion. — Likewise, 
foreign bodies (Fig. 101), which have in any way entered the bladder 



























230 THE RETROGRADE CHANGES. 


from without, may lead to the formation of calculi, through the irritation 
which they excite in the mucous membrane of the bladder. 


Intestinal calculi are much more common in horses and cattle than in man: since 
undigested vegetable material and hairs which have been licked off are of frequent oc- 
currence in the intestinal] canals of these animals and form the starting-point of such 
concretions. The true stones, which occur especially in horses, are rather hard masses 
consisting chiefly of magnesium phosphate; the false stones consist of hairs and vege- 
table fibres which are more or less encrusted. Occasionally balls are found which con- 
sist almost wholly of hair (egagropili or bezoar stone»). In ruminating animals they are 
found chiefly in the rumen or reticulum; in hogs, more frequently in the small intestine. 

According to Schiuberg, the enteroliths of herbivorous animals consist chiefly of car- 
bonates; those of carnivorous. of phosphates. The composition of those found in man 
varies according to the food ingested. 

Urinary calculi are classified according to their composition as follows: 

1. Caleuli composed chiefly of urte acid or uraten. 

Pure wrte-ccid calculi are usually small, yellow, reddish, or brownish in color, and 
hard. 

Stones consisting of uratea are rarely pure. They are usually covered on the surface 
with a coating of calcium oxalate and ammonium-magnesium phosphate. 

2. Caleuli composed chiefly of phosphates and carbonates. 

To this class belong stones composed of caleium phosphate, ammonium-maquest im 
phosphate, and ealeium carbonate, The last two varieties are rare. All these calculi are 
white or grayish-white. The triple phosphate stones are soft and friable, the others 
hard. 

3. Stoner composed of calecnin oxalate, 

These are hard and rough, and of a brown color. 

4. Cystin calenti, 

These are soft, waxy, and of a brownish-yellow color. 

5. Nanthin ealeuli. 

These are cinnabar-red in color, smooth, and have an earthy fracture. 

Fbstein and Meolaier succeeded in experimentally producing urinary caleuli by feed- 
ing animals with oxamide, an ammonium derivative of oxalic acid. The greenish-yellow 
concretions thus produced in the urinary passages of dogs and rabbits consisted essen- 
tially of oxamide; on section they presented a concentric laminated structure showing 
radiating striations. They were found likewise to possess an albuminous stroma, which 
was derived from the necrosis and desquamation of epithelium caused by Ihe action of 
the oxamide during excretion. 


Literature. 


(Free Concretions. ) 


Baumann u. v. Udransky: Ueber das Vorkommen von Diaminen, sog. Ptomainen 
bei Cystinurie. Ber. d. Deutsch. chem. Ges., xxi.; Zeitschr. f. phys. Chem., 1889. 

Brieger u. Stadthagen: Ueber Cystinurie. Berl. klin. Woch., 1889. 

Cushing: (Gall-stones Lit.) Bull. Johns Hopkins Ilosp., 1898. 

Ebstein: Die Natur u. Behandlung der Harnsteine, Wiesbaden, 1884. 

Ebstein u. Nicolaier: Künstl. Darstellung von harnsauren Salzen in der Form v. 
Sphärolithen. Virch. Arch., 123 Bd.; Exper. Erzeugung von Harnsteinen, Wies- 
baden. 1891. 

Fauconneau-Detrésne: Traité de l’affection calculeuse du foie et du pancréas, Paris, 
ISS1. 

Fürbringer: Nephrolithiasis, Caleuli renum, Nierenconcremente. Deut. med. Woch., 
1800. 

v. Genersich: Ilärte der Coneremente. Virch. Arch., 181 Bd., 1898. 

Hahn: Nabeleoneremente. Beitr. v. Bruns, xxvi., 1900 (Lit.). 

Leube: Darmsteine.  Ziemssen's Handb., vii. 

Lewis and Simon: C'ystinuria with Diaminurin. Amer. Journ. of Med. Sc., 1902. 

Mayer: Gallensteinbildung. Virch. Arch., 136 Bd.. 1885. 

Mester: Beitr. z. Kenntniss der Ovstinurie. Zeitschr. f. phys. Chem., xiv., 1889. 

Moreigne: La evstinurie. Arch. de med. exp., i., 1889. 

Naunyn. Die Gailensteinkrankheiten. Verh. d. X. Congr. f. inn. Med., Wiesbaden, 
ISG). Klinik der Cholelithiasis. Leipzig. 1892. 

Posner. Studien über Steinbildune. Zeitschr. f. klin. Med., ix. and xvi. 


THE PATHOLOGICAL FORMATION OF PIGMENT. "231 


Ribbert: Path. Anat. d. Wurmfortsatzes (Bildung v. Kotlisteinen). Virch. Arch., 
132 Bd.. 1898. 

Schuberg: Bau u. chem. Zusammensetzung v. Kothsteinen. Virch. Arch., 90 Bi. 

Bnatiock; Calcul of Calcium Oxalate from a Cyst of the Pancreas, Journ. of Pat, 


Smith Coneretions a id Calculi. Ref. Handb, of Med. Se., 1901. 















Solger: Ablagerungen f. mikr. Anat., 34 Bd, 1889. 

Spiegelberg: Huarnsiu thorenen Arch exp. Puth.. 41 Ba., 1890. 

Steinmann: Schulen- und Kalksteinbildung. Ber. d. Nuturf. Ges. zu Freiburg, iv.. 
1889. 

Stroebe: Arbei Bildung freier Coneremente. CVl. f. allg. Path., i., 1890 (Lit.). 

Studensky: Zur Lehre von der Bildung der Harnsteine. Deut. Zeitschr. f. Chir., vii., 
1877. 





Tross: Faccttirte Speichelsteine. Beitr. v. Ziegler, viii., 1890. 


XIV. The Pathological Formation of Pigment. 


§ 70. Both connective and epithelial tissues in various parts of the 
body contain normally an autochthonous pigment, which lies within the 
cells, and consists either of yellow, brown, or black granules, or forms a 
diffuse yellow or brown coloration of the cells. These autochthonvus pig- 
ments are known as melanin, lipochrome, 
and hemofuscin. In the epithelial tis- 
sues the pigment is found particularly 
in the lowest layers of the rete Malpighii, 
which contains pigment in all the pig- 
mented portions of the skin, also in the 
1 in the pigment-epithelium of the 

and in many ganglion-cells. In 

the pigment-cells of the skin the granules 
are chiefly yellow and brown; in the epi- 
thelium of the retina they are black. In 
marked pigmentaticn of the skin other 
cells besides those of the rete Malpighii 
contain pigment. Among the connective- 
tissue cells, which most frequently con- 
tain yellow or brown pigment-granules, 
are the cells of the choroid, sclera, co- 
rium, heart-muscle, muscularis of the in- 
testine, and pia. 

The normal autochthonous pigments 
may be increased under various physiol- 
ogical and pathological conditions. For 
example, during pregnancy the »igment of 
the skin is usually more or less increased 
(chloaama_uterinum), particularly in bru- 
nettes. In Addison’s disease, a general 
disease leading to cachexia and which is 
dependent upon pathological conditions 
of the adrenals (see § 27), there occurs a 4 
decided pigmentation of the skin asa re- pin. 02. Large halry ent wile 
sult of an increase of then al pigment. over the bet ee ko wt N 
Not infrequently spots of a bronze color shoutders. (After Röhring.) 
appear in the mucous membranes of the 
mouth. Further, in atrophic conditions of the heart there is usually an 
increase of the normal heart-pigment. Yellow pigment-granules also 














232° THE RETROGRADE CHANGES. 

appear in the voluntary muscles in conditions of atrophy; and in old per- 
sons the smooth muscle of the intestine always contains more or less of a 
yellow granular pigment, so that sometimes the outer surface of the in- 
testine may show a vellow or yellowish-brown coloration. 

The most intense grades of pathological pigmentation are met with 
in freckles, lentigines, pigmented moles (Fig. 102) and pigmented warts, and 
in black melanotic tumors (see Chapter VIII). The amount of plement 
may be so great as to give the tissues a pure black color. 

The pigment lies for the greater part inside of tissue-cells (cho omato- 
pnores). more rarely in the intercellular substance. It is composed of 
vellow, brown, or black granules; not infrequently individual cells may 
be diffusely pigmented. In Addison’s disease the pigment-granules are 
found partly in epithelial cells, especially in those lying directly upon 
the connective tissue (Fig. 103, 
A, a, db, and B, a), and part- 
ly in branched connective-tis- 
sue cells (A, ¢, ¢, d), from 
which pigmented processes ex- 
tend up between the epithelial 
cells (B, ec). 

In the pigmented spots of 
the skin and in melanotic sar- 
comata the pigment is partly 
contained in especially differ- 
entiated connective-tissue cells 
of large size, and partly in ap- 
parently normal cells of the 
given tissue, very often in the 
connective-tissue cells in the 
neighborhood of the vessels 


9 
Den co o 


2,2, 
200 





Fic. 18.— A,and B, Pigmented cells of the skin from 


acase of Addison's disease with caseous tuberculosis of 
both adrenals. (Alcohol, carmine.) a. Pigmented epi- 
thelium cells from the deepest layer, in a section cut at 
right angles to the surface. 4. b, Pigmented epithellal 
cells froin a section made parallel to the surface. By bh, 
Epithelial cells containing no pigment: c,c,. nucleated 
pizmented connective-tissue cells, the processes of which, 
in B, push between the epithelial cells; «d, pigmented 
cell- processes, 7.3. 


and in the cells of the vessel- 
walls. 

In the ganglion-cells the 
pigment is composed of brown 
granules. 

The pigments just described 


are products of a specific cell- 
activity; and we must suppose that many connective-tissue cells, gan- 
glion-cells, and muscle-cells are able to form pigment from the material 
brought to them. In the majority of cases the pigment appears to be 
formed in the places where it is found; yet different investigations make 
it probable that the pigment may at times be transported. The pig- 
ment of the epidermis and of the hairs, at least in part, is not formed 
in the epithelial cells themselves, but in branched eonnective-tissue cells 
(Fir. 105 X, eo, d, and B, ce) which lie just beneath the rete, and send 
processes between the epithelial cells, through which the pigment is 
transferred to the latter. 

The fact that the pigment is often found particularly about the blood- 
vessels would seem to indicate that the material from which it is formed 
is derived from the blood, and many authors accept without question the 
view that the pigment is a derivative of the coloring-matter of the blood. 
Against this view is the fact that neither in the blood nor in the neigh- 
borhood of the blood-vessels are there present evidences of an escape of 
the red blood-cells or of a disintegration and solution of the same. It 


THE AUTOCHTHONOUS PIGMENTS. 233 


is, therefore, very probable that the pigment is formed either from the 
cireulating albumin or from the albumin of the cells, 

The attempt has been made to solve this problem by means of chemi- 
cal investigations; and the results obtained up to the present time favor 
the theory that the pigment is a product of cell-activity, and is formed 
from albuminous bodies. The different forms of melanin, in which 
group the pigments of the skin and choroid are usually placed, are, ac- 
cording to the investigations of von Nencki, Sieber, Abel, Davids, and 
Schmiedeberg, nitrogenous bodies rich in sulphur, but vary greatly in 
composition. According to Schmiedeberg these differences depend upon 
their mode of origin, inasmuch as these pigments represent the final prod- 
uct of a long series of metumorphoses of albumin; and in their formation 
may be compared to the development of humus. The genuine albu- 
minous bodies do not furnish the material for the building up of this 
final product (Schmiedeberg), but it is derived from sulphur-containing 
bodies formed by the splitting-up of the albumins, and from which cer- 
tain carbon-containing groups have already been split off, so that there 
arise combinations which in proportion to their carbon-content are very 
rich in sulphur, and from these the melanins are formed. 

The majority of authors regard melanin as an iron-free substance. 
Brandl, Pfeiffer, Mörner, and others, on the other hand, found small 
quantities of iron in melanosarcomata; but this cannot be regarded as: 
proof that the melanin was derived from hemoglobin, inasmuch as a 
tumor may contain besides melanin also iron-containing produets arising 
from the disintegration of red blood-cells. The majority of the pigment 
granules give no reaction for iron. 

Lipochrome is the term applied to the coloring-matter of adipose 
tissue, corpora lutea, ganglion-cells (Rosin), and of the greenish tumors 
known as chloromata (Krukenberg). Of the origin and nature of this 
pigment nothing definite is known. 

Hemofuscin (von Recklinghausen, Goebel) is the iron-free, vellow- 
ish, granular pigment foundin heart-muscle, smooth and striped muscle, 
in the cells of the glands of the stomach and intestine, in the lachry- 
mal, mucous, and sweat glands. According to von Recklinghausen this 
piginent is derived from the blood, but it has not yet been established 
that it is a hsemoglobin-derivative. The sulphur-content (Rosenfeld) 
makes it not unlikely that the hwemofuscin granules belong to the mela- 
Bil group. 


Aehy was the first to express the belief that the epithelial cells themselves do not 
form the pigment, but obtain it from wandering cells which penetrate between the in- 
dividual epithelial cells and there degenerate, the pigment and cellular debris being 
taken up by the epithelium. According to ron Aölliker, “the pigment of the hair and 
epidermis is derived from pigmented connective-tissue cells which lie just beneath the 
deepest layers of the epithelium of the hair-bulbs and of the rete, and send processes 
between the delicate cells of these layers. These processes divide into long fine ramifi- 
cations which lie in the intercellular spaces and may even penetrate into the cells them- 
selves, and in this way transfer their pigment to the latter.” The pigment of the gan- 
glion cells and of the cells of the retina arises, on the other hand, in the ectodermal cells 
themselves. Riehl and Ehrmann agree with ron Kölliker. Karg observed that, follow- 
ing the transplantation of white skin on to the surface of a leg-uleer in a negro, the 
white grafted portions became wholly black in from twelve to fourteen weeks: and he 
concludes that. in the pigmentation of the epidermis, pigmented connective-tissue cells 
penetrate bet ween the epithelial cells and convey pigment to the latter. Microscopical 
examination showed the presence of such pigmented processes between the epithelial 
cells at a time when the latter had not yet become pigmented. Vou Wild has shown 
that in melanosarcomata of the skin pigmented con.eetive-tissne cells may penetrate 
between the epithelial cells. Similar pigmented connective-tissue cells are found in the 


234 THE RETROGRADE CHANGES. 


pigmented portions of the skin or mucous membranes in cases of Addison's discase, 
usually, however, in certain areas only and not every where. 

Histological studies of the mode of formation of the normal pigment in various 
animals, chiefly in fishes, amphibia, and reptiles, have led to different conclusions. 
Thus yarisch is of the opinion that the pigment of the skin and teeth of tadpoles is not 
derived from the blood, but is a product of the protoplasm, while Liat, on the other 
hand, believes that the pigment of the skin of fishes and amphibia is formed from 
hemoglobin, Ehrmann holds that the melanotic pigment of all vertebrates is a hamo- 
globin-derivative. According to Aromayer, the pigment of the skin of mammals is 
derived from the protoplasmic fibrille (spongioplasın) and represents a degeneration- 
product of the same. 

In domesticated animals there occurs a peculiar melanosis of the internal organs, 
occasionally associated with melanosis of the subcutaneous tissue. The affected organs 
(heart, lungs, intestines, etc.) present in varying numbers grayish or black spots, look- 
ing like ink-spots, which are produced by the deposit of pigment in connective-tissue 
cells which otherwise appear normal. 

Under the term ochronosis of cartilage, Virchow described a peculiar iron-free 
pigmentation of the cartilage, tendon-sheaths, and capsules of the joints, in which the 
cartilage shows a brown or black color, caused by the imbibition by the ground-sub- 
stance of some pigment. Virchow believed the condition to be due to the imbibition 
of blood-pigment, and compares the process to the pigmentation of freckles and lentig- 
ines. It is probable that the condition is a more pronounced form of the brown pty- 
mentation, Which occurs especially often in the costal cartilage of old persons. Occa- 
sionally the pigment is deposited ina granular form, and may be found as granules 
within the cells. Of the nature of the pigment and its origin nothing is known: it 
probably belongs to the melanin group. 


Literature. 
(Autochthonous Pigments.) 


Abel: Bemerkungen über thier. Melanine u. das Hamosiderin. Virch. Arch., 120 Bd.. 
1890 


Aeby: Herkunft des Pigmentes im Epithel. Cbl. f. d. med. Wiss., 1885. 

Baumel: Capsules surrenales et melanodermie, Paris, 1888. 

Bonnet: Ucber Eingeweidemelanose. Verh. d. Phys.-med. Ges. zu Würzburg, 24 Bıl.. 
1890. 

Boström: Ueber d. Ochronose der Knorpel. Internat. Beitr., Festschr. f. Virchow, 
ii., 1891. 

Brandl u. Pfeiffer: Farbstoff melanotischer Sarkome. Zeitschr. f. Biol.. 26 Bd., 1890. 

Caspary: Ueber den Ort der Bildung des Hauptpigmentes. Arch. f. Derm., xxiii.. 
1891. 

Ehrmann: Physiol. u. Pathol. d. Hauptpigmentes. Vierteljahrsschr. f. Derm.. 1885, 
1986; Entwickel. u. Wanderung d. Pigmentes bei Amphibien. Arch. f. Derm., 
xxiv., 1892; Das melanotische Pigment, Cassel, 1896; Biol. Chl., xix., 1899. 

Goebel: Pigmentablagerung in der Darmmuskulatur. Virch. Arch., 136 Bd., 1894. 

Halpern: Ueber das Verhalten des Pigmentes in der Oberhaut. Arch. f. Derm., 
xxiii., 1891. 

Hansemann: Ueber Ochronose. Berl. klin. Woch., 1892. 

Heile: Ochronose. Virch. Arch, 160 Pd., 1900. \ 

Jarisch: Herkunft des Oberhautpigmentes. Arch. f. Derni., xxiii.; Ergänzlı., 1891. 

-  XNiv., 1892. 

v. Kahlden: Beitr. z. path. Anat. d. Addison’schen Krankheit. Virch. Arch., 114 
Bd, 1X88, 

Xaposi: Pathogenese der Pigmentirungen, Arch. f. Derm., xxiil., 1891. 

Karg: Ueber Hautpigment u. Ernährung der Epidermis. Anat. Anz., ii., 1887, p. 
377; Studien über transplantirte Haut. Arch. f. Anat. u. Phys., 1888. 

v. Kölliker: Woher stammt d. Pigment in d. EpidermisgebildenY Anat. Anz., ii., 
ISS7; Die Entstehung d. Pig. in d. Oberhautgebilden. Zeitschr. f. wiss. Zool., 
lv... IN87. N) 

Kromayer: Obcrhautpigment. Arch. f. mikr. Anat.. 42 Bd.. 1888; Zur Pigment frage. 
Derm. Zeit... vi, 189%. 

Krukenberg: Grundziige der vergl. Physiol. der Farbstoffe u. d. Farben, Heidel- 
berg, INS87. 

Kunkel: Eisen in Melanomen. Sitzungsber. d. Phys.-med. Ges. zu Würzburg, 1881. 


THE HZEMATOGENOUS PIGMENTS. 235 


List Herkunft d. Pigmentes d. Oberhaut. Anat. Anz., iv., 1889, Biol. Cbl., x., 1890. 

Mackenrodt: Unters. über das Chloasma uterinum. Inaug.-Diss., Halle-a.-Saale, 
1880. 

Mertsching: Studien über Keratohyalin u. Pigment. Virch. Arch., 116 Bd., 1889, 

Meyerson: Zur Pigmentfrage, ib., 118 Bd., 1889. 

Miura: Beitrag zur Kenntniss des Melanins, ib., 107 Bd., 1887. 

v. Nencki: Farbstoffbildung im thier. Körper. Correspbl. f. Schweizer Aerzte, xx., 
1890. 

v. Nencki u. Berdez. Farbstoffe der melanotischen Sarkome. Arch. f. exp. Path., 
xx., 1886. 

v. Nencki u. Sieber: Weitere Beiträge zur Kenntniss des thier. Melanins, jb., xxiv., 
1838. 

Oppenheimer: Pigmentbildung in melanotischen Geschwülsten. Virch. Arch., 106 
Bd., 1886 

Pförringer- Entstehung d. Pigmentes bei Morb. Addisonii. Cbl. f. allg. Path., x., 
1900. 

Philippson: Ueber Hautpigment. Fortschr. d. Med., viii., 1890. 

Post: Pigmentirung der Oberhaut. Virch. Arch., 135 Bd., 1894. 

Raymond: Pigmentation dans Ja maladie d’Addison. Arch. de phys., iv., 1892. 

v. Recklinghausen: Hamochromatose. Tagebl. d. Naturforschervers., Heidelberg, 
1889. 

Biehl: Zur Pathologie des Morbus Addisonii. Zeitschr. f. klin. Med., x.; Zur Kennt- 
niss der Pigmentbildung im ınenschlichen Haar. Vierteljahrsschr. f. Derm. u. 
Syph., 1885. 

Röhring: Pigmentnaevus. Deutsch. med. Woch., 1893. 

Rosenfeld: Das Pigment der Himochromatose des Darms. Arch. f. exp. Path., 48 
Bd., 1900. 

Rosin: Bau der Ganglienzellen. Deutsch. med. Woch., 1896. 

Schmiedeberg: Ueber die Elementarformeln einiger Eiweisskörper und über die 
Zusammensetzung und die Natur der Melanine. Arch. f. exp. Path.. 39 Bd., 
1897. 

Senator: Ueber schwarzen Urin u. schwarzen Ascites. Char.-Ann., xv., 1890. 

Sieber, N.: Pigmente der Chorioidea u. der Haare. Arch. f. exp. Path., xx., 1886. 

Tietze: Beobacht. an einem Falle v. Melanosarkom mit Melanuric, Cassel, 1894. 

Virchow: Allgem. Ochronose der Knorpel u. knorpelähnlichen Theile. Virch. Arch., 
37 Bd., 1866. | 

Vuilleumier: Pigment. de la peau dans quelques cas de melanosarc. Beitr. v. Zieg- 
ler, xxiii., 1898. 

Wallach: Beitr. z. Lehre v. d. Melanosarkomen. Virch. Arch., 119 Bd., 1890. 

v. Wild: Einwanderung v. Pigment in d. Hautepithel bei Melanosarkom. Inaug.- 
Diss., Strassburg, 1888. 

Winkler: Ursprung des Pigmentes. Arb. a. d. embryol. Inst. in Wien, 1892. 


$ 71. Hematogenous pigments—that is, the pigments whose origin 
from the coloring-matter of the blood may be demonstrated beyond any doubt 
—are derived usually from blood whieh has escaped from the blood-ves 
sels, or has undergone coagulation within the vessels, and are, therefore, 
dependent upon local changes. In other cases they may be caused by a 
taking-up of blood-pigment into the blood or by a change in the blood 
itself, whereby granwar pigment iseither formed in the blood, or hemo- 
globin passes into the blood-plasma, so that: pigmentation of the tissuer 
results from metastatic deposits of pigment. Such pigmentations are known 
as hemachromatoses. 

Both large and small extravasates of blood very soon undergo cer- 
tain changes which are visible to the naked eye. Extravasates in the 
skin become first brown, then blue, followed by green, and finally yel- 
low. Small hemorrhages into the tissues, as in the peritoneum, pleura, 
and lungs, may show for a long time as reddish-brown spots; in de- 
composing cadavers their color may be slate-colored or black. Large 
hemorrhages into the tissue, as in the brain or lungs, assume after a cer- 
tain time a rust-brown color, which later changes to an ochre-yellow, 
yellow, yellowish-brown, or brown pigmentation. All these changes of 


236 THE RETROGRADE CHANGES. 


color correspond to certain changes in the hemoglobin and in the iron 
which it contains. 

Whenever a hemorrhage occurs in the tissues or into a body-carvity, 
a certain portion of the blood-plasma and of the red blood-cells may be 
taken up unchanged through the lymph-vessels. Another portion of the 
corpuscles gradually loses its hemoglobin, the pale stroma of the corpus- 
cles remaining. The escaped hemoglobin diffuses through the surrounding 
tissues, and from it there 
are formed the different 
products which give rise 
to the changes of color in 
the neighborhood of the 
extravasate. A part of 
the absorbed hemoglobin 
may be excreted as urobi- 





6... „eg lin (urobilinuria) ; another 
.’ SER part, on the other hand, 
. zug 


may be precipitated in 


the tissues in the form of 

Fıc. 104.— A, Cells containing amorpbous blood-pigment: a, r 
those with few large fragments of red blood-cells; I, c, those granules or cry stals. The 
containing great numbers of small disintegration-products of red Jlatter are yellowish-red or 


blood cells; B, rhombic plates and needles of hsematoidin. ruby-r ed rhombic pla tes and 

needles of hematoidin (Fig. 
104 B); and represent a frequent residuum of hemorrhages. <A portion 
of the diffused hemoglobin may also be taken up by cells, the latter 
thereby acquiring in part a diffuse yellowish pigmentation, or in part 
showing the presence of yellow and brown pigment-granules. 

A third portion of the blood-corpuscles disintegrates at the site of 
the extravasation, and forms yellow and brown granules and lumps. This 
event occurs particularly in larger extravasates in the so-called hemato- 
mata. The pigment-granules and lumps which arise either directly from 
the disintegration of red blood-corpuseles, as well as the crystals and 
granules precipitated from the dissolved hemoglobin, are often taken up 
by cells, partly leucocytes and partly cells derived from proliferating 
tissue; and these form the so-called blood-corpuscle cells and pigment-con- 
taining cells (Figs. 104, A and 105, a, 6). 

At the beginning of the disintegration of the red corpuscles the color- 
ing-matter present is hemoglobin, but this quickly undergoes changes ; 
and the yellow and rusty masses and granules which are found both in the 
cells and Iying free, and which become changed in the course of time into 
darker pigment, are no longer hemoglobin itself, but represent different 
derivatives of hemoglobin. According to their chemical composition 
these derivatives may be divided into two groups, one iron-free, the other 
containing iron. The former is known as hematoidin, the latter as hamo- 
siderin (Neumann). 

Hematoidin (identical with bilirubin) is a ruby-red (Fig. 104, B) or 
reddish-yellow (Fig. 105, b) pigment occurring either in crystalline form, 
or as granules, which may be amorphous, but often show a somewhat 
angular shape (Fig. 105, 6), suggesting rudimentary and imperfect crys- 
tals. Hiematoidin is scluble in chloroform, carbon disulphide, and 
absolute ether; and insoluble in water and aleohol. It would appear to 
be formed especially when hemoglobin is but slightly exposed to the 
action of living cells, as is especially the case in the centre of large ex- 
travasates and in hemorrhages into the body-cavities, as, for example, 


THE HAEMATOGENOUS PIGMENTS. 237 


into the pelvis of the kidney or the subdural space. It may be pro- 
duced artificially by the introduction of glass capsules containing blood 
beneath the skin or into the peritoneal cavity in such a way that the 
blood within the capsules may be exposed to the action of the tissue- 
fluids but not of the cells. 

The granules and crystals of hematoidin are found in the tissues 
either free (Fig. 104, B), or enclosed in cells (Fig. 105, 5). In the lat- 
ter case the granules and crystals are usually taken up by phagocytes 
after they have been formed; though occasionally it may happen that 
the hematoidin while in solution is taken up by fixed connective-tissue 
cells, for example, cartilage or fat-cells, and then precipitated in solid 
form. 

Hzmosiderin, the derivative of the red blood-cells which contains 
tron in demonstrable quantity microscopically, is usually found in the 
tissues as yellow, orange, and brown granules and lumps which become 
darker in the course of time. ‘They are for the greater part contained 
within cells, and in part are formed within the cells. 

When treated with potassium ferrocyanide and dilute hydrochloric 
acid hemosiderin becomes deep-blue through the formation of Berlin 
blue (ferric oxide salt of hydroferrocyanic acid) (Fig. 105, a). When 
treated with ammonium sulphide there is formed a black sulphide of 
iron. 

Heemosiderin appears to be formed particularly (Neumann) when the 
blood in an extravasate or in a thrombus is subjected to the action of 
cells; and it is consequently seen more frequently in small extravasates 
and at the periphery of larger ones. The formation of hemosiderin may 
take place either within the cells or free in the tissue. The pigment en- 
closed within cells (sideroferous cells) may have been formed from the 





Fie. 15.—Cells containing hemosiderin and bwemwatwidin froin an old hemorrhagic focus in the brain. 
(Alcohol, Berlin-blue reaction.) a, Cells containing hemosiderin; b, cells containing bematoidin : c, fat- 
granule cells which have become clear; d, newly formed connective tissue. x. 


remains of disintegrated red blood-cells which have been taken up by 
the cells, or from dissolved hemoglobin which has been absorbed by the 
cells. In favor of the latter mode of formation is the diffuse yellow color 
seen in both wandering and fixed cells, which becomes blue when the 
Berlin-blue reaction is applied. Further, when hemoglobin is exereted 
through the kidneys, iron-containing pigment-granules form in the renal 
epithelium; and moreover fixed cells, as cartilage-cells, for example, 


238 THE RETROGRADE CHANGES. 


which could hardly be supposed to act as phagocytes and take up frag- 
ments of red cells, often contain granules of hemosiderin, even when 
lying outside of the immediate neighborhood of the extravasate. 

The free pigment and the pigmented cells cause a distinct: pigmenta- 
tion of the extravasate and its immediate neighborhood. The pigmented 
cells soon pass into the lymph-vessels and a metastasis of the pigment takes 
place, as a result of which the pigment is found in the lymph-vessels and 
their neighborhood, and in the lymph-glands where it is found first in the 
free cells of the lymph- 
sinus (Fig. 106). Later 
it may be taken up by 
the fixed tissue-cells. In 
the course of time the 
hemosiderin is de- 
stroyed and disappears. 
The view which is held 
by many, that hemosi- 
derin is changed into a 
black melanin, is not 
supported by the actual 
facts. The brownish- 


black granules in the 
1,779, „100. "Acrumulation of, pigment-containing celle in the lungs, which have been 
yinph-gelan. ter on of an extravasate of blood. er’s i S e] 

tuul Carmine.) “a, Cordial nodes, Yuphainus; c calla con  CXPIAINEA as due to such 


taining piginent-granules. X 100. a change, are found 

through high magnifica- 
tion (Neumann) to consist of one or several minute particles of carbon 
surrounded by a coating of hemosiderin. 

Tf hemosiderin is brought into contact with hydrogen sulphide it be- 
comes black; and as the result of such reaction there may be produced 
in the cadaver black and green spots or a more diffuse discoloration, 
which are known as pseudomelanosis. It is observed most often in the 
intestine, peritoneum, and in suppurating wounds, since in these regions 
hydrogen sulphide is more likely to be formed in the course of putrefac- 
tion. 











Arnold has recently declared that, both in hematogenous and exdgenous siderosis. 
(see § 72), the éron-granules of the sideroferous cells (leucocytes, connective-tissue cells, 
i is, ete.) are not iron-granules which have been taken up from without through 
phagocytosis, or which have been precipitated within the cells, but are changed cell- 
plasmosomes which have taken up the iron, converted it, and combined it with them- 
selves. The statements made in the main text ($S 71 and 72) as to the genesis of a por- 
tion of the ‚roferous cells harmonize with Arnold's view, but it must be affirmed 
that a formation of sideroferous cells through phagocytosis also occurs, both in case of 
extravasates and hivmachromatoses due to intravascular destruction of the red blood- 
cells. 

The black pigment of paeudomelanoeia is regarded by many authors as a sulphur 
compound of iron which is formed through the action of hydrogen sulphide upon the 
blood, According to investigations by £ mann, pseudomelanin is not caused by a 
cadaveric decomposition; hut its formation is dependent upon local conditions, the 
chief of which is that the iron-containing products of the destruction of hemoglobin 
must be formed during life, whereby the hemosiderin when exposed after death to the 
action of hydrogen sulphide assumes a black color. According to investigations by 
Ztler, Arnold, and Ernst, black pigment may also be formed during life, through the 
action of bacteria which produce hydrogen sulphide, 































THE HAZMATOGENOUS PIGMENTS. 239 


Literature. 


(Hematogenous Pigments.) 


Arnold: Siderofere Zellen. Anat. Anz., xvii.; Virch. Arch., 161 Bd., 1900. 

Borat; Melanose des Pericardiums (Epithelpigmentirung).” Virch. Arch., 147 Bd., 
1897. 

Cordua: Ueber den Resorptionsmechanismus von Blutergüssen, Berlin, 1877. 

Dürck: Veränderungen . Blutungen im Centralnervensystem. Vire. Arch., 180 

Ernst: 'Pseudomelanose. Virch. Arch., 153 Bd., 1898 (Lit.). 

Gabbi: Le cellule globulifere nei loro rapporti alla fisiologia del sangue, Firenze, 1891. 

Langhans: Resorption der Extravasate u. Pigmentbildung. Virch. Arch., 49 Bd. 


1870. 
hlmann: Pigmentmetamorphose der rothen Blutkörperchen. Virch. Arcı., 126 
., 1881. 
Neumann, E.: Beiträge zur Kenntniss der pathologischen Pigmente, ib., 111 Bd., 
1888; Das Pigment der braunen Lungeninduration, ib., 161 Bd., 1900. 
Perls: Nachweis von Eisenoxyd in gewissen Pigmenten, ib., 89 Bd., 1867. 
Quincke: Deut. Arch. f. klin. Med., 25, 27, and 33 Bd. 
Schmidt: Verwandtschaft d. hämafogenen u, autochthonen Pigmente.  Virch, Arc, 
115 Bd., 1889; Hämorrhagie u. Pigmentbildung. Ergebn. d. allg. Pat 97. 
Skrzeceka: Ueber Pigmentbildung in Extravasaten. Beitr. v. Ziegler, i 
Virchow: Die pathologischen Pigmente. Virch. Arch., 1 Bd., 1847. 
Vossius: Grünliche Färbung der Cornea nach Traumen. Graefe’s Arch., 35 Bd., 1889. 
Zeller u. Arnold: Pseudomelanotische Abscesse. Virch. Arch., 189 Bd., 1895. 
Ziegler: Untersuchungen über die Herkunft der Tuberkelelemente, Würzburg, 1875. 





$ 72. When large numbers of red blood-cells break down in the 
circulating blood, a portion of the dissolved hemoglobin or methemo- 
globin may pass into the plasma, or, on the other hand, fragments of red 
cells may be carried about in the circulation. Such a destruction of red 
cells occurs to a marked degree in poisoning with arsenic, toluylendia- 
min, potassium chlorate, and morels; toa lesser degree in other diseases, 
such as many infections, malaria, pernicious anemia, and in overheating 
of the hody. The passage of 
hemoglobin or methemoglobin 
into the blood-plasma leads to 
the condition of hemoglobin- 
emia, in which the blood- 
plasma is colored red. When 
the amount of dissolved he- 
moglobin in the blood is large, 
a portion may be excreted 
through the kidneys, giving 
rise to haemoglobinuria or meth- 
emoglobinuria, in which con- 
ditions the urine may present x 
a bloody appearance, or a color Kar 
varying from a clear brownish- Fi. 107.—Infitration of the cells of the liver-rods with 
red to a dark reddish-black. elem, beingldern granules, run a car of pernicious 
This occurs particularly in the sate of fatty degeneration.” x 250. 
case of the first-named poisons, 
but also occasionally after the action of other injurious influences, as, for 
example, after exposure to cold (periodical hemoglobinuria). 

When formed products arise from the disintegration of the red cells, 
as, for example, after extensive burns, such fragments collect in the 














HZEMOSIDERIN. 243 


the action of H,S on oxyhsmoglobin (Hoppe-Seyler, Harnack). In the absence of oxy- 
gen, sulphur-hemoglobin is formed, which possesses a dark-red color (Harnack). 


Literature. 
(Hoemochromatosis ; Iron Absorption ; Deposit and Excretion.) 


Afanassiew: Toluylendiaminvergiftung. Zeitschr. f. klin. Med., vi.; Mit Hämoglo- 
binurie und Ikterus verbund. Ver iftungen. Virch. Arch., 98 Bd., 1884. 

Alexander: Eisengehalt d. Milz- u. Lymphdrüssen. Inaug.-Diss., Freiburg, 1895. 

Auscher et Lapicque: Accumul. d’hydrate ferrique dans l’organisme. Arch. de 
phys., viii., 1896. 

Arnstein: Ueber Melanämie und Melanose. Virch. Arch., 61 Bd., 1874. 

Baserin: Eisengehalt der Galle bei Polycholie. Arch. f. exp. Path., xxiii., 1887. 

Biondi: ‚Ablagerung von Hämosiderin bei Hämatolyse. Beitr. v. Ziegler, xviii., 1898 
(Lit.). 

Boström: Intoxication durch die essbare Morchel, Leipzig, 1882. 

Cloetta: Eisenresorption im Darm. Arch. f. exp. Path., 38 Bd., 1897. 

Dutton: Iron in the Liver and Spleen in Malaria. Journ. of Path., v., 1898. 

de Filippi: Unters. über das Ferratin. Beitr. v. Ziegler, xvi., 1894. 

Gaule: Resorption des Eisens. Deutsch. med. Woch., 1896. 

Geyer: Die chron. Hautveränderungen bei Arsenicisınus, Arch. f. Derm., 48 Bd., 
1898 (Lit.). 

Grimm: Urobilin im Harn. Virch..Arch., 133 Bd., 1893. 

Harnack: Einfluss d. Schwefelwasserstoffs auf d. Blutfarbstoff. Zeit. f. phys. Chem., 
26 Bd., 1898. 

Heuss: Keratosis u. Melanosis nach Arsengebrauch. Correspbl. f. Schweizer Aerzte, 


1894. 
Hindenlang: Pigmentinfiltration bei Morb. macul. Werlhofi. Virch. Arch., 79 Bd., 
1880 


Hintze: Hämochromatose. Virch. Arch., 189 Bd., 1895. 

Hochhaus u. Quincke: Eisenresorption u. Ausscheidung im Darm. Arch. f. exp. 
Path., 87 Bd., 1896. 

Hofmann: Eisenresorption u. Ausscheidung. Virch. Arch., 151 Bd., 1898. 

Hoppe-Seyler: Abscheidung des Urobilins in Krankheiten. Virch. Arch., 114 Bd., 
1891. 

Hunter: Action of Toluylendiamin. Journ. of Path., iii., 1895. 

Jacob: Ueber Siderosis. Inaug.-Diss., Freiburg, 1895. 

Kober: Ueber das Eisen in diätetischer Hinsicht. Deut. med. Woch., 1894. 

Kobert: Argyrie u. Siderosis. Arch. f. Derm., 1893. 

Kunkel: Farbstoff im Harn. Virch. Arch., 79 Bd.; Pigmentinfiltration, ib., 81 Bd., 


1880. 

Marchand: Giftige Wirkung d. chlors. Salze. Arch. f. exp. Path., 22 and 23 Bd., 
1886, 1887. 

v. Mering: Das chlorsaure Kali, Berlin, 1885. 

Minkowski u. Naunyn: Ikterus durch Polycholie Arch. f. exp. Path., 21 Bd., 
1886, 

Moroni: Siderosi epatica. Arch. per le Sc. Med., xvii., 1893. 

Müller: Arsenmelanose. Arch. f. Derm., 25 Bd., 1893. 

Nasse: Die eisenreichen Ablagerungen im thierischen Kérper, Marburg, 1889. 

Nathan: Aufnahme u. Ausscheidung d. Eisens d. Eisensomatose. Deut. med. Woch., 
1900. 

Neumann: Bilirubinkrystalle im Blute neugeborener und todtfauler Früchte. Arch. 
d. Heilk., x., 1869; Das melanämische Pigment. Virch. Arch., 116 Bd., 1889. 

Nielsen: Melanosis arsenicalis. Monatsh. f. prakt. Derm., xxiv., 1897. 

Opie: Hämochromatosis. Journ. of Exp. Med., iv., 1899. 

Peters: Eisenablagerungen bei versch. Krankheiten. Deut. Arch. f. klin. Med., 32 Bd., 
1882, 

Ponfick: Hämoglobinämie. Berl. klin. Woch., 1877, 1883. 

Quincke: Zur Pathologie des Blutes. Deut. Arch. f. klin. Med., 25, 27 and 83 Bd. ; 
Perniciöse Anämie. Klin. Vortr., No. 100, 1876; Eisentherapie. Klin. Vortr., No. 
129. Leipzig, 1895. 

Scheimpflug: Beitr. z. pathol. Histologie des Darms. Zeitschr. f. klin. Med., ix., 
1885. 

Schurig: Schicksale des Hämoglobins im Organismus. Arch. f. exp. Path., 41 Bd., 
1898. 





HEPATOGENOUS PIGMENT: ICTERUS. 945 


Icterus is a hepatogenous disease, inasmuch as the bile-pigments have their 
source in the liver. As the result of disease processes in the biliary 
passages or in the liver itself the normal outflow of the bile is hindered, 
and the bile is then taken up into the lymphatics and blood-vessels of 
the liver. Such a damming back of the bile may be caused, for exam- 
ple, by a narrowing or closure of the large bile-ducts through the forma- 
tion of scar-tissue, through gall-stones wedged in the lumen, or through 
tumors developing in the bile-ducts themselves, or arising outside of the 
ducts and compressing them; or through inflammatory processes, ab- 
scesses, connective-tissue growths, or tumors of the liver which compress 
or pull upon, or completely obliterate the smaller bile-ducts, and in this 
way hinder the outflow of blood from the smaller bile-ducts and capil- 
laries. 

When through obstruction of any kind the bile is dammed back into 
the intrahepatic bile-passages, namely, into the bile-capillaries, there 
may occur in the first place a resorption of bile through the lymphatics 
of the liver. As the condition progresses the bile accumulates more and 
more in the intra-acinous bile-capillaries (Fig. 111, a, 5) and in the liver- 
cells themselves (c), so that finally the masses of bile-pigment (g) may 
break through into the blood-capillaries, the point of rupture often being 
demonstrable microscopically. Following this the endothelium of the 
blood-capillaries may also become pigmented (d, d,). — 

According to recent investigations regarding the structure of the 
liver, the intracellular bile-capillaries extend into intracellular secretion- 
racuoles (von Kupffer, Pfeiffer) from which are given off extremely fine 
intracellular secretion-canaliculi (Nauwerck, Stroebe, Browicz) surround- 
ing the nucleus as with a meshwork. On the other side the liver-cells 
stand in the closest relationship to the blood-capillaries. Normally, a 
double secretion takes place in the liver, an external one of bile-acids 
and pigment into the bile-passages, and an internal one of sugar and 
urea (Minkowski) into the blood-vessels. Nauwerck is of the opinion 
that this latter secretion is also carried through a network of extremely 
delicate intracellular canaliculi. It is, therefore, easy to understand that 
disturbances of secretion are of not infrequent occurrence, and that a pas- 
sage of bile into the blood may be caused, not only through a stasis of the 
bile, but also through diseased conditions of the liver-cells due to infee- 
tions or intoxications. Besides the icterus due to stasis of the bile, or stasis- 
parapedesis (Minkowski), there may, therefore, be distinguished an éeterus 
due to a toxic or infectious parapedesis of the bile (paracholia, Pick). It is 
probable that many forms of icterus, which were formerly believed to be 
caused by a catarrhal condition of the bile-passages, are to be interpreted 
as belonging to the second class. 

It is also possible that disturbances of innervation and of the circula- 
tion of the liver may be sufficient to bring about an escape of bile into 
the intra-acinous lymph-channels or into the blood, so that a nervous 
paracholia may also be distinguished. 

In paracholia of long standing and of a marked severity, as occurs 
particularly in cases of permanent closure of the bile-passages, not only 
do the liver-cells become pigmented, but also the endothelium of the 
blood-vessels (Fig. 111, d, d). Asthe result of such pigmentation the 
cells not infrequently become desquamated (e), and lie free in the ves- 
sels. Not rarely degenerative changes, cell-necroses, inflammation and 
proliferation of the connective tissue are also associated with the biliary 
stasis. 





HEPATOGENOUS PIGMENT: ICTERUS. 247 


When au increased destruction of red blood-cells takes place within the 
blood-vessels, hematoidin or bilirubin, in addition to hsmosiderin, is 
formed in different parts of the body (see § 72); but the formation of 
bilirubin outside of the liver is very slight and is not sufficient to cause 
any extensive icteric coloration of the tissue, so that a purely hematoge- 
nous jaundice does not occur. The liver is the great elaborator of bilirubin, 
and in cases of increased destruction of the blood-cells the liver-function 
is increased and there is an increased production and excretion of bile- 
pigment. An icterus due to increased destruction of blood-cells can occur 
only when at the same time there are present in the liver such changes 
as cause a passage of the bile into the blood. 


The question as to whether there is a hsematogenous as well as a hepatogenous 
jaundice has long been an object of discussion, and remains unsettled at the present 
time, in spite of numerous experimental investigations directed toward its solution. 
Since, as a matter of fact, bilirubin may be formed in the most different kinds of tissue 
from extravasated blood, the occurrence of a hematogenous icterus would a priort ap- 
pear very probable. Experimental investigations as to the results of the destruction of 
red cells in the circulating blood, particularly through the action of arsenic, toluylen- 
diamin, and potassium chlorate, have shown that the derivatives of blood-pigment 
which are formed in the tissues and there retained for a long time are essentially iron- 
containing pigments (hemosiderin), while the production of bilirubin is practically con- 
fined to the liver, which for the time being secretes an increased amount of richly pig- 
mented bile. 

According to the investigations of Minkowski and Naunyn, the urine of geese and 
ducks after removal of the liver contains no bile-pigment—a fact which would indicate 
that the transformation of blood-pigment into bile-pigment is ordinarily confined to the 
liver. Theinhalation of arseniureted hydrogen fora few minutes is sufficient to produce 
in geese in a very short time an intense polycholia and hematuria, the urine containing 
hz moglobin in solution, disintegrating red cells and biliverdin. If the liver from such 
a goose be removed, the biliverdin quickly disappears from the urine, and no trace of 
bile- pigment can be demonstrated in the blood. It is therefore evident that in arsenic 
poisoning the formation of the bile-pigment is confined to the liver, in which organ 
leucocytes enclosing iron-containing fragments of broken-down red cells are found to 
be present. 

In so far as it is possible to judge from the experimental investigations which have 
been made up to the present time, a pure hematogenous jaundice does not appear to 
«occur. The mere fact of the occurrence of jaundice after intoxications, inhalation of 
«ther and chloroform, transfusion of blood, snake-bite, septicemia, typhoid fever, yel- 
low fever, paroxysmal hemoglobinuria, etc., cannot be taken as proof of the existence 
of a hematogenous jaundice. There is, indeed, in these conditions an increased destruc- 
tion of red blood-cells; but bilirubin is essentially a product of the liver, and if jaundice 
«ccurs it can be due only to the fact that a portion of the bile-pigment, which is pro- 
«luced in excess, has found its way into the blood. It appears that a change in the con- 
sistency of the bile is sufficient (Stadelmann) to cause an absorption of bile-pigment into 
the . 


Literature. 
(Icterus. ) 


~Auld: Hematogenous Jaundice. Brit. Med. Journ., i., 1896. 
"Birch Hirschfeld: Die Entstehung der Gelbsucht neugebor. Kinder. Virch. Arch., 
., 1882. 
®rowicz: Intracelluläre Gallengänge, etc. Deut. med. Woch., 1897: Cbl. f. allg. 
Path., 1898; Lebercapillaren. Bull. de l’Ac. des sc. de Cracovie, 1900. 
Dastre et Florescu: Pigments biliaires. Arch. de phys., ix., 1897. 
Halter u. Lauterbacher: Resorptionsikterus beim Frosch. Beitr. v. Ziegler, x., 1891. 
Harley: Pathology of Obstructive Jaundice. Brit. Med. Journ., 1892; Leber u. Galle 
während dauernden Verschlusses von Gallen- und Brustgang. Du Bois-Reymond’s 
rch., 1893. 
Hofmeier: Die Gelbsucht der Neugeborenen. Zeitschr. f. Gebh. u. Gyn., viii., 1882. 
Kiener et Engel: Pathogénie de l’ictere et ses rapports avec l’urobilinurie. Arch. de 
phys., x., 1887. 














CYST-FORMATION. 253 


may undergo calcification. Cysts of the thyroid and kidneys contain 
colloid masses, or a clear though occasionally cloudy fiuid. 
Retention-cysts lined with endothelium may develop from blood- 
and lymph-vessels, lymph-spaces, burss, and tendon-sheaths. Here also 
the content of the cyst is dependent upon its place and mode of origin, 
As retention-cysts increase in size the stretching of the cyst-wall 
would ultimately lead to a defect iu the continuity of the wall if no new 
formation of tissue took place. Cyst formation is, therefore, not purely 
a degenerative process; such a new formation of tissue takes place first 
in the epithelial or endothelial lining of the cyst, but the connective- 
tissue elements of the wall also increase, so that in spite of the stretching 





Fe ie ne tie tae perivrerien atneawan. 0, Ceres: 
wre Be stewing Tai Stan se wenn © ve + 
ere es: ing para, 


the wall of the evt beeomes no thinner, and under certain edition 
May «ven inereaw: in thickness. Moreover, cyst formation is 
asseciated with a pathological formation of new glandular tissue, 
rel in this way constitutes a secondary change in hypertrophic or tamer 
Like growths, Tt ia therefore. sometimes imprmible to draw a sharp line 
besween the simple cystic: dilatations of preéxisting gland -sanale and 
ghacet pares. and thee tumors. the cystomata, which are characterized 
bs ovat formation we Cystema. Endihrlial epta may ala derdip ont 
of sorely formed lpmph spares and Ipmph-resels, 

A ened form A est in the degeneration-cyst. which ariee~ throngh 
th partial dintegrarion and liqnefaction A a time. Cys forme in 
ths manner seme in the brain hypertrepbie thyrvids. and in trimers. 
Tet mag enanain a clear on Amis. or af times hamerthayie ecutate. 

A third form ff epete rnit from the formation of a comnective- 
tissue capsaie Armand foreign bodies, which have frend entraner te the 
themes, as. fae erample. abewit a ballet: of ale, alent mecrotic areas, +» 

extravasates. 

















A foarth: rariety eye im former by parasites which am thevvugh 


254 THE RETROGRADE CHANGES. 


a cystic stage in the course of their development in the body, and ::re 
likewise surrounded by a connective-tissue capsule. 


Literature. 
( Retention- Cysts. ) 


Aschoff: Cysten. Ergebnisse d. allg. Path., II. Jahrg., Wiesbaden, 1897 (Lit.). 

Bard et Lemoine: De la maladie kystique essentielle des organes glandulaires, Paris, 
1880. 

Chiari: Genese der sog. Atheromcysten. Zeitschr. f. Heilk., xii., 1891. 

Franke: Blutcyste der seitlichen Halsgegend. Deut. Zeitschr. f. Chir., 28 Bd., 1888 
(Lit.). 

Hennes: Angeb. Auswüchse am Halse. Arch. f. Kinderheilk., ix., 1888 (Lit.). 

Hess: Ueber eine subcutune Flimmercyste. Beitr. v Ziegler, viii., 1890. 

Kühne: Pathol. Histologie der Cystenbildung. Virch. Arch., 158 Bd., 1899. 

Marchand: Cysten. Eulenburg’s Realencyklop., 1894 (Lit.) 

Nordmann: Galaktocele. Virch. Arch., 147 Bd., 1897. 

Philippson: Anatomische Untersuchungen über Nierencysten. Virch. Arch., 111 
Bd.. 1888. 

v. Recklinghausen: Ueber die Ranula, die Cyste der Bartholin’schen Drüse und die 
Flimmercyste der Leber. Virch. Arch., 84 Bd., 1881. 

Richard: Geschwülste der Kiemenspalten. Beitr. v. Bruns, iii., 1888. 

Sabourin: La dégénérescence kystique du foie et des reins. Arch. de phys., x., 1882. 

Sasse: Cysten der Mamma. Arch. f. klin. Med., 54 Bd., 1897. 

Terburgh: Ueber Leber- und Nierencysten. Inaug.-Diss. v. Freiburg, Leiden, 1891. 

Török: Entstehung der Atheromcysten. Monatsschr. f. prakt. Derm., xii. 

Virchow: Die krankhaften Geschwülste, i., Berlin, 1868. 











TISSUE-HYPERTROPHIES OF CONGENITAL ORIGIN. 259 


itself in a premature development of certain organs, the structure remaining 
normal. The external and internal sexual organs are most frequently 
affected. Girls, even in the first years of life, may show a development 
of breasts and external genitals and a growth of hair corresponding to 
that of the sexually ripe woman; and menstruation may be established 
at this early period. 


The size of the entire body as well as of its separate parts and organs shows con- 
siderable variation within physiological limits, according to the race, family, and indi- 
vidual. The variation in the relation of the size of single parts and organs to that of 
the entire body is less marked. 

The average height of the body in well-built individuals is, according to Vierordt 
(* Daten u. Tabellen für Med.,” Jena, 1898), as follows: Men 172 cm., women 160 cm. ; 
of the new-born, males 47.4 cm., females 46.75 cm. The average body-weight in 
Europe is for men about 65 kgm., that of women about 55 kgm., that of the new-born 
about 3,250 gm. 

The average weight of the internal organs is as follows, the figures in parentheses 
being for the new-born: Brain 1,897 (885) gm., heart 804 (24) gm., lungs 1,172 (58) gm., 
liver 1,612 (118) gm., spleen 201 (11.1) gm., right kidney 131, left kidney 150 gm., both 
kidneys 299 (23.6) gm., testicles 48 (0.8) gm., muscles 29,880 (625) gm., skeleton 11,560 
(445) gm. Expressed in percentages of the body-weight the figures for adults and new- 
born are (the latter in parentheses): Heart 0.52 (0.89), kidneys 0.48 (0.88), lungs 2.01 
(2.16), stomach and intestines 2.34 (2.53), spleen 0.346 (0.41), liver 2.77 (4.30), brain 2.37 
(14-34), adrenals 0.014 (0.31), thymus 0.0086 (0.54), skeleton 15.85 (16.17), muscles 43.09 
(28.4). 


Literature. 
( Tissue- Hypertrophy of Congenital Origin.) 


Arnheim: Congen. halbseitige Hypertrophie. Virch. Arch., 154 Bd., 1898 (Lit.). 

Baas: Das Hornhauthorn. Cbl. f. allg. Path., viii., 1897. 

Bartels: Abnorme Behaarung. Zeit. f. Ethnol., viii., 1896; Affenmenschen, ib., xvi., 
1884. 

Behrend: Hypertrichosis. Eulenburg’s Realencyklop., 1896 (Lit.). 

Brandt: Hundemenschen. Biol. Cbl., xvii., 1897. 

Bruns: Ueber Rankenneurom. Virch. Arch., 50 Bd.; Beitr. z. klin. Chir., 1891. 

Busch: Riesenwuchs der Extremitäten. Arch. f. klin. Chir., vii., 1866. 

Carbone: Ictiosi congenita. Arch. per le Sc. Med., xv., 1892. 

Caspary: Ichthyosis congenita. Vierteljahrsschr. f. Derm., xiii., 1886. 

Chiari: Ueber Hypertrichosis. Prag. med. Woch., 1890. 

Demme: Halbe. uskelhypertrophie. 27. Jahresber. d. Jenner’schen Kinderspitals, 

rn, 1890. 

Ecker: Ueber abnorme Behaarung des Menschen, Braunschweig, 1878. 

Esmarch u. Kulenkampff: Die elephantiastischen Formen, Hamburg, 1885. 

Esoff: [chthyosis. Virch. Arch., 69 Bd., 1877. 

Ewald: Hypertrophie der Hand. Virch. Arch., 56 Bd., 1872. 

Fischer: Riesenwuchs der Extremitäten. Deut. Zeitschr. f. Chir., xii., 1880. 

Friedrich: Halbseitige congenitale Kopfhypertrophie. Virch. Arch., 28 Bd., 1863. 

Hornstein: Halbseitiger Riesenwuchs. Virch. Arch., 133 Bd., 1898. 

Hürthle u. Nauwerck: Fibroma mollusc. u. congen. Elephantiasis. Beitr. v. Ziegler, 
i., 1886. 

Jacobson: Universeller Riesenwuchs. Virch. Arch., 189 Bd., 1895. 

Jordan: Pathol.-anat. Beitr. z. Elephantiasis congenita. Beitr. v. Ziegler, iii., 1890. 

Kiwull: Zur Casuistik der halbseitigen Gesichtshypertrophie. Fortschr. d. Med., 
viii, 1890. 

Klein: Pubertas praecox. Deut. med. Woch., 1899. 

Kussmaul: Geschlechtliche Frihreife. Würzb. med. Zeitschr., 1862. 

Mitwalsky: Hauthörner der Augenadnexa. Arch. f. Derm., 27 Bd.,1894. 

Nonne: Elephantiasis congenita hereditaria. Virch. Arch., 125 Bd., 1891. 

Poisson: Hyperostose diffuse des maxillaires supérieures. Sem. méd., 1890. 

Poumayrac: ft. sur I’hypertrichosis, Bordeaux, 1893. 

v. Recklinghausen: Die multiplen Fibrome der Haut, Berlin, 1882. 

Réna: Ichthyosis im Jünglingsalter. Arch. f. Derm., xxi., 1889. 

Spietschka: Ueber Elephantiasis congenita. Arch. f. Derm., xxiii., 1891. 

Trelat ct Monod: De l’hypertrophie unilatérale. Arch. gen. de méd., 1869 

15 











264 THE PROGRESSIVE CHANGES. 


a paw-shaped deformity of the hands and a gigantesque appearance of 
the feet, while Marie, who first described these conditions, attempts to 
draw a sharp line between acromegaly and ostéoarthropathie hypertro- 
phiante. He holds that in acromegaly the hands and feet are not de- 
formed, but are syinmetrically enlarged, the thickening and broadening 
diminishing toward the tips of the extremities, so that the terminal 
phalanges of the fingers and toes are but slightly thickened, while, on the 
other hand, in ost@oarthropathie hypertrophiante the terminal phalanges 
are enlarged so as to resemble drumsticks, and the articular ends of the 
bones are irregularly thickened. In the first affection the lower jaw is 
lengthened, in the latter it is thickened. Marie believes that in many 
cases ostéoarthropathie hypertrophiante is a sequela of inflammatory 
aifections of the lungs and pleure, and designates the condition accord- 
ingly as ostévarthropathie hypertrophiante pneumique, and holds that 
the connection between these processes is to be found in the taking up 
into the body-fluids of poisonous products from the inflammatory foci in 
the lungs, so that the affection of the bones is to be regarded as an infec- 
tious toxie hypertrophie inflammation. 

By other authors the causes of acromegaly and ostéoarthropathie hy- 
pertrophiante are to be sought in a congenital predisposition (Virchow), 
in disturbances of the sexual function (Freund), in a hypertrophy of the 
hypophysis (Henrot, Klebs), in persistence of the thymus (Erb, Klebs), or 
in nervous influences (von Recklinghausen); but none of these hy pothe- 
ses is adequately supported by anatomical and clinical observations. 
From the investigations made up to the present time it follows rather 
that these conditions do not represent an excessive growth similar in 
nature to a partial giant growth, but are acquired diseased conditions, 
which develop either as independent. diseases (acromegaly, pachyakria), 
or as secondary phenomena in the course of other diseases (ostéoarthro- 
pathie hypertrophiante pneumique). 

The cause of the hypertrophic condition of the thyroid gland, occur- 
ring so frequently in many regions, is wholly unknown. 


Literature. 
(Compensatory ITypertrophy of Glands and of the Heart.) 
Beresowsky: Compensatorische Hypertrophie d. Schilddrüse. Beitr. v. Ziegler, xii., 


1892. 
Bizzozero: Accrescimento e rigenerazione nell’ organismo. Arch. p. le Sc. Med., 
xviii., 1894. 


Boström: Beitr. z. path. Anat. d. Niere, Freiburg, 1884. 

Bozzi: Untersuch. über die Schilddrüse. Beitr. v. Ziegler, xviii., 1895. 

Eckhardt: Compensat. Hy pertrophie der Nieren. Vireh. Arch., 114 Bd., 1888. 

Grawitz u. Terael As above, ib., 77 Bd., 1879. 

Hodenpyl: Apparent Absence of the Spleen with General Compensatory Lymphatic 
Hyperplasia, Med. Ree., 1898. 

Horwath: Die Hy pertrephie des Herzens, Wien, 1897. 

Krahé: Comp. Hyp. d. Speicheldrüsen. Inaug. “Diss., Bonn., 1888. 

Leichtenstern: Comp. Nierenhypertrophie. Berl. klin. Woch., 1881. 

Nothnagel: Ucher Anpassunge nou. ‚Ausglciehungen bei pathologischen Zuständen. 
Zeitschr. f. klin. Med., 188} ; INN6; xv., 1888. 

Perl: Comp. Nierenhype rtrephic. Viren. Arch., 56 Bd., 1872. 

Podwyssozky: Exp. Unters. üb. die Regeneration d. Drüsengewebe. Beitr. v. 
Ziegler. i, 1886. 

Ponfick Zur Pathologie der Leber. Virch. Arch., 118, 119, and 188 Dd., 1889-1894. 

v. Recklinghausen: Pathologie des Kreislaufes u. d. Ernährung, Stuttgart, 1887. 

Ribbert: Comp. Nierenhypertrophie.  Virch. Arch., &8 Bd.; Compens. Hypertr. d. 


REGENERATION. 265 


Geschlechtsdrüsen, ib., 120 Bd., 1890; Compens. Hypertrophie u. Regen. Arch. f. 
Entwickelungsmechan., i., 1884. 

Rogowitsch: Veränd. d. Hypophyse nach Entfernung d. Schilddrüse. Beitr. v. 
Ziegler, iv., 1889. 

Sacerdotti: Ipertrotia compens. dei reni. Arch. per le Sc. Med., xx.; Virch. Arch., 
146 Bd., 1896. 

Schuchardt: Compensat. Hypertrophie d. rechten Lunge. Virch. Arch., 101 Bd., 
885. 

Stieda: Verhalten d. Hypophyse nach Entfernung d. Schilddrtse. Beitr. v. Ziegler, 
vii., 1 

Stilling: Compensat. Hypertrophie der Nebennieren. Virch. Arch., 118 Bd., 1899. - 

Simmonis: Compensat. Hypertrophie d. Nebennieren. Virch. Arch., 153 Bd., 1898. 

Tangl: d. Hypertrophie u. d. phys. Wachsthum des Herzens. Virch. Arch., 116 
Bd., 

Velisch: Compens. Hypertrophie d. Nebennieren. Virch. Arch., 154 Bd., 1898. 

Wollmann: Ein Fall von Agenesic der l. Lunge. Inaug.-Diss., Freiburg, 1891. 

Ziegler: Ursachen d. pathol. Gewebsneubildungen. Intern. Beitr., Festschr. f. Vir- 
chow, ii., 1891. 

Zielonko: Stud. üb. die Hypertrophie des Herzens. Virch. Arch., 62 Bd., 1865. 


(Acromegaly, Pachyakria, Ostevarthropathie Hypertrophiante, and Hyper- 
trophy of the Skull. ) 


Arnold: Akromegalie, Pachyakrie oder Ostitis. Beitr. v. Ziegler, x., 1891; Beitr. zur 
Akromegaliefrage. Virch. Arch., 135 Bd., 1893. 

Bamberger: Knochenveränd. bei chron. Lungen- u. Herzkrankh. Zeit. f. kl. Med., 
xviii., 1890. 

Brooks: Acromegaly. Archives of Neurology, New York, i., 1898. 

Chiari: Basale Schädelhy perostose bei Idioten. Verh. d. path. Ges., ii., Berlin, 1900. 

Erb: Ueber Akromegalie. Deut. Arch. f. kl. Med., 42 Bd., 1888. 

Freund: Ueber Akromegalie. Samml. klin. Vortr., Nos. 829-30, Leipzig, 1889. 

Friedreich: Hyperustose des gesammten Skeletes. Virch. Arch., 43 Bd., 1863. 

Fritsche u. Klebs: Ein Beitrag zur Pathologie des Riesenw uchses, Leipzig, 1884. 

Holsti: Akromegalie avec autopsic. Festkrift fr. Pathol. Anatom. Institutet Helsing- 
fors, 1890. 

Lefebvre: Des défornat. ostéoarticulaires conséc. ä des mal. de l’app. pleuropulmo- 
naire, Puris, 1891. 

Marie: Sur deux cas d’ akromégalie, hy pertrophic singuliére non congénitale des ex- 
tremités et cephalique. Rev. de 'med., , 1886; De l’ost&oarthropathie hypertro- 
phiante pneumique. Ib., x., 1890. 

Marie et Marinesco: Sur l’anatomie pathol. de l'akromégalie. Arch. de med. exp., 
iii., 1891. 

Minkowski: Ueber einen Fall von Akromegalie. Berl. klin. Woch., 1887. 

Oestreich: Riesenwuchs und Zirbeldrüsengeschwulst. Virch. Arch., 157 Bd., 1899. 

Rauzier: Ostevarthropathie hypertrophiante d'origine pneumique. Rev. de med., 
xi.. 1891. 

v. Recklinghausen: Ueber Akromegalie. Virch. Arch., 119 Bd., 1890. 

Schütte: Path. Anat. u. Aetiol. d. Akromegalie. Cbl. f. allg. Path., ix., 1898 (Lit.). 

Souza-Leite: De l’akromegalie, Paris, 1890. 

Spillmann ct Haushalter: Ostévurthropathic hypertrophiante. Rev. de méd., x 
1890. 

Sternberg: Die Akromegalie, Wien, 1897. 

v. Strümpell: Zur Pathologie d. Akromegalic. Deut. Zeit. f. Nervenheilk., xi., 1897. 

Thomson: Acromegaly with the Description of a Skeleton. Journ. of Anat. xxiv., 
1X91. 

Verstraeten: L’akromégalie. Rev. de méd., ix., 1889. 

Virchow. Ueber Akromegalie. Berl. klin. Woch. and Deut. med. Woch., 1889. 


§ 79. Regeneration is that process through which tissues which have been 
destroyed are restored. Under especial conditions this restoration may be 
brought about by an enlargement of existing parts of cells (regeneration 
of axis-eylinders), but it is usually the result of new-formation of cells, which 
arise in all cases through the division of preéxisting cells. 

Regeneration presupposes that the injured tissue is capable of pro- 
liferation, and is, moreover, a phenomenon which is in all cases depend- 








270 THE PROGRESSIVE CHANGES. 


its tentacles and anterior extremity, crabs and crayfish their claws and legs. Salaman- 
ders are able to restore their legs, eyes, and tails, and lizards and slow-worms their 
tails, when these are broken off. In the case of frogs, snakes, and fishes, on the other 
hand, the power of regeneration diminishes as the scale of animal life is ascended, yet 
this does not happen equally in the case of all animals, and animals closely related to 
each other may show very different capacities for regeneration. Further, in the same 
animal the regenerative power is not the same in all organs; for example, in tritons the 
regencrative capacity of the internal organs is slight. Moreover, the power to forma 
new portion of the body, asa tail or extremity, for example, does not prove that all 
the tissues of the portion of the body in question possess an especial capacity for pro- 
liferation. In crayfish and crabs the regeneration of the claws and legs takes place only 
from certain places; in injuries occurring to other points, the new extremity is thrown 
off only at that. place, where a new-formation is possible. In tritons, fractures of the 
bones heal very slowly, although they are able to reproduce their extremities. 

Several years ago @raritz advanced the view (“ Ueber die schlummerden Zellen des 
Bindegewebes und ihr Verhalten bei progressiven Ernährungstörungen,” birch. Arch., 
127 Bd., 1892; “ Atlas der pathologischen Gewebelehre,” 1898) that cells may ale arise 
from intercellular substance, He holds that, in the formation of connective tissue, cells 
are transformed into fibres and pass over into a non-nucleated resting-stage, in which 
condition they are invisible under the microscope. From these invisible slumbering-cells 
(Schlummerzellen) new cells may arise in inflammation and tissue-proliferation. In this 
theory of slumbering-cells, Grawitz has brought forward as a new teaching, views 
which were held years ago by Stricker and Heitzmann, and which had been regarded 
as buried; but the work done by him and his pupils in his institute contains nothing to 
substantiate this view. The well-known phenomena of proliferating and inflamed tis- 
sues have been described, but no observations have been published which can be re- 
garded as proving that cells may arise from intercellular substance—that is, from invisi- 
ble slumbering-cells. 


§ 80. The cause of the cell-proliferation underlying all hyperplastic 
and regenerative new-formations of tissue varies according to the condi- 
tions under which the proliferation occurs. If the new tissue-growth 
leading to hypertrophy takes its origin from the anlage of the organism 
concerned or of a portion of the same, no new stimulus is necessary for 
its appearance; the attainment of the abnormal size is dependent only 
upon the condition that the new-formation of tissue does not lead to 
hindranees to growth before the full limit of development is reached. 
When the proliferation appears first at a later period, something addi- 
tional is necessary to cause an increase of the normal tissue-formation or 
to start again into activity the cell-proliferation which becomes quiescent 
at the close of the period of growth. 

In the case of both hyperplastie and regenerative proliferation the 
“ stimulus” may consist simply iu the removal of hindrances to growth. 
Experience teaches that the majority of the cells of the body possess the 
power ina given case to divide, even those (connective-tissue cells, gland- 
cells, muscle-cells) in which the processes of cell-division wholly cease 
for long periods of time. This cessation of proliferation may be ex- 
plained by the assumption that the firm combination of the cells with 
each other and the formation of the intercellular cement inhibit further 
multiplication. It is also possible that chemical and unknown vital 
Influences act in the same manner. Injuries and degenerations of the 
tissues of the most varied kinds can, through the loosening of the cells, 
and through physical and chemical changes in the intercellular cement 
substance and of the tissue-fluids, cause such changes that all hindrances 
to the growth and division of cells are removed. 

In addition to the removal of hindranees to growth there may be 
present at the same time a formative stimulus, which increases both 
the reproductive capacity and the tendency toward reproduction. 
Further, such a stimulus may act independently—that is, without the 


REGENERATION AND REPAIR. 271 


removal of the influences inhibiting growth—and this event is to be 
assumed in those cases in which after the loss of a portion of an organ 
the remaining portion (liver, kidney) undergoes a compensatory hy per- 
trophy. 

The stimuli which are able to excite growth and cell-division are 
known only in part. In those cases in which their action may be recog- 
nized they appear to be identical with the stimuli which excite or increase 
Junctional and nutritive activity. In the case of the muscles hypertrophy 
is brought about by increased contraction following nervous excitation. 
Liver and kidney tissue undergo proliferation when, as the result of a 
loss of a large area of gland-tissue, the remaining portions are obliged to 
do an increased amount of work—that is, they must out of the circulating 
blood produce and secrete those substances which, if life is to be pre- 
served, must be given off either externally or within the body. 

Whether there exist still other formative stimuli cannot be said with 
certainty at the present time. An increased supply of nutrition, which has 
been believed by many to act as a formative stimulus, is not in itself 
sufficient to excite a new-formation of cells and tissue; it gives rise only 
to an increased deposit of fat. The cells of the body are not fed, they 
feed themselves; and an increase of nutrition depends upon the activity 
of the cells. An increase of the temperature of the tissues may hasten the 
process of cell-division and thereby further tissue-proliferation; but it is 
doubtful if it can directly excite proliferation in a resting-tissue. The 
local action of heat, which has been observed to be followed by prolifer- 
ation (for example, in the skin), produces in the first place changes of a 
degenerative nature, so that the occurrence of proliferation may be also 
explained as due to the removal of intluences inhibiting growth. 

Whether there are chemically active substances capable of exciting pro- 
liferation, besides those present normally in the body, cannot be decided 
at the present time. The fact that slight irritation of the skin (painting 
with iodine) can cause proliferation without preceding degenerative 
changes makes this appear probable. But it is more probable that, in 
spite of the negative findings, slight tissue-changes of a degenerative 
nature do occur, and that through these the inhibitory influences are 
weakened. 

Moreover, it must be noted that even the hypertrophy of muscles and 
glands following increased activity cannot be absolutely regarded as the 
direct result of a nervous or chemical stimulus, but rather must we 
assume that with the increased labor there is an excessive consumption of 
cell-elements which excites regenerative processes, the latter leading not only 
to a restoration of the parts lost, but also to an increased building-up of 
the cell-mass and formation of new cells. 


Literature. 
( Regeneration. ) 


Aschoff: Regeneration u. Transplantation. Ergebn. d. allg. Path., v., 1900. 

Bard: La spécificité cellulaire. Arch. de phys., vii., 1886; Intern. med. Congr., 
Berlin, 1890; De l’induction vitale ou influence spécifique a distance des éléments 
cellulaires les uns sur les autres. Arch. de méd. exp., 1890; La specificité cellu- 
laire, Paris, 1899. 

Barfurth: Zur Regeneration de. Gewebe. Arch. f. mikr. Anat., 37 Bd., 1891; Regen- 
eration d. Keimblätter bei Amphibien. Anat. Hefte, Wiesbaden, 1893; Regenera- 
tion u. Involution. Ergebn. d. Anat., Wiesbaden, 1893-1900. 

Beneke: Die Ursachen der Thrombusorganisation. Beitr. v. Ziegler, vii., 1890. 


272 THE PROGRESSIVE CHANGES. 


Bizzozero: Accroissement et régénération dans l’organisme. Arch. ital. de biol., xxi., 
1894; Arch: per le Sc. Med., xviii., 1894; Influence de la température. Arch. ital. 
de biol., xxvi., 1896. 

Caporaso: Sulla rigeneraz. del midollo spinale della coda dei Tritoni. Beitr. v. Zieg- 
ler, v., 1889. 

Carnot: Les régénérations d’organes, Paris, 1899. 

Carriere: Studien über die Regeneration der Wirbelthiere, Würzburg, 1880. 

Cattani: Ueber die Reaction der Gewebe auf specifische Reize. Beitr. v. Ziegler, vii., 
1890. 

Coön: Veränderungen d. Haut nach Einwirkung von Jodtinctur. Beitr. v. Ziegler, 
ii., 1887. 

Cohnheim: Vorlesungen über allgemeine Pathologie, 1882. 

Colucci, F.: Intorno alla rigenerazione degli arti e della coda nei Tritoni, Bologna, 1885. 

Delage: [a structure du protoplasme, Paris, 1895. 

Demarquay: )e la regeneration des organes ct des tissus, Paris, 1874. 

Fraisse: lie Regeneration von Geweben u. Organen bei Wirbelthieren, Berlin, 1885. 

Götte: Ueber Entwickelung u. Regen. des Gliedmaassenskelets der Molche, Leipzig, 
1879. 

Gruber, A.: Beiträge zur Kenntniss der Physiologie und Biologie der Protozoen. 
Berichte der Naturf. Ges. zu Freiburg i. B., 1886; Biol. Cbl., iv., 1886. 

Harrison: Regeneration of the Tail of the Frog Larva. Bull. of Johns Hopkins 
Hosp., x., 1899. 

Haeckel: Ursprung und Entwickelung der thierischen Gewebe, Jena, 1884. 

Hansemann: Studien über die Specificität, den Altruismus und die Anaplasie der 
Zellen, Berlin, 1893; Ueber die Specificität der Zelltheilung. Arch. f. mikr. Anat., 
48 Bd., 189. 

Herbst: Formative Reize. Biol. Cbl., xv., 1895. 

Klaatsch: Stand der Keimblattfrage. Münch. med. Woch., 1899. 

Kölliker: Die embryonalen Keimblätter und die Gewebe. Zeitschr. f. wiss. Zool., 40 
Bd., 1884; 42 Bd., 1885. 

Marchand: Bez. d. path. Anat. z. Entwickelungsgesch. Verh. d. Deut. path. Ges., 
ii., 1900. 

Martinotti: Ueber Hyperplasie u. Regeneration der drisigen Organe in Beziehung 
auf ihre Functionsfähigkeit. Cbl. f. allg. Path., i., 1890. 

Merkel: Bemerkungen üb. d. Gewebe beim Altern. Verh. d. X. intern. med. Congr., 
Berlin, 1891. 

Minot: Vererbung u. Verjüngung. Biol. Cbl., xv., 1895. 

Morgan: Earthworm Regenerating a Tail in Place of a Head. An. Anz., xv., 1899. 

Morpurgo: Sur les rapports de la régénération cellulaire avec paralysie vaso-motrice. 
Arch. ital. de biol., xiii., 1890; Sulla neoproduzione degli elementi cellulari di 
animali nutriti dopo un lungo digiuno. Arch. per le Sc. Med., xiv., 1890: Ueber 
den physiol. Zellneubildungsprocess während der Inanition. Beitr. v. Ziegler, iv., 
1889 


Pekelharing: Ueber Endothelwucherung in Arterien. Beitr. v. Ziegler, viii., 1890. 

Penzo: Influenza della temperatura nella rigenerazione. Arch. per le Sc. Med., xvi., 
1892. 

Podwyssozki, Jun.: Regeneration der Drüsengewebe. Beitr. v. Ziegler, i., ii., 
1886-87. 

Rand: Regenerat. and Regulat. in Hydra viridis. Arch. f. Entwickelungsmech., viii., 
ix., 1899. , 

v. Recklinghausen: Allg. Path. d. Kreislaufs u. d. Ernährung, 1888; Ucber Akro- 
megalie. Virch. Arch., 119 Bd., 1890. 

Ribbert: Das patholog. Wachsthum d. Gewebe, Bonn, 1896; Umbildungen. Virch. 
Arch., 157 Bd., 1899. 

Roemer: Ucber den formativen Reiz der Proteine Buchner’s. Berl. klin. Woch., 1861: 
Chem. Reizbarkeit thier. Zellen. Virch. Arch., 128 Bd., 1892. 

Roux, W.: Der Kampf der Theile im Organismus. Leipzig, 1881; Ueber die Speciti- 
cation der Furchungszellen und über die bei der Postgeneration und Regeneration 
anzunehmenden Vorgänge. Biol. Cbl., xiii.. 1893. 

Samuel: Die Regeneration. Virch. Arch., 50 Bd.; Die histogenetische Energie und 
die Symmetrie des Gewebswachsthums, ib., 101 Bd; Das Gewebswachsthum bei 
Störungen d. Circulation, ib., 108 Bd.; Gewebswachsthum bei Störung d. Inner- 
vation, ib., 113 Bd. 

Sokoloff: Bedingungen d. Bindegewebsneubildung in doppelt unterbund. Gefässen. 
Beitr. v. Ziegler, xiv., 1893. 

Strasser: Zur Kenntniss der functionellen Anpassung der quergestr. Muskeln, Stuttg., 
1883. 








KARYOKINESIS. 275 


the neighborhood of the polar corpuscles themselves the granules of the 
protoplasm present a radial arrangement, giving rise to figures (Fig. 
142) which are known as ray-figures, stars, or attraction-spheres. In the 
following stage of division of the nucleus, which has been designated 
metakinesie, a movement takes place among the chromosomes leading to 
the formation of unequal-sided loops, whose angles are directed toward 
the pole. Later the loops, following the direction of the spindle-fibres, 
move toward the poles and form two stars (Figs. 142, 143) which are 
known as daughter-stars. From the star-figures the daughter-star passes 
successively through the thick-skein and then the fine-skein stage (Fig. 
144, upper part) which finally changes into the nuclear framework (Fig. 
144, lower part). During the later stages of the process of division a 
new nuclear membrane is formed. 

The division of the cell-protoplasm usually takes place at the time 
the daughter-star changes into the ordinary nuclear condition, and con- 
sists in a constriction and separation of the protoplasm (Fig. 144). The 
radiating figures (Fig. 142) about the centrosomes are to be regarded as 
evidences of movements within the protoplasm. It is probable that a 
complicated interrelationship exists between the nucleus and cell-proto- 
plasm; but the nucleus is to be regarded as the more highly organized sub- 
stance, as the centre of cellular potentiality, The nuclei are also the bearers 
of heredity, while the protoplasm governs the relations of the cell with 
the outer world. 

Variations from the typical karyokinesis may consist in the first 
place in the occurrence of a pluripolar division in place of the bipolar, so 
that two to six or more nuclear spindles and a correspondingly increased 
number of equatorial plates (Fig. 145, a) may be formed. Further, in 
place of the simple mother-star there may be formed a complicated figure 
out of the chromatin loops, from which 
several daughter-stars may be evolved. 
Not infrequently there occur asymmetrical 
divisions of the nucleus (Fig. 145, b, c), par- 
ticularly in tumors, but occasionally also 
in regenerative or inflammatory new-for- 
mations of tissue. 

There also not infrequently occur 
divisions of the nucleus which are char- 
acterized by abnormal size, abnormal rich- 
ness in chromatin, and manifold variations 
of form. As types of such division are 
the large oval or bean-shaped (Fig. 146), pıa.116..a.Plurpoiar sviton-tgure: 
knobbed or convoluted, lobulated and d.c, asymmetrical division-Agures. 
branched (Fig. 147), wreath-shaped, 
linked, basket-shaped (Fig. 148), and otherwise-shaped nuclei. Finally, 
there are occasionally found in the cells more or less extensive, indis- 
tinctly-outlined heaps of granular and lumpy chromatin (Fig. 149). 

Such nuclear forms, with the exception of the polynuclear leucocytes, 
are found particularly in the cells of the bone-marrow, spleen, and 
lymph-glands, and also in tumors which arise from the bone-marrow or 
periosteum, but have been also observed elsewhere, particularly in sar- 
comata. Certain of these forms are appearances due to contraction, and 
have nothing to do with cell-division. In other cases these changes of 
size and form precede a division of the nucleus through constriction of 
certain portions, this process occurring sometimes with, sometimes with- 

16 











278 THE PROGRESSIVE CHANGES. 


of the spindle, thus completing the mother-star (Fig. 154). At the same time the 
nuclear membrane disappears while from the poles of the spindle radially-arranged 
fibrils (Figs. 154-156) stream out into the cell-protoplasm (eytaster, attraction-sphere). 

Metakineaia is characterized by a separation of the daughter-threads arising from 
the longitudinal fission, which up to this time have remained parallel with each other: 
and it is completed sometimes by the threads of each pair (Fig. 155) moving toward 
the opposite poles. The new loops arising in this way have their angles directed tow- 
ard the poles, 

The daughter-stars (Fig. 156) are formed by the chromatin loops that have moved 
toward the poles of the spindle, 

The daughter-skeins (dispirem of Flemming) arising from the daughter-stars consist 
of loops of fibrils which are bent back at the point where the poles of the spindle arc 
situated (Fig. 157, a) and leave one polar field (c, d) free from loops. 

The transition from the skein into the framework of the resting-nucleus (Fig. 157, 
b) follows (Rudl) the division of the cell-protoplasm, and is initiated by the chromatic 
fibres sending out processes. According to Flemming, Strassburger, and Retzius, the 
chromatin threads unite directly with one another. 

The significance of the nuclear corpuscles (nucleoli) is still a matter of dispute. 
Flemming and Pfitzner believe that they are different from the nuclear framework, 
while others regard them as much-thickened nodal points of the fibrils of the frame- 
work, In what way they are aguin formed after the division of the nucleus is not 
known. 

The muckar framework forms at its periphery & thick, basket-like layer, on the 
outer side of which lics another membrane, which does not stain. 

The spindle-figure, whose fibres stain but slightly with nuclear stains, is derived. 
according to Flemming and Hertwig, from the above-mentioned achromatic substance 
of the nuclear framework, while Strassburger believes 
that it arises from the cell-protoplasm. 

‘The centrosomes or polar corpuscles, which are always 
present in nuclear segmentation, are found also in rest 
ing-nuclei; but up to the present time they have been 
demonstrated only in a part of the cells, most frequently 
in lymphocytes and the giant-cells of the bone-marro 
At the same time the investigations of ron Kalliker. 
Flemming, M. Heidenhain, and others make it probable 
that the centrosomes are present in all cells, lying sonıc- 
times in the nucleus, sometimes in the protoplasm, where 
on account of their small size they can be demonstrated 
only with difficulty. (The centrosomes do not stain with 
the ordinary nuclear stains, but with acid aniline dyes, as 
acid fuchsin and safranin.) Whether they are elements 
of the protoplasm or of the nucleus has not yet been di 
cided, According to van Beneden, Boveri, and Rabl, the 
mitosis of the nuclear substance is to be referred to a 
Fic. 157. —Danghterakein (a), direct drawing-apart, starting from the divided centro. 
and daughter Jattice-work (1); somes and brought about by the agency of the achro 
Polar area with the remains of he matic fibres, According to M. Heidenkain, the central 
—_ 7 corpuscles are sharply circumscribed granules which 

possesss the power of assimilation, of growth and of 
multiplication by budding, whereby they are accustomed to form groups. Either alone 
or united in groups, they can form the central point of insertion of a system of con- 
tractile fibres (spindle-figures, microsome rays), and consist of a specific substance (in 
a chemical sense) which is not present elsewhere in the cell. 

Flemming designates the cell as a circumscribed mass of living matter, and distin- 
guishes in the eell-inly two different elements, one of which, the protoplasm (filarmass, 
mitome, framework) is somewhat more highly refractive and is arranged in the form of 
threads, while the other, the paraplaam (interfilar mass, paramstome) fills in the remain- 
ing space. ‘The products of metabolism, granules, ‘vacuoles, and other inclusions, 
which the cells at times contain do not belong to the cell-substance. Arnold advances 
the view that many threads contain granules (microsomes, plaemosomes) or break up into 
rows of granules which are united by connecting links. The plasmosomes may also 
become changed into granules (sce $ 66). 

















CELLS AND CELL-DIVISION. 279 


Literature. 
(Cells and Cell-division. ) 


Arnold: Kerne u. Kerntheilungen in den Zellen des Knochenmarkes. Virch. Arch., 
93 Bd., 1888: Ueber Kern- und Zelltheilungen bei acuter Hyperplasie der Lymph- 
drüsen und der Milz. Ib., 95 Bd., 1884; Theilungsvorginge an den Knochenmark- 
zellen. Ib., 97 Bd., 1884; Ueber Kerntheilung und vielkernige Zellen. Ib., 98 Bd., 
1884; Theilungsvorgänge an den Wanderzellen. Arch. f. mikr. Anat., xxx., 1887; 
Kern- u. Zelltheilungen in der Milz. Ib.,xxxi., 1888; Structur und Architektur der 
Zellen. Ib., lii., 1898; Flemming und die Mitosenlehre. Anat. Anz., xvi., 1899. 

Bardeleben: Karyokinese. _Eulenburg’s encyklop. Jahrb., i., 1891. 

Bizzozero: Ueb. die Regeneration. Cbl. f. d. med. Wiss., 1886 (Lit.). 

Boveri: Zellenstudien I-II, 1887-88. 

Cornil: Multiplication des cellulues de la mo&lle des os. Arch. de phys., x., 1888. 

Demarbaix: Division et dégénérescence des cellules geantes. La Cellule. v., 1889. 

Denys: La cytodiérése des cellules géantes et des petites cellules incolores de la moélle 
des os. Cellule, 1886; Division des cellules géantes de la moélle des os d’aprés 

"les travaux de Arnold, Werner, Löwit et Cornil. Anat. Anz., iii., 1888; La Cellule, 
v.. 1889. 

Eberth: Virch. Arch., 67 Bd.; Kern- und Zelltheilung während der Entzündung u. 
Regeneration. Internat. Beitr., Festschr. f. Virchow, ii., Berlin, 1891. 

Fischer: Fixirung, Farbung und Bau des Protoplasmas, Jena, 1899. 

Flemming, W.: Kerntheilung. Arch. f. mikr. Anat., xvi., 1879; xviii., 1880; xx., 
1882; xxiv., 1884; Virch. Arch., 77 Bd.; Zellsubstanz, Kern- und Zelltheilung, 
Leipzig, 1882; Ueber Zeclltheilung. Verh. d. Anat. Gesellsch., München, 1891; 
Beiträge zur Kenntniss der Zelle. Arch. f. mikr. Anat., xxix., 1887; Theilung u. 
Kernformen bei Leukocyten. Ib., xxxvii., 1891; Amitotische Theilung im Blasen- 
epithel des Salamanders. Ib., xxxiv., 1890. 

Frenzel: Zur Bedeutung der amitotischen Kerntheilung. Biol. Cbl., xi., 1891. 

Fuerst: Veränd. d. Epith. durch. Wärme u. Kälte (Riesenzellen durch directe Kern- 
theilung). Beitr. v. Ziegler, xxiv., 1898. 

Galeoti: Chromatin in den Epithelzellen der Carcinome. Beitr. v. Ziegler, xiv., 1893; 
Erzeugung von Unregelmässigkeiten d. kuryokinet. Processe. Ib., 1893; xx., 1896. 

Gruber, A.: Biologie der Infusorien. Ber. d. Naturf. Gesellsch. zu Freiburg, 1886; 
Einflusslosigkeit des Kerns auf Bewegung, Ernährung u. Wachsthum einzelliger 
Thiere. Biol. Cbl., iii., 1883; Zeitschr. f. wiss. Zool., xxxviii., 1883. 

Hansemann: Ueber asymmetrische Zelltheilung in Epithelkrebsen u. deren biologi- 
sche Bedeutung. irch. Arch., 119 Bd., 1890; Ueber pathol. Mitosen. Ib., 123 
Bd., 1891; Stud. üb. d. Specifität, d. Altruismus u. d. Anaplasie der Zellen, 
Berlin, 1893. 

Hertwig, O.: Bildung, Befruchtung u. Theilung d. thier. Eies. Morph. Jalırb., i., 
1875; iii., 1877; iv., 1878; Ei- u. Samenbildung bei Nematoden. Arch. f. mikr. 
Anat., xxxvi., 1890; Die Zelle und die Gewebe, Jena, 1893. 

Hess: Ueber Vermehrungs- u. Zerfallsvorgänge an den grossen Zellen in der acut 
hıyperplastischen Milz der Maus. Beitr. v. Ziegler, viii., 1890. 

Klebs, G.: Ueber den Einfluss des Kerns in der Zelle. Biol. Cbl., vii., 1887. 

Kölliker: Zeitschr. f. wiss. Zool., xlii., 1885. 

Krafft: Histogenese des Callus. Beitr. v. Ziegler, i., Jena, 1886. 

Krompecher: Die Mehrtheilung.. Chl. f. allg. Path., v., 1894; Die mehrfache Kern- 
theilung, Wiesbaden, 1895; Mitosen mehrkerniger Zellen. Virch. Arch., 142 Bd., 
1895. 

Löwit: Neubildung u. Zerfall weisser Blutkörperchen. Sitzber. d. K. Akad. d. Wiss. 
in Wien, 92 Bd., 1885; Neubildung u. Beschaffenheit d. weissen Blutkörperchen. 
Beitr. v. Ziegler, x., 1891; Amitotische Kerntheilung. Biol. Cbl., xi., 1891; Cbl. 

f. allg. Path., i., 1890. 

Meves: Üeber eine Art der Entstehung ringförmiger Kerne, Kiel, 1893. 

Nauwerck u. Steudel: Itegenceration d. quergestreiften Musculatur. Beitr. v. Zieg- 
ler, ii., 1888. 

Nedjelsky: Amitotische Theil. in path. Neubild. Beitr. v. Ziegler, xxvii., 1900. 

Pfe : Bedeutung der Amitose. Ber. d. K. Sächs, Ges. d. Wiss. z. Leipzig, 1899. 

Pfitzner: Arch. f. mikr. Anat., xxii., 1883; Morph. Jahrb., xi., 1885. 

Podwyssozky: Regeneration d. Driisengewebe. Beitr. v. Ziegler, i., ii., 1886-88. 

Rabl: Ucber Zelltheilung. Morph. Jahrb., x., 1885; Anat. Anz., 1888, 1889. 


280 THE PROGRESSIVE CHANGES. 


Reinke: Untersuchungen über das Verhältniss der von Arnold beschriebenen Kern- 
formen zur Mitose und Amitose. Inaug.-Diss., Kiel. 1891. 

Betzius, G.: Studien über die Zelltheilung, Stockholm, 1881. 

Roux, W.: Ueber die Bedeutung der Kerntheilungsfiguren, 1883. 

Schlatter: Stand der Zellenlehre. Biol. Cbl., xix., 1889. 

Schottländer: Ueber Kerntheilungsvorgänge in dem Endothel der artificiell entzün- 
deten Hornhaut. Arch. f. mikr. Anat., xxxi., 1888. 

Schwarz: Zur Theorie der Kerntheilung. Virch. Arch., 124 Bd., 1894. 

Strasburger: Zellbillung u. Zelltheilung, Jena, 1890; Ueber den Theilungsvorgang 
der Zellkerne u. d. Verhältniss der Kerntheilung zur Zelltheilung. Arch. f. mikr. 
Anat., xxi., 1882; Die Controversen d. indirecten Kerntheilung. Ib., xxiii., 1884; 
Das Protoplasma u. die Reizbarkeit, Jena, 1891. 

Stroebe: Kerntheilung u. Riesenzellenbildung in Geschwülsten u. im Knochenmark. 
Beitr. v. Ziegler, vii., 1890; Celluläre Vorgänge u. Erscheinungen in Geschwülsten. 
Ib., xi., 1891; Vorkommen und Bedeutung der asymmetrischen Karyokincsen. 
b., xiv., 1893. 

Tangl: Zellkörper u. Kern während der mitotischen Theilung. Arch. f. mikr. Anat., 
XXx., 1887. 

Verworn: Die physiologische Bedeutung des Zellkerns. Pflüger’s Arch., 51 Bd., 
1892. 

Waldeyer: Ueber Karyokinese. Deut. med. Woch., 1886, 1887. 

Weismann: Das Keimplasma, Jena, 1892. 

Wilson: The Cell in Development and Inheritance, New York, 1897. 

Zander: Ueber d. gegenwärtigen Stand der Lehre v. d. Zelltheilung. Biol. Cbl., xii., 
1892. 

Ziegler, H. E.: Biologische Bedeutung der amitotischen Kerntheilung. Biol. Cbl., 
xi., 1891. 


(Attraction-spheres, Centrosomes, and Nuclear-spinde. ) 


van Beneden: Rech. s. 1. fécondation. Bull. de l’Acad. Roy. Belgique, xiv., 1887. 

Boveri: Zellenstudien I.-II., 1887-88. 

Bürger: Was sind die Attractionssphären und ihre Zellkörper? Anat. Anz., vii., 1892. 

Carnoy: Fecondation. La Cellule, xiv., 1898. 

Flemming: Ueb. Theilung u. Kernformen bei Leukocyten u. über deren Attractions- 
sphären. Arch. f. mikr. Anat., 37 Bd., 1891; Attractionssphären u. Centralkörper. 
Anat. Anz., 1891. 

Fol: Die Centrenquadrille. Anat. Anz., 1891. 

Häcker: Stand der Centrosomafrage. Verh. d. Deut. Zool. Gesellsch., 1894. 

Heidenhain, M.: Centralkörper. Arch. f. mikr. Anat., 43 Bd., 1894; Centralkörper 
u. Attractionssphären. Anat. Anz., 1891; Kern- u. Protoplasma. Festschr. f. 
Kölliker, 1892. 

Hermann: Entstehung der karyokinetischen Spindel. Arch. f. mikr. Anat., 37 Bd., 
1891. 

Hertwig: Die Zelle und die Gewebe, Jena, 1898. 

v. Kölliker: Handb. d. Gewebelehre, i., Leipzig, 1889. 

Lustig u. Galeotti: Cytolog. Studien über pathol. Gewebe. Beitr. v. Ziegler, xiv., 
1893. 

Strasburger: Zu dem jetzigen Stand der Kern- u. Zelltheilungsfragen. Anat. Anz., 


@). 


ll. The Processes of Hyperplasia and Regeneration in the Various 
Tissues. 


§ 82. The morphological changes in the regeneration and hyperplasia 
of epithelium are relatively simple. The karyomitoses (Fig. 158, a—d) 
show for the chief part a typical course. The division of the protoplasm 
takes place either in the later stages of the process of nuclear division 
or follows after the same. Occasionally processes are first formed from 
the proliferating epithelial cells, and into these nuelei later wander. 
Through separation from the mother-cell these processes may become 
independent cells. 





282 THE PROGRESSIVE CHANGES. 


extend to a relatively great distance from the wound. Experimental 
wounds of the liver heal through the formation of connective tissue, into 
which only offshoots of the bile-ducts penetrate, while a local reproduc- 
tion of liver-tissue does not take place. Likewise, in the kidneys, testi- 
cles, thyroid, and ovary the local production of glandular tissue in the 
connective-tissue scar is very slight or wholly wanting, and does not 
lead to the formation of functionating tissue. In the salivary and mu- 
cous glands, on the other hand, there occurs a branching of the gland- 
ducts, and a new-formation of glandular alveoli. 

When portions of the mucosa and submucosa of the intestine are lost 
as a result of ulcerative processes, there occurs during the process of 
healing a glandular proliferation, which, according to the nature of the 
defect, forms partly typical, partly atypical (Fig. 133, ¢) glands which 
grow into the submucosa. The new gland-formation takes its start from 
the old glands, whose epithelium pushes over the edge and base of the 
ulcer (Fig. 133, g, h) and also lines any depressions which may happen 
to be present (kK). In asimilar manner ulcerative defects of the stomach 
mucosa are again made good; and even extensive ulcers may become 
covered over with a gland-containing mucosa, although the glands do 
not for the most part show a typical development—that is, are not trans- 
formed into characteristic gastric glands. 

The epithelial portions of the uterine mucosa which are in part lost, 
as a physiological process, during menstruation and parturition, and are 
afterward replaced, may be restored in a similar manner in the healing 
of pathological defects of the endometrium. The new-formation of epi- 
thelium takes its origin from the glandular remains. 

Compensatory hypertrophy of a kidney or liver, as the result of the 
loss of kidney- or liver-tissue, is brought about through the formation of 
new gland-cells, and the enlargement of existing renal tubules, or liver-rods 
respectively. After extirpation of one kidney the beginnings of compen- 
satory hypertrophy are recognizable even on the third day, by the ap- 
pearance of division figures in the epithelium of the urinary tubules; 
and there then follows a further proliferation, continuing for some time, 
of the epithelium of the uriniferous tubules and glomeruli as well as of 
the cells of the vessel-walls, as a result of which all the parts become 
enlarged. In the liver the lobules are enlarged, but no new-formation 
of these occurs. 


Literature. 
( New-formation of Epithelium and Gland- Tissue. ) 


Arnold: Epithelregeneration. Virch. Arch., 46 Bd., 1869. 

Babes et Manicardite: Prolifér. des cellules hépatiques. Ann. de l’Inst. de path. de 
Boucarest, v., 1899. 

Barbacci: Rigeneraz. fisiol. degli elementi epiteliali. Arch. per le Sc. Med., xiii., 
1889. 

Beltzow: Regen. des Harnblasenepithels Virch. Arch., 97 Bd., 1884. 

Bizzozero: Regen. d. Drüsenzellen. Virch. Arch., 110 Bd.; Arch. per le Sc. Med., 
xi., 1887; Die schlauchförmigen Prüsen d. Magendarmkanals. Arch. f. mikr. 
Anat., 32 Bd., 1893. 

Bockendahl: Regen. v. Flimmerepithel. Arch. f. mikr. Anat., xxiv., 1885. 

Bossi: Reprod. de la muqueuse de Vuterus. Arch. ital. de Biol., xxiv., 1895. 

Coén: Veränderungen der Haut nach der Einwirkung von Jodtinctur. Beitr. v. Zieg- 
ler, ii.; Zur Anatomie der Milchirüse. Ib., ii., 1887. 

Coén e D’Ajutolo: Sulle alterazioni istologiche dei reni, dei muscoli, dello stomaco, 
degli intestini e del fegato nel avvelenamento cronico di piombo. Beitr. v. Ziegler, 
iii., 1888. 





THE NEW-FORMATION OF BLOOD-VESSELS. 283 


Cohnheim: Epithelregeneration. Virch. Arch., 61 Bd., 1874. 

Cornil et Carnot: Régén. cicatricielle des conduits muqueux. Arch. de med. exp., 
x., 1898; Iteg. des cavités muqueuses. Ib., xi., 1899; Cicatrisat. des plaies du foie. 
Sem. méd., 1898. 

Eberth: Epithelre eneration. Virch. Arch., 67 Bd., 1876. 

Fuckel. egen. i Submaxillar- u. Infraorbitaldrüsen. Inaug. Diss., Freiburg, 

896. 

Flemming: Regen. v. geschicht. Plattenepithel, Darmepithel u. Flimmerepithel des 
Eileiters, Follikelepithel des Ovarium. Arch. f. mikr. Anat., xviii., xxiii., xxiv., 
1 rn 


Golgi, C.: Neoformazione dell’ epitelio dei canalicoli oriniferi. Arch. per le Sc. Med., 
vi., 1881; Arch. ital. de Biol., ii., 1882. 

Griffini: Contribut. alla patol. del tessuto epitel. cilindr., Torino, 1884; Arch. ital. 
de Biol., v., 1882; Sulla riproduzione parziale del testicolo. Arch. per le Sc. Med., 
xi., 1887; Sulla riproduzione degli organi gustatori. Rendiconti dell’ Istituto Lom- 


bardo, 1887. . 
Griffini u. Vassale: Ueber d. Reproduction d. Magenschleimhaut. Beitr. v. Ziegler, 
iii., 1888. 
chhaus: Gewebsveränderungen nach Kälteeinwirkung. Virch. Arch., 154 Bd., 
1 


Jatta: Rigen. dell’ epitelio del rene. Arch. per le Sc. Med., xxi., 1897. 

Jung: Reg. d. Uterusschleimhaut nach Verletzung. Cbl. f. Gyn., 1897. 

Kahn: Etude sur la régénération du foie, Paris, 1897. 

Karg: Studien über transplantirte Haut. Arch. f. Anat. u. Phys., 1888. 

Loeb: Regeneration des epithels. Arch. f. Entwickelungmech., 1898; Ueber das 
Wachsthum des Epithels. Ibid., 1901. 

Mall: Healing of Intestinal Sutures. Johns Hopkins Hosp. Rep., i., 1887. 

Martinotti: Ueber Hyperplasie u. Regen. der drüsigen Elemente in Bez. auf ihre 
Functionsfähigkeit. Cbl. f. allg. Patb., i., 1890. 

Mayzel: Theilung der Kerne in Epithelzellen. Chbl. f. d. med. Wiss., 1875. 

~v. Meister: Recreation des Lebergewebes. Beitr. v. Ziegler, xv., 1894. 

Norpurgo: Zelineubildung während der Inanition. Beitr. v. Ziegler, iv., 1889. 

e 


-Neese: Verhalten d. Epithels bei Heilung v. Wunden d. Hornhaut. v. Graefe’s Arch., 
xxxiii., 1887. 

Petrone: Du proc. régén. sur le poumon, sur le foie et le rein. Arch. ital. de Biol., 
v., 1882. 


Piccoli: Rigenerazione parziale della prostata. Arch. per le Sc. Med., xxiv., 1900. 

Pisenti: Sur la cicatrisation du rein, etc. Ib., vi., 1884. 

Podwyssozky: Regen. der Drüsengewebe. Beitr. v. Ziegler, i., ii., 1886-87. 

Poggi: La cicatrisation immédiate des blessures de l’estomac. Ib., iii., 1888. 

Ranvier: Mécanisme de la cicatrisation. Lab. d’histol. du College de France, 1900. 

Ribbert: Regeneration der Mammilla. Arch. f. mikr. Anat., 37 Bd., 1891. 

Sanfelice: Regeneration du testicule. Arch. ital. de Biol., ix., 1888. 

Schlatter: Traumat. Leberverletzungen. Beitr. v. Bruns., xv., 1896. 

Simanowsky: Reg. d. Epithels d. Stimmbandes. Arch. f. mikr. Anat., xxii. 

Stroebe: Acute Leberatrophie. Beitr. v. Ziegler, xxi., 1897. 

Tizzoni: [a fisio-patologia dell’ epitelio pavimentoso stratificato. Arch. ital. de Biol., 
vi.. 1884. 

Vossius: Regen. d. Epithels der Cornea. v. Graefe’s Arch., xxvii., 1881. 

Wath: Regeneration d. Uterusschleimhaut. Arch. f. Gyn., 49 Bd., 1895. 

Wolff: Die Nierenresection u. ihre Folgen, Berlin, 1890; ref. Virch. Arch., 161 Bd. 

v. Wyss: Epithelregeneration. Virch. Arch., 69 Bd., 1877. 

Ziegler: Ursachen d. pathol. Gewebsneubildungen. Intern. Beitr., Festschr. f. Vir- 
chow, ii., Berlin, 1891. 


$ 83. The new-formation of blood-vessels plays a very important 
röle in hyperplasia of the most varied tissues. If connective tissue, 
bone, or glandular tissue is to be reproduced in any considerable 
amount, the new-formation of blood-vessels is essential, since it is only 
through these that sufficient nutrition can be brought to the growing 
tissue. 

The development of new blood-vessels takes place through the forma- 
tion of offshoots from the sides of the walls of preéxisting vessels (Fig. 
160). In the vessel-wall there occurs a proliferation of cells, particu- 


254 THE PROGRESSIVE CHANGES. 


larly of the endothelium (Fig. 161), in which the division of the 
nucleus occurs by karyomitosis. 

As the first step in the formation of a new vessel, there is seen on the 
outer side of some capillary loop a tent-like elevation which terminates 
in a fine protoplasmic thread (Fig. 160, a), standing out from the vessel, 
and gradually becoming longer and longer, while the granular mass like- 





Fig. 160.—Development of blood-vessels by formation of offshoots; from tions taken from in- 
flammatory granulations. «a,b,c, d, Different forms of offshoots, some solid ec), others becoming hol- 
low (a,b, d), some simple (a, d), some branching (b, c). some without nuclei (a, d), some with nuclei 
(b, c); d, offshoot to which fibroblasts have applied themselves. 


wise grows out at the same time. There is thus formed at the beginning 
a solid granular arch of protoplasm, which ends in a protoplasmic thread (a), 
and after a certain time comes to contain nuclei. This thread may 
penetrate into another vessel, or may unite with some other arch which 
it meets, or finally may return to the same vessel from which it started. 

Further, from the solid arch itself new secondary arches may spring 
(Fig. 160, b, ec), or at its end there may be formed a club-shaped swell- 
ing (e). 

The originally solid arch becomes hollow after a certain time (0, a) 
through the liquefaction of its central part, and the space thus formed 
either immediately or very soon comes to communicate with the lumen 
of the blood-vessel (a), or else there is developed from within the vessel 
an extension of the vessel-lumen into the arch. The blood of the mother- 
vessel finds its way at once into the cavity of the daughter-vessel and 
widens it. As the hollowing-out process constantly advances and ex- 
tends to the point of entrance of the protoplasmic arch into another 
blood-vessel, there is finally formed a new capillary loop permeable for 
blood. 

Immediately after the opening of a way for the blood the capillary 
tube possesses a homogeneous wall. After a certain length of time the 
protoplasm groups itself about the nuclei, which have in the mean time 


THE NEW-FORMATION OF BLOOD-VESSELS. 285 


divided and multiplied in the wall, so that ultimately the capillary 
comes to be made up of flattened endothelial cells. As Arnold has 
shown, the boundaries of the individual flattened endothelial cells may 
be made visible through the injection of a solution of silver into the ves- 
sel. At this time the wall for the greater part appears much thickened, 
partly from the proliferation of the cells of the vessel-wall, but also 
partly from the fact that formative cells from the neighborhood heap 
themselves upon the surface of the young vessel (Fig. 160, d), adapt 
themselves to the wall, and so strengthen it. 

At the time of the formation of the offshoots, the endothelial cells of 
the capillaries are swollen, so that they form cells rich in protoplasm, 
which often in proliferating tissues reach such a size that the cross-sec- 
tion of a capillary looks not unlike a gland-tube lined with epithelium 
(Fig. 162, d). At the same time division-figures appear in the endo- 
thelium (Fig. 161, a-c), and later the division of the nucleus and cell- 
protoplasm takes place. 

Just in what relation this proliferation stands to the formation of the 
offshoots is not yet clearly understood; but doubtless the latter spring 
from proliferating cells and represent cell-proc- 
esses of the same. The proliferation of endothe- 
lium, on the other hand, does not always lead to 
a new-formation of vessels, but may result only 
in a thickening of the vessel-wall and finally in 
an obliteration of the lumen. 

In the transformation of newly formed capil- 
laries into arteries and veins—a change which 
must always occur in the case of extensive new- 
growths—the increase of tissue is the result of the 
continued proliferation of the cells of the vessel- 
wall. The individual elements of the arteries 
and veins are then developed from this formative 
material through especial processes of differentia- 
tion. 





papillary body. whose’ endo 
Three carietics of new-formation of blood-ressels are de- y. wi 
scribed by dierent authods the primary secondary, and tesa, cell ae fa proces at 
tertiary, the last of which is described above. painting the back of the foot 

In the primary form the cells of the germ-tissue are With tneture of fodine) (Flem- 
directly transformed into red blood-cells and the elements of piere acid). a, Nucleus with 
the blood vessel walls, in such aa onto Id the germeclls Chromatin framework: b, Dre 
unite to form strands whose axis rtion becomes changed n Vertie q 
to red blood.cells. while the peripieal parts become the  ygereeaireaiasye call wi 
vessel-wall. Such a form of vessel-development, which mononuclear leucocytes. x 
Occurs in the area germinativa, does not take place patholo. 30 

ically. 

Bia ne secondary form, according to Billroth, 0. Weber, Rindfleisch, and Cornil (Le., 
§ 82), spindle-cells unite to form cords in such a way that a canal is formed between 
them. Whether such a mode of vessel-formation actually occurs, appears doubtful. 

It is probable that these observations are based upon errors due to the fact that 
apindle-cells very early arrange themselves upon the vessel-buds, cover them up, and 
form cords of cells about them. 


Literature. 
(New-formation of Blood-vessels.) 
Arnold: Die Entwicklung d. Bluteapillaren. Virch. Arch., 53 Bd., 1871; 54 Bd., 
1872. 


Billroth: Untersuch. über die Entwickelung der Blutgefässe, Berlin, 1856. 
Coön: Veränd. d. Haut nach Einwirkung von Jodtinctur. Beitr. v. Ziegler, ii., 1887. 

















NEW-FORMATION OF CONNECTIVE TISSUE. 291 


tissue, but this does not reach any great size. In the proliferation of cartilage-cells. 
within cartilage the cell-multiplication and new-formation of cartilage occur in the same 
way as in the physiological proliferation of this tissue. Very often the newly-formed 
cartilage is only a transitory tissue, and is soon transformed again into bone and mar- 
row-tissue, or into connective tissue. 

New lymphadenotd tissue may, under pathological conditions, arise either from 
lymphadenoid tissue, or fat-tissue (Bayer) or from fibrillated connective tissue. It is. 

ormed from the latter most frequently in the connective tissue of the mucosa and sub- 
mucosa of the intestinal tract, as well as in the glandular organs; rarely in the inter- 
muscular connective tissue. 

Mucous tissue may develop from any proliferating connective-tissue substance, but 
Tarely appears in large masses, and is usually a transitory form passing over either into. 
fat or connective tissue. 

Fat-tissue develops particularly in those regions normally containing fat, but oc- 
curs also at times in other places, for example, in the reticular connective tissue of 

atrophic lymph-glands, in the perimysium internum of atrophic muscles, etc. 

The close relationship of the connective-tissue substances to each other enables the 
different forms to pass from one to another without the need of an intermediate stage 
of embryonic tissue produced by proliferation. Further details in regard to this point. 

@re contained in the next part. 


Literature. 
New-formation of Connective-tissue and Elastic Fibres.) 


Weltzow: Regeneration der Sehnen. Arch. f. mikr. Anat., xxii. 

Busse: Heilung asept. Wunde der Haut. Virch. Arch., 184 Bd., 1898. 

Dmitrijeff: | Yeränd. d. elastischen Gewebes b. Arteriosklerose. Beitr. v. Ziegler, 
xxii., 1897. 

Fischer: Exper. Unters. üb. d. Heilung von Schnittwunden d. Haut. Inaug.-Diss., 
Tübingen, 1888. 

ing: Z. Entwickelungsgesch. d. Bindegewebsfibrillen. Festschr. f. Virch., i., 

Berlin, 1891. 

@3ardner: Histogenese d. elastischen Gewebes. Biol. Cbl., xvii., 1897. 

“rasen: Feinere Vorgänge bei Verwachsung peritonealer Blätter. Zeit. f. Chir., xxvii.,. 
1 


Haasler: Regenerat. d. Rückenmarks. Arch. f. klin. Chir., 1., 1895. 
Hamilton soon the Presence of New Elastic Fibres in Tumors. Trans. Chicago, Path.. 
Soc., 1900. 
Hansen: Genese einiger Bindegewebsgrundsubstanzen. Anat. Anz., xvi., 1899. 
Homen: Regeneration der fixen Hornhautzellen. Fortschr. d. Med., i., 1883. 
wWores: Neubildung elast. Fasern. Beitr. v. Ziegler, xxiv., 1898; xxvii., 1900. 
Klemensiewicz: Karyokinese in den fixen Hornhautzellen. Cbl. f. d. med. Wiss.,. 
1884. 
Xromayer: Regen. d. elast. Fasern in Hautnarben. Monatsh. f. Derm., xix., 1895. 
Lwoff: Entwickelung d. Fibrillen des Bindegewebes. Wiener Sitzber., 98 Bd., 1889. 
Melnikow: Unters. üb. d. elastischen Gewebe. Beitr. v. Ziegler., xxvi., 1899. 
Merkel: Histogenese d. Bindegewebes. Verh. d. Anat. Gesellsch., v., 1896. 
Neelsen u. Angelucci: Untersuch. über Keratoplastik. Klin. Monatsbl. f. Augenhk.,. 


1880. 
Neumann ni : Entwickelung d. Bindegewebes in pleuritischen Schwarten. Arch. d. 
eilk., 1869. 
Mikiforof: Bau u. Entwickelung des Granulationsgewebes. Beitr. v. Ziegler, viii.,. 
1 


Oliver: Elastic Tissue in Cirrhosis of the Liver. Trans. Chicago Path. Soc., 1902. 

Passarge u. Krösing: Regen. d. elast. Gew. d. Haut. Derm. Stud. v. Unna, xviii., 
1894. . 

Pearce: The Increase of Elastic Tissue in the Lung in Chronic Congestion. Jour. of 
Med. Res., 1901. 

Podwyssozki: Regeneration der Drüsengewebe. Beitr. v. Ziegler, i., ii., 1886-87. 

Poljakoff: Anat. d. Bindegewebes. Arch. f. mikr. Anat., 45 Bd., 1895. 

Ranvier: Mécanisme de la cicatrisat. Lab. d’histol. du Collége de France, 1900. 

Spuler: Histogenese der Bindesubstanz. Anat. Hefte, xxi., Wiesbaden, 1896. 

Stroebe: Heilung von Rückenmarkswunden. Beitr. v. Ziegler, xv., 1894. 

Tillmanns: Exp. u. anat. Unters. über Wunden der Leber u. Niere. Virch. Arch.,. 


292 THE PROGRESSIVE CHANGES. 


Yamagiva: Zellenstudien an sich regenerirendem Sehnengewebe. Virch. Arch., 135 

., 1894. 

Zachariades: Tissu conjonct. Lab. d’histol. du Collége de France, 1900. 

Ziegler: Untersuch. über pathol. Bindegewebs- u. Gefässneubildung, Würzburg, 1876. 
See also Intlammatory New-formations of Tissue. 


(New-formation of Cartilage. ) 


Bardeleben: Knorpel. Eulenburg’s Realencyklop., 1896. 

Ewetzky: Entzündungsversuche am Knorpel. Arb. a. d. pathol. Instit. in Zürich., 
iii., Leipzig, 1875. 

Gies: Heilung v. Knorpelwunden. Deut. Zeitschr. f. Chir., xviii., 1882. 

Kassowitz: Die norınale Ossification, etc., Wien, 1881. 

Peyrand: Etudes exper. sur. la regen. des tissus cartilagineux et osseux, 1869. 

Schleicher: (Knorpelzelltheilung.) Arch. f. mikr. Anat., xvi. 

Schottelius: Die Kehlkopfknorpel, Wiesbaden, 1879. 

Sieveking: Wachsthum u. Regen. d. Knorpels. Morph. Arbeiten v. Schwalbe, ii., 
1891. 

Solger: Ueber Knorpelwachsthum. Fortschr. d. Med., vii., 1889. 

Spuler: Bau u. Entstehung d. elast. Knorpels. Inaug. Diss., Erlangen, 1895. (Lit.) 


( New-formation of Bone.) 


Barth: Knochenimplantation. Beitr. v. Ziegler, xvii., 1895. 
Bonome: Knochenregeneration. Virch. Arch., 100 Bd., 1885. 
Bruns: Die Lehre v. d. Knochenbrüchen. Deut. Chir., Lief. 27, Stuttgart, 1886. 
Busch: Knochenneubildung. Deut. Zeit. f. Chir., viii.; Arch. f. klin. Chir., xxi., 1877. 
Kassowitz: Die normale Ossification, etc., Wien, 1881, 1882. 
Kölliker: Die normale Resorption des Knochengewebes, Leipzig, 1872; Gewebelebre, 
1889. 
Krafft: Zur Histogenese des periostal. Cullus. Beitr. v. Ziegler, i., 1886. 
Steudner: Beiträge zur Lehre von der Knochenentwickelung, Halle, 1875. 
Strelzoff: Die Histogenese der Knochen. Unters. a. d. pathol. Institut in Zürich, 1873. 
Troja: Expériences sur la régénération des os, Paris, 1890. 
Wolff. Unters. üb. d. Entwickelung d. Knochengewebes, Leipzig, 1874; Virch. 
Arch., 101 Bd., 1885. 
Ziegler: Proli feration, Metaplasie u. Resorption d. Knochengewebes. Virch. Arch., 
73 Bd., 1878. 
See also Pathological Anatomy of the Bones. 


( Formation of Lymphadenoid Tissue and Spleen-tissue. ) 


Bayer: Regeneration u. Neubildung der Lymphdrüsen. Prager Zeitschr. f. Heilk., 
vi.. 1885; Ueber kranke Lymphdrüsen. Langenbeck’s Arch., 49 Bd., 1895. 

Ceresole: Regeneration de la rate. Beitr. v. Ziegler, xvii., 1895. 

Czermack: Entwickelung d. Lymphndtchen d. Darmwand. Arch. f. mikr. Anat., 42 
Bd., 1893. 

Galland: The Development of Lymphatic Glands. Jour. of Path., ii., London, 1894. 

Laudenbach: Totale Milzregeneration. Virch. Arch., 141 Bd., 1895. 

Ribbert: Regeneration u. Entzündung der Lymphkdrüsen. Beitr. v. Ziegler, vi., 
1889, 

Saxer: Entwickelung d. Lymphdrüsen. Anat. Hefte, Wiesbaden, 1896. 

Stöhr: Die Enwickelung des adenoiden Gewebes. Anat. Anz., vi., 1891; Entwick- 
elung der Darmlymphknötchen. Arch. f. mikr. Anat., 41 Bd., 1898. 

Warthin: The Changes Produced in the Hemolymph Nodes of the Sheep by Splenec- 
tomy. Jour. of Med. Res., 1902; The Relation of the Hemolymph es to Adi- 
pose Tissue. Trans. Phil. Path. Soc., 1903. 

Zehnder: Ucber regenerative Neubildung der Lymphdrüsen. Virch. Arch., 120 Bd., 
L890. 


&§ 85. The new-formation of the white blood-cells occurs, in the first 
place, within the lymphadenoid tissue of the lymph-glands, spleen, and 
the intestinal tract, and there are contained within the lymph-nodes 
areas sharply outlined from their surroundings, in which there are 


NEW-FORMATION OF RED BLOOD-CELLS. 293 


always present numerous cell-division figures which belong for the most 
part tofree cells. These areas have been designated germ-centres (Flem- 
ming). Further, leucocytes are also produced in the bone-marrow and 
gain entrance to the blood through the vessels of the marrow. Moreover, 
division of leucocytes occurs in the lymph-vessels of the lymph-; glands 
and the tissues, and there is now no doubt that leucocytes may divide in 
the circulating blood and in the tissue-spaces. Whether there may arise 
from the proliferation of connective-tissue cells such forms of cells as 
have the power of wandering into the blood-vessels, and which there 
may be regarded as white blood-corpuscles, is not yet settled. 

The division occurs chiefly through mitosis; but amitotic division also 
takes place, and upon this phenomenon depends the fact that a large 
part of the leucocytes contain peculiar lobulated, wreath-shaped nuclei 
or even nuclei which have broken up into small fragments. 

Mitotic division is the form of division which leads to the formation 
of viable cells. In how far amitotic division (fragmentation of the nu- 
cleus) is followed by a cell-division isa diffi- 
cult question to decide, but it is to be as- 
sumed that leucocytes with fragmented nuclei 
represent elements undergoing a retrograde 
change. Consequently the transformation 
of mononuclear into polynuclear leucocytes 
is to be taken as an evidence of approach- 
ing dissolution. 

The new-formation of red blood-cells 
takes place (Bizzozero, Neumann, Flemming) 
through mitotic division of nucleated young 
forms of red blood-cells, the erythroblasts. 
In the human adult this process is limited 
to the bone-marrow, and the same is true in P 
the case of mammals, birds, reptiles, and nal centre of mente ind ite 
the tailless amphibia, while in the tailed am- Sts ear sine ant um 

hibia and in fishes the spleen also takes part cleat ‘afvision or nuclear tmgmentar 
in the formation of red cells. In embryos nucleus“ tingible bodies" and small 
the formation and multiplication of red cells inQnQ'EMent granules, whose sig- 
occurs throughout the entire vascular sys- 
‘tem; later this activity is confined to the spleen, liver, and bone-marrow, 
and finally to the last alone. 

Neumann holds that the multiplication of the young forms of the red 
sells occurs in the lymphoid marrow. According to Bizzozero and 

Denys the increase, under normal conditions, takes place only in the 
vessels of the marrow, and the complete development of the red cells is 
«arried out in the same location. The change of the nucleated cells into 
the non-nneleated is brought about, rding to the majority of ob- 
servers, by the disappearance of the nucleus. According to Rindfleisch, 
Howell, Malassez, and Maximow the nucleus is extruded from the cell. 
According to Maximow there may be distinguished in the protoplasm of 
erythroblasts possessing old pyknotie nuclei, a granular substance lying 
elose to the nucleus and a homogeneous peripheral substance. After the 
extrusion of the nucleus the inner granular substance, which stains with 
neutral red and other stains, remains preserved for atime, but vanishes 
during the ripening of the red blood-cells. 

The origin of the nucleated red cells has not yet been satisfactorily 
explained. According to Bizzozero the young forms of the red cells are 

17 




















294 THE PROGRESSIVE CHANGES. 


of a peculiar type which constantly contain hemoglobin and have no 
colorless antecedents. Denys, Löwit, Howell, and Pappenheim hold, on 
the contrary, that they arise from nucleated, colorless cells containing no 
hemoglobin (basophile leucocytes according to Pappenheim), which ac- 
cording to Denys increase within the marrow-vessels; while Lowit, on 
the other hand, holds that the colorless antecedents of the red cells, 
dividing by mitosis, and which he calls erythroblasts, occur in the 
lymph-glands and spleen, as well as in the bone-marrow, and are found 
both within the vessels and in the meshes of the reticular tissue. 

Flemming, who agrees with Bizzozero concerning the hemoglobin 
content of the nucleated young red cells, is inclined to assume that the 
young forms present in later life are direct descendants of the young 
forms of the embryonic period. Neumann holds that this hypothesis is 
not sufficient to explain all the phenomena of later life; as, for example, 
the replacement of fatty marrow, which contains no nucleated red cells, 
by blood-forming lymphoid marrow, and the formation of blood-cells in 
newly developed marrow. He finds himself driven to the assumption 
that either a development of the nucleated red blood-cells takes place 
from the leucocytes of the blood which are carried to the marrow after 
birth by the arteries, or that they arise from the tissue-elements of the 
bone-marrow. 

In case of an increased formation of red cells, as occurring after loss 
of blood, and also in severe chronic anzinia and leuksemia, nucleated 
red cells may appear also in the circulating blood outside of the bone- 
marrow, while under normal conditions they are not found there. The 
fatty marrow acquires in such cases the character of lymphoid marrow, 
and this change is brought about by the disappearance of the fat through 
dilatation of the vessels with increased supply of blood, and through an 
increase in both the colorless and red cells of the marrow. 


Ehrlich (Zeitschr. f. klin. Med.,i.; Charite Annal., 1884; Verhandlung d. Phys. 
Ges. zu Berlin, 1878-79; Deutsch. med. Wochenschr., 1883) and Einhorn (“ Veber d. Ver- 
halten der Lymphocyten zu den weissen Blutkörperchen,” Inaug.-Diss., Berlin, 1884, 
ref. Fortschr. der Med., iii.) distinguish among the leucocytes of the normal blood: (1) 
small lymphocytes with deeply staining nuclei of relatively large size, aud with little 
protoplasm ; (2) large lymphocytes with large nuclei that stain lightly and with abundant 
protoplasm; (3) mononuclear transitional forms with irregular nuclei; (4) polynuclear 
nentrophile leucocytes with polymorphous nuclei or with several nuclei, and containing 
neutrophile granules (granules which stain with a neutral dye, obtained by mixing acid 
fuchsin with basic methyl-green), these forming about seventy per cent of all the white 
calls of the blood, and migrating in purulent inflammations; (5) eostnophile cells, whose 
protoplasm contains numerous granules staining with acid dyes (eosin); (6) mst-cells 
(0.5 per cent of the white cells) having basophile granulation. 

Lörit distinguishes among the colorless cells of the blood two different forms which 
he designates leucoblasts and erythroblasts, and which he believes to have a wholly 
different significance and not to pass over from one form to the other. The leucoblasts 
are the lymphocytes with chromatin arranged in clumps, which do not undergo mitotic 
division, but pass overinto the polynuclear leucocytes through fragmentation of the 
nucleus. The erythroblasts are the colorless voung forms of the red cells, which divide 
by mitosis, and are distinguished from the lymphoid cells by their homogeneous char- 
acter and slight contractility of the protoplasm. The transformation into hemoglobin- 
containing cells oceurs partly in the blood, and partly in the bone-inarrow. 

Flemming regards Loit’s views as incorrect, claiming that the observations of the 
latter give no evidence of a transformation of colorless erythroblasts into red cells, and 
that leucocytes which do not become changed into red cells also divide by mitosis. 
Neumann also is unable to agree with Zörrit. 

Howell holds that the bone-marrow contains numerous colorless erythroblasts, 
which change in the marrow into nucleated cells which later through the extrusion of 
the nucleus are transformed into non-nucleated red blood-cells. 

Petrone believes that the red blood-cells of the mammals are only apparently non- 


NEW-FORMATION OF RED AND WHITE BLOOD-CELLS. 295 


nucleated, and that it is possible by means of especial methods of fixation and staining 
to render the nucleus visible. Negrt has tikewise found similar structures in red cells, 
but does not believe them to be nuclei. .Walassez believes that the red cells arise from 
buds of nucleated cells of the marrow. According to Denys, with whom Z. H. Ziegler 
agrees, the red blood-cells have a peculiar origin; and in birds are formed from the wall 
of the venous capillaries of the bone-marrow, which have a germinal layer of red blood- 
cells in the form of a cellular coating of many layers, which give off into the blood- 
stream cells, which then come to contain hemoglobin. 


Literature. 
(New-formation of Leucocytes. ) 


Arnold: Theilungsvorgänge an Wanderzellen. Arch. f. mikr. Anat., 30 Bd., 1887; 
Knochenmarkzellen. Virch. Arch., 144 Bd., 1896. ' 

Bizzozero: Bau d. Knochenmarks bei Vögeln. Arch. f. mikr. Anat., 35 Bd., 1890; 
Arch. ital. de Biol., xiv., 1890. 

Dekhuyzen: Mitosen in frei im Bindegewebe gelegenen Leukocyten. Anat. Anz., 
vi., 1891. 

Denys: La structure de la moélle des os. La Cellule, iv., 1887. 

Drews: Zellvermehrung in der Tonsilla palatina. Arch. f. mikr. Anat., 24 Bd., 1885. 

Ehrlich u. Lazarus: Die Anämie, i., Wien, 1898. 

Flemming: Zellvermehrung in Lymphdrisen, Theilungsarten der Leukocyten. Arch. 
f. mikr. Anat., 24 Bd., 1885; Theilung u. Kernformen bei Leukocyten. Ib., 87 Bd., 
1891. 

Hayem: Du sang et de ses altérations organiques, Paris, 1889. 

Joas: Ueber entzündliche Leukocytose. Beitr. v. Ziegler, x., 1891. 

Jolly: Diff. types de glob. blancs. Lab. d’hist. du Coll. de France, 1900. 

Lawdowsky: Unters. einiger Lebensvorgänge des Blutes. Virch. Arch., 96 Bd., 1884. 

v. Limbeck: Klin. Pathologie des Blutes, Jena, 1896. 

Löwit: Neubildung u. Zerfall weisser Blutkörperchen. Sitzber. d. K. Akad. d. Wiss. 
in Wien, 92 Bd., 1885; Anat. Anz., i., 1886; Neubildung u. Beschaffenheit d. 
weissen Blutkörperchen. Beitr. v. Ziegler, x., 1891; Die Anordnung von Leuko- 
blasten u. Erythroblasten in d. Blutzellen bildenden Organen. Anat. Anz., vi., 
1891; Arch. f. mikr. Anat., 38 Bd., 1891. 

Maurel: Rech. experimentales sur les leucocytes, Paris, 1891. 

Möbius: Zellvermehrung in der Milz. Arch. f. mikr. Anat., 24 Bd., 1885. 

Müller: Zur Frage der Blutbildung. Wien. Sitzber., 1889; Zur TLeukämiefrage. 
Deut. Arch. f. klin. Med., 48 Bd., 1891; Mitose an eosinophilen Zellen. Arch. f. 
exp. Path., 29 Bd., 1891. 

Neumann: Bed. d. Knochenmarks für die Blutbildung. Centralbl. f. d. med. Wiss., 
1868; Arch. d. Heilk., x., 1869. 

Oppel: Die Entstehung der rothen u. weissen Blutkörperchen. Cbl. f. allg. Path., 
1892 (Lit.) 

Pappenheim: Bez. d. farblosen Blutkörperchen, zu einander. Virch. Arch., 160 Bd., 


1900. 

Paulsen. Zellvermehrung in Lymphdrisen u. Tonsillen. Arch. f. mikr. Anat., 24 
Bd.. 1885. ‘ 

Roemer: Formativer Reiz der Proteine Buchnet's auf Leukocyten. Berl. klin. Woch., 
1891. 

Saxer: Abstammung d. weissen u. rothen Blutkérper von primären Wanderzellen. 
Chi. f. allg. Pathol., vii., 1896. 

Schedel: Zellvermehrung in der Thymus. Arch. f. mikr. Anat., 24 Bd., 1883. 

Spronck: Regencratie van Leukocyten in het circuleerende Bloed. Fortschr. d. Med., 
vii., 1889. 

Zenoni: Entstehung versch. Leukocytenformen. Beitr. v. Ziegler, xvi., 1894. 


(Formation of Red Blood.cells). 


Arnold: Himoglobinhaltige Knochenmarkzellen. Virch. Arch., 144 Bd., 1896. 

Bizzozero Gaz. Med. Lombarda, 1869, No. 2: Centralbl. f. d. med. Wissensch., 1869, 
1880, 1881: Arch. der le Sc. Med., iv.; Arch. ital. de Biol. i., iv., xiv.; Virch. 
Arch., 95 Bd.: Bau des Knochenmarks bei Vögeln. Arch. f. mikr. Anat., 35 Bd., 
1890. 

Bizzogero u Torre Entstehung d. rothen Blutkörp. Virch. Arch., 95 Bd., 1884. 

Cadet Etude physiolog. des éléments figures du sang. These de Paris, 1881. 


296 THB PROGRESSIVE CHANGES. 


Denys: La genése du sang chez les oiseaux. La Cellule, iv., Louvain, 1888. 

Eberth: Ueber die Vermelirung der rothen Blutkörper. Fortschr. d. Med, iii., 1885. 

Ehrlich u. Lazarus: Die Anämie, i.. Wien, 1898. 

Engel: Embryon. rothe Blutkdrp. Arch. f. mikr. Anat., 52 Bd., 1898; 54 Bd., 1899; 
Fortschr. d. Med., xvi., 1898. 

Feuerstack: Entwickelung d. r. Blutkörperchen. Zeitschr. f. wiss. Zool., xxxvii, 
1883. 

Flemming: Zelisubstanz, Kern- u. Zelltheilung, 1882; Ueber Theilung und Kern- 
formen bei Leukocyten. Arch. f. mikr. Anat., 87 Bd., 1891. 

Hayem: Du sang et de ses altérations, Paris, 1889. 

Howell: The Life History of the Formed Elements of Blood. Jour. of Morph., iv., 
Boston, 1890, ref. Cbl. f. allg. Path., 

Israöl u. Pappenheim: Entkernung d. Erythroblasten. Virch. Arch., 143 Bd., 1896. 

Kuborn: Devel. des vaisseaux et du sang dans le foie de l’embryon. Anat. Anz., v., 
1890. 

Löwit: Wiener akad. Sitzungsber., 88 Bd., 1888: 92 Bd., 1885; 95 Bd., 1887. 

Malassez: Gaz. méd. de Paris, 1874 and 1878; Arch. de 'phys., ix., 1882. 

Maximow: Structur u. Entkernung d. r. Blutkorp. Arch. f. ‘Anat., 1899. 

Mondino: Sulla genesi degli elementi del sangue, Palermo, 1888; Arch. ital. de Biol., 
xii., 1889. 

Mosse: Umwandlung d. rothen Blutkörperchen in Leukocyten. Virch. Arch., 109 

d., 1887 

Negri: "Persistenz des Kernes r. Blutkörp. Anat. Anz., xvi., 1899. 

Neumann: Bedeutung des Knochenmarks für d. Blutbildung. Cbl. f. d. med. Wiss., 
1868, 1869; Arch. d. Heilk., xv.; Arch. f. mikr. Anat., xi.; Entwickelun rother 
Blutkörperchen im neugebild. Knochenmark. Virch. Arch., 119 Bd., 1890; Blut 
bildung b. Fröschen. Ib., 143 Bd., 1896. 

Oppel: Die Entstehung rother u. weisser Blutkörperchen. Chbl. f. allg. Path., 1892 
(Lit.). 

Prppenheim: Entwickelung d. Erythroblasten. Virch. Arch., 145 Bd., 1896 (Lit.); 
Entstehung d. rothen Blutzellen. Virch. Arch., 151 Bd., 1898. 

Petrone: L’esistenza del nucleo nell’ emasia adulta dei mammiferi, Catania, 1897; 
L’apparenze dj cellule nel globulo rosso. Bull. dell’ Accad. di. Sc. Nat. in Catania, 
1900. 

Reinert: Die Zählung der rothen Blutkörperchen, Leipzig, 1891. 

Bindfleisch: Knochenmark u. Blutbildung. A Arch. f. mikr. Anat., xvii., 1879. 

Sanfelice: Genese des corp. rouges dans la mo&lle des os. Arch. ital. de Biol., xiii., 
1890 

Schmidt: Ueber Blutzellenbildung in Leber u. Milz. Beitr. v. Ziegler, xi., 1892. 

Spuler: Ueb. d. intracelluläre Entstehung rother Blutkörper. Arch. f. mikr. Anat., 40 
Bd., 1892. 

Timofejewsky : Regenerat. d. rothen Blutkörperchen. Cbl. f. alle. Path., vi., 1895. 

Tizzoni: Fonction h¢matopoctique de la rate. Arch. ital. de Biol., , 1882. 

Trachetti: Glob. ressi ed emoglobina nelle anemie sperim. Arch. “per le Sc. Med., 
1896. 

Ziegler, E. H.: Entstehung d. Blutes d. Wirbelthiere. Ber. d. Naturf. Ges. zu Frei- 
burg, iv., 1889. 


& 86. The new-formation of transversely striated muscle-fibres 
takes its start from portions of old muscele-fibres; and although, after 
injury to a muscle, the intermuscular connective tissue may be excited 
to active proliferation, there is formed in consequence only connective 
tissue, or probably also the sarcolemma of new fibres, but never new con- 
tractile substance. 

The first signs of a formative activity of the muscle-fibres after injury 
appear in the muscle-nuclei, in that these become elongated and then 
divide into a varving number of fragments (Steudel, Nauwerck). Even 
on the second day there may occur mitotie division (Fig. 171, a, 6) of the 
musele-nuclei This form of division seems to be the only way in which 
multiplieation takes place, and under favorable conditions it oceurs very 
actively after the second day. 

The behavior of the contractile substance of the muscle differs very 
markedly according to the nature and extent of the injury. In the case 


REGENERATION OF MUSCLE. 297 


of traumatic, toxic, and anemic injuries it suffers a fragmentation into 
larger and smaller portions, so that the muscle-cells come to lie in spaces 
of varying size between the detritus of the muscle-fibres. Crushing and 
tearing can bring about a wide separation of the parts of the contractile 
substance. The ends of the pieces of muscle-fibres, in such a case, may 
be conical, oblique, transverse, or torn in an irregular edge, but not infre- 
quently after a short time the ends become split into two or more pointed 
filaments (Fig. 171, a). 

The mitotic division of the muscle-nucleus takes place, not only in 
nuclei that rest upon living fibres (a), but also in the muscle-cells lying 
free in the spaces between the separated muscle-fibres (b); and in both 
places leads to the production of large multinuclear cells, which form 
multinuclear protoplasmic masses on the ends of the muscle-fibres (e, f) 
as well as on the body of the fibres (c). Into these masses the trans- 





Fig. 171,—Portions of muscle-Abres showing regenerative proliferation, from 1“. wounds of dif- 
ferent axes (Flemming’s, safranin). a, Pointed ends of the aplit slump of a niusch ith nuclear divi- 
sion-figures, three days after laceration of the muscle: , proliferated muscle-nuclel transformed Into cells 
rich in protoplasın, one of which ts In process of mitotic division: c, plece of a muscle-fbre eight days after 
!ying the muscle: d. etantcells, enclosing necrotic places of muscle, from a muscle-scar twenty-six days 

3 ¢.f, musele-Abres ending in protoplasmic masses (mus €, from a musclesrar ten days old, 
$- Hoi one twenty-one days oid Qc dividing’ moselechbres froma tnuseoscar forty-three days old. > BI. 

















versely striated muscle-substance passes without a sharp line of demarca- 
tion. There occurs, therefore, at the same time with the multiplication of 
the nuclei an increase of the sarcoplasm of the musele-fibres, and this becomes 
distinctly visible ; it is probable, also that muscle-fibrilla may become 
changed back into sarcoplasm. 

The muscle-cells not connected with living contractile substance be- 
come changed into large epithelivid cells with large nuclei (b). Through 
continued division of the nucleus these cells become transformed into 
multinuclear protoplasmic masses (d); and a scar, consisting of prolifer- 
ating connective tissue, of from eight to thirty days old, contains such 
giant-cells which often enclose the remains of old musele-fibres (d) in 
large numbers. 

The new muscle-fibres develop for the chief part from the richly nucleated 
sarcoplasm, which appears in the continuity and at the ends of the muscle- 
fibres, in connection with the formation of numerous large nuclei, and 
which through its increase of size causes an increase in the thickness and 
length of the muscles, which has been designated budding by Neumann. 








REGENERATION OF NERVE-TISSUE. 299 


certain limits, is of very frequent occurrence. In the pregnant uterus 
the size of the muscle-cells may reach five to ten times the ordinary size. 
Of other organs the bladder most frequently shows a marked hypertro- 
Phy of smooth muscle. 


Literature. 


(Regeneration of Striped Muscle.) 


8B3arfurth: Zur Regeneration der Gewebe. Arch. f. mikr. Anat., 37 Bd., 1891. 
—BDoré: De la regen. du tissu muscul., etc., Paris, 1881. 
—EFelix: Wachsthum der quergestr. Musculatur. Zeitschr. f. wiss. Zool., 48 Bd., 1889. 
=£Jaleotti u. Levi: Regen. d. quergestr. Muskels. Beitr. v. Ziegler, xiv., 1893. 
7. Kahlden: Regen. d. quergestr. Muskeln (Referat). Cbl. f. allg. Path., iv., 1893. 
Kirby: Unters. üb. Degeneration u. Regeneration d. Muskelgewebes. Beitr. v. Zieg- 
ler, xi., 1892. 
Kölliker: Gewebelehre des Menschen, i., 1889. 
ke: Unters. über die Regeneration der quergestr. Muskelfasern, Halle, 1879. 
—Leven: Regeneration der quergestr. Muskelfasern. Deut. Arch. f. klin. Med., Ixiii., 
1888. 
‘Morpurgo: Ipertrofie funzionali dei muscoli. Arch. per le Sc. Med., xix., 1895; xxii., 
1898; Virch. Arch.. 150 Bd., 1897; Kernwucherung beim Längenwachsthum. 
Anat. Anz., xvi., 1899. 
Nauwerck: Ueber Muskelregeneration nach Verletzungen, Jena, 1890. 
Neumann: Ueber den Heilungsprocess nach Muskelverletzungen. Arch. f. mikr. 
Anat., 1868. 
Panet: Die Entwickelung der quergestr. Muskeln aus Sarkoblasten, Wien. 1886. 
Robert: Wiederbildung quergestr. Muskelfasern. Beitr. v. Ziegler, x., 1891. 
Schaffer: Histol. u. Histogenese der quergestr. Muskelfasern, Wien, 1893. 
Steudel u. Nauwerck: Itegeneration der quergestr. Musculatur. Beitr. v. Ziegler, 
ii., 1888. 
Valle: Rigeneraz. dei muscol. volont. Arch. per le Sc. Med., xxiv., 1900. 
Volkmann: Regeneration des quergestr. Muskelgewebes. Beitr. v. Ziegler, xii., 1898. 
Zaborowski: Regen. d. quergestr. Musk. Arch. f. exp. Patlı., xxv., 1889. 
Zenker: Uvber die Regen. des quergestr. Muskelgewebes, Leipzig, 1864. 


(Regeneration of Smooth Muscle, and of JIeart-musele.) 


Askanazy, 8.: Ucber die Regeneratior glatter Muskelfasern. Inaug.-Diss., Königs- 
berg, 1891. 

Aufrecht: Herzhypertrophie. Pathol. Mittheil., ii., Magdeburg, 1883. 

Berent: Heilung von Herzwunden. Inaug.-Diss., Königsberg, 1892. 

Bonome: Heilung von Herzwunden. Beitr. v. Ziegler, v., 1889. 

Busachi: Ueber die Neubildung von glattem Muskelgewebe. Beitr. v. Ziegler, iv., 
1X8. 

Goldenberg: Hypertrophie der Herzmuskeln. Virch. Arch., 103 Bd., 1886. 

Herczel: Muskelhypertrophie bei Darmstenosen. Zeitschr. f. klin. Med., xi., 1886, 

Jakimowitsch: Regen. glatter Muskeln. Cbl. f. d. med. Wiss., Wien, 1879, 

Kölliker: Gewebelehre des Menschen, i., 1889. 

Martinotti: Sugli effetti delle ferite del cuore. Giorn. della R. Accad. de Med. di 
Torino, 1880. 

Poggi: La cicatrisation immédiate des blessures de l’estomac. Beitr. v. Ziegler, iii., 
18: 


Ritschl: Heilung v. Wunden d. Magens, Darmkanals u. Uterus. Virch. Arch., 109 
Bıl., 1887. 

Stilling ı. Pfitzner: Regen. glatter Muskeln. Arch. f. mikr. Anat., 28 Bd., 1886. 

Tangl: Hypertrophie des Herzens. Virch. Arch., 116 Bd., 1889. 


8 87. Regenerative new-formation of the nerve-elements of the 
central nervous system through the new-formation of ganglion-cells 
most probably does not occur in man and mammals in post-embryonal 
life. According to the investigations of Stroebe, on the other hand, 
dirided nerre-fibrils (in Mammals) may grow lengthiise to a certain extent 











REGENERATION OF NERVE TISSUE. 308 


these assertions. The results obtained by Grunert in experimental work with pigeons 
agree with the conclusions arrived at by Zschistowitsch. 

Monti and Fieschi could demonstrate no evidences of regeneration in the ganglion- 
cells of the sympathetic after injuries. Zvrelli found only degenerative changes in 
the ganglion-cells of the intervertebral ganglion after injury of the same. 

he new-formation of peripheral nerve-fibres has been made very frequently 
the subject of experimental research, and ditferent observers have come to very diifer- 
ent concl:ısions (see Stroebe, l.c.). ‘The above-described mode of new-formation I regard 
as firmly established, in so far as its essentials are concerned, upon the ground of per- 
sonal investigations. I have been unable to contirm the views of Neumann, Dobbert, 
Duszkierriez, Cattant, Weir Mitchell, Gluck, Beneke, von Büngner, Wieting, and others, 
who hold that the new fibres in the distal portion of the severed nerve rise autochthon- 
ously from the nuclei of the sheath of Schwann, or from the old axis-cylinder, or from 
a protoplasmic mass formed by a chemical transformation of the medullary sheath and 
axis-cylinders (Neumann-Dobbert). Likewise, the attempt made by Neumann and 
Wieting (Marchand) to bring iuto accord the established fact of the outgrowth of the 
axis-cylinders of the proximal portion into the scar uniting the severed ends, with the 
theory of the origin of new nerve-fibres from the nuclei of the sheath of Schwann, or 
from the remains of old fibres, or from both, by the assumption that the axis-cylinders 
growing from the proximal end convey a stimulus from the nerve- centres to the distal 
portion and thereby make possible the development of new fibres, I regard as unsuc- 
cessful, and hold to the above-given view. Iam further of the opinion that the medul- 
lary sheath is not formed by the cellsof the sheath of Schwann, but represents a product 
of the axis-cylinders; but further investigations as to this point are needed. According 
to Nissl, Marinesco, and others (see Barbacei, !. ce.) there occurs, after the severing of a 
nerve, first a degeneration in the corresponding ganglion-cells with disintegration of 
the Niss!'s bodies, and this may lead to the destruction of individual cells. Later, 
progressive changes with new-formation of chromatin take place, and may lead to 
hypertrophy of the cells (Warineseo); these changes reach their maximum in about 
pinety days, after which time there is a return to the normal condition. 

The regenerative new-formation of the tissues of the eye has in recent years 
been repeatedly an object of research. According to Wolff, Müller, and Kochs the lena 
of tritons may regenerate, after removal, by means of a proliferation of the epithelium 
of the inner layer of the iris. According to Zöötkig, the same thing occurs in the trout. 
Gonin observed in rabbits, after the lens had been removed in such a manner that the 
capsule and some of the equatorial lenticular fibres and epithelium of the anterior wall 
were left behind, that there occurred a proliferation of this epithelium, leading to the 
union of the anterior and posterior walls through cells resembling connective-tissue 
cells. A new-formation of lenticular fibres from these cells does not take place. 
Remains of the lenticular fibres may form a rudimentary, useless lens, which in the 
case of young animals may become somewhat enlarged through the growth of the fibres. 
Randolph obtained somewhat better results in guinea-pigs. In the human eye similar 
formations are seen after removal of the lens, and are known under the name of “ Krys- 
tallwulst " (Baas). According to Franke, Krückmann, and Stoewer, the sclera possesses 
but slight power of proliferation. Wounds of the same are healed chiefly through 
proliferation of the choroid and episcleral tissue. 

According to Baquis, there occurs, in the injured retina of the rabbit. division of 
both ganglion and neuroepithelial cells. According to Kräckmann, the pigment- 
epithelium is capable of extensive regeneration, but neuroepithelium, on the other 
hand, is not again formed. 


Literature. 
( Regeneration of the Elements of the Central Nervous-System. ) 


Barfurth. Zur Regeneration der Gewebe. Arch. f. mikr. Anat., 37 Bd., 1891. 

Caporaso. Rigenerazione del midollo spinale della coda dei Tritoni. Beitr. v. Ziegler, 
v., 1889. 

Coen. Ueber die Heilung von Stichwunden des Gehirns. Beitr. v. Ziegler, ii., 1889. 

Dentan: Rech. sur la regénération de la moßlle épiniére. Diss. in Berne, 1875. 

Eichhorst un Naunyn: Ueber die Regeneration u. Veränderungen im Rückenmark 

‚ nach streckenweiser totaler Zerstörung desselben. Arch. f. exp. Path., ii., 1874. 

Friedmann: Progressive Veränderungen an den Ganglienzellen bei Entzündungen. 
Arch. f. Psych., xix., 1887: Zur Histologie der acuten Encephalitis. Neurol. Cbl., 
1X89 

Grunert Itegenerationsfähigkeit d. Gehirns. Arb. a. d. path. Inst. Tübingen, ii., 
1894. 


304 THE PROGRESSIVE CHANGES. 


His: Histogenese u. Zusammenhang d. Nervenelemente. Verh. d. X. intern. med. 
Congr., ii., Berlin. 1891; Die Neuroblasten u. deren Entstehung im embryonalen 
Mark, Leipzig, 1889. 

Keresztszeghy u. Hanns. Regenerationsersch. im Rückenmark. Beitr. v. Ziegler, 
xii., 1892. 

Masius et Vanlair: Regen. d. Rückenmarks bei Fröschen. Mém. de l’Ac. de Bel- 
gique, T. 21, 1870. 

Mondino: Sulla cariocinesi delle cellule nervose. Rend. R. Istituto, Lombardo, 1885. 

Monti ct Fieschi: Guérison des bless. des ganglions sympathiques. Arch. ital. de 
Biol., xxiii., 1895. . 

Müller, H.: Regen. d. Wirbelsäule u. d. Rückenmarks v. Eidechsen u. Fischen, 
Frankfurt, 1864. 

Banerelli: Les proc. de réparat. dans le cerveau et dans le cervelet. Arch. ital. de 

iol., xiii. 

Schiefferdecker: Ueb. Reg., Deg. u. Architektur d. Rückenmarks. Virch. Arch., 67 
Bd., 1876. 

Stroebe: Heilung v. Rückenmarkswunden. Beitr. v. Ziegler, xv., 1894; Histol. d. de- 
gen. u. regen. Processe im centralen Nervensystem. Cbl. f. allg. Path., 1895 
(Lit.). 

Sgobbo: Sulle rigen. del midollo spinale. La Psichiatria, viii., 1891. 

Tedeschi: Regen. d. Gewebe d. Centralnervensystems. Beitr. v. Ziegler, xxi., 1897. 

Tirelli: Proc. répar. dans le ganglion intervertébral. Arch. ital. de Biol., xxiii., 1895. 

Vitzou: La néoform. des cell. nerveuses dans le cerv. du singe. Arch. de phys., ix., 
1897. 


(Regeneration of the Peripheral Nerves. ) 


Barbacci: Die Nervenzellen (Veränd. nach Nervendurchschneid.). Cbl. f.a. Path., x., 
1899 (Lit.). 

Beidl: Verh. d. Nerven u. ihrer Centren nach Durchschneidung. Wien. klin. Woch., 
1897. 

v. Büngner: Regenerationsvorgängean Nerven nach Verletzungen. Beitr. v. Ziegler, 
x., 1891. 

Cattani: Sulla deg. e neoformaz. delle fibre nervose. Arch. per le Sc. Med, xi., 
18837. 

Demoor: Contrib. & l’etude de la fibre nerveuse, Bruxelles, 1891. 

Eichhorst: Ueber Nervendegeneration u. Regeneration. Virch. Arch., 59 Bd., 1874. 

Forssmann: Ursache der Wachsthumsrichtung d. periph. Nervenfasern. Beitr. v. 
Ziegler, xxiv., 1898; Neurotropismus. Ib., xxvii., 1900. 

Galeotti u. Levi: Neubildungen nerv. Elem. im regen. Muskelgewebe. Beitr. v. 
Ziegler, xvii., 1895 (Lit.). 

Gessler: Die motorischen Endplatten, Leipzig, 1885. 

His: llistogenese u. Zusammenhang d. Nervenelemente. X. intern. med. Congr., ii., 
Berlin, 1891. 

Huber: A Study of the Operative Treatment for Lossof Nerve Substance in Peripheral 
Nerves. Jour. of Morph., vol. xi., 1895. 

Kolster: Regen. durchschn. Nerven. Arch. f. mikr. Anat., 41 Bd.. 1893; Histogenese 
und Regen. periph. Nervenfasern. Beitr. v. Ziegler, xxvi., 1899. 

Laveran: Itech. exper. sur la regencration des nerfs, Strasbourg, 1867. 

Marinesco: Path. génér. de la cellule nerveuse. La Presse med., 1897. 

Neumann: Degeneration u. Regeneration nach Nervendurchschneidung. Arch. d. 
Heilk., ix., 1868; Nervenquetschung u. Nervenregeneration. Arch. f. mikr. 
Anat., xviii., 1880; Axencylindertropfen. Virch. Arch., 158 Bd.. 1898, 

Nissl: Veränd. d. Ganglienz. d. Fac. nach Ausreissung d. Nerven. A. Zeit. f. Psych., 
48 Bd. 

v. Notthafft: Regenerationsprocesse am verletzt. periph. Nerven. Zeit. f. wiss. Zool., 
55 Bd., 1893. 

Peterson: Peripheral Nerve Transplantation. Amer. Jour. of Med. Sc., 1899. 

Ranvier: l.econs sur l’histologie du syst. nerveux, Paris. 1878. 

Santi Sirena: Ricerche sperim. sulla riproduz. d. nervi, Palermo, 1880. 

Stroebe: Desreneration u. Regeneration periph. Nerven. Beitr. v. Ziegler, xiii., 1893; 
Cbl. f. allg. Path., vi., 1895 (Zusfass. Ref. üb. Regen. d. Nerven u. d. Endap- 
parate). . 

Tillmanns: Ucber Nervenverletzung u. Nervennaht. Arch. f. klin. Chir., xxvii, 
1881. 

Tizzoni: Sulla patol. del tessuto nervoso. Arch. per le Sc. Med., iii., 1879. 

Vanlair: Arch. de biol. de van Beneden et van Bambeke, 1882-85; Arch de phys., x., 


\ 


TRANSPLANTATION AND IMPLANTATION. 305 


1883; vi., 1885; viii., 1886; Compt. rend. de l’Acad. des sciences, 1885; Sur l’in- 
nervat. indirecte de la peau. Ib., 1886; De l’organisat. des drains de caoutchouc, 
etc. Revue de Chir., 1886; La suture des nerfs, Bruxelles, 1889; La persistance de 
Vaptitude régénératrice des nerfs. Bull. de l!’Acad. Roy. de Belgique, 1888; Rech. 
chronométriques sur la regen. des nerfs. Arch. de phys, vi., 1894. 

Vulpian: Note sur la regen. dite autogénique des nerfs. Arch. de phy., i., 1874 

Wieting. Regen. periph. Nerven. Beitr. v. Ziegler, xxiii., 1898. 

Wolberg: Nervennaht. Deut. Zeitschr. f. Chir., xviii. and xix., 1883. 


(Regeneration of the Tissues of the Eye.) 


Baas: Linsenregeneration. Minch. med. Woch., 1899. 

Baquis: Etude expér. sur les rétinites. Beitr. v. Ziegler, vi., 1888. 

Coluzzi: Rigen. parziale dell’ occhio nei tritoni. Mem. Acc., Bologna, i., 1891. 

Fischel . Regen. d. Linse. Anat. Anz., xiv., 1898. 

Gonin: Regen. du cristallin. Beitr. v. Ziegler, xix., 1896 (Lit.). 

Kochs. Regen. d. Organe bei Amphibien. Arch. f. mikr. Anat., 49 Bd., 1897. 

Krückmann: Pigmentzellen der Retina. Arch. f. Ophthalm., 48 Bd., 1899. 

Müller: Regen. der Linse bei Tritonen. Arch. f. mikr. Anat., 48 Bd., 1896. 

Bandolph: The Regeneration of the Crystalline Lens. Johns Hopkius Hosp. Rep., 
ix., 1900. 

Stoewer: Heilungsvorg. bei Wunden d. Auges. Arch. f. Ophthalm., 46 Bd., 1899. 

Wolff: Linsenregeneration bei Tritonen. Biol. Cbl., xiv., 1896; An. Anz., xviii., 1900. 


Ill. The Results of Transplantation and Implantation of Tissues and 
Organs. 


§ 88. The local regeneration of tissue is, as mentioned in the last part, 
very often but slight, so that losses of tissue may be followed by perma- 
nent defects, and in place of the original structures there may appear 
only a cicatricial tissue of a lesser value. Consequently, from practical 
reasons, many attempts have been made, through transplantation and 
implantation of tissue, to aid and to improve the healing-process; and 
such attempts have in part been successful. At the same time tlıey have 
also thrown light upon the individual life of the tissues and upon the 
behavior of the organism toward implanted living tissue. 

The most. successful results have been obtained in the transplantation 
of tissues which remain connected with their nutrient vessels, since the same, 
at the point of union between the transplanted portion and the under- 
lving tissues upon which it is placed, grow together with the latter in 
essentially the same manner as do the edges of the wound in the case of a 
eut. This method is utilized most frequently in the case of plastic oper- 
ations upon the surface of the body, but it finds application also in inter- 
nal surgery. For example, wounds of the bladder, intestine, ureters, 
tubes, etc., may be easily closed through implantation of the omentum; 
and the surface presenting upon the lumen of the organ coneerned 
becomes very quickly covered over by the neighboring epithelium, which 
extends over it from the edges, or is also transplanted from the opposite 
epithelial surface (Cornil, Carnot); while the omentum itself grows to 
the adjacent wound-surfaces, and thus through changes in its structure 
completely closes up the defeet. Very often such an implantation of the 
omentum oecurs spontaneously, as, for example, in the ease of traumatic 
or ulcerative perforations of the intestine, stomach, gall-bladder, ete., 
and even large openings may be elosed in thismanner. As experimental 
investigations have shown, portions of intestine provided with blood- 
vessels may be implanted into other portions of the intestines, into the 
bladder (Enderle), stomach (Reerink), and can heal perfectly in these 











TRANSPLANTATION AND IMPLANTATION. 809 


absorbed (equally so in either case, whether living bone or dead and 
macerated bone is implanted), and is replaced by new bone arising from 
the neighboring periosteum and bone-marrow. In this way there may 
be obtained a better healing of the bone-defect, and such implantations 
of bone or cartilage may also be made use of in the case of other tissues, 
for the stimulation of a more abundant production of tissue for the pur- 
pose of filling up tissue-defects. 

The transplantation of nerves has never resulted in the new-formation 
of a nerve from the transplanted piece. The attraction which the prod- 
ucts of disintegration of a nerve (Forssmann) exert upon the axis-cylin- 
ders growing into the wound may be utilized to direct the course of the 
growing nerves into certain channels. 


Literature. 
(Transplantation and Implantation.) 


Alessandri: Innesti di tessuti viventi. Ref. Cbl. f. allg. Path., viii., 1897. 
Barth: Knochenimplantationen. Arch, f. klin. Chir., 46 Bd., 1893; Beitr. v. Ziegler, 
xvii., . 
y: Transplant. v. Hautstücken, auf Thiere e. and, Species. Beitr. v. Zieg- 
ler, xii., 1892. 
‚Hirschfeld u. Garten: Verh. impl. embryonaler Gewebe. Beitr. v. Ziegler, 
xxvi., 1899. 


Böhm: Traumat. Epithelcysten. Virch. Arch., 144 Bd., 1896 (Lit.). 
Braun: Anheilung ungestielter Hautlappen. Beitr. v. Bruns, xxv., 1899. 
Bruns, P.: Transplantation von Knochenmark. v. Langenbeck’s Arch., xxvi., 1881. 
Busse: Fortleben losgetrennter Theile. Virch. Arch., 149 Bd., 1897. 
. a: De la greffe thyröoidienne. Arch. de phys., vii., 1885; Jour. de phys., 
., 1901. 
net u. Maas: Implantation v. Periost. in die Blutbahn. Virch. Arch., 70 Bd., 


Diatschenko: Transplantation der Schleimhäute. Cbl. f. d. med. Wiss., 1890. 

hardt: Transplantation der Milz. Inaug.-Diss., Königsberg, 1892. 

v. Eiselsberg: Einlieilung der Katzenschilddrüse. Wien. klin. Woch., 1892. 

Enderlen: Einheilung v. Pfropfungen. Deut. Zeitschr. f. Chir., 45 Bd., 1898; An- 
heilung getrockn. u. feucht aufbewahrter Hautlappen. Ib., 48 Bd., 1898; Trans- 

lant. v. Schilddrüsen in die Bauechhöhle. Mittheil. a. d. Grenzgeb., iii., 1898; 

implant. d. resec. Intermediärknorpels. Deut. Zeit. f. Chir., 51 Bd., 1899; 

Transplant. d. Netzes auf Blasendefecte. Ib., 55 Bd., 1900; Deckung von Magen- 
defecten durch Netz. Ib., 55 Bd., 1900. 

Féré: La famille teratoplastiyue (Implant. v. Blastoderm). Rev. de chir., 1895. 

Foa: Trapiant. delle ovarie. Riv. per le Sc. Biol., ii., 1900; La greffe des ovaires. 
Arch. ital. de biol., xxxiv., 1900. 

Garré: Traumatische Epithelcysten. Beitr. v. Bruns, xi., 1894; Vorgänge bei An- 
heilung d. Thiersch’schen Transplant. Beitr. v. Bruns, iv., 1889. 

Goldmann: Die künstliche Ueberhiutung offener Krebse durch Hauttransplantation. 
Cbl. f. allg. Path., i., 1890; Schicksal der verpflanzten Hautstücke. Beitr. v. 
Bruns, xi., 1894. 

Goldzieher: Implantationen in die vordere Augenkammer. Arch. f. exp. Path., ii., 
1874. 

Grawitz: Widerstandsfihigkcit leb. Gewebe. Deut. med. Woch., 1891. 

ieff: Schwangerschaft bei Transpl. v. Ovarien. Arch. f. Gyn., 22 Bd., 1897. 

Grohé: Vita propria d. Zellen d. Periosts. Virch. Arch., 155 Bd., 1899. 

Hedon: Greffe souscutanée du pancréas. Arch. de phys., 1892. 

Henle u. Wagner: Transplant. ungestielter Hautlappen. Beitr. v. Bruns, 24 Bd., 


1899. 
Herlitzka: Transplant. des testicules. Arch. ital. de biol., xxxii., 1899; Ovarien- 
transplant. Biol. Cbl., xx., 1900; Arch. ital. de biol., xxxiv., 1900. 
Joachimsthal: Schnentransplant. Eulenburg’s Jahrb., viii., 1898 (Lit.). 
Junge gel: Die Hauttransplantation. Verl. d. Phys.- med. Ges. zu Würzburg, 25 
., 1891. 
Karg: Studien über transplantirte Haut. Arch. f. Anat. u. Phys., 1888. 
18 


310 THE PROGRESSIVE CHANGES. 


Kaufmann: Enkatarrhaphie v. Epithel. Virch. Arch., 97 Bd., 1884. 

Knauer: Ovarientransplantation. CLl. f. Gyn., 1896; Wien. klin. Woch., 1899. 

Laurent: Rech. sur la greffe osseuse, Bruxelles, 1893. 

Leopold: Transplant. v. Knorpel. Virch. Arch., 85 Bd., 1881. 

Wungren: Lebensdauer d. lluutepithels ausserh. d. Organismus. Deut. Zeit. f. Chir., 
47 Bd., 1898. 

Leob: Transpl. v. weiss. Haut auf Defecte in schwarzer u. umgek. Arch. f. 
Entwicklungsmech., vi., 1898. 

Lubarsch: Zur. Lehre v. d. Geschwülsten u. Infectionskrankh., Wiesbaden, 1899. 

Marchand: Knochentransplantation. Verh. d. Deut. path. Ges., ii., Berlin, 1900. 

v. Mangoldt: Ueberhiutung von Wunden durch Epithelaussaat. Deut. med. Woch., 
1895; Einpflanz. v. Rippenknorpel in Kelilkopf. Langenbeck’s Arch., 50 Bd., 1899. 

Minkowski: Unters. fiber Diabetes mellitus.- Arch. f. exp. Path., 31 Bd., 1893. 

Morpurgo: Vita propria d. Periostzellen. Virch. Arch., 157 Bd., 1899. 

Mossé: La greffe osseuse heteroplast. Arch. de phys., viii., 1896. 

Neumann: Nierentransplantation. Arch. f. Entwickelungsmechan., vi., 1898. 

Ollivier: Traité exper. et clin. de la régénérat. des os, 1867; De la greffe osseuse chez 
homme. Arch. de phys., 1889. 

Pascale: Innesti ossei. XI1. Congr. Chir., Roma, 1897. 

Plessing: Hautverpflanzung nach Thiersch. Langenbeck’s Arch., 37 Bd., 1888. 

Raehlmann: Anheilung transplant. Lippenschleimhaut. Beitr. v. Ziegler, xxvi., 
1899. 

Beerink: Experimente über Transplantationen am Magen. Beitr. v. Ziegler, xxviii., 
1900. 

Beverdin: De la greffe epidermique, Paris, 1872 (u. Gaz. des höp., 1870, 1891); 
Trauspl. de peau de grenouille sur des plaies humaines, Arch. de med. exp., iv., 
1892. 

Ribbert: Das patholog. Wachsthum d. Gewebe, Bonn, 1896; Veränd. transplant. 
Gewebe. Arch. f. Entwickelungsmech., vi.; Transplant. v. Ovarium, Hoden, 
Mamma. Ib., vii., 1898; Exp. Erzeugung von Epithel- u. Dermoidcysten. Deut. 
Zeit. f. Chir., 47 Bd., 1898. 

Rutkowski: Harnblasenplastik. Cbl. f. Chir., 1899. 

Saltykow: Transpl. zusammenges. Theile. Arch. f. Entwickelungsmech., ix., 1900. 

Scheff: Die Replantation der Zähne, Wien, 1890. 

Schloffer: Osteoplastik bei Defecten d. Tibia. Beitr. v. Bruns, xxv., 1899. 

Schüller: Schalenhaut des Hihnereies. Monatssch f. Unfallheilk., 1899. 

Schultz: Transp]. v. Ovarien auf männ!. Thiere. Cbl. f. allgem. Path., xi., 1900. 

Stransky: Sensibilität transpl. Hautstücke. Wien. nıed. Woch., 1899. 

Sultan: Transpl. v. Schilddrüsen. Cbl. f. allgem. Path., 1898. 

Schweninger: Ueber Transplant. u. Implant. v. Haaren, München, 1875. 

Tietze: Netzplastik. Beitr. v. Bruns, xxv., 1899. 

Valan: Sull’ innesto dell’ osso sul cranio. Arch. per le Sc. Md., xxii., 1898; Arch. 
it. de biol., xxxi. 

Weiss: Transplant. v. Bindehaut auf Hornhaut. Arch. f. Augenh., 33 Bd., 1896 

Wentscher: Eigenleben menschl. Epidermiszellen. Beitr. v. Ziegler, xxiv., 1898. 

Wetzel: Transplantationsversuche mit Hydra. Arch. f. mikr. Anat., lii., 1897. 

Zahn: Sur le sort des tissus implantes dans l’organisme. Congrés med. Internat. de 
Genéve, 1876; Schicksal in den Organismus implant. Gewebe. Virch. Arch., 95 
Bd., 1884. 


IV. The Metaplasia of Tissues. 


§ 89. Metaplasia of a tissue is that process by which an already fully- 
developed tissue is changed into another tissue without passing through an 
intermediate cellular stage—that is, through the stage of an embryonic 
or formative tissue. Such a transformation occurs only in tissues which 
are closely related to each other, particularly in the connective tissues, 
All the tissues belonging to this group may, under pathological condi- 
tions, be transformed, one into another, without the occurrence of any 
intermediate proliferation—a phenomenon which in itself is not surpris- 
ing, as such transformations occur also under normal conditions, Mu- 
cous tissue becomes changed to adipose tissue through the conversion of 
the stellate connective-tissue cells into round fat-cells through the tak- 
ing-up of fat, while the mucous ground-substance disappears. Lymph- 








METAPLASIA. 313 


orrhcea), nose (ozena), and of the trachea, whereby the cylindrical epithe- 
lium becomes changed into flattened. 

This transformation takes place through a change in the character of 
the regenerating epithelium as the result of repeated loss of the original 
epithelium. In the stratified squamous epithelium of a mucous mem- 
brane there may occur also a cornification of the uppermost layers of cells, 
both in regions where squamous epithelium is normally present, and also 
in regions which normally possess none, as, for example, in the ureters, 
as well as in places where it has been formed pathologically, as in the 
nose and uterus. 


Literature. 
( Metaplasia. ) 


Finger: Die chronische Urethralblennorrhde. Arch. f. Derm., Er Anzungsheft, 1891. 

Hansemann: Studien üb. Specificität, Altruismus u. Anaplasie d. Zellen. Berlin, 1893. 

Hildebrandt: Ueber einen Katarrh d. weibl. Geschlechtsorgane. Sammi. klin. 
Vortr., No. 82. 

Kanthack: Stud. üb. d. Histologie d. Larynxschleimhaut. Virch. Arch., 119 and 120 
Bd., 1890. 

Küstner: Plattenepithel auf Uteruspolypen. Cbl. f. Gyn., 1884. 

Liebenow: Ueber ausgedehnte Epidermisbildung der Harnwege. Inaug.-Diss., Mar- 
burg, 1891. 

Neelsen: Histol. Veränd. i. d. chron. entzündet. Urethra. Vierteljahrsschr. f. Derm., 
1887. 

Ohloff: Epithelmetaplasie u. Krebsbildung in Gallenblase u. Trachea. Inaug. Diss., 
Greifswald, 1891. 

Sangalli: Die Metaplasie d. krankh. Gewebe. Int. Beitr., Festschr. f. Virchow, ii., 

rlin, 1891. 
Schmiedeberg: Die chemische Zusammensetzung des Knorpels. Arch. f.exp. Path., 


1891. 

Schuchardt: Ueber d. Wesen d. Ozaena. Samml. klin. Vortr., No. 340, Leipzig, 
1891. 

Virchow: Gesammelte Abhandl., Frankfurt, 1856, pp. 500, 509; Cellularpathol., iv. 
Aufl., p. 70. Virch. Arch., 8 and 97 Bd.; Deut. med. Woch., 1884. 

Zeller: Plattenepithel im Uterus. Zeitschr. f. Geburtsh.. ~i., 1885. 


Men lere en eu. 


CHAPTER VII. 


Inflammation. 
I. The Early Stages of Acute Inflammation. 


§ 90. Under the designation inflammation are grouped those patho- 
logical phenomena which represent a combination of different patholog- 
ical processes, consisting on the one hand of tissue-degenerations and 
tissue-proliferations, and on the other of pathological exudations from 
the blood-vessels. Degenerations of tissue and pathological exudations init- 
tate the process ; with these tissue-proliferation is sooner or later associated, 
the latter leading in the further course of the process to a compensation 
for the disturbance—that is, to healing. The proliferation of tissue may, 
therefore, be regarded as regenerative, but such new-formation of tissue 
may be in excess of that which is useful to the body. The tissue-degen- 
erations and proliferative processes described in the previous chapters 
appear for the greater part as participating factors in inflammation; the 
process acquiring tts inflammatory character through the combination of tissue- 
degenerations and tissue-proliferations with pathological exudations. 

Deeper tissue-lesions—that is, injury of tissues containing blood-vessels— 
which in some way or other affect the vascular system, will, therefore, 
constantly bear at some time during their course the character of an inflamma- 
tion. The formation of scar tissue, the healing of transplanted tissucs, as 
briefly described in the last chapter, always take place through processes 
essentially inflammatory in nature. 

Exudation in acute inflammation is constantly associated with a 
pronounced hyperemia, which appears even before the beginning of the 
exudation, and hence ushers in the latter. As a result of the combina- 
tion of hyperemia and exudation the inflamed tissue becomes reddened 
and swollen. When situated on the surface of the body, where a cooling 
of the tissues takes place, the increased flow of warm blood from the 
deeper tissues causes a local increase of temperature. If the tissue af- 
fected contains sensory nerves, the sensation of pain will be produced as 
the result of the changed conditions in the inflamed area. 

Redness, swelling, increased warmth, and painfulness of the in- 
flamed tissue are phenomena which even in ancient times were regarded 
by physicians as the signs of inflammation; and rubor, tumor, calor, and 
dolor were designated by Celsus, at the beginning of our era, as the 
cardinal symptoms of inflammation. To these four was then added 
still a further symptom, functio lesa, altered function of the inflamed 
tissue. 

The causes of inflammation may lie either in mechanical, thermal, 
electrical, or chemical influences, as well as in the influence of parasites. 
The common characteristic of all these injurious agencies is the produe- 
tion, in the first place, of a local tissue-degeneration, which, when of a certain 
extent and intensity, is associated with disturbances of the circulation and of 
the vascular secretion. The causes of inflammation are not specific; any 

314 


THE EARLY STAGES OF ACUTE INFLAMMATION. 315 


injurious agent may excite inflammation if on the one hand its action is 
sufficiently intense to cause certain disturbances of circulation in asso- 
ciation with tissue-degenerations, but on the other hand not so intense as 
completely to destroy the tissue and stop the circulation. 

The great majority of the causes of inflammation reach the human 
organism from the outside, but excitants of inflammation may be formed 
also within the body. In the first place bacteria which have penetrated 
into the tissues very often form within their protoplasm or from sub- 
stances present in the body certain products which are capable of excit- 
ing inflammation. Moreover, substances that excite inflammation may 
arise within the organism without the aid of parasites; particularly as 
the result of the death of large masses of tissue from any cause, as, for 
example, as the result of ansmia, or when as the result of disturbances 
of metabolic processes (gout) products of metabolism are deposited in 
the tissues. . 

The causes of inflammation may act upon the tissues either from the 
portions of the body accessible from without, or from the lymph and the 
blood; and we may, therefore, distinguish ectogenous, lymphogenous, 
and hematogenous inflammations. Through the spread of an inflam- 
mation to neighboring tissues there arises an inflammation by con- 
tinuity ; as the result of the transportation through the lymph or blood 
stream of an agent causing inflammation, there are produced metastatic 
inflammations. If injurious substances are discharged through the 
excretory organs, excretory inflammations may arise. 

When a local injury to tissues has reached such a degree as to pro- 
duce the exudation characteristic of an inflammation, there is usually 
found in the first place a congestive hyperemia, as a result of which 
the blood flows through the dilated blood-channels with increased veloc- — 
ity. After a short time there is a lessening of the speed of the circula- 
tion which leads finally to an abnormal slowing of the blood-current. 

The first disturbances of circulation, which find expression in the 
congestive hyperemia, may be due either to a stimulation or paralysis 
of the vasomotor system or to a direct action upon the vessel-walls, par- 
ticularly upon the arterial walls, leading to a dilatation of the lumen. 
Although these disturbances very frequently precede the inflammatory 
exudation, they do not form an essential characteristic of inflammation, 
and occur very often without being followed by an inflammatory exuda- 
tion. Further, they may be absent during the course of an inflammation. 
The circulatory disturbances characteristic of inflammation are shown 
only when the slowing of the blood-current and the pathological 
exudation from the blood-vessels set in. The slowing of the blood- 
stream in the dilated channels and the pathological exudation are de- 
pendent upon a change in structure, an alteration of the vascular walls, 
through which there results a lasting dilatation of the vessel and an 
adhesion of the blood to the vessel-wall, causing an increase of friction- 
resistance and an increased permeability of the vessel-wall. In the capil- 
laries the persistent dilatation is in great part the result of relaxation of the 
connective tissue surrounding the capillaries, inasmuch as the thinness of the 
capillary walls makes this tissue bear the greater part of the blood-press- 
ure resting upon them. 

The tissue-lesion which leads to the phenomena of inflammatory dis- 
turbances of circulation and exudation usually affects all parts of the 
tissue, but under certain conditions may be limited to the vessel-wall, 
particularly in the case of a hematogenous inflammation, in which the 











THEORIES OF INFLAMMATION. 319 


pressed-out blood-serum; while a part, which is chiefly taken up by the “irritated” 
cells, is to be regarded as a product of an increased drawin of the blood-elements 
through the tissues, as a kind of nutritive educt. Of the cells collecting in the in- 
flamed area, he believed that all originate from a proliferation of the tissue-cells oc- 
curring as the result of the action of the inflammatory irritant. 

The recognition that the formation of the exudate is to be referred to an injury of 
the vessel-walls we owe chiefly to Cohnheim, whose investigations along various lines 
were completed by Samuel, Arnold, Thoma, Binz, and others. Cohnheim also showed 
that in inflammation the colorless corpuscles emigrate, and form an essential constituent 
of the inflammatory exudate. 

Dutrochet (“ Rech. anatomiques et physiologiques sur la structure interne des ani- 
maux et des végétaux et sur leur motilité,” Paris, 1842, p. 214) and Waller (Philosoph. 
Magaz., xxix., 1846, pp. 271, 398) had as early as the years 1842 and 1846 already de- 
scribed the escape of colorless corpuscles from the blood-vessels. These observations 
had, however, fallen completely into oblivion until Cohnheim, in 1867, rediscovered the 
phenomenon. 

According to researches of Schklarewsky (Pfliger’s Arch., Bd. i.), the peripheral dis- 
position of the leucocytes in the veins is purely a physical phenomenon. If fluids, in 
which are suspended finely powdered substances of different specific gravity, are made 
to flow through tubes, it will be found that at a certain degree of retardation of the 
current, the bodies of lighter specific gravity pass over into the peripheral zone, and at 
a more marked retardation the heavier bodies also enter this zone. 

For the occurrence of the emigration of the white corpuscles, it is necessary, 
according to the researches of Binz, Thoma, and Lavdousiy, that they be capable of 
motion and of adhering to the vessel-wall. According to these observers, the emigra- 
tion of the white blood-cells is not a purely passive, but isin part at least an active 
process. If the amaboid power of the white cells be lessened by means of irrigation 
of the mesentery with a 1.5-per-cent. solution of salt (Juma), or if the vital energy 
of these cells be lowered by means of quinine or iodoform (Binz, Appert, Kerner), 
there results an inhibition of emigration. On the other hand, Pekelharing believes 
that quinine, oil of eucalyptus, and salicylic acid cause a contraction of the veins, 
lessen the permeability of their walls, and thereby hinder the passing-out of the white 
cells. This view is rejected, however, by Disselhorst, who observed a dilatation of 
the veins after irrigation of the tissues with quinine, carbolic acid, salicylic acid, and 
mercuric chloride. As there occurs in this case a retardation of the current after a 
transitory acceleration, without an emigration of the leucocytes collected in the periph- 
eral zone; and as, on the other hand, leucocytes from blood-vessels that have been irri- 
gated foran hour with quinine still retain complete vitality (berth), Disselhorst is of the 
opinion that the drugs mentioned so change the inflamed vessel-wall that an adhesion of 
the leucocytes rolling along the wall either cannot occur at all or only with difficulty. 

It is very probable that a lesion of the vessel-wall is not absolutely necessary for 
the emigration of leucocytes (Thoma). Since vasomotor disturbances of the circulation 
can produce migration (von Recklinghausen, Thoma), it is probable that all of the con- 
ditions necessary for this process are furnished by a slowing of the blood-stream with 
peripheral disposition of the colorless corpuscles and the ability of the leucocytes to 
perform amewboid movements and to adhere to the vessel-walls. It is possible that 
differences in the water-content of the tissues (Toma) also exert some influence, since 
an increased amount of water causes increased amaboid movement. It is also possible 
that the presence, in the tissue-fluids, of substances having active chemotactic proper- 
ties may cause emigration of those leucocytes in the peripheral zone which ere adherent 
to the vessel-wall. 

According to the investigations of Arnold, Thoma, and Engelmann, there is present 
between the edges of the endothelial cells a soft cement-substance which suffers a change 
in the circulatory disturbance associated with cell-migration. This change may some- 
times, but not always (Zöwit), be recognized, on histological examination, in the form 
of numerous circumscribed widenings of these intercellular areas (Engelmann). If leu- 
cocytes pass through these places in great numbérs the cement-substance becomes still 
more permeable, and may then permit red cells also to pass through in rapid succession 

homa). 

Wandering cells are found normally in many tissues (von Itecklinghausen), and 
wander from these partly into the lymph-vessels (Hering, Thoma), and under certain 
conditions also into the blood-vessels (Bubnoff, Schulin, Rantier, Senftleben), or onto the 
surface of the mucous membranes, where they penetrate between the epithelial oells. 
They are found constantly in large numbers about the nodes of Jymphadenoid tissue 
in the mucous membranes, and wander from these through the epithelium onto the 
surface. According toobservations by Aunkel and Siebel, small numbers also reach the 
free surface of the alveoli of the lungs. 


— 


sn 4 


320 INFLAMMATION. 


The inflammatory disturbances of circulation and the formation of exudates may 
be most easily followed in the transparent membranes of cold-blooded animals, particu- 
larly in the mesentery, or the extended tongue or the spread-out web of the frog. In 
the frog’s mesentery, which has been spread out ona suitable glass plate, circulatory 
disturbances and inflammation develop simply through exposure to the air and the 
resulting evaporation: in the case of the tonguc and web, it is necessary to cauterize in 
order to produce an inflammation. By the employment of suitable apparatus the cir- 
culation of the blood and the formation of the inflammatory exudate may also be ob- 
served under the microscope in the thin membranes of mammals (mesentery of rabbit, 
wing-membrane of bat), and observations thus made harmonize wholly with those made 
upon the frog. 


Literature. 
(Inflammation. ) 


Aufrecht: Ueber Entzündung, Pathol. Mittheilungen, i., Magdeburg, 1881. 

Brault: Etude sur l’inflammation, Paris, 1888. 

Cohnheim: Ueber Entzündung und Eiterung. Virch. Arch., 40 Bd., 1876; Neue 
Untersuchungen über Entzündung, Berlin, 1873; Noch einmal die Keratitis. 
Virch. Arch., 61 Bd., 1874; Vorles. über allg. Pathologie, Leipzig, 1882. 

Cornil et Ranvier: Man. d’histol. patholog., i., Paris, 1901. 

Councilman: Inflammation. Ref. Handb. of Med. Sciences, 2d ed., 1902. 

Franke: Die menschliche Zelle, Leipzig, 1891. 

Grawitz: Atlas der pathol. Gewebelehre, Berlin, 1893. 

Hektoen: Old and Modern Theories of Inflammation. Phil. Med. Jour., 1898. 

Henle: Handb. d. ration. Pathologie, Braunschweig, 1844. 

Janowski: Die Ursachen der Eiterung. Beitr. v. Ziegler. xv., 1894. 

Landerer: Zur Lehre von der Entzündung. Volkmann’s Sammi. kl. Vo:tr., No. 259, 
1885; Die Gewebsspannung, Leipzig, 1884. 

Leber: Die Entstehung der Entzündung, Leipzig, 1891. 

Letulle: L'Inflammation, Paris, 1893. 

Löwit: Entstehung des Lungenödems. Beitr. v. Ziegler, xiv., 1894. 

Lubarsch: Entzündung. Ergebn. d. allg. Path., iii., 1897; Deut. med. Woch., 1898. 

Metschnikoff: Lec. sur la pathologie comparée de l’inflammation, Paris, 1892. 

Neumann: Ueber den Entzindungsbegriff. Beitr. v. Ziegler, v., 1889. 

Ponfick: Die Entwickelung der Entzündungslelire im. 19. Jahr. Berl. klin. Woch., 
1900. 

v. Recklinghausen: Handb. d. allg. Path. d. Kreislaufs u. d. Ernährung, Stuttgart, 
1883 


Rokitansky: Lehrb. d. path. Anatomie, Wien, 1855. 

Roser, K.: Entzündung und Heilung, Leipzig, 1886. 

Ribbert: Das pathologische Gewebswachsthum, Leipzig, 1896. 

Samuel: Der Entzündungsprocess, 1873; Entzündungsherd und Entzündungshof. 
Virch. Arch., 121 Bd. ; Ueber anämische, hyperämische u. neurotische Entzündung. 
Ib. 121 Bd.; Die Selbstheilung der Entzündungen und ihre Grenzen. Ib., 126 

., 1891. 

Thoma: Ueber die Entzündung. Berl. klin. Woch., 1886; Pathol. Anat., i., 1894. 

Virchow: Cellularpathologie u. Handb. d. spec. Path., i., 1854; Die Rolle der Gefässe 
und des Parenchyms bei der Entzündung. Virch. Arch., 149 Bd., 1897. 

Weiss: Beiträge zur Entzündungslehre, Wien, 1893. 

Woronin: Untersuchungen über die Entzündung, Moskau, 1897. 

Ziegler: Historisches u. Kritisches über die Lehre von der Entzündung. Beitr. v. 
Ziegler, xii., 1892: Entzündung. Eulenburg’s Realencyklop., vii., 1895; Inflam- 
mation, Twentieth Century Practice of Medicine, xvi., New York, 1899. 


(Migration of Leucocytes, and Inflammatory Exudation. ) 


Appert: Der Einfluss des Chinins auf die Auswanderung der weissen Blutkörperchen 
bei der Entzündung. Virch. Arch., 71 Bd., 1877. 

Arnold: Ueber Diapedese. Virch. Arch., 58 Bd., 1873; Verhalten der Blutgefässe 
bei der Emigration weisser Blutkörper. Ib., 62 Bd., 1875; Ueber die Kittsubstanz 
der Endothelien. Ib., 66 Bd., 1876; Saftbahnen des Bindegewebes. Ib., 68 Bd., 
1876. 

Binz: Der Antheil des Sauerstoffes an der Eiterbildung. Virch. Arch., 59 Bd., 1874, 
and 73 Bd., 1878; Verhalten der Auswanderung farbloser Blutzellen zum Jodo- 


INFLAMMATORY EXUDATION. 321 


form. Ib., 89 Bd., 1882; Zur Salicylsäure- und Chipinwirkung. Arch. f. exp. 
Path., vii., 1877; Ueber einige Wirkungen ätherischer Oele. Ib., viii., 1877. 
Borisow: Chemotakt. Wirkung versch. Subst. Beitr. v. Ziegler, xvi., 1894. 
Bunzel: Einfluss d. vasomotor. Nerven auf die Entzündung. Arch. f. exp. Path., 87 
., 1896. 

Cohnheim: L. c., Untersuchungen fiber die embolischen Processe, Berlin, 1872. 

Dekhuyzen: Ueber Emigration v. Leukocyten. Verh. d. Anat. Ges., Jena, 1891. 

Disselhorst: Emigration farbloser Zellen aus dem Blute. Virch. Arch., 118 Bd., 1888, 

Engelmann: Verh. d. Blutgefässendothels bei Auswanderung farbl. Blutkörp. Beitr. 
v. Ziegler, xiii., 1893. 

Goecke: Exper. Entzündung der Hornhaut. Beitr. v. Ziegler, xx., 1896. 

Hauser: Entsteh. d. fibrindsen Exsudates bei d. croupösen Pneumonie. Beitr. v. 
Ziegler, xv., 1894. 

Heidenhain: Ueber Lymphbildung. Verh. d. X. internat. med. Congr., ii., Berlin, 
1891; Histologie u. Physiologie d. Dünndarmschleimhaut. Arch. f.d. ges. Phys., 
43 Bd, Suppl.-Heft, 1888; Versuche u. Fragen zur Lehre v. d. Lymphbildung. Ib. 
49 Bd., 1891. 

Heller: Ueber die feineren Vorgänge bei der Entzündung, Erlangen, 1869. 

Hoffmann, F. A.: Eiweissgehalt der Ascitesflissigkeiten. Virch. Arch., 78 Bd., 1879. 

Hoppe-Seyler: Ueber seröse Transsudate. Virch. Arch., 9 Bd., 1856. 

Klemensiewicz: Fundamentalversuche über Transsudation, Graz, 1883; Entzündung 
u. Eiterung. Festschr. f. Rollet., Jena, 1893. 

Kronacher: Die Aetiologie u. d. Wesen der acuten eiterigen Entzündung, Jena, 1891. 

Lassar: Ueber Ovdem u. Lymphstrom bei der Entzündung. Virch. Arch., 69 Bd., 
1877. 

Lavdowski: Auswanderung farbloser Blutelemente. Virch. Arch., 96 Bd.; Die Aus- 
wanderung d. Leukocyten u. die Frage nach dem Schicksale derselben. Ib., 97 Bd., 
1884. 

Löwit: Bezich. d. Blutgefässendothels zur Emigration. Beitr. v. Ziegler, xvi., 1894. 

Maximow: Thermoelektrische Messung von Entzündungsherden. Wiener med. 
Jahrb., 1886. 

Middeldorpf u. Goldmann: Exp. Untersuchungen üb. Croup u. Diphtherie, Jena, 
1891. 

Pekelharing: Diapedese d. farblosen Blutkörp. bei d. Entzündung. Virch. Arch., 
104 Bd., 1886. 

Ranvier: Traite techn. d’histologie, Paris, 1875-88; Beitrag z. Lehre v.d. Entzündung 
u. den dabei auftretenden corpusculären Elementen. Virch. Arch., 72 Bd., 1878. 

v. Recklinghausen: Das Lymphgefässsystem. Stricker’s Handb. d. Gewebelehre; 
Ueber Eiter und Eiterkörperchen. Virch. Arch., 28 Bd., 1863. 

Ribbert: Zur Anatomie der Lungenentzündung. Fortschr. d. Med., xii., 1894. 

Schklarewski: Zur Extravasation der weissen Blutkörperchen. Pflüger's Arch., i., 
1869. 

Schumacher: Pharmakol. Studien über die Auswanderung der farblosen Blutkörper- 
chen. Arb. a. d. pharmakol. Institut zu Dorpat, x., 1894. 

Senftleben: Verschluss d. Blutgefässe nach d. Unterbindung. Virch. Arch., 77 Bd., 
1879. 

Siebel: Ueb. d. Schicksal v. Fremdkörpern in d. Blutbahn. Virch. Arch., 104 Bd., 
1886 


Stöhr: Ueber Mandeln u. Balgdrüsen. Virch. Arch., 97 Bd., 1884. 

Thoma: Entzündl. Störungen d. Capillarkreislaufs bei Warmblütern. Virch. Arch., 
74 Bd., 1878; Die Ueberwanderung farbloser Blutkörper v. d. Blut- ind. Lymph- 
gefiisssystem, lIeidelberg, 1873. 

See also SS 91-9. 


8 91. The cellular and fluid exudates secreted by the vessels collect: first 
in the immediate neighborhood of the vessels (Fig. 180), but soon spread 
out in the vicinity, mass themselves in the lymph-spaces of the tissue, and 
thus form a tissue-infiltrate (Figs. 181, e; 182, 5; 185, p). When the 
exudate is very abundant it may spread into and infiltrate the neighbor- 
ing sound tissue that has not been injured by the inflammatory irritant. 
This infiltration may be so marked that new disturbances of circulation 
and nutrition may be produced, and the area of tissue-degeneration and 
inflammatory exudation becomes increased in extent. 

The erudate present in a tissue may be in part absorbed by the tissue- 











THE ORIGIN OF THE CELLS IN THE EXUDATE. 325 


tissnes immediately about it the prefixes “ peri” and “para” are placed 
before the Greek names with the termination “itis.” Thus, for example, 
are formed the words perimetritis, parametritis, periproctitis, perityph- e x... 
litis, paranephritis, and perihepatitis. | 

For certain forms of inflammation especial names are used, as, for 
example, inflammation of the lungs is called pneumonia, and inflamma- 
tion of the palate and tonsils, angina. 


Since Cohnheim taught that the migration of leucocytes en masse is an important 
feature of inflammation and serves as a source for the cells in the exudate, the ques- 
tion of the origin of the cells present in the exudate of acute inflammations has been 
many times the subject of discussion. While some have regarded all the cells in the 
exudate as extravasated leucocytes, others have held that the leucocytes arising from 
the blood-stream form only an unessential element, and that the main part of the cells 
in the exudate have arisen on the spot from the tissue “irritated” by the cause of the 
inflammation. 

Stricker held the opinion that the swelling and hardening of the tissues in inflamma- 
tion are not caused by the collection of exudate, but by the swelling of the cell-reticulum 
which was thought to traverse the tissues; and that these changes represent a phenome- 
non of growth of the cells and their processes which is characterized by swelling. The 
cellular exudate—that is, pus—he accounts for partly through the segmentation and 
division of the cell-reticulum swollen by the inflammation, and partly through a trans- 
formation of connective-tissue fibrille into pus-corpuscles. Heitzmann regarded the 
inflammatory tissue-changes asa reversion of the tissue to the embryonal condition, and 
believed that the living material is not contained in the cells alone, but infiltrates the 
entire ground-substance, and increases, in the progress of an inflammation, with the 
liquefaction of the ground-substance. Connective-tissue cartilage and bone become 
resolved during inflammation into those elements from which they are formed—i.e., 
into cells—which then immediately reproduce their kind. Grarrcttz believes that both 
the celular infiltrate and pus are formed without any participation of the leucocytes 
worth mentioning. Everywhere in the tissue, according to his view, there lie concealed 
in great numbers cells, which he designates slumber-cells, and which are not affected 
by our nuclear stains and therefore not recognizable (according to him, ony from five 
to ten per cent. of the tissue-cells are Known to us); these cells awake in inflammation, 
and again come into sight—that is, increase in size, stain with nuclear stains, and there- 
fore again become recognizable. 

According to the results of an unprejudiced and careful examination of inflamed 
tissues, there can be no doubt that the description of the origin of the inflammatory in- 
filtrate given by Stricker, Hettzmann, Gravitz, and their pupils, does not correspond to 
the conditions as they actually exist. The cells which lie in recently inflamed tissue 
consist in part of leucocytes which have wandered from the vessels and in part of 
tissue-cells which are more or less degenerated, and are often separated from the under- 
lying tissues. Later, to these there are added newly formed cells which have arisen 
through the division of pre éxisting tissue-cells. 


Literature. 


( The Processes Occurring in the Tissues during Inflammation, and the Origin 
of the Cells in the Exudate. ) 


Alexander-Levin: Histologie d. acut. bakteriellen Entzündung. Arb. a. dem Inst. 
v. Baumgarten, i., 1891. 

Baumgarten: Herkunft d. in Entzündungsherden auftret. lymphkorperart. Elemente. 
Chl. f. allg. Path., i.. 1890. 

Böttcher: Entstehung der Eiterkörperchen bei der traumatischen Keratitis. Virch. 
Arch., 58 Bd., 1873; Ueber die circumscripte Keratitis. Ib., 62 Bd., 1875. 

Cattani: Ueber die Reaction der Gewebe auf specifische Reize. Beitr. v. Ziegler, vii., 
1891. 

Coön: Veränderungen der Haut nach Einwirkung von Jodtinctur. Beitr. v. Ziegler, 
ii., 1887. 

Eberth: Entzündung d. Hornhaut. Unters. a. d. path. Inst. in Zürich, Leipzig, 1874 
and 1875; Kern- u. Zelltheilung bei Entzündung. Internat. Beitr., Festschr. f. 
Virchow, ii., Berlin, 1891. 

Ehrhardt: Muskelveränderungen bei d. Trichinose. Beitr. v. Ziegler, xx., 1896. 

19 





CATARRHAL INFLAMMATION. 327 


horny layer of the epidermis with the liquefaction of the soft layers of 
epithelium lead to the formation of vesicles and blisters with clear con- 
tents (Fig. 183, d, f). 

When the exudation of fluid on the surface of a mucous membrane is 
associated with a marked mucoid degeneration of the superficial epithe- 
lium (Fig. 185, b, ¢, c,), and of the mucous glands (n), there arises a 





Fi. 18%.- Catarrhal secretion of different mucous membranes. 4, Secretion from mucous membranes 
with columnar cells: 2B. from the mouth; C, from the bladder. 1. Round cells (pus-cells); 2, large round 
cells with bright nuclei, from the nose; 3, mucoid columnar cells from the nose; 4, spirillum from the nose; 
5. mucoid cells with cilia, from the nose ; 6, goblet-cells from the trachea; 7, round-cells with spherules of 
Inucus from the nose; & epithellal cells containing pus-corpuseles, from the nose, 9, fatty cells; 10, cells 
containing coal-piginent, from the sputum; ll and 12, squamous epithelium from the mouth; 13, mucoid 
pus-orpuseles : Ir microcoeci; 15, bacteria; 16, leptothrir buccalis; 17, »pirochate denticola : 18, super- 
Beial, 19, middle layer of bladder epithelium ; 20, puscorpuseles; 21, achizompcctes. X 400. 


mucous catarrh (d, f, f,, 9). If a marked desquamation of the epithe- 
lium, with or without a mucoid change, occurs (Fig. 186, @), the condi- 
tion is termed a desquamative catarrh ; and such a process may occur 
not only on mucous membranes, but also in the respiratory parenchyma 
of the lungs, on serous surfaces (Fig. 180, 4, f,), in the kidney-tubules, 
etc. If many pus-corpuscles are present in the exudate it may be spoken 
of as a desquamative purulent (Fig. 186, a), or finally as a pure purue 
lent catarrh, in which condition the exudate becomes white or yellow- 
ish-white, milky or creamy. 

The form and charaeter of the cells of a catarrhal secretion vary with 
the location and the variety of catarrh (Fig. 187). Bacteria are often 
present in the cells of the exudate (Fig. 187, 4, 14, 15, 16, 17, 21). 

If ina fluid exudate there oceurs a deposition of fibrin or coagula- 
tion, there are formed fibrinous and serofibrinous exudates, which are 
often designated as croupous. These occur chiefly upon the surface of 
serous and mucous membranes, and in the lungs; but masses of fibrin 














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CATARRHAL, SEROUS, AND FIBRINOUS INFLAMMATION. 333 


writers who have expressed opinions upon this subject that the deposits are exuda- 
tive fibrin. The illustrations which Neumann has presented in his work are in no man- 
ner confirmatory of his view, but enable us rather to affirm that Neumann had before 
him in his preparations exudative fibrin. In very severe inflammations fibrin may 
indeed be precipitated in the connective tissue of the serous membranes; and, when 
treated with stains, may occasion a peculiar staining of the tissue, but in such a case 
we have to deal with a deposit of exudative fibrin, and not with a fibrinoid degenera- 
tion of connective-tissuc fibres. 


Literature. 


(Catarrhal, Serous, and Fibrinous Inflammation, and Formation of Inflam- 
matory Blebs. ) 


Abramow: Fibrinöse Entzünd. d. serösen Häute. Beitr. v. Ziegler, xxiii., 1898. 

Appel Fi Ueb. d. Herkunft. d. Fibrins auf serösen Häuten. Inaug.-Diss., Göttingen, 
1895. 

Arnold: Morphologie d. extravascul. Gerinnung. Virch. Arch., 150 Bd., 1897. 

Baginsky: Diphtherie u. diphtheritischer Croup, Wien. 1898. 

Baumgarten: Pathogenese der diphtherischen Membran. Berl. klin. Woch., 1897. 

Borst: Fibrinöse Exsudation u. fibrinoide Degeneration. Zeit. d. Phys.-ıned. Ges. 
Würzburg, 1897. 

Cornil: Intlamm. des membranes sereuses. Arch. de med. exp., 1897. 

Ernst: Ueber das Vorkommen des Fibrins in Nicrencylindern. Beitr. v. Ziegler, xii., 
1893. 

Gaylord: Fibrinous Exsudates. Jour. of Exp. Med., iii., 1898. 

Georgiewsky: Fibrin. Entzünd. seröser Hitute. Beitr. v. Ziegler, xxv., 1899. 

Graser: Die erste Verklebung seröser Häute. Langenbeck’s Arch., 50 Bd., 1895. 

Hauser: Pathol. Fibringerinnung. Deut. Arch. f. klin. Med., 50 Bd., 1893; Entsteh. 
d. tibrin. Exsudates bei der croup. Pneumonie. Beitr. v. Ziegler, xv., 1894: Gerin- 
nungscentren, Virch. Arch., 154 Bd., 1898. 

Heinz: Jod u. Jodverbindungen. Virch. Arch., 155 Bd., 1899; Entsteh. d. Fibrins. 
Ib., 160 Bd., 1900. 

Herxheimer: Fibrinöse Entzündungen. Virch. Arch., 160 Bd., 1900. 

Heubner: Ucber die diphtheritische Membran. Jahrb. f. Kinderheilk., xxx., 1889; 
Verh. d. Congr. f. inn. Med., viii., 1889. 

Jatta: Genése de la fibrine duns les inflam. de la plévre. Arch. ital. de biol., xxxi., 
1898. 

Israel: Die aniimische Nekrose der Nierenepithelien. Virch. Arch.. 123 Bd., 1891. 

Kossel: Ueber Schleim und schleimbildende Stoffe. Deut. med. Woch., 1891. 

Kramer: Veränderungen d. Rachen- u. Kehlkopfschleimhaut b. Diphtherie. Inang.- 
Diss . Freiburg, 1890. 

Marchand: Fibrinöse Exsudation bei Entzündungen. Virch. Arch., 145 Bd., 1896. 

Middeldorpf u. Goldmann: Exp. u. path.-anat. Unters. üb. Croup u. Diphtherie, 
Jena, 1891. 

Müller: Veriind. d. Blutkörp. bei extravascul. Gerinnung. Cbl. f. allg. Path., viii., 
1897. 

Neumann: Pikrokarminfärbung und ihre Anwendung auf d. Entzündungslehre. 
Arch. f. mikr. Anat., xviii., 1880: Fibrinoide Degeneration d. Bindegewebes bei 
Entzündungen. Virch. Arch., 144 Bd.; Fibrinoide Degenerat. u. fibrin. Exsuda- 
tion. Ih., 146 Bd.. 1896. 

Oertel: Pathogenese der epidemischen Diphtherie, Leipzig, 1887. 

Ribbert: Zur Anatomie der Lungenentzündung. Fortschr. d. Med., xii., 1894. 

Saltykow: Entzündungen der serösen Häute. Beitr. v. Ziegler, xxix., 1900. 

Schweninger: Diphtheritis. Mittheil. a. d. path. Institute in München, 1878. 

Touton: Vergl. Unters. über die Entstehung der Hautblasen, Tübingen, 1882. 

Weigert: Auat. Beitr. zur Lehre von den Pocken, Breslau, 1874: Ueber Croup u. 
Diphtheritis. Virch. Arch., 70 Bd., 1877: 72 Bd., 1878; Ueber d. pathol. Gerin- 
nunesvorginge. Ib., 79 Bd., 1880; Methoden zur Färbung von Fibrin. Fortschr. 
d. Med.. v.. 1887. 

Wlassow: Die histol. Vorgänge bei der Gerinnung u. Thrombose. Beitr. v. Ziegler, 
vv. 1894. 

Zahn: Beiträge zur pathol. Histologie der Diphtheritis, 1878. 

Zenker: Intravenöse Fibringerinnung. Beitr. v. Ziegler, xvii., 1895. 

Ziegler: Ucb. dd. Entzündung der serösen Häu'e. Beitr. v. Ziegler, xxi., 1897. 

See also SZ 90 and 98. 

























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seme Gite or 











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dr ufkamec 


ue 
Hoss 6 


radwal.s 


the tissne 








sf 
net im 
character of a putrid gangrene 
dirty Vieh. tunen She ann» wh 
dor. « 


e putrid 














“ Tinatie 
dran 








als sometimes 


Literature. 


Necratie Inflammation, 


Busch .\u: 












4a TL, sae 
dle phys. Vo. 





Cornil As 


ii 
Hartmann £5) 
bury Imdl 














Hoffmann Taten uber ad pathe! 
Int 

v. Kuhlden Di Avtivingic u Genes oder a 
Im 


Kaufmann Die Sutin Bres 

Kelsch (mit i) 

Lesser Viv 
Bd 1n8I 

Letulle + Vuquez Kanpeisnmenwert par ! 
1889 














340 INFLAMMATION. 


served payticularly often in the intestine (Fig. 202), but occurs also in 
other mucous membranes, as in those of the vagina, the descending uri- 
nary passages, and the region of the throat, where the tonsils are espe- 
cially frequently affected, ete. The necrotic tissue forms white, or 
grayish-white, or, through the admixture of blood or bile or other im- 
purities, dark green, yellow, brown, or otherwise colored sloughs, which 
are surrounded by reddened and inflamed tissue. If some time has 
already elapsed since its formation, and if a liquefaction of the tissue at: 
the boundary between the living and dead tissues has occurred, with a 
separation of the latter, the necrosed parts form loosely attached or 
wholly free deposits lying on the surface of the membrane, these con- 
sisting at times only of small flakes, 
at other times of larger sloughs, 

Diphtheritis of mucous membranes 
be associated with croupous de- 
s (Fig. 203, e, d), so that the 
necrosis (d) may be covered 
over with fibrin (e). 

Wound-granulations may also ne- 
erose in the same wa} do inflamed 
mucous membranes; such a condi- 
tion may therefore be called wound- 
diphtheritis. 


FIG. 204.—Diphtheritic necrosis within a Acute tissue-necroses caused by 


Fe aa aT, TAT uno infection oceur in the case of the 
between the necrotic cells. 300, internal organs, chiefly in the Iymph- 
4), spleen and” bone- 


glands (Fig. 

marrow, and ueterized by the formation of opaque & 
white, yellow or dirty-gray sloughs. Not infrequently fibr 
exudations are seen within the necrotic tissue (Figs. 203, d; 204). 

In the necrosis caused by tuberculosis the destruction of the 
oceurs gradually, and bears the ch: cter of a caseation. 

When an inflammatory focus contains bacteria which excite putrid 
decomposition of albuminoid bodies, the inflammation may take on the 
character of a putrid gangrene ; and the tissue may disintegrate into a 
dirty gray or black, tinder-like mass which gradually dissolves and gives 
off an extremely disagreeable odor. Gas-bubbles are also sometimes 
developed in the focus. 



















re 


















Literature. 


(Necrotie Inflammation.) 


nat. u. klin. Untersuchungen über Diphtherie. Virch. Arch., 45 Bil.. 1869. 
Anat. pathol. des ulcérations intest. dans la dysenterie. Arch. de phys 








1883. 

Hartmann: Exper. Untersuchungen über Chromsäurenephritis. Inaug.-Diss., Frei 
burg, 1891. 
ffmann: Unters. über. d. pathol.-anat. Veränd. der Organe bei Abdominalty phus, 


1869. 





vy. Kahlden: Die Actiologie u. Genese der acuten Nephritis. Beitr. v. Zi x, 
1892. 
Kaufmann: Di 





ablimatvergiftung, Breslau, 1888. Vireh, Arch. 117 Bd. 1889. 

Vanat. pathol. de la dysent Arch. de phys.. v.. 1 

Lesser: Die ant. Verind. d. Verdauungskanales durch Actzgift 
1881. 








Virch. Arch... 88 


Bil., 
Letulle ct Vaquez: 
1889. 





unement par Vacide chlorhydrique, Arch. de phys. i 


THE PROCESSES OF HEALING. 341 


Marchand: Darmveränderungen bei Typhus abdominalis. Cbl. f. allg. Path., i., 
1890. 

Matzenauer: Hospitalbrand. Arch. f. Derm., 55 Bd., 1901. 

Neuberger: Wirkung des Sublimats auf die Nieren. Beitr. v. Ziegler, vi., 1889. 
See also SS 90-93. 


Il. The Termination of Acute Inflammation in. Healing. 


§ 95. Should there occur in any tissue whatsoever an acute inflamma- 
tion, sooner or later there always arise processes which have in aim the 
removal of the changes established and a restoration of the degenerated 
tissue, and which may therefore be regarded as processes of repair. If 
the cause which excited the inflammation is no longer present, these 
processes consist essentially in the cessation of the pathological exudation 
and its replacement by the normal vascular secretion, the removal or absorp- 
tion of the exudate present and of the necrotic tissue, and the restoration of the 
destroyed tissue. If the exciting cause of the inflammation is still present in 
the tissue and active, it must be removed or rendered inert. 

The cessation of the alteration of the vessel-walls is brought about 
through the restoration of the normal blood-supply to the damaged blood- 
vessels, so that the nutrition of the vessels again becomes normal. If the 
alteration was slight, and if the exciting cause of the inflammation had 
acted only for a short time—if it is the case, for example, only of the 
brief action of a trauma, or high temperature, or chemical substance, that 
was quickly removed—the restoration of the vessels may take place in a 
very short time, i.e., ina time that may be measured in minutes and hours. 

When the exciting cause of the inflammation acts for some length of 
time—as, for example, in the ease of bacteria which live and multiply in 
the tissues, or if changes are brought about through the inflammation 
itself, which act in such a manner as to alter the vessels—if there has 
been, for example, a tissue-necrosis—the vessels are subjected for some 
time to a continued harmful action, which hinders the complete restora- 
tion of their functions. 

The absorption of the exudate occurs in many cases easily and 
quickly, in that it is taken up by the lymph-stream, eventually «Iso by 
the blood. This takes place most quickly in the case of serous exudates, 
vet in many places fibrinous exudates may also be quite rapidly removed, 
but this oeeurs only when the coagula soon liquefy. Firmer fibrinous 
exudates, such as are formed especially upon the serous membranes, and 
also large collections of pus usually offer considerable resistance to ab- 
sorption and are the cause of the prolonged course of the inflammation, 
although the character of this may become changed from what it was in 
the beginning. Im very many cases absorption is accomplished by the 
simultaneous substitution, for the exudate, of embryonie tissue which 
later beeomes changed into connective tissue. 

The sequestration and absorption of necrosed tissue, with the ex- 
ception of the casting-off of dead epithelium, which may be very quickly 
accomplished, always require a certain length of time, which varies 
according to the nature, situation, and extent of the necrosed tissue. In 
general, the inflammation persists as long as necrotic tissue is still pres- 
ent. Superfieial necrosed tissues may be cast off after sequestration—that 1s, 
after the separation of the dead from the living tissues. In the case of 
deep-seated tissue-necroses in which the tissue does not soon undergo 
total liquefaction, absorption is usually slow, and is brought about 
through a gradual substitution of living tissue for the dead. 


842 INFLAMMATION. 


The regeneration of the degenerated tissue is dependent, for its oc- 
currence, partly upon the degree and extent of the degeneration, partly 
upon the nature of the tissue, and partly upon the mode of action of the 
agent exciting the inflammation. 

If the tissue-cells of the inflamed area are but slightly degenerated, 
they are quickly restored when the nutrition becomes normal. If single 
cells are lost but the organization of the whole is not disturbed, there can 
take place in most tissues a rapid renewal of cells through a regenerative 
growth of the reinaining cells. This is true particularly of the different 
forms of connective tissue, the surface epithelium, liver- and kidney-cells, 
while ganglion-cells, bone-cells, cartilage-cells, and heart-muscle cells 
possess but little or no power of regeneration (see Chapter VI.). Ex- 
tensive destruction of tissue with solutions of continuity, wounds, frae- 
tures, suppurations, necrotic inflammations, ete., lead to tissue-prolifer- 
ations, which are indeed sufficient to close the defect, but for the greater 
part do not lead to a restoration of the normal tissue, but to the forma- 
tion of a tissue of a lower grade, which in its earliest stages is known as 
granulation tissue, in its mature form as cicatricial tissue. Of the 
same character is also the tissue which in thecourse of time is substi- 
tuted for exudates and tissue-necroses that are absorbed with difficulty. 

With the entrance of regenerative proliferation and the formation of 
granulation tissue, there appears in the course of the inflammation a 
phenomenon which later gives to the inflammation an especial charac- 
ter, so that it: may be designated a proliferating inflammation. 

The phenomena of proliferation begin in inflamed tissues, at the 
earlies: after eight hours, but are usually first clearly recognizable after 
from twenty-four to forty-eight hours. 

In general, they appear the more rapidly the milder the inflamma- 
tion and the more quickly the pathological exudation is overcome or 
diminished. Suppuration, necrosis, and gangrene of the tissues hinder 
proliferation and retard the beginning of repair, or at least confine the 
reparative processes to the neighboring tissues, 

Every tissue capable of proliferation furnishes formative cells for 
tissue of its own kind or for one closely related to it. Pus-corpuscles are 
not formed by the tissue-cells; on the other hand, cells newly developed 
From the tissue-cells by proliferation may become mixed with the exudate, 
degenerate in the same, and die. Thus not all the cells newly developed 
through proliferation fulfil their function of producing new tissue. 

The removal of the exciting cause of inflammation takes place very 
differently in different. cases, and depends in the first place upon the 
nature of the cause. Many traumatisms and thermal Influences act but 
for a short time, and have no further influence upon the course of the 
inflammation. Many substances acting chemically may be quickly taken 
up by the tissue-juices and made inert, or excreted, while others remain 
locally active for alonger time. Of the bacteria producing inflammation, 
many soon die, while others live and constantly produce new generations 
which in turn cause new inflammation, often in such a way that in the 
first diseased focus the inflammation may subside and healing take place, 
while in the neighborhood, or even in more distant regions, metastatic in- 
AHammations develop. 

On account of the great differences which exist both in the nature and 
the behavior of the exciting cause of the inflammation, as well as in the 
eourse of the inflammatory tissue-degeneration and the exudation, and in 
the course of the healing processes, it is easy to understand that the whole 


THE INFLAMMATORY NEW-FORMATION OF TISSUE. 343 


course of an inflammation, even to its termination in healing, may vary 
greatly in different cases, so that all the possibilities of its course can 
hardly be reviewed. At the same time it is not difficult to comprehend 
the decline of the different forms of inflammation, since ultimately the 
Whole process is always made up of the same factors—that is, of tissue- 
degeneration, pathological exudation, and of proliferative processes, the 
last. of which are calculated to remove the disturbances caused by the 
first two factors. 


Venmann groups under the term inflammation all those phenomena which develop 
locally after a primary tissue-lesion, and are directed toward the healing of this lesion. 
Aceording to this view, regeneration is, therefore, the most important part of the in- 
flammatory process, in that it is especially adapted to restore the defect of tissue caused 
by the primary tissue-lesion, or, as Newuann puts it, to restore the uninterrupted con. 
tinuity of the tissue. Such an identitication of inflammation with regeneration I hold 
as inadmissible, in the first place because tissue-regenerations occur which clinically 
and anatomically in no way bear the character of an inflammatory process. Then also 
the inflammatory pathological exudations cannot be regarded as phenomena that can 
be compared with regeneration, and that like it, have for an end the healing of the 
primary tissuc-lesion. Even if they act favorably in individual cases, this is not 
always true. Much more often do they cause serious damage which increases that 
established by the primary tissue-lesion, and often enough form a hindrance to the 
rapid entrance of the healing process. 

In my opinion the tissue-proliferations do not form an essential part of inflamma- 
tion: the inflammation already exists before they are established. Only in the late 
stares of inflammation do they form a part of the inflammatory process, and represent 
that part of the same which can bring about the healing. It is of no especial signiti- 
cance Whether the processes of proliferation be regarded as a part of the later stages of 
inflammation or as a necessary sequela of the inflammatory tissue-degeneration, sepa- 
rated from the inflammation in a narrow sense, and considered under the point of view 
of tissue-repair. 


lil. The Inflammatory New-formation of Tissue, Substitution of 
Exudates and Tissue-necroses by Connective Tissue. 


$96. The inflammatory proliferation of tissue is essentially a 
revenerative process which has for its aim the compensation of the tissue- 
lesions produced by the causes of inflammation. Under especial condi- 
tions it leads not. infrequently to a hyperplastic proliferation ef connec- 
tive tissue, frustrates its own aim, and causes new damage. This is 
particularly the case when, as the result of the persistence of the cause 
of the inflammation in the organism (chronic infection), or the persistence 
of the residue of the acute inflammation (exudate, abscess, tissue-necro- 
sis), there is kept up a permanent condition of inflammation. 

The inflammatory new-formations of tissue develop in essentially the 
same manner as the regenerative and hyperplastic tissue-proliferations 
described above (33 82-87). They are distinguished, however, from the 
simple regenerations by the fact that they are accompanied, at least dur- 
inva part of their course, by disturbances of circulation and pathological 
exudations, and especially by an emigration of leucocytes, these factors 
exerting a modifving influence upon their course. 

The granulation tissue, which forms in the course of an inflamma- 
tion, is nothing more than an embryonic tissue arising through cell- 
proliferation and infiltrated with leucocytes. Primarily it consists of 
cells and newly formed vessels which at first depend for their support upon 
the ground-substance of the tissue from which they develop, but soon 
form for themselves a new ground-substance. 

The cells of the granulation tissue are partly proliferated tissue- 








346 INFLAMMATION. 


polynuclear form, are found in all the layers of the skin in fresh granula- 
tions, but heap themselves particularly in the superficial strata, and, 
embedded in fibrin, cover over the surface of the granulation tissue (0). 

The freshly formed fibroblasts are round cells; later there develop 
cells partly club-shaped, partly spindle-shaped, partly with many 
branched processes (Fig. 205, d, c, d), which in various ways unite the 
cells. At the same time the number of the large formative cells in- 
creases, so that they finally surpass the small round cells in number, and 
in places come to lie closely together. When their number has reached 
a certain point, the development of connective tissue begins—i.e., the 
formation of the fibrillar intercellular substance (Figs. 205, d, e; 207, «) 
— which is completed in the manner described in $ 34. When a certain 
degree of fibrille-formation has been reached the process comes to a 
standstill, the remains of the fibroblasts with their nuclei remain as fixed 
connective-tissue cells (Fig. 205, e), continue to live, and attach them- 
selves to the surface of the bundles of fibrille. The process has then 
reached its termination—the granulation tissue has become scar tissue. 

In open wounds of the skin, when infection does not disturb the 
course of healing, the formation of granulation tissue lasts until the 
wound is again covered with epithelium. The regeneration of the latter 
proceeds from the edges, the epithelium gradually pushing itself over the 
granulations. With the formation of connective tissue the reproductive 
processes essentially terminate, but transformation processes continue in 
the cicatricial tissue for some length of time. Shortly after its formation 
the cicatrix is rich in blood and appears red; later it loses a portion of 
its vessels through their obliteration, becomes pale, and eontracts to a 
volume much less than the original. Large scars of the skin show per- 
manently a smooth surface, since the papillary bodies are not again 
formed or only imperfectly (Fig. 209, e). The tissue of the scar remains 
for several months abnormally rich in cells, but in the course of time 
becomes poorer in cells and harder, and comes to contain elastie fibres. 

When the healing of a wound occurs in such a manner that the tissue- 
defect is closed by the formation of a granulation tissue visible to the 
naked eye, the process is designated repair by second intention (per secun- 
dam intentionem). 

The healing of incised wounds of the skin, whose edges, united by 
sutures, grow together by first intention, takes place in essentially the same 
manner as the healing of an open wound by second intention; but the 
processes of inflammation, proliferation, and new-formation of tissue are 
less prominent, partly because they take place below the skin, and partly 
because they are of much less extent and intensity. 

The result of such a cut is always a more or less abundant exudation 
on the surfaces of the wound, forming a coagulated mass often contain- 
ing blood (Fig. 208, ce), which glues together the opposing wound-sur- 
faces. Very soon there arises an inflammatory infiltration of the edges 
of the wound, which varies greatly in different cases, and when the course 
of repair is aseptic never reaches any significant degree (g, Ah), attaining 
its maximum in from two to four days, diminishing from the fifth to the 
seventh day, and completely disappearing at or soon after the end of 
the second week. The inflammatory infiltration is usually greater in the 
neighborhood of the wound-sutures than at the edges of the wound. 

As early as the second day regenerative processes of proliferation 
begin in the connective tissue and in the vessels, and lead, in the course 
of several days, to the formation of an embryonic tissue, which lies partly 























INFLAMMATORY PROLIFERATION OF TISSUE. 355 


Hallwachs: Ueber Einheilen von organischem Material. Langenbeck’s Arch., 24 Bd., 

1879. 

Hamilton: On Sponge Grafting. Edinburgh Med. Jour., xxvii., 1881-82. 

Haug i gu eber die Organisationsfahigkeit der Schalenhaut des Hühnereies, München, 
1889. 

Herbert: The Young Plasma-Cell in Chronic Inflammation. Jour. of Path., vii., 
1900. 

van Heukelom: Sarkome u. plastische Entzündung. Virch. Arch., 107 Bd., 1887. 

Hinsberg Betheil. d. Peritonealepithels bei Einheilung v. Fremdkörp. Virch. Arch., 
15 ., 1898. 

Jacobsthal: Histologie der Arteriennaht. Beitr. v. Bruns, xxvii., 1900. 

Justi: Die Unna’schen Plasmazellen. Virch. Arch., 150 Bd., 1897. 

Karg: Entzündung und Regeneration. Dtsch. Zeitschr. f. Chir., xxv., 1887. 

Kiener et Duclert: Formation et guérison des abscés. Arch. de med. exp., v., 1898. 

Klemensiewicz: Bau und Tbätigkeit der Eiterzellen. Mitth. d. Ver. d. Aertze v. 
Steiermark, 1898. 

Krafft: Zur Histogenese des periostalen Callus. Beitr. v. Ziegler, i., Jena, 1886. 

Krompecher: Plasmazellen. Beitr. v. Ziegler, xxiv., 1898. 

Krückmann: Heilung v. Lederhautwunden. v. Graefe’s Arch., 42 Bd., 1896. 

Küster: Wunden. Eulenburg’s Realencyklop. xxvi., 1901. 

Lejars: Sections. Traité de path. gén., i., Paris, 1895. 

Marchand, F.: Einheilung von Fremdkörpern. Beitr. v. Ziegler, iv., 1888; Betheil- 
igung d. Leukocyten an d. Gewebsneubildung. Verh. d. X. internat. med. Congr., 
ii., Berlin, 1891. 

Marschalk6: Dic Plasmazellen. Arch. f. Derm., 30 Bd., 1895; Cbl. f. allg. Path., x., 
1899. 

Marwedel: Veriind. d. Knochenmarks bei Gewebsneubildung. Beitr. v. Ziegler, 
xxiii., 1898. 

Muscatello: Condiz. necess. alla produz. di aderenze periton. Arch. per le Sc. Med., 
xx., 1896. 

Nikiforoff: Bau u. Entwickelungsgesch. d. Granulationsgewebes. Beitr. v. Ziegler, 
viii., 1890. 

Ostry: Karyokinesen in entzündlichen Neubildungen der Haut. Zeit. f. Heilk., iv., 
1883 


Podwyssozki: Ueber die Regeneration der Drisengewebe. Beitr. v. Ziegler, i. and 
ii., 1884-87. | 

Poggi: La cicatrisation immédiate des blessures de l’estomac. Ib., iv., Jena, 1888. 

Ranvier: Möcanisme hist. de la cicatrisation. Lab. d’hist. du Collége de France, 1900. 

Reinke: Proliferation u. Weiterentwickelung der Leukocyten. Beitr. v. Ziegler, v., 
1889. 

Ribbert: Das patholog. Wachsthum d. Gewebe. Bonn, 1896; Beitr. z. Entzündung. 
Virch. Arch., 150 Bd., 1897 

Roloff: Rolle d. Pleuroperitonealepithels bei d. Entsteh. d. Bindegewebsadhäsionen. 
Arb. a. d. Inst. v. Baumgarten, ii., 1897. 

Salzer: Ueber Einheilung von Fremdkörpern, Wien, 1890. 

Scheltema: Veränderungen im Unterhautbindegewebe bei Entzündung. Deut. med. 
Woch., 1886. 

Schottländer: Kern- u. Zelltheilung im Endothel d. entzünd. Hornhaut. Arch. f. 
mikr. Anat., xxxi., 1888; Ueber Einstichstuberkulose, Jena, 1897. 

Schujeninoff: Veränderungen d. Haut nach Aetzungen. Beitr. v. Ziegler, xxi., 1897. 

Senftleben: Verschluss der Gefässe nach der Unterbindung. ‚Virch. Arch., 77 Bd., 
1879. 

Sherrington u. Ballance: Entstehung d. Narbengewebes. Cbl. f. allg. Path., i., 
1890. " 

Tillmanns: Exp. u. anat. Unters. über Wunden der Leber u. Niere. Virch. Arch., 
18 Bd., 1879. 

Vermorel: Rech. sur l’inflamm. pleurale, Paris, 1898. 

Ziegler: Exper. Unters. über die Herkunft der Tuberkelelemente, Würzburg, 1875; 
Unters. über pathologische Bindegewebs- u. Gefässneubildung, Würzburg, 1876; 
Bethieligung der Leukocyten an der Gewebsneubildung. Verh. d. X. internat. 
med. Congr., ii., Berlin, 1891; Die Ursachen der pathologischen Gewebsneubil- 
dungen. Festschr f. Virchow, ii., Berlin, 1891; Historisches u. Kritisches über die 
Lehre von der Entzündung. Beitr. v. Ziegler, xii., 1892; Entzündung. Eulen- 
burg’s Realencykl., 1894; Entzündung der serösen Häute. Beitr. v. Ziegler, xxi., 
1897. 

See also §3 90 and 98. 


856 INFLAMMATION. 


IV. Phagocytosis Occurring in the Course of Inflammations, and 
the Formation of Foreign-body Giant-cells. 


§ 98. The presence in the tissues of the human body of small foreign 
bodies or of dead tissue-elements and tissue-detritus leads very often 
to a marked collection of cells about the embedded substance. At first 
these cells are leucocytes which have wandered out from the vessels, but 
later proliferating tissue-cells which have become motile wander into the 
neighborhood of the foreign body or dead tissue-remains. 

According to investigations by Leber, Buchner, Massart, Bordet, 
Gabritschewsky, and others, it is certain that the collecting of the cells 
is in part due to chemotazis—i.e., by an attraction exerted by substances 





Fi. 218.—Granular cells in a focus of degeneration in the brain (teased preparation treated with omic 
acid). a, Blood-vessel with blood; b, media; ¢, adventitia with Iymph-aheath; d, unchanged glia-cells; 
¢, fatty giiacells: J. gliacells with two nuclel; g. sclerotic theue: Mi. round-cells; Ny, roundcells with few 
fat-droplets; hg, fat-droplet apherules ; hs, pigment-granule spberules. x 300. 





3 


which have been dissolved out of the foreign body or the tissue-detritus; 
but without doubt other factors may determine the place where the cells 
collect. 

If the material while still undissolved comes within the neighborhood 
of the motile cells, it is very often taken up by the latter, and there 
occurs that phenomenon which is known as phagocytosis. If the proc- 
ess be observed under the mieroseope—as may very easily be done by 
mixing the richly cellular tissue-lymph of the frog with granules of soot 
—one sees that the mobile cells pour their protoplasm around the foreign 
bodies and through the union of the pseudopodia extended over the bod- 
ies receive them wholly into their protoplasm. Among the foreign 
bodies which penetrate from without are particularly the different forms 
of dust (especially soot) which are taken into the lungs with the inspired 








PHAGOCYTOSIS, RESORPTION, AND ENCAPSULATION. 359 


Barth: Knochenimplantation. Beitr. v. Ziegler, xvii., 1895. 

Bordet: Phagocytose. Ann. de l’Inst. Pasteur, x., 1896. 

Cassaet: De l’absorption des corps solides. Arch. de méd. exp., iv., 1892. 

Fleiner i Resorption corpusculärer Elemente durch Lunge u. Pleura. Virch. Arch., 
1 “ . 

Hamilton: On Sponge Grafting. Edinburgh Med. Jour., xxvii., 1882. 

Haug: go eber die Organisationsfahigkeit der Schalenhaut des Hühnereies, München, 


Hallwachs: Ueber Einheilen von organischem Material. Langenbeck’s Arch., 24 Bd., 

1879. 

Heidenhain i „ulistologie u. Physiologie d. Dünndarmschleimhaut. Pflüger’s Arch., 

., 1888. 

Hektoen: Absorption and Incrustation of Elastic Fibres in Giant Cells. Jour. of 
Med. Res., 1902; The Fate of the Giant Cells which Form in the Absorption of 
Coagulated Blood Serum, etc. Jour. of Exp. Med., 1898; The Fate of the Giant 
Cells in Healing Tuberculous Tissue. Ib., 1898. 

Hildebrand, : Secundäre Implantation v. Haaren in Dermoidcysten. Beitr. v. Ziegler, 
vii., 1890. 

Hoffmann u. Langerhans: Verbleib in d. Circulat. eingeführten Zinnobers. Virch. 
Arch., 48 Bd., 1869. 

v. Ins: Exper. Unters. über Kieselstaubinhalationen. Inaug.-Diss., Berne, 1876. 

Kölliker: Die normale Resorption des Knochengewebes, Leipzig, 1887. 

Krückmann: Fremdkérpertuberkulose. Virch. Arch., 138 Bd., Suppl. 1894. 

Langhans: Beobachtungen über Resorption der Extravasate. Virch. Arch., 49 Bd., 
1870. 

Latis: Riassorbimento del catgut. La Riforma Med., 1891. 

Le Count: Cholesterin Giant Cells. Jour. of Med. Res., 1902. 

Lesser: Ueber das Verhalten des Catgut im Organismus. Virch. Arch., 95 Bd., 1884. 

Looss: Degenerationsercheinungen im Thierreiche, bes. über die Reduction des Frosch- 
larvenschwanzes, Leipzig, 1889. Ref. Biol. Cbl., ix. 

Marchand, E.: Bildungsweise der Riesenzellen um Fremdkörper. Virch. Arch., 98 

., 1883. 

Marchand, F.: Einheilung von Fremdkörpern. Virch. Arch., 93 Bd., 1888. 

Metschnikoff: Unters. üb. die intracelluläre Verdauung, Wien, 1883; Biol. Cbl., ii., 
1883; Pathologie comparée de l’inflammation, Paris, 1892; La phagocytose mus- 
culaire. Ann. de l’Inst. Pasteur, vi., 1892; La résorption des cellules. Ib., 1899. 

Meyer: Fremdkörperperitonitis mit Bildung von riesenzellenhaltigen Knötchen durch 
Einkapselung von Cholesterintafeln. Beitr. v. Ziegler, xiii., 1893. 

Muscatello: Aufsaugungsvermögen des Peritoneums. Virch. Arch., 142 Bd., 1895. 

Nikiforoft : Bau und Entwickelung des Granulationsgewebes. Beitr. v. Ziegler, viii., 
1890. 

Noetzel: Histolyse. Virch. Arch., 151 Bd., 1898. 

Ochotin: Transplantation todter Knochentheile. Virch. Arch., 124 Bd., 1891. 

Ponfick: Studien üb. d. Schicksale körniger Farbstoffe im Organismus. Ib., 118 Bd., 
1890. 

v. Recklinghausen: Ueber Eiter und Eiterkörperchen. Ib., 28 Bd., 1868. 

Rindfleisch: Experimentalstudien über die Histologie des Blutes, 1868. 

Roser, K.: Beiträge zur Biologie niederster Organismen, Marburg, 1891. 

Ruppert: Exper. Unters. üb. Kohlenstaubinhalation. Virch. Arch., 72 Bd., 1878. 

Salzer: Ueber Einheilung von Fremdkörpern, Wien, 1890. 

Slavjansky: Exper. Beitr. z. Pneumonokoniosislehre. Virch. Arch., 48 Bd., 1869. 

Sudakewitsch: Riesenzellen und elastische Fasern. Virch. Arch., 115 Bd., 1889; 
Modifications des fibres musculaires par la trichinose. Ann. de l’Inst. Pasteur, vi., 
1892. 

Virchow: Die Bildung der patholog. Pigmente. Virch. Arch., 1 Bd., 1847. 

Wasilieff-Kleimann: Resorption körn. Subst. durch. d. Darmfollikel. Arch. f. 
exp. Path., 27 Bd., 1890. 

Ziegler: Exper. Unters. über die Herkunft der Tuberkelelemente, Würzburg, 1875; 
Unters. über pathologische Bindegewebs- u. Gefässneubildung, Würzburg, 1876; 
Ueber Proliferation, Metaplasie u. Resorption des Knochengewebes. Virch. Arch., 
73 Bd., 1878; Historisches u. Kritisches über die Lehre von der Entzündung. 
Beitr. v. Ziegler, xii., 1892; Ueber die Zweckmässigkeit der pathol. Lebensvorgänge. 
Münch. med. Woch., 1896. 


See also § 97; and for further literature concerning the behavior of body-cells 
toward bacteria, see Chapter X.; and for further literature concerning the fate of trans- 
planted living tissue, see § 88. 




















CHAPTER VIII. 


Tumors. 
I. General Considerations. 


8 100. A neoplasm, or autonomous new-growth (Thoma), or tumor 
in the narrower sense, is a new-formation of tissue, apparently arising and 
growing independently, having an atypical structure, inserted uselessly into the 
organism, possessing no function of service to the body, and showing no typical 
termination to its growth. The atypical character of the structure of a 
tumor is shown in its external appearance as well as in its internal or- 
ganization in that a true tumor departs more or less in structure from 
that of a normal organ. When this departure is but slight, the structure 
of the tumor approaches closely to that of the tissue-hypertrophies; and 
there occur cases in which the difference in structure is so little that it 
becomes very difficult to decide whether an excessive new-growth of tis- 
sue is to be classed as a tumor or an hypertrophy. 

Tumors may develop in any tissue of the body which is capable of 
growth, and arise through the proliferation of the tissue-cells, asso- 
ciated with a new-formation of blood-vessels. Not infrequently there 
occurs also an emigration of leucocytes into the tumor, and exudative proc- 
esses and inflammatory tissue-proliferations may take place in its neigh- _ 
borhood, but these phenomena form no essential part of the development 
of the tumor. Ä 

The processes of cell-division and new-formation of blood-vessels are 
the same as those described in $$ 81 and 83—i.e., the division of the cells 
takes place by karyomitosis, and the new vessels are formed from buds 
given off by the proliferating cells of the walls of old vessels. The 
mitoses are for the greater part typical (Fig. 230, 5), but there are also 
found relatively often atypical forms, such as asymmetrical divisions, 
nuclear figures with abnormally large chromatin masses (so-called giant 
mitoses), pluripolar mitoses, and forms of nuclear fragmentation, and 
also direct segmentation. 

In their fully developed condition tumors are for the greater part well 
defined from the surrounding tissues, but in some cases they may pass into the 
neighboring tissue without any sharply defined border of transition. Further, 
an entire organ may become transformed into a tumor, or large portions of 
tissue not sharply outlined from their surroundings may take on the character 
of atumor. Through the disintegration of tumor tissue there very fre- 
quently arise ulcers. 

The difference between the structure of a tumor and that of normal 
tissue is usually recognizable even macroscopically, but there are also 
tumors which so closely resemble the parent tissue from which they arise 
that the difference can be made out only through a more careful exami- 
nation. 

The circumscribed tumors are usually nodular (Figs. 231, d; 233, d, e; 
234, a). The size of the single nodules varies, according to the kind of 

366 








GENERAL CONSIDERATIONS. 369 


Combinations of epithelial proliferations with proliferations of the 
connective tissue, which exceed the ordinary amount of supporting tis- 
sue or bear a sarcomatous character, lead to the formation of epithelial 
mixed tumors, 

The teratoid tumors and cysts form a group which is especially 
characterized on the one hand by the fact that they contain the most 
varied kinds of tissue which may be derived from all three germ-layers 
(teratoid mired tumors), and on the other hand by the presence of tissue 
formations in regions where they donot normally occur. Tumors, there- 
fore, which according to their structure may be placed in one of the other 
groups, may be considered as teratomata on account of their situation. 
Further, there are also included in the group of teratoid tumors certain 
formations which according to their structure, origin, and physiological 
relations ought not to be classed with the tumors. 

Tumors usually develop singly; but it also happens that within a 
certain tissue system there may appear either coincidently or in succes- 
sion a great number of tumors of the same kind, so that it must be 
assumed that the conditions requisite for the development of these tu- 
mors were present in different parts of the system affected. At times 
there develop in different organs of the same individual two entirely dif- 
‚ferent varieties of tumors, which stand in no relation to each other, and 
whose coincident appearance is purely accidental. 


— dem 


The exact determination of what should be included under the term tumor is 
hardly possible; and consequently the designation tumor is applied to many different. 
formations which, according to their etiology, genesis, and life-characteristics, have not 
the same significance. The idea of tumor is, therefore, very differently conceived by 
different authors. I regard it as advisable, and also as based upon the life-characteris- 
tics of the tissue-formations which we are about to consider, to exclude in the first place 
from the class of tumors all hyperplastic proliferations, and further all retention-cysts 
which arise purely through the retention of secretions and show no independent new- 
formation of tissue. Further, according to my view, there should be separated from the 
true tumors all proliferations of tissue due to the presence of parasites or to infection, par- 
ticularly the infectious granulomata which occur in tuberculosis, syphilis, leprosy, etc. 
Should it be proved—which so far has not been done—that some of the new-growths 
now included with the true tumors are caused by infection, they should also be ex- 
cluded from the category of true tumors. 

The above classification of tumors is based essentially upon their histological 
character and histogenesis. They may of course be classified according to other points 
of view. Lubarach has offered the following classification with reference to the growth 
and behavior of the tumor: (1) Tumors which differ from the parent tissue in the 
arrangement of their elements, but for the chief part present no recognizable increase 
or at most only a transitory growth (various teratoid new-growths, misplaced tissue 
anlage, congenital nevi, many adenomata, myomata, fibromata, lipomata, chondro- 
mata, and osteomata); (2) tumors which show a certain autonomy and independence in 
their structure, but yet on the whole obey the normal laws of life in that they always 
respect the physiological tissue boundaries (myomata, adenomata, angiomata, lipomata) ; 
(3) tumors which are wholly emancipated from the physiological laws of life and rule 
in the tissues in total lawlessness of growth (carcinoma, sarcoma). 

The atypical structure of tumors is not given so much prominence by all au- 
thors as has been done above. This is particularly true with reference to those tumors 
which are similar in structure to the parent tissue from which they arise, and which are 
accordingly designated Aomoplaatic tumors. It should be noted, however, that even in 
these tumors (chondroma, osteoma, fibroma, etc.) there occur in general, both in the 
histological structure, coarser organization, and external form, pronounced departures 
from the normal; and, moreover, it may also happen that inflammatory proliferations 
caused by infection may show a structure similar to that of tumors. It is therefore 
not always easy to determine positively whether a new-growth is to be regarded as a 
tumor. 

Tumors are in no sense useful to the organism as many tissue-hypertrophies 
may be. Tumor tissue does not possess the specific activity of that tissue from which 


310 TUMORS. 


R spri ev thet tumors can in no way be regarded as useful new -formations of tissue. 
ht bepress. indesd. that in certain tumors there occur precesses :{ secretion which 
ourrespnd to pormal secretions—thus. epithelial tumor: may proiuce maceas or horny 
or sılloid material (uayruid tumere,. or bile-pigment :liver-tumurs.. even in metastatic 
oder but from these facts we can conclude only that. in manr tumors which do net 
difl-r um greatly im structure from the parent tissue. the cells may retain to a certain 
den». tur a sumber of generations. the functimal capecities of the parent tissue. 
Thete in. buwerer, no basis fur believing that new useful tissue is formed os in the case 
of by pertrophy from increased labor: the products are fur the chief part of no use to 
the body. and though perhaps in especial cases the culkad cr bile & produced mar be 
made use of. such a function must surely be of much less value tian tust Cf the nurmal 
The tumors arising from the mesoderma! epithelium <-f the ser us membranes or of 
the glands arising from tbese are included in tie group ef cpitieciial tumers. This is 
justified by the fact that such tumors ved in their structure and clinical be- 
havior to the epithelial tamors of the ecto entoderm. I have also consilered the 
question whetber it would pot be advisable tas Hausmann bas propused) to class als 
amony the epithelial Tumors—ie.. the adenumata and carcinomata—tbose tumors which 
have a framework of connective tissue, the spaces of which are filled. in a manner sug- 
gesting epithelial tissues. with cell nests arising frum ube proliferating endothelium of 
the blood- and Ivmpb-vessels. Aside from the similarity in the structure of these tumors 
with the ordinary adepumata and carcinomata, there may be taken in favor of this new 
the fact that from the anatomical side the endothelium of the blond- and Iymph-vessels 
is often designated us mesodermal epithelium. Against such a grouping of the endo 
thelial with the epithelial tumors may be urged the facts that. aside from tbe general 
aceeptance of the term endotbelioma. the bebavior of the endothelium of the bloud- and 
ly mph- vessels under pathological conditions is very different from that of epithelium. 
and that in many tumors it is impossible to separate the products of the growth of the 
endutbelium of the bluod- and lymph- vessels from the products of proliferation of con- 
nective-tissue cells. 


Literature. 
(Development of Tumors.) 


Adami: (Classification of Tumors.) Jvuur. of Path. and Bacı., 1902. 

Alberts: Das Carcinom, Jena. 1887. 

Aoyoma: Indirecte Kerntheilung in verschiedenen Neubildungen. Virch. Arch., 106 
Bd., 1886. 

Arnold: Kerntheilungen in den Zellen der Geschwülste. Virch. Arch.. 78 Bi.: Kern- 
theilung und vielkernige Zellen. Ib., 9% Bd.. 1884. 

Berd: Anatomie pathol. generale des tumeurs. Arch. de pbys., v., 1855. 

Brault: (sycog&ne dans kes tumeurs. Arch. des Sc. Med., 1896: Le pronostic des 
tumeurs. L’(Euvre med.-hir., 1899; Des tumeurs. Man. d’hist. path. de Cornil 
et Ranvier, i.. 1901. 

Bucher: Multiple Carcinome. Beitr. v. Ziegler, xiv.. 1898. 

: Geschwülste bei Thieren. Ergebn. d. allg. Path , iii., 1898. 
Cornil: Division indirecte des noyaux et des cell. dans les tumeurs. Arch. de phys., 


1886. 
Asymmetrische Zelltheilung in Epithelkrebsen. Virch. Arch.. 119 Bd., 
1890 ; Pathologise be Mitosen. Ib., 123 Bd.. 1891: Die Anaplasie der Geschwulst- 
zeiten u. die asymmetrischen Mitusen. Ib., 129 Bd., 1892: Die mikrosk. Diagnose 
der Geschwülste, Berlin, 1897. 
Hauser: Das Cylinderepithelcarcinom, Jena, 1890. 
van Heukelom: Sarkome u. plastische Entzündung. Virch. Arch., 107 Bd., 1887. 
Kaufmann: Multiplicitat d. prim. Carcinoms. Virch. Arch., 75 Bd. ‚1878. 
k: Renal Growths, Edinburgh, 1898. 
Eicke. Allgeın. pathol. Morphologie, Jena. 1889. 


Lancoreate, Traite d’anat. pathol., i., Paris. 181%. 
Langhans: Ueber Glykogen in pathologischen Neubildungen. Virch. Arch., 120 
31., 1900. 


Lennois «t Courmont: Deux cancers primit. du tube digestif. Rev. de méd., 1894. 

Lubarsch: Hy perplasie u. Geschwülste. Ergebn. d. allg. path. Morph., W iesbaden, 
1495: Zur Lehre v. d. Geschwülsten, Wiesbaden, 1899. 

Luecke u. Zahn: Chirurgie d. Geschwülste, i. Stuttgart, 1896. 

Marchand: }ezich. d. path. Anat. z. Entwickelungsgesch. Verh. d. Deut. path. 
Ges., i., Berlin, 1900. 


ETIOLOGY OF TUMORS. 371 


Martin: Zur Kenntniss der indirecten Kerntheiking. Virch. Arch., 86 Bd., 1881. 

Müller: Celluläre Vorgänge in Geschwülsten. Virch. Arch., 180 Bd., 1892. 

Müller, J.: Ueber den feineren Bau und die Formen der krankh. Geschwülste, 1883. 

Paget: Lectures on Tumors, 1852. 

Petrone: Breve guida allo studio dei tumori, Catania, 1890. 

Pfitzner: Zur patholog. Anatomie des Zellkerns. Virch. Arch., 108 Bd., 1886. 

Schimmelnnach: Multiples Auftreten prim. Carcinome. Langenbeck’s Arch., 89 

Schmidt: Secretionsvorgiinge in Krebsen. Virch. Arch., 148 Bd., 1897 (Lit.). 

Senn: Pathology and Surgical Treatment of Tumors, 1895. 

Strobe: Kerntheilung und Riesenzeilenbildung in Geschwülsten. Beitr. v. Ziegler, 
vii., 1890; Celluläre Vorgänge u. Erscheinungen in Geschwülsten. Ib., xi., 1891; 
Neuere Arbeiten über Histogenese u. Actiologie des Carcinoms. Cbl. f. allg. 
Path., ii., 1891. 

Thiersch: Der Epithelkrebs der äusseren Haut, 1865. 

Thoma: Allgem. patholog. Anatomie, Stuttgart, 1894. 

Trambusti: Bau u. Theilung der Sarkomzellen. Beitr. v. Ziegler, xxii., 1897. 

Virchow: Die krankhaften Geschwülste, i.-iii., 1863-67. 

Wells: Multiple Primary Tumors. Jour. Path. and Bact., 1900 (Lit.). 

White: The Definition, Terminology, and Classification of Tumors. Jour. of Path., 
vi., 1899. 

Williams: The Principles of Cancer and Tumor Formation, London, 1889. 

Wilms: Die Mischgeschwülste, i., ii., Leipzig, 1899, 1900. 

See also §§ 101 and 102. 


§ 101. The etiology of tumors is by no means uniform, and very 
often cannot be determined with certainty. In the majority of cases, 
however, the conditions, at least, under which the new-growth appeared 
can be assigued and we may accordingly establish different groups of 
tumors. Infection is indeed very frequently advanced as a cause of tu- 
mors, but such etiology has not in any case been demonstrated beyond 
doubt. 

Als the first group of tumors, according to etiology, may be taken those 
arising from especial congenital anlage, so that we may in a certain sense 
regard them as local malformations of tissue. They develop either in 
uterine life, and are present at birth, or later in extra-uterine life, dur- 
ing the period of growth or even later, in which case trauma not infre- 
quently gives the immediate occasion for the beginning of the develop- 
ment of the tumor from the preexisting anlage. 

To this group belong in the first place many osteomata, chondromata, 
angiomata, gliomata, fibromata (of the nerves and skin), sarcomata and 
adenomata. Further, many teratoid tumors and cysts are also to be 
included in this group, inasmuch as they represent in part either re- 
mains of fatal structures, transpositions or monogerminal inclusions of 
embrvonic tissue, implantations of rudimentary portions of a twin em- 
bryo (bigerminal implantations), or probably also the results of disturb- 
ances of the earliest stages of the development of the ovum. 

A second group develops after traumatic injuries of the tissues ; and it has 
been reckoned that in about seven to fourteen per cent of cases a trau- 
matic origin can be assigned; particularly in the case of sarcoma, carci- 
noma, and osteoma. The causes of the tumor-formation may be a single 
injury, a stab, a blow, crushing, fracture, ete., as well as repeated me- 
chanical irritation, such as rubbing, scratching, ete. 

In a third group the development of the tumor follows inflammation, par- 
ticularly the formation of granulation tissue with subsequent cicatrization. The 
inflammation and ulceration may be caused by non-specific as well as by 
specific injurious agents. For example, cancer of the gall-bladder (Fig. 
233, d, e) almost invariably develops only in gall-bladders which contain 





ETIOLOGY AND GENESIS OF TUMORS. 373 


and on the other hand, of a lessening or removal of hindrances to growth. But it still 
remains a problem why there should not be formed typical tissues which would so fit 
into the organization of the body that they would be of service to the latter. In the 
attempt to explain this phenomenon, which is at the same time associated with an in- 
crease in the vital and reproductive capacities of the cells, even under pathological con- 
ditions (metastasis of the cells through the blood- and lymph-vessels), many writers 
have sought and would recognize as the cause the presence of parasites (sec Etiology 
of Carcinoma); but our present knowledge does not in any way justify us in attributing 
the development of true tumors, of autonomous new-growths, to the influence of para- 
sites. On the contrary, the development and life-history of tumors, and in particular 
the formation of metastases, which without doubt arise through the multiplication of 
living tumor-cells transported in the lymph- or blood-stream, speak against the hy poth- 
esis of the parasitic nature of tumors. 

Cohnheim advanced the theory that all true tumors arose from especial tumor- 
anlage which had their origin in the persistence of foci of embryonal tissue. Neither 
the results of clinical observation nor of the anatomical investigation of the tissues 
speak in favor of such a theory. 

Ribbert is of the opinion that the cause of the pathological proliferation which leads 
to tumor-formation is to be found particularly in a separation of cells or cell-groups 
from their organic relations, such a separation occurring either as the result of intra- 
uterine disturbances of development or later under the influence of external agencies. 
Nevertheless, such transplantations or separations of cell-groups take place very fre- 
quently in intra-uterine life, or after trauma, after ulceration, in scars and in infectious 
granulomata, without any subsequent development of a tumor. These transplanta- 
tions of tissue conatitute only one of the predisposing causes of tumor-formation, but some 
other factor is necessary to excite the atypical progressive tissue-proliferation—i.e., the 
development of the tumor. The development of a tumor ts, therefore, in no wise depen- 
dent upon a transplantation of tissue ; rather does the tumor-proliferation take tts origin in 
cella which are normally situated ; and this may be actually demonstrated, particularly 
in the case of epithelial tumors. 

Our knowledge of the causes of tumor-decelupment at the present time may be summed 
up as follows: Inherited and acquired conditions of certain cells and cell-groups, which 
assert themselves in a tendency to increased formative activity with the production of 
atypical tissue, lead to the formation of tumors. In many cases this proliferation is 
prepared for, favored, and excited by the transplantation of cells and cell-groups, but 
often also through changes in the neighborhood of the cells concerned. No general 
scheme applicable to the development of all tumors can be given. On the contrary, 
the conditions vary not only with the different forms of tumors, but also with the indi- 
vidual cases of the same tumor-type. Moreover, it should not be forgotten that the 
formations which we class as tumors do not all possess the same significance, and that 
many of the same ought more properly to be classed with other phenomena of growth 
(malformations). 


Literature. 
(Etiology and Genesis of Tumors. ) 


Adami: On Growth and Overgrowth, etc. Med. Chron., 1900; Concerning the Causa- 
tion of Cancerous and Other New-Growths. Yale Med. Jour., 1901. 

Askanazy: Geschwülste d. in d. Niere eingeschloss. Nebennierenkeime. Beitr. v. 
Ziegler, xiv., 1893. 

Beneke: Neucre Arbeiten z. Lehre vom Carcinom. Schmidt’s Jahrb., 234 Bd., 1892. 

Bögehold: Entwickelung von malignen Tumoren aus Narben. Virch. Arch., 88 Bd., 
1882, 

Boll: Das Princip das Wachsthums, Berlin, 1876. 

Bonnet: Zur Actiologie der Embryome. Mon. f. Gebh., 1901. 

Borsch: Pathogenese d. malignen Geschwilste. Virch. Arch., 162 Bd., 1900. 

Buxton: Enzymes in Tumors. Jour. of Med. Res., 1903. 

Cohnheim: Vorlesungen tiber allgemeine Pathologie, Berlin, 1882. 

Crone: Lupuscarcinom des Kehlkopfs. Arb. a.d. path. Inst. v. Baumgarten, ii., 1894. 

Czerny: Warum dürfen wir die parasit. Theorie für die bösart. Geschwülste nicht 
aufgeben? Beitr. v. Bruns, xxv., 1899. 

Foa: Sui parassiti et sulla istologia patologica del cancro. Arch. per le Sc. Med., 
xvii., 1893. 

Gerhardt: Das Gliom. Festschr. zur dritten Säcularfeier d. Universität, Würzburg, 
ii., 1882. 


37% TUMORS. 


Maberers Daten zur Lehre ron den Calustumsren. Langenbers : Awa 45 Bi. 


Nesecmena Sperificitas Alartismns 1. Anasiasie der Zeilen. Bertin. ei 

Hauser imacamn Mageagewhwir. Leipzig. is. Tee Cv lindereoithe'rarce m les 
Maras d. Darma Jeza. 1). Husernese 1 Plaienepiiieizeners Bers + 
Zersr 183i. LS. 

hie Acting ‘rest. Gesenwiiste. Ber. z ei. 2. 1S). 
Theune tea Carringnmea Chi. f. aiiz Pasa. vi I 

v. Karwowski: User (aöinstumemn. Inauz Ira Freiburg. 18. 

Kenibachieff- (arin.m naca Lopus Inaug -Die. Freiburz. 188 

Kirmisson ( hirurziwne Krankheiten angeborenen Cxprimgs. Stas zar. 99. 

Kocher Kranıh. 3. ndanl. (eschierhiwrzane. Desch. Chirurzie. Lief eh. ivet 

Küster Yrazeo 4. pach. Pflanzenana: mir -Gallenbdiaiczaz. Bee Ch. xx.. 9 

Liebe Theer. 107 Parafinkrrtm. Sehmii:'s Jahrb.. 238 Bi. 

Levin. (ii Prrüiferatiea under Pathological Conditions with Epoche: Reference -. the 
Eriierzy of Tamer. stnrties from Depe of Path. C-ıambia University. air 

. Traumazische Entstehung v. Geachwilsten. Arch kin (her.. 4¥ Bi. 
195. 

Petersen :ı Exner. Hefrpilze u. Gesrhwulsthibiung. Beitr. v. Brür«. xır.. 

Pianese: Pei:r. z. Hisusisgie u. Actiniogie d Caremoms. Beitr. v. Zesaer. Spel. 
1 =i 

Teck lingheusen : Adenranrome u. Cystadencare d. Uterus. Bertin. 1%. 

Ribbert: Hisuigeneswe d. Carcinomas. Virch. Arch.. 135 Bd. 194. Die Enzstehun: 4 
Gewhwijiate. Deut. mei. Woch.. 1995: Das pathok.z. Wachsthum d. Gewche. 
Berlin. 16. Urber Rückbikiung v. Zelen u Geweben u. die Entstebuns v. 
Geschsfilsten. Stuttgart. 199%. 

Schubert. Ueber den primären Gallenblasenkrebs. Inaug.-Dis.. Freiburg. 1%. 

Schuhardt. Entstehung der Carcinome aus chron. entzündlichen Zuständen. Leij-zig. 


I 
Schulthess: Statistiw-be Untersuch. Gb. d. Aetiologie d. Carcinoms. Beitr. v. Bruns. 
v. Isl 


Artislogie des Gallenblasenkrebses. Virch. Arch.. 132 Bi... 1893. 

Stern Maligne Tumoeren im Kindessiter. Deut. med. Woch.. 192. 

Strobe: Neuere Arbeiten über Histogenese u. Aetiologie des Carcinoms. Cbi. f. alle. 
Patb.. ii., 1991: Die parasitären Protozoen in ihren Beziehungen zur menschl. 
Pathologie. insbes. zur Histogenese u. Actinlogie des Carcinoms (Ref... IT... 
14. Entstehung d. Gliome. Beitr. v. Ziegler. x viii. 1%95. 

Tauffer: surkome auf narbig lupdsem Boden. Virch. Arch.. Supp! . 151 Bd.. 189s. 

Volkmann: Krebs d. Extremitäten. Samm. klin. Vortr.. Nos. 334. 335. 189. 

Weisflog: Urber Callustumoren. Beitr. v. Bruns, x., 1893. 

Wilms Pie teratoiden Geschwülste d. Hodens. Beitr. v. Ziezler. xix.. 1996. 

v. Winiwarter: Beitr. z. Statistik d. Carcinome. Stuttgart. 1878. 

Wieland Primär« multiple Knochensarkome. Inaug.-Diss.. Basel, 1898. 

Wolff, Zur Ent-tehunz d. Gechwiilste nach traumatischen Einwirkungen. Inau:r.- 
Dies. Berlin. 1474. " 

Würz Traumat. Ent-tehung der Geschwülste. Beitr. v. Bruns, 36 Bd.. 1We Lit... 

Zahn Zur Actiologie der Fpithelkrebse. Virch. Arch... 117 Bad... 1889. 

Zenker Jer Kretm d. Gallenblase. Deut. Arch. f. klin. Med.. £4 Bl. 1889. 

Ziegler, P.: Wezieh v. Traumen zu malignen Geschwülsten. Münch. med. Woch., 
In 
Ser ala zZ IM. 


£102. When once a tumor has arisen in any tissue and has reached a 
certain stage of development it may become quiescent in growth, and 
remain for a life-time without undergoing further change. This is true 
particularly of those tumors which according to their origin are re- 
ganled as local tissue-malformations: but tumors which develop first in 
later life may also come to a standstill after attaining a certain size. 

The growth of a tumor takes place independently, and in many 
cases continues even until death occurs. 

From the surrounding tissues the tumor acquires both its blood-ves- 
sels and thereby its food inaterial, but may besides grow independently 
je, through an inerease of the cells which form the elements of the 
tumor. fan thy cases the tumor increases in size essentially through an 














MALIGNANCY. 379 

The malignant tumors, on the whole, coincide with those tumor 
forms which are known as carcinoma and sarcoma. It must, however, 
be borne in mind that the malignancy of a tumor depends not only upon 
its character, but also upon its location. A benign tumor takes ona 
malignant character as soon as its presence interferes with the functions 
of vital organs. Hence every tumor of the brain or meninges becomes a 
dangerous affection at the moment when it gives rise to disturbances of 
the cerebral functions. Under certain conditions such benign tumors as 
tibromata of the uterus become destructive growths as soon as they reach 
such a size as to displace and compress the neighboring organs. 

After a tumor has existed for a certain period there results very 
frequently a marked lowering of the general nutrition, a marasmus, 
which is usually designated tumor-cachexia. This occurs chiefly in 
association with the malignant growths known as cancer and sarcoma; 
and may depend, in part at least, upon the great demands made upon the 
food supply by the rapid growth of the tumor, particularly in the case 
of formation of metastases. A still more important cause may lie in the 
fact that the tumor may interfere with the taking-in of food. In cancer 
of the cesophagus, stomach, and intestine the function of the affected 
organ is greatly interfered with, and the assimilation of food may be 
entirely prevented or nearly so. Further, it should be borne in mind 
that through the degeneration of the tumor and the continuous secretion 
from the resulting ulcers large amounts of albuminous material may 
often be lost from the body; and that through putrid decomposition 
there may arise substances which, when absorbed, may act injuriously 
upon the organism. Finally, the pain which is often felt in a tumor 
may rob the patient of his sleep. Whether the tumor itself, in certain 
cases, produces substances harmful to the organism is yet unknown, but 
is, however, not improbable. 


Literature. 


( Tumor- Metastasis. ) 


Acker: Zur Pathogenese d. Geschwulstmetastase. Deut. Arch. f. klin. Med., xi., 
1873. 

André: Entsteh. d. Geschwulstmetastasen auf embolischem Wege. Virch. Arch., 61 
Bd, 1874. 

Arnold: Ueber rückläufigen Transport. Vireh. Arch., 124 Bd., 1891. 

Audibert: De la généralisat. du cancer de l’estomac, Paris, 1877. 

Beneke: Freies Wachsthum metast. Geschwulstelemente in serösen Höhlen. Deut. 
Arch. f. klin. Med., 64 Bd.. 1899. 

Geissler: Uebertragbarkeit d. Carcinoms. Langenbeck’s Arch., 46 Bd., 1898. 

Goldmann: Verbreitungswege bösartiger Geschwülste. Beitr. v. Bruns, xviii., 1897. 

Hanau: [Erfolgreiche exp. Uebertrag. v. Carcinom. Fortschr. d. Med., vii., 1889 

Just: Ucb. d. Verbreit. d. melanot. Geschw. im Lymphgefässsystem. Inaug.-Diss., 
Strassburg, 1888. 

Kantorowicz: Pathogenese der allgemeinen Carcinomatose. Cbl. f. allg. Path., iv., 
1493. 

Lanz: Uebertragbarkeit melanot. Geschwülste. Festschr. f. Kocher, Wiesbaden, 1891. 

Morau: Rech. exp. sur la transmissibilité de certains néoplasmes. Arch. de med. 
exp., 1594. 

Perls: Beitr. z. Geschwulstlehre. Virch. Arch., 56 Bd., 1872. 

Petrick: Verbreitung d. Carcinoms in den Lymphdrüsen. Deut. Zeitschr. f. Chir., 
32 Bd.. 1891. 

Rieder: Ueber die embol. Geschwulstmetastase. Inaug.-Diss., Dorpat, 1878. 

Velich: Ucbertrag. v. Rattensarkom auf andere Ratten. Wien. med. Bl., 1898. 

Virchow: Die krankh. Geschwülste, i.-iii., 1863-67. 

Weber: Zur Geschichte des Enchondroms, namentl. in Bezug auf (dessen hereditäres 








382 TUMORS. 


Moreover, it is not uncommon to see within a tumor several centres of 
growth—that is, the mass of the tumor is made up of several nodules or 
bands held together by ordinary connective tissue (Fig. 241, 5). Fibro- 
mata are malignant only through their size and position. 

Fibromata may undergo fatty degeneration or may soften and disiiite- 
grate, so that cavities may be formed within them. They may also break 
through and give rise to ulcers. Their blood-supply varies greatly, at 
times being scanty, at other times abundant. Occasionally the blood- 
vessels are ectatic, so that the tissue is interspersed with wide channels 
and clefts, from which blood escapes when the tumor is examined in a 
fresh state. In other cases dilated lymplh-channels are seen. 

Keloid is the designation applied to a hard, nodular, or flat and 
banded, or stellate growth of the skin, which in its fully developed state 
consists of dense fibrous tissue without elastic fibres. The direction of 
the fibres is often at right angles to the surface of the skin, or at least 
does not accord with that of the normal fibres. It usually develops after 
injuries or inflammations (cicatrix-kelvid), but it may also appear without 
such association (spontaneous keloid). The cause of the keloid growth is 
not known; the tendency to recurrence after removal, the multiple oc- 
currence, and the fact that many cases frequently occur in the same 
family (Hutchinson) speak in favor of a special predisposition on the 
part of the skin. 


Literature. 


(Fibroma and Keloid.) 


Aschoff: Geschwilste. Ergebn. d. allg. Path., v., 1900. 

Jacobson: Keloid. Arch. f. klin. Chir., xxx., 1884. 

Jores: Elastische Fasern in Bindegew ebsgeschwülsten. Beitr. v. Ziegler, xxvii., 
1900, p. 389. 

Joseph: Ueber Keloide. Arch. f. Derm., 49 Bd., 1899. 

Jürgens: Primäre Herzgeschwülste. Berl. klin. Woch., 1891. 

Langhans: Keloid. Virch. Arch., 40 Bd., 1867. 

Lison: Sur la chéloide inguinale spontanée, Puris, 1887. 

Peterson: Ovarian Fibromata. American Gynecology, 1902 (Lit.). 

v. Recklinghausen: Ueber die multiplen Fibrome der Haut. Berlin, 1882. 

Schütz: Wahres Keloid combin. mit Narbenkeloid. Arch. f. Derm., 29 Bd., 1894. 

Thorn: Spontanes Keloid. Arch. f. klin. Chir.. 51 Bd., 1895. 

Unna: Die Histopathologie d. Hautkrankheiten, Berlin, 1894. 

Wilms: Pathogenese des Keloids. Beitr. v. Bruns, 23 Bd., 1899. 
See also § 112. 


(b) My.roma. 


$ 104. A myxoma is a tumor which consists essentially of mueous 
tissue, and is made up of cells and a fluid or gelatinous intercellular sub- 
stance containing mucin. Thecells of the tumor are for the greater part 
polymorphous, with processes of varying length (Fig. 242) which anas- 
tomose with one another (Fig. 243, a). The tissue is markedly trans- 
lucent, soft, and the blood-vessels are easily seen through it. From the 
cut surface gelatinous masses or a stringy fluid, which swell up in water, 
may be obtained. 

No tumor is ever wholly made up of myxomatous tissue; the latter 
is usually combined with other forms of tissue, particularly with fibrous 
connective tissue, fat tissue, cartilage, and sarcomatous tissue. For this 
reason such tumors are properly designated fibromyxoma, lipomyxoma 
(Fig. 245), chondromyxoma (Fig. 248, c), and myxosarcoma (Fig. 243). 





384 ‘TUMORS. 


These forms are all benign tumors, which rarely produce metastases. 
Myxosarcomata, on the other hand, have the characteristics of sarcomata 
and may form metastases. 


Literature. 
(Myzoma.) 


Myxome de l’oreillette guache. Arch. de med. Sr: 1898. 
an Myxom im rechten Seitenventrikel. Virch. Arch., 49 1870. 

Heyfelder: Zur Resection des Oberkiefers. Virch. Arch., 11 Bd., 1857. 

Jürgens: Primäre Herzgeschwülste. Berl. klin. Woch., 1891. 

Köster: Myxom u. ödemat. Bindegewebe. Sitzber. d. "Niederrhein, Ges. f. Naturk., 


Müller, J.: Myxom. Arch. f. Anat. u. Phys., 1836, 
Orth: Schleim u. Schleimgeschwülste. Ges. d. Wissensch. zu Gottingen, 1895. 
Robin: Myxome du caur. Arch. de méd. exp., 1898. 
Bumler: Ueber Myxom. Inaug.-Diss., Bonn, 1881. 
Virchow: Myxom. Yirch, Arch. 11 Bd. ; Geschwülste, | 1808. 
‘agner: Collonema im Gehirn. Virch. Arch., 8 Bd., 1855. 
Weichseibeum: Myxom d. Oberschenkels m. secund. Knoten in d. Lunge. Virch. 
Archiv, 54 Bd., 


(ec) Jipoma. 


§ 105. A lipoma is a tumor consisting of adipose tissue (Fig. 244). 
These tumors are sometimes soft, sometimes firm, usually nodular and 
lobulated, and very often attain a very great size. In structure they 
are very similar to the subcutaneous adipose tissue—that is, they consist 
of fat-lobules held together by thick or narrow connective - tissue 
trabeculae. 

Histologically, the tissue of a lipoma resembles the fat-lobules of 
the subcutaneous panniculus (Fig. 244), although the tendency to form 
typical grape-like clusters of fat-cells is wanting. If, as not infrequently 
happens, mucous tissue is also 
formed in connection with the 
fat tissue, or if the latter, fol- 
lowing a disappearance of its 
fat, becomes changed into myxo- 
matous tissue, the tumor is des- 
ignated a lipomyxoma (Fig. 
245); if there is an abundance 
of fibrous tissue present, it is 
called a lipofibroma or fibroli- 
poma. 

Lipomata develop most com- 
monly from adipose tissue, but 
may arise also from connective 
tissue which normally contains no 
fat. Calcification, necrosis, gan- 
ig 244-—Lipoms of shoulder region, wit relatively grene, and sloughing are of not 
amall fatceils (Müllers Sula: hactiatosyiin)e. x infrequent occurrence in lipomata 

of large size. These tumors do 
not produce metastases, but are occasionally of multiple occurrence. A 
complete disappearance of a lipoma does not take place in the case of 
extreme general emaciation of the individual. 

Lipomata are sometimes observed even in new-born children—for 





LIPOMA. 385 


example, as tumors developing in or over the cleft-formations of spina 
bifida—but they occur much more frequently in later years. The most: 
common seats of these growths are the subcutaneous tissues of the back, 


AINE OMAN Lp 
alee. 


a 





Fic. 245.—Lipomyzoma of the beck (Müller's Auld, Yan, Gtegon's), a, Lange fat-oells; D, e, fatoells in 
whieh the fat is broken up into little droplets; d, mucous tissue; ¢, blood-versel. 


buttocks, neck, axilla, abdomen, and thigh; but they are found also in 
the intermuscular connective tissue, subserous fat tissue, in the kidneys, 
intestine, mammary gland, under the aponeurosis of the forehead, in 
the meninges, skin, fingers, lymph-glands, joints, ete. They may occur 
as multiple growths, and in such cases may be symmetrically distributed. 
In man there occurs a rare formation of fat tissue about the neck and 
throat, leading to nodular and lobulated disfigurations of the skin of this 
region, and giving occasion for the designation fatty collar (Madelung). 
The development of fat in these cases takes place partly in the subeuta- 
neous tissue, partly in and under the fascia and between the muscles. 
An abnormal development of fat in an extremity may give rise toa 
condition of lipomatous elephantiasis. Should the process extend to the 
trunk and upper extremities, etc., conditions are established which re- 
semble very closely general obesity. 





Literature. 


(Lipoma.) 
Adami: Retroperitoneal Lipoma. Mont. Med. Jour., 1897. 


Alveoli: La genesi del lipoma. Policlinico, 1900. 
Askanazy: Entsteh. multipler Lipome in I,ymphärüsen. Virch. Archiv, 188 Bd., 


1899. 
Blaschko: Erbliche Lipombildung. Virch. Arch., 124 Bd., 1891. 

Statistik der Lipome, Würzburg, 1886. 
Xanthelasmen u. Lipome. Beitr. v. Bruns, iv., 


Goebel: Ueber multiple Lipome. Cbl. f. allg. Path., vi., 1895 (Lit,—Uebers). 
Grosch: Studien über das Lipom. Dtsch. Zeitschr. f. Chir., xxvi., 1887. 

Koettnitz: Symmetr. Auftreten der Lipome. Zeitschr. f, Chir., 38 Bd., 1894, 
Langer: Multiple symmetrische Lipome. Arch. f. klin. Chir., 46 Bd., 1898, 









































4 TUMORS. 


Lymphangiomata are sometimes congenital: at other times they make 
their first appearance at a later period of life. 

The congenital forms occur particulariy as different varieties of 
ectasia of lymph-vewels, and are found chietly in the tongue | macro- 
glossia, palatal arch, lips ( macrocheilia), skin (narus lymphaticus:, sub- 
cataneons tissue, in the neck (hygroma colli cungeritum), vulva, etc. The 
lymphangiomata of the skin spread over more or less extensive areas of 
the skin, and form either smooth or irregular elevations of the same. If 
the blood-vessels are numerous the growth may have a red color. The 
rupture of dilated Iymph-vessels lying immediately beneath the epithe- 
liumm (Fig. 264, d) may give rise to a moist condition of the surface and 








M10, 255, Lymphangioma cavernosum mubentaneum (alcohol, alum-carmine). a. Fetatic Iymph-vessels: 
b connective Umsue; €, adipose Umsue el, large blood-veaely; ¢, cellular areas. Y 2. 





Iymphorrheea. The extension of the cavernous develop- 
-vessels over large areas of the skin and subcutaneous: 
tissue may give rise to elephantiasis-like disfigurations of the part affected. 
Not infrequently the intervening connective tissue also takes part in the 
hypertrophic growth, or there develops a fibrous elephantiasis in connec- 
tion with 1 

In rare eas yle-eontaining growths (ehylangiomata) are found in 
the intestinal wall or mesentery. Cystic lymphangiomata are also found 
rarely in the peritoneum, 

The pathological formations which may be classed as hypertrophic 
lymphangiomata represent. peculiar changes of the , Which are 
either congenital or develop in early youth. They are commonly known 
as pigmented moles, lentigines, freckles, and fleshy warts, 

The pigmented moles, or nevi pigmentosi, ov mclanomata, form larger or 
smaller smooth areas which are not: e| above the general surface of 
the skin (nevus spilux), or pi (merus prominens, 
nerus verrucoxus), When cove frequently the case, 
they are led hairy moles (nevus pilosus). In color they are usually 
light: brown or dark brown, or even black (Fig. 266); and are usually 


eventually to 









































LYMPHANGIOMA. 403 


of the cells); though often the pigment lies chiefly within the connec- 
tive tissue cells of the fibrous portions of the growth. 

The cells of the cell-nesis are relatively large (Fig. 268), possess an 
abundant protoplasm, and a bright, bladder-like nucleus. Their posi- 
tion and appearance justify the assumption that they represent the prod- 
ucts of the proliferation of the endothelial cells of the lymph-vessels. In 
rarer cases Similar formations arise from the blood-vessels (hamangioma 
hypertrophicum). Accordingly, it would seem proper to class these 
growths with the endotheliomata or lymphangiosarcomata, but their lim- 
ited growth makes their classification as lymphangiomata more appro- 
priate (see § 115). The cell-nests of the hypertrophic lymphangioma 
may in part spread out more diffusely through the tissues (as is the case 
with the hypertrophic hemangioma), so that the peculiar structure of 
the growth may be lost. In rare cases there may develop a combination 
of hypertrophic lymphangioma and lipoma. 


Unna, Kromayer, Delbanco, and Marchand held the view that the cell-nests of the 
cellular nevi are of epithelial origin, and represent misplaced portions of the surface 
epithelium; and Aromayer goes so far as to assume a metaplasia of epithelium into 
connective tissue. Preparations showing the first stages of the development of nevi 
are not accessible to me; but a thorough study of nevi and fleshy warts of a later stage 
does not show any connection between the cell-nests and the epithelium; and conse- 
quently I hold the opinion—notwithstanding the investigations of the above-named 
authors—that the view given above in the text, in regard to these nevi and fleshy 
warts, harmonizes most perfectly with their anatomical nature and clinical behavior, 
both in their fully developed condition as well as when they undergo a transformation 
into malignant sarcomata. That in individual cases the cell-nests lie close to the epi- 
thelium is no proof of a genetic relationship, since the ordinary lymphangiomata also 
lie cluse to the epithelium (Fig. 264, d). 


Literature. 


(Lymphangioma and Cellular Nevi.) 


Arnold: Zwei Fälle von Hygroma colli congenitum. Virch. Arch., 32 Bd., 1865. 

Arnstein: Zur Casuistik der Makroglossie. Virch. Arch., 54 Bd., 1872, 

Bauer: Endotlieliale Naevi. Virch. Arch., 142 Bd., 1896. 

Bayer: Bedeut. d. Fettgewebes f. d. Aufbau d. lymphat. Neubildungen. Zeit. f. 
Heilk., xii., 1891. 

v. Biesiadecki: Untersuch. aus dem pathol. Institut., 1872. 

Bircher: Aetiol. d. Naevus pilosus (untergegangenes Zwillingsgeschwister). Arch. f. 
Derm., 41 Bd., 1897. 

Bogoliubsky: Die Pigmentflecken der Haut. Inaug.-Diss., Bern, 1887. 

Delbanco: Epitlielialer Naevus. Monatsh. f. prakt. Derm., xxii., 1896. 

Demieville: Ueber Pigmentflecken der Haut. Virch. Arch., 81 Bd. , 1880. 

Freudweiler: Lymphang. cystoides cutis. Arch. f. Derm., ‘41 Bd., 1897. 

Frobenius: Ueber einige angeb. Cystengeschwülste des Halses. Beitr. v. Ziegler, vi., 
1889. 

Gaucher et Lacapére: Lymphangiome circonscrit. Arch. de med. exp., 1900. 

Hebra u. Kaposi: Handb. d. Hautkrankh., ii., 1872. 

Köster: Ucb. Hygroma colli congenitum. Verh. d. Würzb. phys.-med. Ges., iii., 
1872. 

Kromayer: Histogenese d. weichen Hautnaevi. Derm. Zeitschr., 1896; Erwiderung 
un Ribbert. Beitr. v. Ziegler, xxii., 1897. 

Kruse: Ueber das Chylangioma cavernosum. Virch. Arch., 125 Bd., 1891. 

Küttner: Intermittir. Entzündung d. Lymphangiome. Beitr. v Bruns, xviii., 1897. 

Langhans; Lymphangiom d. unt. Extremität. Virch. Arch., 75 Bd., 1875. 

Lesser u. Beneke: Lymphangioma tuberosum multiplex. Virch. Arch., 123 Bd., 
1891. 

v. Lesser: Lymphangioma diffusum multiplex. Zeitschr. f. Chir., 34 Bd., 1893. 

Lion: Lymphcysten d. Ligam. uteri latum. Virch. Arch., 144 Bd., 1896 (Lit.). 

Loewenbach: Histogenese der weichen Naevi. Virch. Arch., 157 Bd., 1899. 

Nasse: Ucber Lymphangiome. Langenbeck's Arch., 34 Bd., 1887. 





406 TUMORS. 


and others, multiple ınyomata of the skin may take their origin either 
from the arrectores pilorum or from the muscle-cells of the sweat-glands. 

A certain amount of connective tissue always takes part in the for- 
mation of a myoma, and often assumes such importance that the tumor 
may with propriety be called a fibromyoma or myofibroma. For 
example, the majority of the uterine myomata are fibromyomata. The 
fibrous connective-tissue portions of the tumor appear glistening white, 
the muscular portions more reddish-white or clear reddish-gray. The 
spindle-shaped muscle-fibres may be isolated by teasing a bit of the 
tumor or by maceration of the same for twenty-four hours in a twenty- 
per-cent nitric-acid solution or for twenty to thirty minutes ina thirty- 
four-per-cent solution of potassium hydroxide. In longitudinal sections 
the muscle-fibres are most: easily recognized by their rod-shaped nuclei 
(Figs. 270, 271), as well as by the regular structure of the cells in bands 
or strands. In cross-section the muscle-cells appear as small flattened 
cells containing in their centres the transversely cut nuclei (Fig. 270) 

The leiomyomataare benign tumors, but often reach avery large size, 
and sometimes undergo a sarcomatous proliferation. In fibromyomata of 
the uterus there not infrequently occur fatty degeneration and softening, 
which may lead to the disintegration of the growth or to the formation 
of cystic cavities. Calcification may also occur. Through degeneration 
and atrophy of the muscle-fibres a myofibroma may become transformed. 
into a fibroma. 

A rhabdomyoma (Zenker), or myoma striocellulare, is on the whole 
a rare tumor. Its most characteristic feature is the preseuce of stri- 
ated muscle-fibres, which in part are fully developed and in part un- 








Tee aa 





Fia. 272.—Cells from a rhabdomyoma, (After Ribbert and Wolfensberger.) a, b. c. d. Striated bres 
of varying thickness ; «l, small nucleated übre without striatlo spindle-cell with longitudinal striation ; 
f, xpindle-cells with longitudinal and transverse striation indlecells, without striation, with elon 
sted processes h, I, Pound cells with concentric and radial station. 








developed. When well developed the musele-fibres form multinuclear 
bands of varying width, which present a cross-striation (Fig. 272, a, b, 
ec), and in part also a longitudinal striation (e, f). The undeveloped 
forms consist of narrow bands without transverse striations (d); of 
spindle-cells with long-drawn-out thread-like processes without transverse 
striation (g) or with partial striation (/); or, further, of round cells of 


MYOMA. 407 


different sizes, which present either a radial or a concentric fibrillation 
or striation (h, i). Besides these there are also cells which possess no 
especial characteristics, so that it is impossible to decide whether they 
are young undeveloped muscle-cells or connective-tissue cells. The 
bands as well as the spindles are usually arranged in interlacing bundles. 
It is usually not possible to demonstrate with certainty the presence of a 
sarcolemma on the surface of the fibres; but various delicate membranes 
have been described by different authors, which probably are to be re- 
garded as representing portions of a sarcolemma. 

Rhabdomyomata of the heart, in so far as they do not consist of a 
formation of delicate transversely striated muscle-fibres, are made up of 
a delicate network supported by connective-tissue bands, in the clear 
spaces of which network there lie spider-like cells, whose processes are 
partly free, and partly continuous with the reticulum. According to 
Seiffert, these cells are to be regarded as enlarged embryonal musele- 
cells, which, in the event of an overproduction of the structureless pro- 
toplasmic portion, have formed no transversely striated covering. 

Rhabdomyomata occur most frequently in the kidney or its pelvis, 
in the testicles, and uterus; more rarely in other regions, as, for exam- 
ple, in the vagina, bladder, muscles, heart, nerves, subcutaneous tissue, 
mediastinum, oesophagus, ete., and form nodular, or, in case they are 
situated on the surface of a mucous membrane, papillomatous and poly- 
poid tumors, which vary greatly in size. They develop from striped 
muscle, possibly also from smooth muscle (uterus). In the kidneys and 
testicles they either form circumscribed nodules, or lead to a total 
destruction of theorgan. The origin of the tumor in these cases is prob- 
ably from misplaced anlage of muscle-tissue; and accordingly such 
growths are most frequently congenital. They may, however, develop 
first at an advanced age. Occasionally they enclose other tissues, for 
example, cartilage. Moreover, muscle-fibres of corresponding stages of 
development occur in the complex tumors of the testicles and kidueys 
(see Teratoma). 

If a tumor contains only a few cells which can be definitely recog- 
nized as muscle-fibres, while the majority of the cells have no specific 
character, the tumor is ordinarily designated a rhabdomyosarcoma. 


Literature. 


(Leiomyoma and Rhabdomyoma. ) 
Arnold: Glykogenhaltiges Myoma striocellulare des Hodens. Beitr. v. Ziegler, viii., 
1890. ; 


Becker: Muskelgeschwülste des Hodens. Virch. Arch., 163 Bd., 1901. 

Brodowski: Myosarkom des Magens. Virch. Arch., 67 Bd., 1876. 

Cesaris-Demel: Rabdomioma del cuore. Arch. per le Sc. Med., xix., 1895 (Lit. ). 

Cohen: Histogenese der Myome. Virch. Arch., 158 Bd., 1899. 

Cohnheim: Congenitales quergestreiftes Muskelsarkom der Niere. Virch. Arch., 65 
Bd., 1875. 

Eberth: Myoma sarcomatodes renum. Virch. Arch., 55 Bd., 1872. 

Fujinami: Rhabdomyosarkom im Muskel. Virch. Arch., 160 Bd., 1900. 

Gebhard: Myome d. Uterus. Handb. v. Veit, ii., Wiesbaden, 1897 (Lit.). 

Helbing: Rhabdomyom an Stelle der I. Lunge. Chbl. f. allg. Path., ix., 1898. 

Herzog: Cutancous Myoma. Journ. of Cutan. and Genito-urinery Dis., 1897 (Lit.). 

Hess: Ein Fall von multiplen Dermatomyomen an der Nase. Virch. Arch., 120 Bd., 
1890. 

Huber u. Boström: Myosarkom der Niere. Deut. Arch. f. klin. Med., 23 Bd. 

Jadassohn: Zur Kenntniss der multiplen Myome der Haut. Virch. Arch., 121 Bd., 
1890. 


408 TUMORS. 





Kunze: Zur Casuistik der Myome des Magens. Arch. f. klin. Chir.. 40 Bd., 1890. 

Lartigau and Larkin: Multiple Leiomyomata of the Kidney. Journ. of Med. Res., 
1901. 

Lukasiewicz: Multiple Dermatomyome. Arch. f. Derm., 1892. 

Marc: leiomyoma subcutaneum congenitum. Virch. Arch., 125 Bd., 1891. 

Marchand: Myosarcoma striocellulare der Niere. Virch. Arch. 73 Bd.. 1878; Ueber 
eine Geschwulst mit quergestreiften Muskelfasern. Ib., 100 Bd., 1885. 

Neumann: Myoma striocellulare des Hodens. Virch. Arch., 103 Bd., 1886; Multiple 
Dermatomyome. Arch. f. Derm.. 39 Bi, 1807. 

Orlandi: Rabdomioma del nervo ischiadico, Arch. per le Sc. Med.. xix., 1895 (Lit.). 

Paviot et Bérard: Cancer musculaire lisse (maligne Myo! Arch, de méd. ex 
1897. 

Pernice: Myomreoinn striocellulare des Uterus. Virch. Arch., 118 Bd., 1888, 

Prudden: Rhubdomyom d. Parotis, Amer. Jour. of the Med, Sciences, April, 1883. 

v. Recklinghausen: Die Adenomyome u. Cystadenome des Uterus, Berlin, 1896. 

Ribbert: Myosurcoma striocellulare des Nierenbeckens. Virch. Arch., 106 Bd.; Zur 
Kenntn. der Rhabdomyome. Ib.. 180 Bd.. 1892. 

Ricker: Actiologie der Uterusgeschwülste. Virch, Arch., 142 Bd., 1895. 

Beiffert: Multiple Rhabdomyome des Herzens. Beitr. v. Ziegler. xxvil., 1900. 

Smith: Fibromyomatous Tumors of the Vagina. Amer. Journ. of Obst., 1902. 

Steiner: Myome d. Magendarmkanales. Beitr. v. Bruns, xxii., 1898 (Lit.). 

Tusini: Rabdomioangioma del dorso. Arch. per le Sc. Med., xx., 1896. 

Virchow: Die krankhaften Geschwilste, fi., 1865. 

Williams: Histogenese d. Uterussarkome (Myoma sarcomatodes). Zeitschr. f. Heilk., 
xv., 1894. 

Wolfensberger: Rhabdomy«m der Speiseröhre, Beitr, v. Ziegler, xv.. 1894, 

Zenker, K.: Rhabdomyosarkom der Örbita. Virch. Arch., 120 Bd., 1890. 





























(h) Glioma and Neuroglioma Ganglionare. 


$ 111. A glioma is a tumor which develops from the cells of the sup- 
porting tissue of the central nervous system (neuroglia), and in its fully 
developed condition consists essentially of 
these cells. In the brain the gliomata form 
tumors, which for the most part are not 
sharply defined from the normal brain-sub- 
stance, but pass into the 
latter by insensible gra- 
dations. At times they 
appear simply as local 
swellings of the brain, 
and only the difference in 
eolor and the disappear- 
ance of the normal tissue- 
contrasts between the dif- 
ferent elements of the 
brain, give evidence to 
the eye that a tumor is 
present. In the spinal 
B cord they arise most: fre- 
Fig. 273.-Glioma cerebri. A, Cells isolated by wasing and quently in the neighbor- 
sn alone. ood of the central canal, 
and may extend over a 

large portion of the cord. 

Their appearance varies greatly; sometimes they are light-gray, 
somewhat translucent, and similar in color to that of the cortex, and 
moderately firm in consistence; at other times they are more grayish: 
white, denser, and firmer; and again they are not infrequently grayish- 
red or dark red in color. In the last case they are traversed by numerous 





GLIOMA AND NEUROGLIOMA. +09 


large vessels. Gliomata well supplied with blood often contain hemor- 
rhagic areas. Fatty degeneration, softening, and destruction of the tissue 
are also of common occurrence. 

A section of a fully developed glioma shows under the microscope a 
network of extremely delicate glistening fibrille (Fig. 273, B), in which 
are imbedded numerous short oval nuclei. About the nuclei there is 
but a scanty amount of protoplasm, and this can be distinguished only 
with difficulty. When examined in the fresh state or after maceration 
in Miiller’s fluid it may be seen dis- 
tinetly that these nuclei belong to 
cells (astrocytes) which are charac- 
terized by a great number of fine 
processes extending in all directions, 
and often branching (Fig. 273, A). 
By proper staining-methods the con- 
nection between some of the fibres 
may be demonstrated also in sections 
(Fig. 274). 

The cells are very similar to nor- 
mal glia-cells; but are not infre- 
quently much larger, occasionally 
more plump, and some may Possess pig, 274, section of a giioma of the cerebrum, 
two, three, or four nuclei. with ‘astrocytes (Müller's fluid, haematoxylin, 

Investigations as to the develop. “Tr metal) 5m. 
ment of gliomata have proved that 
the glia-cells are the mother-cells of the tumor-cells. The ganglion-cells 
do not take any part in the proliferative process. Within the tumor 
there may be found cavities lined with ependyma-epithelium (Stroebe), 
and this may be regarded as evidence of their connection with some dis- 
turbance of development of the brain or spinal cord. The mumber of 
cells in a glioma varies greatly. At times the cells greatly predominate, 
at other times the fibrille. A simultaneous proliferation of the cells of 
the perivascular connective tissue leads to the formation of gliosarcomata. 

The glioma usually oceurs singly, and does not produce metastases, 
Traumatism may furnish the exciting cause for its development. 

The term glioma is also applied to certain tumors of the retina oceur- 
ring during childhood. These growths, a certain portion of which are 
of congenital origin, are evidently to be referred to some disturbance in 
the development of the retina. They form cellular, soft, white or reddish 
tumors, the greater part of which consi of small, round or irregular 
cells poor in protoplasm, resembling the cells of the stratum granulosum. 
In part they possess smaller or larger processes. These cells are found 
best preserved in the neighborhood of the blood-vessels, while in other 
portions of the tumor they often show retrograde changes. The tumor 
may also contain ganglion-cells, cylindrical cells, and peculiar rosette 
and ribbon-like cell-formatious (Wintersteiner), these latter being re- 
garded as aggregations of rods and cones. Wintersteiner has, therefore, 
designated the tumor a neuroepithelioma. 

The glioma of the retina often shows areas of necrosis in its central 
portion. In its growth it may break into the retrobulbar space, or for- 
ward through the cornea and sclera; it recurs after operation, and gives 
rise to metastases. 

A neuroglioma ganglionare (Fig. 275) is a tumor of the central 
nervous system, composed of hyperplastic glia-tisaue, ganglion-cells, and 










































NEUROMA AND NEUROFIBROMA. 411 


Literature. 
(Glioma and Neuroglioma. ) 
Baumann: Zur Kenntniss der Gliome u. Neurogliome. Beitr. v. Ziegler, ii., 1888, p. 


Eisenlohr: Gliom der Netzhaut. Virch. Arch., 128 Bd., 1891. 

Emanuel: Gliom d. Pars cil. retinae. Virch. Arch., 161 Bd., 1900. 

Ernst: Missbildung d. Kleinhirns. Beitr. von Ziegler, xvii., 1895. 

Gayet ct Poncet: Gliome de la rétine. Arch. de phys., ii., 1875. 

Gerhardt: Gliome. Festschr. z. Säcularfeier der Universitat, Wtrzburg, 1882. 
Greeff: Bau d. Glioma retinae. Deut. med. Woch,, 1896. 

Heller: Hirngliom. Tagebl. d. Naturforschervers. in Freiburg, 1883. 
Hoffmann: Gliom. Zeitschr. f. rat. Med., 84 Bd.. 1869. 

Klebs: Hirngliom. Vierteljahrsschr. f. prakt. Heilk., 125 Bd. 

Neumann: Gliom der Substantia perforata. Virch. Arch., 61 Bd., 1874. 
Petrina: Gliom. Prager Vierteljahrsschr., 133, 134 Bd. 

Pusey: The Genesis of Glioma Retin in Neuroglia. Johns Hopkins Hosp. Bull., 1902. 
Reisinger: Uchber das Gliom des Rückennarks. Virch. Arch., 98 Bd., 1884. 
Rosenthal: Neurocpithelioma gliomatosum. Beitr. v. Ziegler. xxvii., 1900. 
Schüppel: Gliom u. Gliomyxom des Rückenmarks. Arch. d: Heilk., viii., 1867. 
Simon: Spinnenzellen u. Pinselzellen im Gliom. Virch. Arch., 61 Bd., 1874. 
Steinhaus: Netzhautgliome. Cbl. f. allg. Path., xi., 1900. 

Stolpe: Eigenartiges Gliom. Festschr. d. Krankenh., Dresden, 1899. 

Stroebe: Bau u. Entstehung der Gliome. Beitr. v. Ziegler, xix., 1896. 

Thomas and Hamilton: Neuroglioma of the Brain. Journ. of Exp. Med., ii., 1897. 
Virchow: Die krankhaften Geschwülste, ii., 1864. 

Wintersteiner: Neuroepithelioma (Glioma) retinae, Wien, 1896 (Lit.). 


(i) Neuroma and Neurofibroma. 


$112. The tumors designated neuromata occur most frequently on 
the ends of amputated nerves, where they form more or less prominent 
swellings, either circumscribed or blending into the surrounding tissue 
without any clearly defined demarcation. Froin the conditions of their 
origin they are known as amputation-neuromata (Fig. 276, 5b). Thedevel- 
opment of these neuromata is to be referred to the changes taking place 
after the nerves have been severed; during the development of connective 
tissue in the stump the ends of the axis-cylinders of the proximal portion 
of the affected nerve divide and grow longitudinally, so that the scar- 
tissue comes to be penetrated by nerves which at first have no sheaths, 
but are soon surrounded by medullary sheaths. The mass of nerves 
penetrating into the granulation tissue may be large or sınall, so that the 
connective tissue after a certain length of time may contain a very rich 
supply of nerves, which, radiating from the end of the old nerve, extend 
into the connective tissue in all directions (Fig. 276, 6). The process 
is, therefore, an example of a useless regenerative proliferation of a nerve- 
stump exceeding the physiological needs. 

As another form of so-called neuromata are classed those growths 
developing spontaneously, without external cause, along the course of 
nerves; and which consist essentially of an increase in the connective tissue 
of the nerve, usually of the outer, more rarely of the inner layer of the 
endoneurium. 

At the point of tumor-growth the nerve-bundles become surrounded 
by a more or less thick layer of connective tissue, which is usually loose, 
more rarely dense (Fig. 277, b, d), or the bundles may be split apart 
into their individual fibres (c). Occasionally the perineurium takes 
part in the proliferation. In the case of large nerve-trunks the epineu- 
rium may be affected in association with the endoneurium and perineu- 


413 TUMORS. 


rium of the individual bundles, although the process is most frequently 
confined to the endoneurium. . 

According to their structure these tumors are not true neuromata, 
but are neurofibromata or fibromata of the nerves. They are usually 
of multiple occurrence, and may extend throughout the entire peripheral 
nervous system, but are more often limited to a definite area of nerve- 
distribution. In very rare cases they occur in the nerve-roots and spinal 
cord. The nodules are sometimes situated along the course of the 
nerve-trunks, sometimes on the finer 
branches, most frequently of the cutai.e- 
ous nerves; and in the skin form more or 
less numerous, larger or smaller, tumor- 
nodules, for the greater part of soft con- 
sistence, to which the designation multi- 
ple fibromata of the skin is usually 
applied. The smallest nodules can be 
seen only with the microscope; the ma- 
jority vary in size from that of a pea to 
that of a hazel-nut. Individual tumors 
may reach the size of a man’s fist, the 
nerve-fibres being wholly lost sight of in 
the great mass of connective tissue. At- 
rophy of the fibres may be caused by the 
increasing connective tissue, the fibres 
finally vanishing completely. In addi- 
tion to the formation of circumscribed 
nodules there may occur also in the af- 
fected area a diffuse thickening of the nerves 
from hypertrophy of their connective tissue. 
Moreover, with this condition there may 
be associated a hypertrophic prolifera- 
tion of the connective tissue of the skin 
and subcutaneous tissue, leading to ele- 
phantiasis-like thickenings of the skin, 

A third form of false neuroma is the 
cirsoid neuroma (Bruns) or plexiform 
neuroma (Verneuil), a tumor formation 
which is characterized by the develop- 
ment in the domain of one or more nerve- 
Dranches of a convolution of tendril-like, 
Fig, 226 tn of he twisted or interwoven, thickened and 
70, Lengitudinal section. a. nodular nerv ands (Fig. 278). When 
n been hardened in examined in detail this formation is also 

found to depend essentially upon a fibro- 

matosis of the nerves (Fig. 277), the pro- 

liferation of the endoneurium resulting partly in a diffuse and partly 
in a nodular thickening of the nerves. In addition, it may be found 
in such formations that the nerves of the affeeted area are lengthened 
and thereby rendered tortuous, while at the same time the nerves are in- 
creased in number, that the number of the nerves of the skin and 
subcutaneous tissues is greater than under normal conditions. The con- 
dition must, the pre, be regarded as one of true neuroma, a neuroma 
verum associated with a fibromatosis. The nerves are for the greater part 
medullated (neuroma myelinieum). It is very diflicult to determine to 



































414 TUMORS. 


glion-cells. These tumors consist of connective tissue, non-medullated 
and medullated nerve-fibres, and ganglion-cells which resemble those of 
the sympathetic ganglia. 

Both the neurofibroma and the true neuroma are, as regards their origin, 
to be referred to a congenital anlage. They form no metastases, but cases 
occur in which neurofibromata take on a sarcomatous character and 
thereby become malignant. 


Literature. 


(Neuroma and Nesrofibroma. ) 


Aschoff: Geschwülste. Ergebn. d. allg. Patlı., v., 1900. 

Beneke: Gungliöse Neurome. Cbl. f. allg. Path., ix., 1898. 

Borst: Neuroma ganglionare. Sitzber. d. phys.-med. Ges., Würzburg, 1897. 

Bruns, P.: Ueber das Rankenneurom. irch. Arch., 50 Bd., 1870; Beitr. z. klin. 
Chir., viii., 1891; Arch. f. klin. Chir., 42 Bd., 1892. 

v. Büngner: Multiple Neurofibrome. Langenbeck's Arch., 55 Bd., 1897. 

Busse: Neuroma gangljocellulare d. Sympathicus. Virch. Arch., 151 Bd., Suppl., 
1898. 

Courvoisier: Die Neurome, Basel, 1886. 

Czerny: Neurotibrom. Arch. f. klin. Chir., xvii., 1874. 

Esmarch u. Kulenkamp: Die elephantiastischen Formen, Hamburg, 1885. 

Goldman: Beitr. z. Lehre von den Neuromen. Beitr. v. Bruns, x., 1892. 

Haenel: Neuroganglioma myelinicum. Arch. f. Psych., 31 Bd.. 1898. 

Herczel: Ueber Fibrome u. Sarkome der peripheren Nerven. Beitr. v. Ziegler, viii., 
1890. 

Jordan: Elephantiasis congenita. Beitr. v. Ziegler, viii., 1890. 

Knauss: Echte multiple Neurome. Virch. Arch., 153 Bd., 1898. 

Krause: Ueber maligne Neurome, 1887. 

Lecroix et Bonnaud: Névrome plexiforme amyélinique. Arch. de med. exp., ii., 
1880. 

Petrén: Multiple allgem. Neurome. Nordiskt Med. Ark., 1897. 

Preble and Hektoen: Multiple Fibromata of the Nerves, etc. Trs. Ass. of Amer. 
Phys., 1900 (Lit.). 

v. Recklinghausen: Ucber die multiplen Fibrome der Haut. Berlin, 1882. 

Schmidt: Ganglienzellenhalt. wahres Neurom d. Sympathicus.  Virch. Arch. 155 
Bd., 1899. 

Stiénon: Etude sur In structure du nevrome, Bruxelles, 18883. 

Strube: Combinat. v. Neurofibrom mit Gliom. d. Rückenmarks. Virch. Arch., 151 
Bd., Suppl., 1898. 

Thomson: On Neuroma and Neurofibromatosis, Edinburgh, 1900. 

Verneuil ct Depaul: Bull. de la soc. anat., Paris, 1857. 

Virchow: Die krankh. Geschwülste, iii.; Das wahre Neurom. Virch Arch., 13 Bd., 
1858. 

Westphalen: Multiple Fibrome der Haut. u. der Nerven mit Uebergang in Sarkom, 
und Metastasenbildung. Virch. Arch., 110 Bd., 1887. 

Weichselbaum: Gangliöses Neurom der Nebenniere. Virch. Arch., 85 Bd., 1881. 


(k) Sarcoma. 


x 113. A sarcoma is a connectire-tissue tumor whose elements, either 
because of their number or often because of their size, predominate over the 
intercellular substance. Sarcomata are closely related to the undeveloped 
connective tissues, so that sarcomatous tissue may be compared with em- 
bryonal tissue. 

Sarcomata develop either in previously normal tissue belonging to 
the connective-tissue group—as, for example, in the skin, subeutaneous 
tissue, Intermuscular connective tissue, periosteum, spinal cord, menin- 
ges, connective tissue of the glands, ete.—or in some preéxisting con- 
nective-tissue tumor, as a fibroma, myoma, chondroma, hypertrophic 
Iymphangioma, ete. The transformation of the parent tissue into tumor 





SARCOMA. 415 


tissue takes place through tlıe growth and multiplication of the existing 
cells. The division of the cells takes place chiefly by mitosis, and mitoses 
are the more abundant the more rapid the growth of the tumor. In 
addition to typical mitoses there are frequently observed atypical forms, 
also nuclear fragmentation, and more rarely segmentation. 

In their fully developed state sareomata form more or less sharply 
circumscribed growths. They may appear in any portion of the body 
where connective tissue is present; but are found in certain tissues more 
frequently than in others. Thus, for example, they are found much 
oftener in the skin, faseia, intermuscular connective tissue, bone-inar- 
row, periosteum, brain, and ovaries, than in the liver, intestines, uterus, 
and Jungs. 

The development and form of the cells vary greatly in different 
sarcomata. The intercellular substance is sometimes very scanty, soft, 
and deheate; at other times more abundant and in character resembling 
the ground-substance of the mature normal connective-tissue substances. 

The amount of the intercellular substance has a marked influence 
upon the consistence and color of the tumor. The medullary forms are 
soft and very cellular, and poor in intercellular substance; on section 
they present a marrow-like white or grayish-white surface. The hard, 
dense forıns, on the other hand, are poor in cellsand rich in fibrous inter- 
cellular substance; they pass by insensible gradations into fibromata: 
Transition-forms are known as fibrosarcomata. The cut surface of a 
sarcoma presents a nearly uniform appearance, in case retrograde changes 
or differences in the blood-content do not cause alterations of the same; 
it is usually uniformly smooth, in the medullary forms milk-white, in 
the firmer varieties clear grayish-white, somewhat translucent, or more 
of a clear grayish-red or grayish-broyn color. The hard forms are glis- 
tening white or yellowish- white. 

The development of the blood-vessels varies greatly; sometimes the 
vessels are very numerous, large, aud ectatic (teleangiectatic sarcoma). 
Usually the vessels have walls easily distinguishable from the tumor tis- 
sue; but the tumor-cells may also constitute the outer cells of the vessel- 
wall; and in such a case the cells of the vessel-walls also take part in 
the growth of the tumor. | Lymph vessels have not been demonstrated in 
Sarcornata. 

Retrograde changes—such as fatty degeneration, mucous degenera- 
tion, liquefaction, caseation, necrosis, hemorrhage, gangrene, ulceration, 
ete. —are of frequent occurrence in sarcomata. 

The sarcomatous tumors may be divided into three classes. The first 
of these includes the simple sareomata, or sarcomata in the narrower sense 
—that is, tumors of the type of embryonal connective tissue, showing a. 
more or less uniforin distribution of the cells without the formation of 
distinet groups of cells. The second class ineludes those sarcomata 
which show a special arrangement and grouping of the individual elements, 80 
that tumor-formations arise which are very similar to the epithelial 
tumors. The third class is characterized by the appearance of secondary 
changes in the cells, in the intercellular substance, and inthe blood-vessels, these 
changes giving to the tumors concerned a characteristic appearance. 

The etiology of sarcomais not a simple one. Itoccurs more frequently 
in youth than in old age. Some sarcomata develop even in embryonic 
life, and the origin of such may be referred to some local malformation. 
Occasionally trauma appears to be an exciting cause. A parasitic origin 
has not been demonstrated (see Etiology of Carcinoma). Usually only 








418 TUMORS. 


pure white color. In general, these sarcomata are more benign than the 
round-celled varieties, but their character in this respect varies according 
to their location and their richness in cells. 

According to the size of the cells there may be distinguished large 
spindled-celled and small spindle-celled sarcomata. Through the teas- 
ing of small pieces of the tumor the cells may in part be isolated, and in 
this way very long spindles may be obtained (Fig. 283). The cells lie 
side by side with their flat sides approximated, and are grouped in bun- 
dies, which, in sections, are cut partly longiiudinally, partly transversely, 
and partly obliquely—evidence that they are interwoven in different 
directions. 

The arrangement of the spindles in bundles is often very striki 
in other cases it is wanting; and the spindles for considerable dist: 
run in the same direction. Sometimes the direction of the spind 
determined by the direction of the blood-vessels—that is, the indiv 
bundles form sheaths about their respective blood-vesse 

Between the spindles there is often but a very scanty intercellular 
substance, or it may not be possible to demonstrate in sections the pres- 
ence of such. In other cases it may be more abundant, and show a fibril- 
lar character. The cells in such cases have less protoplasm, so that often 
it is scarcely possible to demonstrate any protoplasm around the nucleus, 
and the processes at the poles of the cells seem to spring directly from 
the nucleus (nuclear fibres). Such varieties are dense and hard. They 
represent the connecting-link bw 
tween sarcomata and fibromata, 
and are designated fibrosarcomata. 

Sarcomata with polymorphous 


& 
2 


Fig. 29. Spindle-cells from a large spindle-celled sarcoma of the ch 












Fig, 2h 





ek ‘teased preparation), X 409, 
Fig, 24. Cells fron a myelogenous giantcelied sarcoma of the bla. (Hiematoxylin.) < 400, 





n spin- 
1-forms 


cells are found also among the spindle-celled forms; and con 
dle-shaped, pyramidal, prismatic, stellate, and very irregular ce) 
(Fig. 284). 

Both in polymorphous- and spindle-celled 
found more or less numerous giant cells ( 
the designation giant-celled sarcoma may be 








mata there may be 
>82, 284, and 285), so that 
applied to these tumors, 








420 TUMORS. 


v. Karwowski: Ucber Callustumoren. Inaug.-Diss., Freiburg, 1895. 

Langhans: Das maligne Lymphosarkom. Virch. Arch., 49 Bd., 1872. 

Lartigau: Primary Sarcoma of Thyroid. Amer. Journ. of Med. Sc., 1901 (Lit.). 

Linser: Sarkom der Haut mit Schrumpfung. Beitr. v. Bruns, 26 Bd., 1900. 

Lowenthal: Traumat. Entstehung d. Geschwilste. Langenbeck's Arch., 49 Bd., 
1875. 

Manz: Riesenzellensarkom d. Brustdrüse. Beitr. v. Bruns, xiii., 1895. 

Neumann: Sarkome mit endothelialen Zellen. Arch. d. Heilk., xiii., 1892. 

Paltauf: I,ymphosarkom. Ergebn. d. allg. Path., iii., 1897. 

Pawlowski: Parasitäre Einschlüsse in sarkomatésem Gewebe. Virch. Arch., 133 Bd., 
1893. 

Perl: Surkom der Vena cava inferior. Virch. Arch., 53 Bd., 1871. 

Putiata-Kerschbaumer: las Sarkom des Auges, Wiesbaden, 1900. 

Sänger: Sarcoma uteri deciduo-cellulare. Arch. f. Gyn., 64 Bd., 1898 (Lit.). 

Schmidt: Ueber das Angiosarkom der Mamma. Langenbeck’s Arch., xxxvi., 1888. 

Sokolow: Ueber die Entwickelung des Sarkoms in den Muskeln. Virch. Arch., 57 
Bad... 1873. 

Spiegelberg : Multipel auftretende Knockensarkome. Inaug.-Diss., Freiburg, 1894. 

Steudener: Beiträge zur Onkologie. Virch. Arch., 59 Bd., 1874. 

Tillmanns: Beitr. z. Lehre v. d. Sarkomen. Arch. d. Heilk., xiv., 1873. 

Trambusti: Bau u. Theilung d. Sarkomzellen. Beitr. v. Ziegler, xxii., 1897. 

Virchow: Die krankhaften Geschwülste, 2 Bd., 1864. 

Wieland: Primär multiple Knochensarkome. Inaug.-Diss., Basel, 1893. 

Williams: Histologie u. llistogenese d. Uterussarkoms. Zeitschr. f. Heilk., iv., 
1304 (Lit.). 

See also 8$ 115-117. 


$ 115. Sarcomata which present an organoid structure appear in 
those forms known as alveolar and tubular sarcomata. These are con- 
nective-tissue tumors in which the cellular elements, especially the larger 
cells, are arranged in groups, so that it is possible to distinguish a vas- 
cular connective-tissue stroma and strands or nests of cells. According to 
their genesis, these growths may be divided into two types: lymphangiosar- 
coma and hemangiosarcoma. There are, however, also alveolar sarcomata 
which possess stroma and cell-nests, but which, in so far as their devel- 
opment is concerned, cannot be included with the above-named types. 

The lymphangiosarcomata are tumors which arise from a prolifera- 
tion of the endothelium of the lymph-vessels and lymph-spaces. They may 
accordingly be designated as lymphangioendotheliomata or as endo- 
theliomata in the narrower sense. They may develop either in previously 
normal tissue, or in preexisting tumor-like formations, such as the hy- 
pertrophic lymphangioma in particular (pigmented moles and warts, 
see $109), and also from myxochondromata. The first occur particularly 
in the meninges of the brain, and in the serous membranes of the great 
body-cavities; but may develop also in other organs; the second are 
found chiefly in the skin; while those arising from myxochondromata 
develop in the mixed tumors of the salivary glands, palate, and orbit. 

The endotheliomata of the inner meninges of the brain and spinal cord 
occur partly as nodular growths and partly as flattened proliferations; 
they develop through the transformation of the flattened endothelium, 
which covers the connective-tissue net work of the subarachnoideal tissue 
and pia, into cubical or even cylindrical cells (Fig. 286, d, e). In con- 
sequence, the new-growth at first presents the appearance of gland-like 
formations; in the event of a more active proliferation solid nests of cells 
are formed. Inasmuch as the pia is continued as a lymph-sheath around 
the cerebral vessels, there are formed around the latter strands of large 
epithelial-like cells (Fig. 286, f, 9, h). 

The endothelioma of the dura mater arises through a proliferation of the 
endothelium of the lymph-vessels, and leads, through the filling up of 















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Taw f Fostoria rn Mute Mace Med Jucm 


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Nnart- Wipe Ensraisen erXrtarı Lesers ich 36 Bad. 1987. 
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Schalz, R.: fru Brsrrevar fa. ar. IS 
Teneke Fniciwoee mad Han. Dent. Zeitsesr. f. Chir. 51 BL, 1500. 
Tuizura. 1.7 (an.ii un prinams Peomeniituesms Imng.-Dim. Freibare. 


Volkmann. Errskeiiaie fach . Dent Zeitschr. 2. Chir.. 41 Bd. 1906 (Lit... 
. Waslsch A... weinen Narticnterh. bina. Gschw. Arch f Derm. 49 Bd. 1509. 
" Warthin: Foveie cma of the Lachrymal Glesi Arch .f Upbth. 1901. 

Bram, £2 11M acad 156, 





2116. The hemangiosarcomata represent a group of organoid sar- 
wnnata, in which the walls of the blood-vessels and their surrounding 





Fie TO tien seemed ene 
Fu baad 





lina of the kidney (formalin, haem 
rain Ulieel With proliferated cnduthe 


oxsiin, eosin). a, Versels Lil 
Leells, A SW. 














ENDOTHELIOMA. 427 


may so occur that the tumor throughout bears the character of a heman- 
giosarcoma; but it also happens that such proliferations of the vessels 
form only asingle feature of other 
tumors (Figs. 293, c, d; 300, d); 
and though this feature indeed 
gives character to individual por- 
tions, it is, on the whole, over- 
shadowed by other features of the 
growth—as, for example, & fibro- 
cellular tissue, cartilage (Fig. 
293, a, b), or myxomatous tissue 
(Fig. 300, a). 
Lymphangiosarcomata and 
hemangiosarcomata cannot al- 
ways be sharply differentiated 
from each other, and tumors 
oceur to which both designations 
may be applied with propriety. 
The perivascular development of 
the endothelial proliferation with- 
in the brain in endothelioma of 
the pia (Fig. 286, f, gh) would 51, 4 srvootar melanatie sarcoma of the skin 
justify also the application of the (alcohol, hematoxylin). a, Mononuclear, a), multl- 
term hemangiosarcoma. ee arama colgf eat ae DEE, 
If in a lymphangiosarcoma of and pigment. x 30. 
the skin there is such a rapid de- 
velopment of the cell-nests that the space between the vessels becomes 
wholly filled with cells, so that the framework of the tumor comes to 
consist only of blood-vessels (Fig. 294), it becomes an open question as 
to whether the tumor should be called a Iymphangioendothelioma or a 
hemangiosarcoma. 





Literature. 
(Hemangiosarcoma [ Endothelioma]. ) 


Arnold: Primäre Angiosarkome der Leber. Beitr. v. Ziegler, viii., 1890. 
Borrmann: Blutgefässendotheliom. Virch. Arch., 151 Bd., 1898; Wachsthum d. 
Gefässgeschwülste. Ib., 157 Bd., 1899. 
Harris: Malignant Disease of the Pleura. Journ. of Path. 
vy. Heinleth: Perithelioma gland. caroticae. Cbl. f. allg. 
Hildebrand: Tubuläres Angiosarkom der Knochen. Deut. Zeitsel 
1890; Nierentumoren. Arch. f. klin. Chir., 47 Bd., 1894. 
v. Hippel: Zur Casuistik der Angiosarkome. Beitr. v. Ziegler, xiv., 1898. 
Jarisch: Hautgeschwülste (Hämangioendotheliom). Arch. f. Derm., 28 Bd., 1894. 
Jolly: Angiome sarcomateux. Arch. de med. exp., vii., 1895. 
Kolaczek: Ueber das Angiosarkom. Deut. Zeitschr. f. Chir., ix. and xiii, 
Limachet: Blutgefässendotheliom. Virch. Arch., 151 Bd., Suppl., 1898. 
Low and Lund: Tubular Perivascular Sarcoma. Journ. of Med. Res., 1902. 
d: Anat. d. Glandula carotica. Intern. Beitr., Festschr. f. Virchow, ii., 
1891. 
Maurer: Beitr. z. Kenntniss des Angiosarkoms. Virch. Arch., 77 Bd., 1879. 
Neumann: Ucber Sarkome mit endothelialen Zellen. Arch. d. Heilk., 
Paltauf: Geschwülste der Glandula carotien (Angiosarkom), Betr. v. Ziegle 
1892, 








„ 1893. 
th., xi., 1! 















1900. 
Chir., 31 Bd., 











xi., 


de Paoli: Primäres Angiosarkom der Niere. Beitr. v. Ziegler, x., 1891. ri 

Putiata: Ueber Sarkome der Lymphärüsen. Virch. Arch., 69 Bd., 1877. 

Ritter: Fetthaltiges Endotheliom der Knochen. Zeitschr. f. Chir., 50 Bd., 1899. 

Sailer: Primary Endothelioma of Left Sup. Pulm. Vein. Cont. from the Willian 
Pepper Labor., 1900. 





430 ‘TUMORS. 


ence in the cells of small shining spherules which give the microchemical 
reactions of fat. In harmony with this view is the fact that the color 








Fra. png Jarge-cellod sarcoma of the tibia (MOller’s Nuld, hematoxylin, coatn). a. Poty- 
morphous tunorecin’ b, altcolar stroma; © Lraprulle of srume ooutsioloRalaall calcareous Sones. 
Uons; d, petrifying trabecube of the stroma. "x 38. 


disappears in alcohol. On the other hand, von Recklinghausen holds 
that the color is a property of the parenchyma. 

Osteoid sarcomata develop in the bone-marrow and periosteum, and 
are characterized by a thickening of the ground-substance in certain 
areas, so that there are formed trabecule of osteoid tissue (Fig. 297, db). 
Such tumors are closely related to the osteosarcomata but differ from 
them in the absence of deposits of lime-salts. 

Petrifying sarcomata likewise occur most frequently in connection 
with the skeleton, and are characterized by the development between the 
tumor-cells of trabecule of a deli- 
cate ground-substance (Fig. 298, 
c), through the calcification (d) of 
which the tumor tissue becomes 
hardened, although no typical 
bone is formed. 

Psammomata or sand tumors 
(acervulomata) are sarcomata or 
fibrosarcomata of the dura, in- 
ner meninges, or pineal gland, 
which contain concretions of lime- 
sults in greater or less abundance. 
Some of these concretions are sim- 
ilar in. structure to the normal 
0. 290. Section from a psammoma of the dur  brain-sand, the basis of their for- 


mater (alronoly pierie acid, hematoxstn, ein). te in-sand, f 
ited spherule inclosing calcareous con: mation being concentric layers of 
‘porter Inckontin torn connective tie Cells Which have undergone hya- 
Penner tisues deapieute of Im In the inner Line degeneration (Fig. 299, a, 
tive tissue; ¢, splculé with three concretions. < 18. d, €). Occasionally the chalky 
spherules lie inside of individual 
cells and represent hyaline products of the cells which have later become 
ealeified. Others are more of the nature of spicules (d), and arise 
through the deposit of lime-salts in connective tissue or blood-vessels 
which have undergone hyaline degeneration. 





















432 TUMORS. 


Ribbert regards the melanosarcoma as an especial form of tumor arising from the 
chromatophores, and would for this reason separate it from the sarcomata as an individ- 
ual tumor-type. It is to be noted, however, that in the development of the melanotic 
sarcoma other cells besides the chromatophores take on proliferative activity: so that 
melanotic sarcomata can be regarded only as sarcomata in whose development certain 
cells, which possess the power to form pigment, have taken part. 


Literature. 


( Melanotic Sarcoma. ) 


Achenbach: Orbitales Melanosarkoın. Virch. Arch., 143 Bd., 1896. 

Dietrich: Beitr. z. Statistik u. klin. Bed. melanot. Geschwülste. Arch. f. klin. Chir., 
xxv., 1867. 

Dobbertin: Melanosarkom d. Kleinhirns. Beitr. v. Ziegler, xxviii., 1900. 

Eberth: Ueber die embolische Verbreitung der Melanosarkome. Virch. Arch., 58 Bd., 
1878. 

Gonin: Sarcome pigmenté de la cornée. Beitr. v. Ziegler, xxiv., 1898. 

Hirschberg u. Birnbacher: Sarcoma melan. corp. cil. et chorioideae. Cbl. f. 
Augenheilk., 1884. 

Just: Ueb. d. Verbreit. d. melanot. Geschw. im Lymphgefässsystem. Inaug.-Diss., 
Strassburg, 1888. 

Kolaczek: Zur Lehre von der Melanose der Geschwilste. Deut. Zeitschr. f. Chir., 
xii. 

Leber: Aderhautsarkome. Arch. f. Opbthalm., 44 Bd., 1897. 

Martens: Entwickelung d. Melanosarkoms d. Chorioidea. Virch. Arch., 138 Bd., 
1894. 


Maurer: Beitr. z. Kenntniss der Angiosarkome. Virch. Arch., 77 Bd., 1879. 

Mörner: Zur Kenntn. d. Farbstoffes in melan. Geschw. Zeitschr. f. phys. Chem., 11 
Bd., 1887. 

Oppenheimer: Pigmentbildung in melanot. Geschwülsten. Virch. Arch., 106 Bd., 
1886. 


Putiata-Kerschbaumer: Das Sarkom des Auges, Weisbaden, 1900. 

Ribbert: Das Melanosarkom. Beitr. v. Ziegler, xxi., 1897. 

Schalek: Contribution to the Histogenesis of Melanotic Sarcoma of the Skin. Journ. 
of Cutan. and Genito-urinary Diseases, 1900. 

Steinmetz: Ein Fall von Melanosarkom mit ausgedehnter Metastase. Inaug.-Diss., 
Freiburg, 1891. 

Virchow: Die krankhaften Geschwülste, ii., 1864. 

Wagner: 19 Fälle von Melanosarkom. Münch. med. Woch., 1887. 

Wallach: Beitr. z. Lehre vom Melanosarkom. Virch. Arch., 119 Bd., 1890. 

Wiener: Melanosarkom d. Rectums. Beitr. v. Ziegler, xxv., 1899. 

Williams: Melanotisches Uterussarkom. Zeitschr. f. Heilk., xv., 1894. 


(Chloroma. ) 


Chiari: Chlorom. Zietschr. f. Heilk., iv., Prag, 1883. 

Dock: Chloroma and its Relation to Leukemia. The American Journ. of the Med. 
Sc., 1893. 

Dressler: Ein Fall v. sogenanntem Chlorom. Virch. Arch., 35 Bd., 1866. 

Höring: Zur Kenntn. d. Chloroms. Arb. her. v. Baumgarten, i., Braunschweig, 
1891. 

Huber: Ueb. d. sog. Chlorom. Arch. d Heilk., xix , 1878. 

v. Recklinghausen: Tagebl. d. 58 Naturforschervers. in Strassburg, 1885. 

Virchow: Die krankh. Geschwülste, ii., 1864. 

Waldstein: Chlorolymphom. Virch. Arch., 91 Bd., 1888. 


( Psammoma. ) 


Arnold: Zur Lehre v. d. Bau u. d. Entwickelung d. Psammome. Virch. Arch., 52 
Bd., 1871. 

Ernst: Ueber Psammome. Beitr. v. Ziegler, xi., 1892. 

Golgi: Bau u. Entwickelung des Psammoms. Virch. Arch., 51 Bd., 1870. 

Levi: Untersuch. über d. Bau u. d. Entstehung d. Concretionen in Psammomen der 
Dura mater cerebri u. d. Kalkplättchen der Arachnoidea spinalis. Inaug.-Diss., 
Freiburg, 1891. 


THE EPITHELIAL TUMORS. 438 





Linser: Verkalkte Endotheliome. Beitr. v Bruns, xxvi., 1900. 
Petroni: Sarcome angiolithique. La Roumaine méd., 1898. 

Steudener: Zur Kenntnis der Sandgeschwülste. Virch. Arch., 51 Bd., 1870. 
Virchow: Die krankhaften Geschwülste, ii., 1864. 


(Sarcoma with Hyaline Formations.) 


Billroth: Untersuchungen über die Entwickelung der Blutgefässe, 1866. 
Dagonet: Cylindrome de la dure-mére, Arch, de méd. exp. Iv., 189% 
bowsky: Cylindrom der Nase. Zeitschr. f. Chir., 88 Bd., 1891. 

Ewetsky: Zur Cylindromfrage. Vi 877. 

Franke: Beitr. zur Geschwulstiehre. Virch. Arch., 121 Bd., 1890. 

Friedlander: Geschwülste mit hyaliner Degenerati 

Koester: Kankroid mit hyaliner Denegeration. Virch. Arcl 

Lubarsch: Krebs des Ileums. Virch. Arch., 111 Bd.; Cy 
1890. 

Maier: Beitrag zur Cylindromfrage. Virch. Arch., 14 Bd., 1858. 

Malassez: Sur les cylindromes. Arch. de phys., 1888. 

Marchand: Endetheilom d. Antrum Highmori mit hyalinen Kugeln. Beitr. v. 
iegler, xiii. 

Pagenstecher: Beitrag zur Geschwulstichre. Virch. Arch., 45 Bd., 1889. 

Sattler: Ueber die sog. Cylindrome, Berlin, 1874. 

See also &$ 115 and 116. 












67 Ba., 1876. 
1887. 
Tb., 122 Bd, 








2. THE EPITHELIAL Tumors. 
(a) General Remarks. 


§ 118. The epithelial tumors are new growths, in the formation of 
which both vascular connective tissue and epithelial cells—that is, cells 
which are derived from either superficial or glandular epithelium—take 
part. The distribution of epithelium and connective tissue follows in 
general the normal arrangement of these tissues, the connective tissue 
either forming a basement structure whose surface is covered with epi- 
thelium (skin and mucous membranes), or forming a network or stroma, 
in the meshes of which the epithelial cells are disposed (glands). The 
imitation of the first-named structure leads to the formation of papillary 





Fro, 91,—Papillarg epithellom or Ichthyotie wart of the skin (Miller's Auld. hematoxylin, eosin). a, 
Pia fut br enlarged paplilary body; cy laminated horny layer. 


new-growths; that of the second, to the formation of more or less 
sharply circumscribed nodules or to extensive superficial thickenings 
of tissue. 

According to the physical characteristics and grouping of the epi- 
thelial cells, as well as the clinical behavior of these tumors, epithelial 
new-; “growths may be divided into two groups; one group including the 





PAPILLARY EPITHELIOMA. 435 


layers lie at right angles to the surface of the skin, leads to the forma- 
tion of a eutaneous horn or cornu eutaneum (Figs. 123 and 124). 

Papillary epitheliomata of the mucous membranes occur either 
in the form of warty, nodular formations (Fig. 303, e, f), or in that of 
long, slender, papillary excres- 
cences (Fig. 304, a), which, 
springing from a narrow base, 
are often repeatedly branched. 
The former variety is found es- 
pecially frequently in the lar- 

















Fig, 308. FIG, 304. 
Fic. 38.- Papillury eplthelioma of the 
lage: d, track 






nx. a, Epigiottix : D. omitled erieold cartilage ; ¢, thyrold carti- 


papillary proliferations. Natural size. 


Fic, 301.- Papillary epithelioma of the urinary bladder. a, Eplthetioma Bc, enlarged prostate; dy 
thickened bladder-wall. Five-sixths natural size, " 





ynx, more rarely in the nose and urinary bladder ; the latter most frequent- 
ly in the urinary bladder and pelvis of the kidney, vaginal portion of the 
uterus, and more rarely in the ureters, gall-bladder, and biliary passages. 

In both e: theexerescencesare formed of slender, connective-tissue 
papille (F ) which contain blood-vessels, and are covered by a 
thie er of epithelium. The character of the epithelium corresponds 
in general to that of the part in which the growth occurs, but papillomata 
covered with stratified squamous cells are sometimes seen in regions 
which normally possess cylindrical epithelium (nose). 




















Papillary epitheliomata in dilatation-cysts, which are also called 
papillary cystomata, occur most frequently in cysts of the ovary and 
in cysts of the ducts of the mammary gland, more rarely in atheromata 
) of the skin. Within the 
1 


(dermo 
vations or cauliflow 
fill the entire eyst-ca 





t are formed small, warty ele- 
¢ tumors, which under certain conditions may 
ty. Their structure corresponds to that of the 








PAPILLARY EPITHELIOMA. CHOLESTEATOMA. 437 


replaced the cylindrical epithelium, and under especial conditions (chronic inflamma- 
tions) produces the formations above described. It is probable that in rare cases they 
arise from epidermoidal cells which during the period of embryonic development have 
found their way into the cavities in question. 

The intracranial cholesteatomata are found at the base of the brain (very rarely in the 
spinal canal), in the region of the olfactory lobe, tuber cinereum, corpus callosum, in 
the choroid plexus, in the pons, medulla oblongata, and cerebellum. In these regions 
the cholesteatomata appear on the surface as silk-like, shining nodules of varying size 
which extend more or less deeply into the brain-substance. The nodules are single, 
but cholesteatoma-masses may become separated from the chief nodule and displaced 
into the neighboring tissue. According to Bustrom, it is always possible to demon- 
strate, at some point, a connection between the pia and the cholesteatoma, where the 
scales composing the cholesteatoma take their origin from a cell-layer lying upon the 
vascular connective tissue, the cells of this layer throughout bearing the character of 
epidermoidal cells. The cholesteatomata of the pia may therefore be designated as 
epitheliomata or as epidermotds (Bostrém); and their origin may be explained by the as- 
sumption that in the early period of development epidermal germs are misplaced into 
the anlage of the pia. According to Bostrom, this takes place in the time between the 
closure of the medullary canal and the separation (by a process of constriction) of the 
secondary vesicle of the fore-brain from the fore-brain or the ’tween-brain, and the separa- 
tion of the after-brain vesicle from the hind-brain (fourth to fifth week). These 
epidermoids may therefore be classed with the teratoid tumors (see Teratoma). 


Literature. 


(Papillary Epithelioma. ) 


Albarran: Les tumeurs de la vessie, Paris, 1892. 

Bergengrün: Verruca dura laryngis. Virch. Arch., 118 Bd., 1892. 

Hellmann: Papilloma durum d. Nasen- u. Stirnhöhlenschleimh. Arch. f. Laryng., 
vi., 1897 (Lit.). 

Hopmann: Warzengeschw. d. Respirationsschleimhiiute. Klin. Vortr., No. 315, 
Leipzig, 1888. 

Israel: Epithelioma folliculare cutis. Festschr. d. Assist. f. Virchow, Berlin, 1891. 

Kürsteiner: Papillome u. Krebse d. Blase. Virch. Arch., 130 Bd., 1892. 

Küster: Harnblasengeschwülste. Samml. Klin. Vortr., No. 267-68, Leipzig, 1886. 

Lange: Papillome der Mundhöhle. Deut. Arch. f. klin. Med., 40 Bd. 

Marchand: Zur Kenntniss d. Ovarientumoren, Halle, 1879. 

Pfannenstiel: Die papillären Geschwülste d. Eierstocks. Arch. f. Gyn., 48 Bd., 
1895. 

Spietschka: Histologie des Cornu cutaneum. Arch. f. Derm., 42 Bd., 1898. 

Stratz: Die Geschwülste d. Eierstocks, Berlin, 1894. 

Tschistowitsch: Wachsthum d. Zottenpoly pen d. Harnblase. Virch. Arch., 115 Bd., 
i8Sy, 

Werner: Beitr. z. Kenntniss d. Papillome d. Kehlkopfs, Heidelberg, 1894. 

Williams: Papillomatous Tumors of the Ovary. Johns Hopkins Hosp. Rep., iii., 
Baltimore, 1892. 

Zarniko: Histologie d. Nasengeschwülste. Virch. Arch., 128 Bd., 1892. 


(Cholesteatoma.) 


Beneke: Meningeale Cholestentome. Virch. Arch., 142 Bd., 1895: 149 Bd., 1897. 

Beselin: Cholesteatomat. Desquamation im Nierenbecken b. Tuberculose.  Virch. 
Arch., 99 Bd., 18805. 

Boström: Die pialen Epidermoide, Dermoide u. Lipome u. duralen Dermoide. Cbl. 
f. alle. Path., viii., 1897 (Lit.). 

Chiari: Cholesteatome des Rückenmarks. Prag. med. Woch., 1883. 

Glaeser: Untersuch. über das Cholestentom. Virch. Arch., 122 Bd., 18%. 

Gross: Contrib. ä l’Ctude des tumeurs perles, Paris, 1885. 

Haug: Das Cholesteatom der Mittelohrräume. Cbl. f. allg. Path., vi., 1895 (Lit.). 

Nehrkorn: Meningeale Perlgeschwulst. Beitr. v. Ziegler, xxi., 1891 (Lit.). 

Thomas: Cholesteatomata of the Brain. Jour. of Med. Res., 1901 (Lit.). 

Virchow: Ueber Perlgeschwülste. Vireh. Arch., 8 Bd.. 1859. 


x 120. The adenomata are usually nodular tumors with sharply 
defined borders; and are situated within glands, or in the skin or mucous 








40 TUMORS. 


normal gland tissue. The cause of the new-formation of gland tissue 
within normal organs is wholly unknown. Glandular new-formations 
developing in tissues which have been altered by inflammation, and 
which lead to tumor-like growths, may in the beginning bear the charac- 
ter of a regenerative or hyperplastic new-formation, and for this reason 
the adenomata cannot be sharply differentiated from regenerative and hyper- 
plastic proliferations. 

Tubular adenomata represent the most common form of the adeno- 
mata. They occur particularly in mucous membranes (Figs. 306 ; 307, f) 
provided with tubular glands (intestine, uterus); but are found also in 
such glands as the breast (Fig. 308), liver, ovary, and not infrequently 
in the kidneys. They are characterized by the formation of simple and 
branched gland-tubules (Figs. 306, a,b; 307 f; and 308, a, b) which are 
lined by simple columnar or eubieal epithelium and form nodular tumors 
varying in size from that of a pea to that of an apple or a man’s fist, or 
rarely even larger. 

The alveolar adenomata arise from glands (mamma, ovary, thyroid, 
sebaceous glands); and are characterized by the formation of numerous 
terminal berry-like alveoli (Fig. 309, a), as well as gland-ducts (5). 

Papillary adenomata arise through the formation within the tabules 
of an adenoma, of little elevations of epithelium into each of which a 
connective-tissue papilla grows. Through the extensive formation of 
such papille the gland-tubules may become wholly filled or even dilated 
(Fig. 310, b, e). 

The stroma of an adenoma is at times well developed, at other times 
but slightly, and consequently adenomata may be divided into hard 
(mammary gland) and soft varieties (kidney, liver, ovary, testicle). An 











FiG. 310.— Adenomu 
stroma; 2, sinuous glat 
2. 


tubulare papiliifermm (Miller's Auld, hematoxylin). a. Connective-tissue 
pules; ¢, gland-tubules with marked development of puplliary excrescences, 








especially marked development of the connective tissue leads to the for- 
mation of fibro-adenomata or fibrous adenomata. Such forms oecur most 
frequently in the mammary gland. 

If, as happens not infrequently in the man y gland, the connee- 
tive-tissue proliferation in an adenoma is not of a diffuse character but 
takes place particularly around the canaliculi (see Fig. 241), the tumor 











442 TUMORS. . 


Literature. 


( Adenoma.) 


Barlow: Adenomata sebacea. Deut. Arch. f. klin. Med., 53 Bd., 1805 (Lit.). 
Beneke: Leberadenom. Beitr. v. Ziegler, ix., 1801. 

Billroth: Tumoren der Brustdrisen. Haudb. d. Frauenkrankh., fii, Stuttgart, 1886. 
Bock: Ueber ein Adenom der TulgdrOsen, Berlin. 1890. 

Bonome: Contr. allo studio degli adenomi del fegato. Arch. per le Sc. Med., xili, 


Brinaud: Du polyadénome gastrique. Arch. gen. de méd., 1885. 
Eberth: Das m der Leber. Virch, Arch., 48 Bd., 1868. 
intestinalis adenomatosa. Deut. Arch. f. klin. Med., 55 Bd., 


1 der Leber. Virch. Arch., 89 Bd., 1867. 
Kelsch et Kiener: Contrib, a hist, de Vadénome du foie. Arch. ds phys., 1878. 
polyp des Tieums, Virch. Arch.. 88 Bd., 1 

d. Geschwülste d. Brustdrüsen. Beitr. v. Ziegler, ii., 1888. 
D » gustriques. Arch. de phys., 1., 1888. 
Nissen: Leberadvnom bei Cirriöse. Innug. Diss, Freiburg, 1898. 
v. Noorden: Dus verkulkte Epitheliom. . v. Bruns, 1888. 
Y. Recklinghausen: Die udeuoinyome u. Cystadenome d. Uterus u. d. Tube, Berlin, 


schwülste der Niere. Cbl. f, allg. Path., vii., 1807. 
1 il. Arch. f. Heilk., v., 1864. 
ig] oso del fegato. Arch. per le Se. Med., vil., 1888. 
Simmonds: Die knot. Hyperphsie u. d. Adınom d. Leber. Ärch. £. klin. Med., 34 
.. 1804. 
Bteudener: Adenom der Brustärtisen. Yirch. Arch., 42 Bd., 1968, 
Sturm: Ueber das Adenom der Niere. Arch. d. Heilk., xvi., 1875, 
Weichselbaum u. Greenish: Adeuom der Niere. Wiener med. Jahrb., 1888. 
Weigert: Adenocarcinoma congen. rents, Virch. Arch., 07 Ba, 1876. 
See also $8 119 and 121 


x 121. A cystadenoma or adenocystoma is an adenoma whose gland- 
spaces have undergone cystic dilatation through the accumulation of secretions. 
Such tumors are usually com- 
posed of numerous cysts, and 
are, therefore, designated as 
multilocular cystomata. Ac- 
cording to the character of the 
eyst-wall there may be distin- 
guished a smooth-walled or simple 
customa (cystoma simplex), or a 
papilliferous cystoma (cystoma pap- 




































Small amounts of secretion 
are often seen in the ordinary 
adenomata (Fig. 306), and the 
of both simple and pap- 
y adenomata are often so 
wide (Figs. 308, a; 311) that 
t once attract the eye on 
‘tion of the growth. In 
adenomata such eyst-forma- 
n is the predominating feat- 



















FIG. 312. Section of weystadenoma evar papiiiferum €) 
(Müller’s uid, Meematoxytiny. 






The earl) sof the cysts are ted by gland-tubules of vary- 
ing shape (Figs. 312 and 313, ), hlie in a more or less richly 
developed connective-tissue stroma, ‘Through the accumulation of seere- 




















PAPILLARY CYSTADENOMA. 447 


ance similar to that of a mucous membrane. If the excrescences develop 
in cysts of small size, they may fill these, and the tissue may thereby take 
on the appearance of a dense, non-cystic, medullary tumor, though from 
the cut surface more or less mucus can usually be obtained. 

Larger papill® are always more or less branched (Fig. 320), and con- 
sist of a cellular stroma (a), whose surface is usually covered with tall 





WA 


Fic. 321.—Paplllary adenocystoma of the ovary with myxomatous degeneration of the connective tissue 
of the people, (Müller’s Guid, hematoxylin). a, Fibrous stroma; d, pepiliae which have undergone 
myxomatous change; ¢, epithelium. 


columnar cells (c) of the character of goblet-cells. The contents of the 
cysts consist of ropy mucus (d) mingled with more or less numerous 
desquamated cells which have undergone mucous degeneration, or the 
remains of such cells. In rare cases the connective tissue of the papille 
may undergo a mucous degeneration (Fig. 321, a, b), and may swell to a 
marked degree, and finally become changed into myxomatous spheres 
covered externally with epithelium. 

Adenocystomata of the liver, testicles, and kidneys usually form no 
papille, or at most very small ones. In the papillary adenocystomata of 
the mammary gland the exerescences are usually broad and plump (Fig. 
322), as is the case with those of the papillary adenomata (Fig. 311). 
Accordingly, on the cross-section of such tumors the cyst-spaces are found 
to be filled with polypoid proliferations of various forms (Fig. 322), 
which are often flattened through mutual pressure, and give to the sur- 
face of such a cross-section a laminated appearance. 

Since in these tumors the connective-tissue elements predominate over 
the epithelial, these growths are often classed with the connective-tissue 
tumors, and designated, according to the character of the connective tis- 
sue, as cystofibroma, cystomyxoma, or cystosarcoma. When showing a 
structure of leaf-like layers they have received the name of sarcoma 
phyllodes. 

The papillary adenocystomata show a certain malignancy, even when 
the papille are covered with a simple epithelium (see cystocarcinoma). 


CARCINOMA AND CYSTOCARCINOMA. 449 


Burckhardt: Genese d. multilocul. Ovarlalcysten. Virch. Arch., 144 Bd., 1896. 

Coblenz: Kystome der Ovarien. Zeitschr. f. Geb. u. Gyn., vii., 1882; Genese u. 
Entwickelung von Kystomen. Virch. Arch., 84 Bd., 1881. 

Dmochowski u. Janowski: Totale cystische Entartung d. Leber. Beitr. v. Ziegler, 
xvi., 1894. 

Flaischlen: Multiloculäre Flimmerepithelkystome der Ovarien. Zeitschr. f. Gyn., 
vi., 1881. 

Goebel: Kieferstumoren v. Zahnsystem ausgehend. Cbl. f. allg. Path., 1897 (Lit.). 

Hess: Ucber eine subcutane Flimmercyste. Beitr. v. Ziegler, viii., 1890. 

v. Hippel: Multiples Cystenadenom der Gallengänge. Virch. Arch., 123 Bd., 1891. 

Israel: Epithelioma folliculare cutis. Festschr. d. Assist. f. Virchow, Berlin, 1891. 

v. Kahlden: Genese der multiloc. Cystenniere u. d. Cystenleber. Beitr. v. Ziegler, 
xiii., 1893; Congen. Adenom beider Nieren. Ib., xv., 1894; Entsteh. d. Ovarial- 
eysten. Ib. xxvii. 1900. 

Kocher: Die Krankheiten des Hodens, Stuttgart, 1882. 

Labbe ct Coyna: Traite des tum. bénignes du sein, 1876. 

Leser: Beitr. z. pathol. Anatomie d. Geschwülste d. Brustdrüsen. Beitr. v. Ziegler, 
ii,. 1888. 

Malassez: Maladies kystiques du testicule. Arch. de phys., 1875. 

Marchand: Beitr. z. Kenntniss der Ovarialtumoren, 1879. 

Michalowicz: Dégénérescence kystique des reins et du foie, Paris, 1877. 

Monod et Terillon: Traité des maladies du testicule, Paris, 1889. 

Nagel: Genese der epithelialen Eierstocksgeschwülste. Arch. f. Gyn., 33 Bd., 1888. 

Nauwerck u. Hufschmid: Uch. d. multilocul. Kystome d. Niere. Beitr. v. Ziegler, 
xii., 1892. 

Olshausen: Die Krankheiten d. Ovarien. Handb. d. Frauenkrankheiten, ii., Stutt- 
gart, 1886. 

Pfannenstiel: Die Pseudomueine der cystischen Ovarialgeschwülste. Arch. f. Gyn., 
88 Bd., 1890; Neubildungen des Eierstocks. Handb. d. Gynäk. v. Veit, iii., 1898. 

Ruge: Papilliformes Atherom. Virch. Arch., 136 Bd., 1894. 

Sabourin: Dégénérescence kystique du foie et des reins. Arch. de phys., x., 1882. 

Sasse: Cysten u. cystische Tumoren der Mamma. Langenbeck’s Arch., 54 Bd., 1897. 

Schmidt: Cystosarkom der Mamma. Arch. f. Gyn., xxii., 1884. 

de Sinety ct Malassez: Sur la structure, l’origine et le développement des kystes de 
l’ovaire. Arch. de phys., 1878, 1879, 1880, 1881. 

Spiegelberg: Drüsenschläuche im fötalen Eierstock. Virch. Arch., 30 Bd., 1864. 

Stratz: Die Geschwülste des Eierstocks, Berlin, 1894. 

Terburgh: Ueber Leber- u. Nierencysten. Inaug.-Diss., Freiburg, Leiden, 1891. 

v. Velits: Genese der Flimmerepithel-Kystome des Eierstocks. Zeitschr. f. Geb., 
xvii., 1891. 

Zöppritz: Multiloculäre Kiemengangscysten. Beitr..v. Bruns, xii., 1894. 

See also S 120. 


(c) Carcinoma and Cystocareinoma. 


X 122. The carcinomata are malignant epithelial tumors characterized 
by infiltrative growth and the formation of metastases. 

They develop: 

(1) In the skin, mucous membranes and in glands, all of which ap- 
peared to be normal, before the development of the carcinoma. 

(2) In the skin, mucous membranes, and in glands, which have 
already suffered chauges before the development of the carcinoma. 

(3) In already existing papillary epitheliomata, adenomata and ade- 
noeystomata. 

(4) From the remains of foetal epithelial structures, and from epithe- 
lial tissues which have been misplaced through disturbances of develop- 
ment, and have already developed into pathological formations. 

(5) From the epithelial tissues of the chorionie villi and placenta. 

The most. essential characteristic of the development of a carcinoma 
is that presented by atypical proliferations of epithelium which sooner 
or later penetrate into the tissue bordering upon the affected glands 
or surface-epithelium. This phenomenon is usually accompanied by a 
proliferation of connective tissue ; but this is not absolutely essential 


450 TUMORS. 


to the development of a carcinoma. Thetissue invaded by the epithelial 
proliferation— whether glandular tissue, muscle, bone, etc. —is sooner or 
later destroyed by the growth. 

The cause of the atypical growth of epithelium is not known with 
certainty; it can only be said that certain conditions favor such growth. 
Thus, for example, old age predisposes to the development of carcinomata 
of the skin, inasmuch as in this period of life the connective tissue of the 
skin undergoes a certain amount of atrophy and becomes looser in struct- 
ure, while the epithelium, at least in part, continues to increase, and 
under certain conditions shows here and there distinct evidences of 
increased activity (formation of heavier hairs upon the nasal septum, 
lobes of the ears, and in the eyebrows). Likewise carcinomata of the 
mucous membranes and the glands usually appear in the later years of 
life, although they may occur earlier in life, even in childhood. 

Further, the misplacement and separation of epithelium predisposes to 
the formation of cancer. Such condition may easily happen during the 
healing of ulcers, and also at the borders or on the surface of both infec- 
tious and non-infectious growths of granulation-tissue. Consequently 
carcinomata not infrequently arise in ulcers, scars, infective granulomata 
(for example, in tuberculous lupus of the skin and mucous membranes), 
or in tissues which have been changed by inflammation of any kind (for exam- 
ple, in a cirrhotic liver). 

All these predisposing factors do not constitute the unique cause of 
the development of a carcinoma. They may exist for a long time with- 
out giving rise to a cancer. It appears that something else must be 
added to cause the unlimited atypical proliferation of epithelium, and 
what this something is, is at present unknown. 

In recent years the opinion has been many times advanced and main- 
tained that parasites cause carcinomatous and sarcomatous prolifer- 
ations. But the majority of the appearances which have been described 
as parasites (as protozoa, especially sporozoa, and as yeast-fungi) have 
not been parasites at all, but degenerated nuclei and nuclear division- 
figures, or leucocytes inclosed within tumor-cells, or degeneration-prod- 
ucts of such, or products of cell-protoplasm, particularly keratohyalin 
and colloid, or epithelial hyalin and mucin. In the few cases in which 
true parasites were present in the tissues, this occurrence could very well 
have heen a secondary infection, which in no way could be regarded as a 
cause of the development of the tumor. Jn not a single case has it been 
proved beyond all doubt that parasites have been the cause of either carcinoma 
or sarcoma. 

Certain portions of the intestinal tract—the rectum, the flexures of 
the colon, the pylorus and cardia of the stomach, the csophagus, 
pharynx, tongue, and gums—are favorite seats for the development of 
cancer. Cancer may develop in any portion of the skin, but it occurs 
more frequently on the lips and nose than on the remaining portions of 
the face, or on the extremities, and on these again more frequently than 
on the trunk. Of thesexual apparatusthe parts most commonly affected 
are the mammary gland and cervical portion of the uterus; less fre- 
quently, though relatively often, the ovary, testicles, body of the uterus, 
vulva, vagina, and penis. The liver, kidneys, bladder, trachea, bronchi, 
lungs and pancreas occupy a middle ground; while the larynx and 
‘ gall-bladder are, on the other hand, more frequently affected. 

Cancer usually develops in the form of nodules, which are not sharply 
differentiated from the neighboring tissues; on the mucous membranes 


CARCINOMA. 451 


they are not infrequently elevated above the surface in the form of 
sponge-like, or polypoid, or papillary growths. From the point of origin 
they spread by an infiltrative growth of the epithelial proliferations, 
by which either the nodules increase in size or there are formed diffuse 
superficial thickenings, as in the case of the intestinal wall. The ovaries, 
testicles, uterus, kidneys, etc., may be partly or wholly transformed into 
carcinomatous tissue. Often the boundaries of the organ originally 
affected are overstepped, and the epithelial infiltration extends into 
neighboring tissues and organs. Thus, for example, a carcinoma of the 
mamma may infiltrate the neighboring fat, skin, and muscle; one of the 
gums, the maxillary bone; one of the uterus, the vagina, parametrium, 
bladder, and rectum; a cancer of the gall-bladder may involve the liver; 
one of the thyroid, the trachea; and one arising in the bronchi, the 
lungs, ete. 

The formation of metastases may take place either through the 
lymph- or blood-vessels, and is of very frequent occurrence by both 
routes. It leads to the development of secondary nodules in different 
organs; but it may happen that large lymphatic areas—as, for example, 
the lymphatics of the lung—may be simply dilated by the new-growth, 
without the formation of circumscribed nodules. The transportation of 
ecancer-cells to the bone-marrow may lead to a carcinomatous degener- | 
ation of the marrow of an entire bone or of several associated bones. 
Moreover, it should be noted that probably not every transportation of 
cancer-cells is followed by the development of a cancer, but that many 
of the cells so transplanted die. 

The tissue of a carcinoma is sometimes white and soft like marrow, 
sometimes firm and dense; but it is almost always possible to obtain from 
the cut surface more or less of a whitish, cloudy fluid called cancer juice 
or cancer milk. Very often the cut surface presents a tough, fibrous 
framework in the meshes of which the softer masses lie; and from which 
the latter may be squeezed out by pressure either in the form of fluid, or 
as plugs or as erumbling masses, 

The masses obtained from the cut surface through pressure and scrap- 
ing consist, for the chief part, of atypically proliferating epithelial 
cells, the so-called cancer-cells, which are found in a great variety of 
forms, and usually show degenerative changes, particularly fatty de- 
generation. A true secretion of these epithelial cells is usually not 
found; but cancers occur—particularly in the mucous membranes, 
ovaries, mammary glands, and thyroid—which produce mucin, pseudo- 
mucin, orcolloid. Theamount of secretion may at times be so abundant 
as to lead to the formation of cysts and thereby to cystocarcinoma. 

Retrograde changes occur very often in cancers at an early stage. 
They are caused partly by the feeble vitality of the new-growth, partly 
by circulatory disturbances, which may be due to the filling-up of capil- 
laries and veins by the ingrowing cancer-cells, and partly by external 
causes. These changes lead, in the first place, to a destruction of cancer- 
cells in certain portions of the tumor, so that, after resorption of the dead 
material, the tissues often sink in, and in this way depressions are caused 
over the surface of the tumor-nodules. Such depressed areas are seen 
particularly upon primary cancer-nodules in the mammary gland, and 
on secondary nodules in the liver, hings, and other internal organs, and 
are often spoken of as cancer-umbilications. ; 

The retrograde changes often lead to complete destruction of tumor- 
tissue, and thereby to the formation of ulcers. This occurs particularly 

25 


452 TUMORS. 


in cancers of the mucous membranes, these growths at the patient’s 
death usually revealing a more or less extensive ulceration; but such 
ulcerations also take place in carcinomata of the mammary glands and 
skin. In the latter situation the cancer may take on the appearance of 
a rodent ulcer. The edge of such ulcers is sometimes elevated and re- 
sembles a wall, or it may be studded with nodules; at other times it is 
more sharply defined and only slightly infiltrated. The base of the ulcer 
is sometimes fissured and ragged, and covered with necrotic tissue; at 
other times it is smooth. 


The question as to the etiology of carcinoma and sarcoma has led in recent 
years to numerous histological and experimental investigations, and publications in 
this line have been made by Sunfelice, Aleroli, Secchi, Plimmer, Wlaef, Sjübring, 
Schiller, Curtis, Leopold, Fahre-Domerque, Petersen and Exner, Sternberg, and others. 
While the earlier writers believed that sporozoa were to be regarded as the cause of 
carcinoma and sarcoma, recent investigators have sought to prove the etiological rela- 
tionship of yeasts or rhizopods (Sibring). Against these views, I believe, in common 
with Fabre-Domerque, Sternberg, Petersen, and Ferner, that many of the formations 
which have been described as yeasts were not such, but were cell-products resembling 
them. 

Likewise, the appearances described as protozoa are of a very doubtful nature. 
Sjobring describes them as very delicate, clear bodies which cannot be fixed; Schiller, 
as large, round, bladder-like bodies of a gold-yellow or brownish color. 

The results of attempts at cultivation and of animal experiments have shown only 
that, outside of the human body, perhaps also by chance in tumors, there are forms of 
Saccharomycetes (Saccharomyces neoformans of Sanfelice), which when injected into ani- 
mals cause inflammations and proliferations of granulation-tissue, and in part also pro- 
gressive diseases leading after weeks or months to death. The statements of Wlaeff, 
Leopold, Sanfelice, and others, that they have also produced true tumors, adenomata, 
adenocarcinomata, carcinomata, and sarcomata, give rise to well-founded doubts con- 
cerning the correctness of their interpretations, Inasmuch as the appearances described 
may very well have been inflammatory proliferations within which glands have also 
proliferated (intestinal glands, bile-ducts). The assertion of Leopold that he had been 
able, through the injection, into the testicle of a rat, of yeasts cultivated froman ovarian 
cancer, to produce a giant-celled sarcoma in the form of multiple nodules in the peri- 
toneal cavity of the animal, can hardly be taken as evidence of the parasitic nature of 
cancer. Likewise, the statement of Sjöhring that he had been able to produce in four 
mice, by means of rhizopods, a cylindrical-celled and squamous-celled carcinoma, a 
colloid cystoma, and an adenoma of the sebaceous glands respectively, is of no value, 
because of the meagreness and inaccuracy of his description. 


Literature. 


(Etiology of Carcinoma.) 


Alberts: Das Carcinom, Jena, 1887. 

d’Anna: L’eziologia del cancro. Tl Policlinico, Roma, 1894. 

d’Arcy: Some Effects of Chronic Irritation upon Living Tissues. British Med. Journ., 
ii., 1893. 

Binaghi: Blastomyceten in Epitheliomen. Zeitschr. f. Hyg., xxiii., 1896 (Lit.). 

Borrel: Sur la signification des figures décrites comme coccidies. Arch. de méd., ii., 
1890. 

Bosc: l.e cancer, mal. infect.  sporozoaire. Arch. de phys., x., 1898. 

Brosch: Genese der malignen Geschwillste. Virch. Arch., 162 Bd., 1900. 

Burchardt: Ein Coccidium im Schleimkrebs des Menschen. Virch. Arch., 181, 1893. 

Chaintre: De l’epithelioma des eicatrices. Lancet, ii., 1889. 

Claessen: Ueber die in Carcinomzellen gefundenen Eiuschlüsse. Beitr. v. Ziegler, 
xiv., 1893. 

Clarke: Observat. on the Histol. of Cancer. Chl. f Bakt., xvi., 1894. 

Debenedetti: Eziologia del cancro, Torino, 1887. 

Fabre-Domergue: Les cancers epitheliaux, Paris, 1898. 

Firket: De l’origine du cancer. Ann. de la Soc. belge d. microse., xvi., 1891. 

Foa: Sui parassiti et sulla istologia patologica del cancro. Arch. per le Sc. Med., 
xvii.; Arch. ital. de biol., xx., 1893. 


DEVELOPMENT OF CARCINOMA. 453 


Foulerton: Pathogenic Action of Blastomycetes. Journ. Path. and Bact., 1899. 

Gaylord: The Protozoon of Cancer. Amer. Journ. of Med. Se., 1901. 

Greenough: Plimmer’s Bodies in Carcinoma. Journ. Bost. Soc. Med. Sc., 1900; Cell 
Inclusions. Journ. of Med. Res., 1902. 

Hauser: Das chron. Magengeschwir, sein Vernarbungsprocess u. dessen Bezieh. zum 
Magencarcinom, Leipzig, 1883; Das Cylindcrepithelearcinom d. Magens u. d. 
Darms, Jena, 18%. 

Karg: Ueber das Carcinom. Deut. Zeitschr. f. Chir., 34 Bd.. 1892. 

Lack: Experim. Production of Cancer. Journ. of Path., vi., 1899. 

Le Count: Analogies Between Plimmer’'s Bodies and Certain Structures found Nor- 
mally in the Cytoplasm. Journ. of Med. Res., 1902. 

Leopold: Actiologie dl. Carcinoms. Arch. f. Gyn., 61 Bd., 1900. 

v. Leyden u. Schaudinn: Leydenia gemmipara. Sitzber. d. Akad. d. Wiss., Berlin, 
1896. 

Liebe: Ueber den Paraflinkrebs. Schmidt’s Jahrb., 236 Bd., 1892. 

Nepveu: Rech. hist. sur la pathogénie du cancer. Marseille méd., 1892. 

Nichols: First Annual Report on the Etiology of Cancer. Journ. Bost. Soc. Med. 
Se., 1900: Second Report. Journ. of Med. Res., 1902. 

Petersen u. Exner: Hefepilze u. Geschwulstbildung. Beitr. v. Bruns, xxv., 1899. 

Pfeiffer: Untersuchungen über den Krebs, Jena, 1893. 

Pianese: Beitr. z. Histologie u. Actiologie dl. Carcinoms, Jena. 1896. 

Plimmer: On the Etiology and Histology of Cancer. The Practitioner, 1899, 1900. 

Roncali: Actiologie des Krebses. Cbl. f. Bakt., xxi., 1897. 

Rosenthal: Mikroorganismen in Geschwülsten. Zeitschr. f. Hyg., v., 1889. 

Ruffer: Les parasites des tum. epitheliales. Traite de path. gen., ii., Paris, 1896. 

Ruffer and Plimmer: Parasitic Protozoa in Cancerous Tumors. Journ. of Path., i., 
1892; ii.. 1898. 

Sanfelice: Wirkung d. Blastomyceten. Zeitschr. f. Hyg., xxi., 1895; xxii., 1896; 
XXix., 1898. 

Schiller: Zur Aetiologie d. Geschwülste. Cbl. f. Bakt., xxvii., 1900. 

Schütz: Protozoen- u. coccidienart, Mikroorganismen in Krebszellen. Münch. med. 
Woch., 18%. 

Schulthess: Stutist. Unters. üb. d. Aetiologie d. Mammacarcinoms. Beitr. v. Bruns, 
iv., 1881. 

Schwarz: Ueber den Carcinomparasitismus, Wien, 1895. 

Sjöbring: Mikroorganismen in Geschwülsten. Cbl. f. Bakt., xxvii., 1900. 

Steinhaus: Ucber Carcinomeinschlüsse. Virch. Arch., 126, 127 Bd., 1891. 

Sternberg: Zelleinschlüsse in Carcinomen. Beitr. v. Ziegler, xxv., 1899 (Lit.). 

Steven and Brown: On the So-called Parasitic Protozoa of Cancer. Journ. of Path., 
ii., 1898. 

Strobe: Histozenese n. Aetiologie des Carcinoms. Cbl. f. allg. Path., ii., 1891 (Lit.); 
Die parasitären Sporozoen in ihren Beziehungen zur menschl. Pathologie, insbes. 
zur Histogenese u. Aetiologie d. Carcinoms. Ib., v., 1894 (Lit.). 

Thoma: Parasitiire Organismen in d. Epithelzellen d. Carcinome. Fortschr. d. Med., 
Vil., 1889. 

Volkmann: Ueb. d. primären Krebs d. Extremitäten. Samml. klin. Vortr.. No. 
334-335, 1890. 

Wlaeff: Röle des Blastomycetes dans l’organisme. Soc. An. Paris, 1900; Cbl. f. allg. 
Path., 1900. 

Zenker: Der primäre Krebs der Gallenblase u. seine Beziehung zu Gallensteinen u. 
Gallenblasennarben. Deut. Arch. f. klin. Med., 44 Bd., 1889. 


$ 123. The development of carcinoma of the skin takes place most 
often from the surface epithelium, and is characterized essentially by the 
growth of the interpapillary portions of the same into the deeper por- 
tions of the skin, in the form of epithelial plugs (Fig. 323, d) which fill 
up the connective-tissue spaces. The stratum corneum (c) may also 
undergo hypertrophy along with the cells of the rete Malpighii, and 
penetrate into the deeper tissues with the epithelial plugs (d). More- 
over, the horny cells which get into the deeper tissues may form epithelial 
pearls (e). 

Besides the surface-epithelium, the epithelium of the hair-follicles and 
sebaceous glands may also take part in the development of the cancer; 
and there occur carcinomata of the skin, which develop entirely from 











GENESIS OF CARCINOMA. 459 


stains, in an altered position and arrangement of the cells, and in their changed rela- 
tions toward the surrounding tissues. 

The traumatic displacement of surface-epithelium in wounds may lead to the forma- 
tion of the so-called traumatic epithelial cysts—that is, cysts varying in size from 
that of a hemp-seed to that of a nut, which are lined with epithelium, and, in case they 
arise from the epidermis, contain a pultaceous mass of desquamated epithelium. They 
occur most frequently after puncture-wounds of the volar surface of the fingers and 
in the hollow of the hand. 


Literature. 
(Genesis of Carcinoma. ) 


Alberts: Das Carcinom, Jena, 1887. 

Bandler: Chorioepithelioma. Amer. Journ. of Obst., 1902. 

Bayha: Lupuscarcinom. Beitr. v. Bruns, iii., 1888. 

Beneke: Neuere Arb. z. Lehre v. Carcinom (1886-89). Schmidt’s Jahrb., 234, 1892. 

Bozzi: Zungencarciuom nach Psoriasis. Beitr. v. Bruns, xxii., 1899. 

Bucher: Beitr. z. Lehre v. Carcinom. Beitr. v. Ziegler, xiv., 1898. 

Cullen: Cancer of the Uterus, New York, 1900. 

Fabre-Domergue: Les cancers épithéliaux, Paris, 1888. 

Fiessinger: La pathologénie du cancer. Rev. de méd., 1893. 

Flemming: Ueber Bau u. Entstehung der Drüsen. Arch. f. Anat. u. Phys., 1888. 

Fränkel: Vom Epithel d. Chorionzotten ausgeh. Carcinom. Arch. f. Gyn., 48 Bd.; 
Blasenmolen. Ib., 49 Bd., 1895; Chorionepitheliom. Encvklop. Jahrb. v. Eulen- 
burg, ix., 1900. 

Franke: Carcin. entart. Epidermoid des Daumens. Virch. Arch., 121 Bd., 1890. 

Friedlander: Ueber Epithelwucherung u. Krebs, 1877. 

Gaylord: Malignant Growths of the Chorionic Epithelium. Amer. Journ. of Obst., 
1898. 

Hansemann: Ueber asymmetrische Zelltheilung in Epithelkrebsen. Virch. Arch., 
119 Bd., 1889; Die mikroskop. Diagnose bösartiger Geschwülste, Berlin, 1897. 
Hauser: Das Cylinderepithelcarcinom des Magens u. des Dickdarms, Jena, 1890; His- 
togenese d. Krebses. Virch. Arch., 188 Bd., 1894, 141 Bd., 1895: Polyposis in- 
testinalis adenomatosa. Deut. Arch. f. klin. Med., 55 Bd., 1895; Histogenese des 
Plattencpithelkrebses. Beitr. v. Ziegler, xxii., 1897; Neue Arb. über d. Carcinom. 

Cbl. f. allg. Path., ix., 1898. 

Heidemann: Bedeut. d. kleinzelligen Infiltration in Carcinomen. Virch. Arch., 129 
Bd., 1892. 

Israél: Ueber die ersten Anfänge des Magenkrebses. Berl. klin. Woch., 1890. 

Jung: Zur Lehre vom Carcinom. Langenbeck’s Arch., 51 Bd., 1895. 

v. Kahlden: Destruirende Placentarpolypen. Cbl. f. alle. Path., ii., 1891. 

Karg: Ueber das Carcinom. Zeitschr. f. Chir., 34 Bd., 1892. 

Klebs: Ueber das Wesen u. die Erkennung der Carcinombildung. Deut. med. Woch., 
1890. 

Köster: Die Entwickelung der Carcinome, Würzburg, 1869. 

Lubarsch: Primärer Krebs des Deums (Carcin. cylindromatosum). Virch. Arch., 
111 Bd., 1888. 

Marchand: Deciduale Geschwülste. Monatsschr. f. Gebh., 1895. 

Noeggerath: Beitr. z. Structur u. Entwickelung des Carcinoms, Wiesbaden, 1892. 

v. Notthafft: Entstehung d. Carcinome. Deut. Arch. f. klin. Med., 54 Bd., 1895. 

Perez: Branchiogenes Carcinom. Beitr. v. Bruns, 23 Bd., 1899. 

Ribbert: Histogenese des Carcinoms. Virch. Arch., 135 .Bd., 1894, 141 Bd., 1895; Cbl. 
f. allg. Path., v., 1894; Das pathologische Wachsthum, Bonn, 1886; Die Entste- 
hung d. Geschwülste. Deut. med. Woch., 1895. 

Schimmelbusch: Ueber multiples Auftreten primärer Carcinome. Langenbeck’s 
Arch., 49 Bd. 

Schmidt, M. B.: Plexiformes Epitheliom der Haut mit hyaliner Degeneration. Beitr. 
v. Ziegler, viii., 1890. 

Schuchardt; Beiträge zur Entstehung der Carcinome, Leipzig, 1885. 

Schütz: Mikroskopische Carcinombefunde, Frankfurt, 1890. 

Schwalbe: Carcinom in einer tuberkulösen Caverne. Virch. Arch., 149 Bd., 1897. 

Snow: A Treatise on Cancers and the Cancer Process, London, 1898. 

Ströbe: Histogenese u. Actiologie d. Carcinoms. Cbl. f. allg. Path., ii., 1891 (Lit.); 
Celluläre Vorgänge in Geschwülsten. Beitr. v. Ziegler, xi., 1891. 

Tauffer: Carcinom. Degeneration von Dermoideysten. Virch. Arch., 142 Bd., 1895. 

Thiersch: Der Epithelkrebs, namentl. der äuss. Haut, 1865. 

Tillmanns: Actiologie u. Histogenese d. Carcinoms. Langenbeck’s Arch., 1., 1895. 

















VARIETIES OF CARCINOMA. 467 


Through the development of mucoid or colloid-like masses within the 
cancer-cell nests, the latter may become studded with hyaline drops, and 
thereby acquire a mesh-like appearance (Fig. 341). Such formations 
were formerly designated as 
eylindromata, and classified 
with the corresponding sar- 
comata. Should it be thought 
desirable to retain this no- 
menclature, such a tumor may 
be designated carcinoma cylin- 
dromatosum ; but it seems un- 
necessary to separate these 
growths from the mucoid and 
colloid carcinomata. 

When the cancer-cells at- 
tain an extraordinarily large 
size, as occurs, for example, cin of the mation (Millers Bald. Bismarck brown), 
in flat-celled cancers or in % Ordinary cancer-cells; b. byd € cells containing drops 
cancers of the breast, the tu- wandering cells. x 300. uo oe 
mor may be termed a carci- 
noma gigantocellulare. If the enlargement of the cells is not due to 
an inerease in the amount of protoplasm, but to a swollen condition of 
the cells or to a collection of drops of fluid in the cells and their nuclei 
(Fig. 342), the cells are designated physalides (carcinoma physaliferum). 

Myxomatous degeneration of the connective-tissue stroma may occur in 
portions of a cancer, so that the cancer-cells become separated from each 
other by myxomatous tissue (Fig. 343). Such growths may be called 
carcinoma myxomatosum. 

Hyaline degeneration of the connective tissue occurs in different. 
forms of cancer, but is usually confined to small areas of the tumor. 








Deposits of lime-salts in carcinomata occur chiefly as concretion-like 
masses, similar to those found in psammomata. The concretions may 
form either from the cells or in the connectivetissue. They are observed 











TERATOID TUMORS AND CYSTS. 413 


The daughter-nodules grow partly by expansion and partly by an 
appositional growth through the infiltration of the neighboring blood- 
vessels and lymph-spaces. 

In general the cancer-metastases retain a nodular form. In the serous 
membranes and in the skin diffuse proliferations of tissue may occur, 








_ Metwatutte collection of Foung cancer-cells within u lver-capillary, arising from a prima 
oma of the stomach (alcohol, hematoxylin). ». 30. “ur Primus 


‘Metastatle development of cancer within the e Nrercapttarte, arising from a primary caret 


Fig. 351 
noma of the pancreas (alcohol, carmine). Both connective tissue and nests of carcinomu cells have de- 
veloped within the capillaries. "X 250. 





leading to dense thickenings which inclose only small cancer-nodules. 
Likewise, the bone-marrow of entire bones or groups of bones may pre: 
sent a diffuse carcinomatosis, in which process there is formed in the 
place of the bone a cancer-tissue, the stroma of which not infrequently 
contains newly-formed osteoid tissue. . 

Portions of living cancer-tissue when transplanted from one animal 
to another of the same species may continue to grow and form daughter- 
nodules, in the same manner as in the formation of metastases in the 
individual originally affected. 





Literature. 


(Metastasis of Cancer.) 


Cunéo: De lenvahiss. du syst. lymph. duns le cancer de I’estomac, Paris, 1900. 
Ely: A A Study of Metastat. Carcinoma of the Stomach. Am. Journ. of the Med. Be., 








Goldmann: Verbreitungswere bgsartiger Gesehwülste. Beitr, v. Bruns, av 
Gussenbauer: v. Langenbeck’s Arch.. 14 Bd.. 1872. 
Hanau: Erfolgreiche Cebertragung von Carving. Fortschr, 4 Med. 













Stiles: Dissem. of Cancer of the Breast. Brit. M 

Wehr: Careinomimpfungen von Hund zu Hv 39 Bd.. 1889, 
Zehnder: Ueber Krebsentwickelung in Lymphdrüsen. . Arch., 119 Bd., 1890. 
See also 02. 


3. Tue TERATOID TUMORS AND Cysts. 


§ 127. Under the head of teratoid tumors and cysts may be grouped 
those tumor: like formations which are characterized by the fact that the 


TERATOID TUMORS AND CYSTS. 475 


cord adipose tissue (Fig. 352, ¢) and muscle-tissue (4) may find their way 
into the spinal canal and the arachnoideal sac and grow around the 
nerves. Arnold observed transposition of fat-tissue, gland-tissue, carti- 
lage and neuroglia at the lower end of the trunk, in a case of myelocyst 
with complete absence of the lumbar, sacral, and coccygeal portions of 
the spinal column. He also found in a lipomatous teratoma of the 
frontal region that the intracranial portion of the tumor communicated 
with the extracranial through a defect in the cranium. 

The teratoid cysts may be divided into two great groups: the ecto- 
dermal on the one hand, and the entodermal and mesodermal epithelial cysts 
on the other. 

The ectodermal cysts vary ın size from that of a pea to that of a 
man's fist. Their walls present ectodermal characteristics, either in that 
they consist only of a smooth connective-tissue membrane, covered with 
stratified squamous cells—the so-called epidermoids ; or the cyst walls 
may present all the characteristics of skin—that is, contain papille, seba- 
ceous glands, hair follicles, hairs and sweat-glands, and often also subcu- 
taneous fat—the so-called dermoids or dermoid cysts or dermatocysts. 

The cyst-contents consist. either of desquamated horny cells alone, or 
of such cells, fat, and blond hair. 

Epidermoids and dermoids are found chiefly in the skin and subcuta- 
neous tissues, where they present themselves in the form of tumors contain- 
ing a pultaceous material, which resemble atheromata, i.e., tumors caused 
by the retention of secretion in the excretory ducts of the sebaceous 
glands and in the hair-follicles. They are also found at the sides of the 
neck and in the median line either above or below the hyoid bone; 
further, in the thoracic cavity, particularly in the mediastinum, in the pert- 
toneal cavity (rarely), pelvic cellular tissue, coccygeal region, and in the raphé 
of the perineum. Finally, they also appear within the cranium, in the dura 
or in the hypophysis. Of frequent occurrence are the intracranial forma- 
tious which are known as cholesteatoma or as pearl tumors. These 
growths vary in size from that of a pea to that of an apple; they form 
spherical or nodular tumors, having a white satiny surface, and consist 
for the chief part of thin, non-nucleated, scale-like cells, arranged in 
closely crowded lamin®. They are invariably situated at some point on 
the pia (Bostrom), and at such places the vascular pia is covered with 
stratified squamous cells, which in the course of years produce the deli- 
cate epithelial scales of which the tumor is composed. The neighboring 
brain tissue and the arachnoid, which may in part extend over the growth, 
are not concerned in the formation of the horny scales. In rare cases 
cholesteatomata may contain sebaceous material and fine hairs in addition 
to the horny seales and cholesterin. In these cases there may be found 
seated here and there upon the pia dermal structures, i.e., true skin tissue 
containing sebaceous glands and hair-follicles, from which the sebaceous 
material and hairs found in the growth arise. The simple cholesteato- 
mata may therefore be designated as epidermoids (Bostrom), those 
containing hair as dermoids. Cholesteatomata occur at the base of the 
brain, in the neighborhood of the olfactory lobe, tuber cinereum, corpus 
callosum, choroid plexus, pons, medulla oblongata (very rarely in the 
spinal cord), and in the cerebellum. 

The dermoids and epidermoids under consideration doubtless owe 
their origin to a transplantation of epithelial germs to the sites in 
question. In the case of the epidermoids probably only embryonal epi- 
thelial cells are transplanted; in dermoids embryonal dermal tissue is 





478 TUMORS. 


celled carcinomata may take their origin. Cysts, cystadenomata, and car- 
cinomata may develop in the jaw from misplaced portions of the epithelial 
anlage of the teeth. 


Literature. 


(Ectodermal, Entodermal, and Mesodermal Teratoid Cysts, Tissue-transplan- 
tations, and Misplacements.) 


Albrecht: Nebenmilzen. Beitr. v. Ziegler, xx., 1896. 

Arnold: Hygroma colli congenitum. Virch. Arch., 83 Bd., 1865; Angeb. lipomatöser 
Teratom der Stirn. Ib., 43 Bd., 1868; Congenitales zusammengesetztes Lipom der 
Zunge und des Pharynx mit Perforation in die Schidelhdhle. Ib., 50 Bd., 1870; 
Behaarte Polypen der Rachenmundhöhle. Ib., 111 Bd., 1888; Ein Knorpelhaltiges 
angeborenes Fibrom des Scheitels mit Hypertrichosis. Beitr. v. Ziegler, viii., 1890; 
Myelocyste, Transposition von Gewebskeimen u. Sympodie. Ib., xvi., 1894. 

Aschoff: Cysten, Ergebn. d. allg. Path., ii., 1897 (Lit.); Cystisches Adenofibrom d. 
Leistengegend. Monatsschr. f. Gebh., ix., 1899. 

Askanazy: Die bösartigen Geschwülste der in der Niere eingeschlossenen Neben- 
nierenkeime. Beitr. v. Ziegler, xiv., 1893. 

Boström: Piale Epidermoide, Dermoide u. Lipome u. durale Dermoide. Cbl. f. allg. 
Path., 1897 (Lit.). 

Beneke: Zur Lehre v. d. Versprengung von Nebennierenkeimen in den Nieren nebst, 
Bemerkungen zur allg. Onkologie. Beitr. v. Ziegler, x., 1891. 

Brunner: Spina bifida mit Hypertrichosis. Virch. Arch., 129 Bd., 1892. 

Bruns, P.: Branchiogene Carcinome. Mittheil. a. d. chir. Klinik zu Tübingen, i. 
1884. 

Buttersack: Congen. Knorpelreste am Halse. Virch. Arch., 106 Bd., 1886. 

Chiari: Genese d. Atheromcysten. Cbl. f. allg. Path., 1890; Zeitschr. f. Heilk., xii., 
1891. 

Cohnheim: Allgemeine Pathologie, i., Berlin, 1882. 

Cullen: Adenomyoma of the Round Ligament. Johns Hopkins Hosp. Bull., 1892. 

Dehler: Atheromcysten am Halse. Beitr. v. Burns, xx., 1898. 

Deichert: Knorpel u. Knochen in d. Tonsillen (Reste d. 2 Keimenbogens). Virch. 
Arch., 141 Bd., 1895. 

Demoulin: De quelques productions hétérotopiques & Cpithelium prismatique cilie, 
Paris, 1866. 

Döderlein: Embryon. Drüsengeschwulst d. Nierengegend. Cbl. f. Krankh. d. Har- 
norg.. 1894. 

Dössekker: Urachuscysten. Beitr. v. Bruns, x., 1893. 

Eberth: Flimmerepithelcysten d. Leber u. d. Gehirns. Virch. Arch., 35 Bd., 1866. 

Frank. Cholesteatom d. weichen Ilirnhäute. Inaug.-Diss., Marburg, 1897. 

Franke: Das Atherom. Arch. f. klin. Chir., 34 Bd., 1887; Virch. Arch., 121 Bd., 
1890. 

Frobenius: Ucber einige angeb. Cystengeschwülste des Halses. Beitr. v. Ziegler, 
vi., 1889. 

Goebel: Vom Zahnsystem ausgehende Kiefertumoren. Cbl. f.allg. Path., 1897 (Lit.). 

Grawitz: Ueber die sog. Lipome der Nieren. Virch. Arch., 93 Bd., 1888. 

Gurlt: Die Cystengeschwülste des Halses, Berlin, 1855. 

Haffter: Ueber Dermoide. Arch. d. Heilk., xvi., 1875. 

Hasse: Die Beziehungen der Morphologie zur Heilkunde, Leipzig, 1880. 

Hektoen: Vitelline-Duct Remains at the Navel. Amer. Journ. of Obst., 1898. 

Helbing: Rhabdomyom an Stelle d. 1. Lunge. Cbl. f. allg. Path., ix.. 1898. 

Hess: Ueber eine subcutane Flimmercyste. Beitr. v. Ziegler, viii., 1890. 

Heusinger: Hals-Kiemenfisteln mit Knorpelresten. Virch. Arch., 29 Bd., 1864. 

Hildebrand: Unters. über Spina bifida (Gewebstranspositionen). Deut. Zeitschr. 
f. Chir., 36 Bd., 1893; Langenbeck’s Arch., 46 Bd., 1893; Cysten u. Fisteln d. 
Halses. Ib., 49 Bd., 1894: Spina bifida (Gliom in Hydrencephalocele). Deut. 
Zeitschr. f. Chir., 36 Bd.. 1893. 

Hueter: Anveb. Darmgeschwulst. Beitr. v. Ziegler, xix., 1895. 

Joachimsthal: Spina bifida occulta mit Hy pertrichosis. Virch. Arch., 131 Bd., 1893. 

Kelly: Hypernephromas of the Kidney. Phil. Med. Journ., 1898. 

Köster: Hygroma colli congenitum. Verh. d. Würzb. phys.-med. Ges., iii., 1872. 

Kühne: Zur pathol. Histologie d. Cystenbildung. Virch. Arch., 158 Bd., 1900. 

Lannelongue ct Achard: Traitc des kystes congenitaux, Paris, 1886. 


COMPLEX TERATOMATA. 479 


Lesage ct Legrand: Des néoplasics nerveuses d'origine centrale. Arch. de phys., 
1888, 


Malassez: Sur se role des debris epitheliaux paradentaires. Arch. de phys., 1885. 

Mallory: Sacrococcy geal Dimples, Sinuses, and Cysts. Am. Journ. of the Med. Sc., 
13992. 

Marchand: Rhabdomyom der Dammgegend. Virch. Arch., 100 Bd., 1885. 

Mermet Lis kystes congen. du raphe genito-perincal. Rev. de chir., 1895. 

Meyer: Ueber epitheliale Gebilde im Myometrium, Berlin, 1899. 

Mintz: Nabeladenom. Deut. Zeitschr. f. Chir.. 51 Bd., 1899. 

Neumann: Myoma striocellulare d. Hodens. Virch. Arch.. 108 Bd., 1886 

Paltauf: Schilddrüsentumoren im Kehlkopf, u. d. Luftröhre. Beitr. v. Ziegler, xi., 
1891. 

Perez: Branchiogene Carcinome. Beitr. v. Bruns, 23 Bd., 1899. 

Permann: Cystöses Sacrococcy gealteratom (grosse Myelocyste). Arch. f. klin. Chir., 
49 Bd, 1895. 

Pflam: Dermoideysten des Mediastinums. Zeitschr. f. Heilk., xvii., 1896. 

‘ Phöle: Angeb. Cysten d. Genitoperinealraphe. Beitr. v. Bruns, xx., 1898. 

Pick Adenomyome d. Leistengegend u. d. Scheidengewölbes. Arch. f. Gyn., 57 Bd., 
1IN9Y. 

v. Recklinghausen: Untersuchungen über ‘Spina bifida. Virch. Arch., 105 Bd., 
1886. Die Adenomyome u. Cystadenome d. Uterus, Berlin, 1896. 

Reinhold: Oelcyste auf d. Schläfenschuppe. Beitr. v. Bruns, viii., 1892. 

Ribbert Spina bifida occulta. Virch. Arch., 132 Bd., 1898. 

Richard: Geschwülste der Kiemenspalten. Beitr. z. klin. Chir., v. Bruns, iii. 

Samter: Ein Beitrag z. Lehre v. d. Keimengangsgeschwülsten. Virch. Arch., 112 
Ba, 1888. 

Sänger: Dermoideysten.d. Beckenbindegewebes. Arch. f Gyn., 37 Bd., 1895. 

Schmidt: Ueber die Flimmercysten d. Zungenwurzel, Jena, 1896. 

Schoch: Congen. zahnhaltige Cyste der Unterlippe. Inaug.-Diss , Basel, 1898. 

Schulz: Embry on. Arschnürungen v. Epidermis. Virch. Arch., 95 Bd., 1884. 

Virchow: Die krankhaften Geschwülste. Berl. ak. Monatsber.. 1875; Ueber einen 
Fall von Hygroma cysticum glutacale congenitum. Virch. Arch.. 102 Bd., 1885. 

Volkmann: Branchiogene Carcinome. Cbl. f. Chir., xxii., 1885. 

Westenryk: Mediastinalcysten. Prag. med. Woch., xxv., 1900. 

Wette: Fisteln u. Cysten d. Sacrococcy gealgegend. Langenb. Arch., 47 Bd., 1894. 

Wyss: Zur Kenntniss heterologer Flimmercsyten. Virch. Arch., 51 Bd., 1870. 

Zahn: Kiemengangscysten. Deut. Zeitschr. f. Chir., xxii., 1895; Myxosarkom der 
Wange bei sechsmonatl. Fötus. Deut. Zeitschr. f. Chir., xxii., 1885; Congen. 
Knorpelreste am Halse. Virch. Arch., 115 Bd: Flimmerepithelcysten des Oeso- 
phagus d. Leber u. d. Pleura. Vireh. Arch., 143 Bd., 1896 (Lit.). 

Zöppritz: Multiloculäre Kiemengangscysten. Beitr. v. Bruns, xii., 1894. 

Sce also SS 128 and 147. 


x 128. Teratoid cysts of a complicated structure and solid tera- 
tomata are found, outside of the sexual glands, in the same regions as 
the simple teratoid cysts, but show a particular predilection for the region 
of the coceyx. The complex character of the cysts is shown by the pres- 
ence in the eyst-wall of cartilage, bone, fat tissue, mucous glands, smooth 
and striped muscle fibres, nerve-tissue, and tissue of a sarcomatous or 
earcinomatous nature. Dermoid cysts may also contain teeth, and further 
also ciliated epithelial eysts. The solid teratomata occur, in the first 
place, as hairy polypi (nose, throat, and mouth)—that is, as polypoid tu- 
mors covered with hairy skin, and consisting essentially of adipose 
tissue, which may also contain muscle fibres, cartilage, bones, teeth, and 
evsts. Another group consists of those kidney-tumors which, in addition 
to tubular glands, inclose sarcomatous tissue, cartilage, fibrous tissue, 
adipose tissue, and muscle tissue, in rare cases also ectodermal tissues. 
In the ragina and cervix uteri of children there occur tumors, for the 
greater part of a raeemose character, which, in addition to connective 
tissue, myxomatous tissue, round and spindle-celled tissue, also contain 
smooth and striped muscle-fibres, and in rare cases also cartilage. Fi- 
nally, there occur tumor-like growths of a very complicated structure in 


480 TUMORS. 


the cranium, thorax, abdomen, neck, lower jaw, and especially in the region 
of the coccyx. They contain the most varied forms of tissue: connective 
tissue, adipose tissue, cartilage, bone, gland tissue, muscle, nerve and 
brain substance, as well as ectodermal and entodermal cysts. They may 
further inclose rudimentary, or completely formed, or at least easily 
recognizable, portions of the body. 

Both the complex teratoid cysts and the solid teratomata are in 
many cases to be regarded as local disturbances of development char- 
acterized by a misplacement of tissue or a separation of tissues by 
constriction within a single individual (monogeminal lissue-implanta- 
tion, autochthonous teratoma). The hairy polypi of the throat, the cystic or 
solid teratomata at the base of the skull or in the hypophysis may be ex- 
plained by the assumption of a misplacement of ectodermal tissue. The 
presence of cartilage and mucous glands in teratoid cysts of the medias- 
tinum may be explained by the proximity of the trachea. The teratoid 
mixed tumors of the kidney may-be explained by the assumption that: in 
the kidney region, in addition to kidney-tubules and remains of the 
Wolffian body, products of the mesenchyma arising from the myotome 
may undergo proliferation. The occurrence of squamous-celled forma- 
tions in such tumors must depend upon the fact that ectodermal tissue 
has found its way into the kidney anlage. The presence of striped 
muscle-fibres of cartilage in tumors of the vagina and uterus is explaina- 
ble by the assumption of an implantation of myotome or of anlage of the 
vertebrae (sclerotome) ; but many writers hold the opinion that striped 
muscle may be formed from unstriped. Wilms believes that the Wolffian 
duct and its development give occasion to and are the cause of the im- 
plantations into the cervix and vagina. In the ease of the teratomata of 
the coccygeal region the manifold character of these growths may be ex- 
plained by the fact that portions of the terminal vertebrie, of the pelvis, 
and of muscular tissue, as well as remains of the neuroenterie canal, 
the hind-gut, and the medullary canal, take part in the formation of the 
tumor. Inthe intracranial teratomata, as well as in the simple dermoids, 
tissue-implantations probably form the basis for the growth. Moreover, 
there exists indeed the possibility of another mode of origin for these 
growths—namely, the presence of a rudimentary twin, a bigeminal im- 
plantation. Such an assumption is well founded in all those cases in 
which the teratoma contains fully developed or rudimentary parts of the 
body, or tissue-formations which cannot be explained by the assumption 
of a misplacement of the tissue elements of a single foetus at the spot in 
question. Ekehorn regards the complex dermoids of the mediastium, 
which contain skin, eartilage, bone, and the constituents of mucous ment- 
branes, as bigeminal implantations. Lexer emphasizes such a mode 
of origin for the teratoid mixed tumors of the abdominal cavity (see $$ 
129, 132, and 147). 


Literature. 


(The Complex Teratoid Cysts and Tumors. ) 


Arnold: Behaarte Poly pen der Rachen- Mundhöhle. Vireh. Arch., 111 Bd., 1888. 

Aschoff: Cysten. Ergehn. d. alle. Path., ii., 1897 (Lit). 

Beck: ‘Teratom d. Hypophysis cerebri. Zeitschr. f. Heilk., 1883. 

Borst: Die angeb. Geschwülste d. Sueralregion. Cbl. f. alle. Path., ix., 1898 (Lit.). 

Birch-Hirschfeld: Nierengeschwiilste. Beitr. v. Ziegler, axiv., 1898. 

Boström: Piale Epidermoide, Dermoide u. Lipome u. durale Dermoide. Cbl. f. allg. 
Path., 1897 (Liät.). 


TERATOMATA OF OVARY AND TESTICLE. 481 


Braun: Die Doppelbildungen u. die angeb. Geschwülsted Kreuzbeingegend, Leipzig, 
1862 


Buzzi: Angeb. Geschwülste der Sacrococcygealgegend. Virch. Arch., 109 Bd., 1887. 

Christian: Dermoid Cysts and Teratomata of the Ant. Mediast. Jour. of Med. Res., 
1902. 

Eberth: Intracranielles Teratom. Virch. Arch., 153 Bd., 1898. 

Ekehorn: Dermoidcysten des Mediastinums. Arch. f. klin. Chir., 56 Bd., 1898. 

Engelken: Embr. Drüsengeschwulst d. Nierengegend. Beitr. v. Ziegler, xxvi., 1899. 

Frank: Tumor sacralis (Teratom m. Dermoid- u. Flimmercysten). Prag. med. Woch., 
1894. 

Fiirstenheim: Kiemengangauswüchse m. Knorpel-Gerüst. Jahrb. f. Kinderheilk., 
1885. 

Hennig: Congen. Sacraltumoren. Beitr. v. Ziegler, xxviii., 1900. 

Hertzog and Lewis: Embryonal Renal Adenosarcoma. Amer. Journ. of Med. Sc., 
1900. 

Jastreboff: Angeb. Geschwülste in der Gegend des Kreuzbeins. Virch. Arch., 99 Bd., 
1885. 

Jores: Dermoidcyste mit Cystosarkom der Lunge. Virch. Arch., 183 Bd., 1898. 

Kirmisson: Chirurg. Kranxheiten angeb. Ursprungs, Stuttgart, 1899. 

Kolaczek: Dermoid d. Ovariums mit Bauchfellmetastasen. Virch. Arch., 75 Bd., 
1879. 

Koslowski: Hodensack-Teratom. Virch. Arch., 148 Bd., 1897. 

Lexer: Teratoide Geschwülste d. Bauchhodhle. Arch. f. klin. Chir., 61 Bd., 1900; 
Fötale Inclusionen in der Bauchhöhle. Ib., 62 Bd., 1900. 

Linser: Sacralteratome. Beitr. v. Bruns, xxix., 1901. 

Marchand: Sacraltumoren. Eulenburg’s Realencyklop., xxv., 1899. 

Marwedel: Ein Fall von persistirendem Urmund (Retroanal entwickeltes Darmstück 
mit sacralem After). Beitr. v. Bruns, xxix., 1901. 

Middeldorpf: Angeb. Geschwülste in der Gegend des Kreuzbeins. Virch. Arch., 
100 Bd., 1885. 

Montgomery: A Terat. of the Abdom. Cavity. Journ. of Exp. Med., iii., 1888. 

Moussaud: Des inclusions foetales. Thése de Paris, 1861. 

Nasse: Genese der sacrococcygealen Teratome. Langenb. Arch., 45 Bd., 1893. 

Otto: Ueber einen congenit. behaarten Rachenpolypen. Virch. Arch., 115 Bd., 1889. 

Pommer: Teratologische Mittheilungen. Cbl. f. allg. Path., i., 1890. 

Ritschl: Angeb. Sacralgeschwülste. Beitr. v. Bruns, viii., 1892. 

Rolleston: Adeno-chondrosarcoma of the Mediastinum. Journ. of Path., iv., 1896. 

Saxer: Teratom im III. Ventrikel. Beitr. v. Ziegler, xx., 1896 (Lit.). 

Schmidt: Bezieh. d. Steissgeschwülste zu d. Steissdrüse. Virch. Arch., 102 Bd., 
1888; Zwei Fälle von Geschwülsten in der Gegend des. Schwanzbeines. Arb.a. d. 
chir. Universitätspoliklinik v. B. Schmidt, Leipzig, 1891. 

Siegenbeek van Heukelom: Tum. cong. du cou. Rev. de trav. du Lab., Boer- 
haave, 1899. 

Stolpe: Angeb. Geschw. d. Kreuzsteissbeingegend. Deut. Zeitschr. f. Chir., 50 Bd., 
1899. 

Strasemann u. Strecker: Ein Teratom im rechten Seitenventrikel. Virch. Arch., 
108 Bd. 

Sutton: Dermoids or Tumors containing Skin, Hair, Teeth, etc., London, 1889. 

Virchow: Teratoma myomatodes mediastini. Virch. Arch., 53 Bd., 1871. 

Weigert: Teratom d. Zirbeldrüse. Virch. Arch., 65 Bd., 1875. 

Wilms: Dermoidcysten u. Teratome. Deut. Arch. f. klin. Med., 55 Bd., 1895 (Ui); 
Die Mischgeschwülste der Niere, Leipzig, 1899; der Vagina u. der Cervix, Leipzig, 


1900. 
See also 83 127 and 147. 


§ 129. The teratomata of the ovary and testicle occur partly in the 
form of dermoid cysts, and partly as solid tumors in which multiple cys- 
tic formations are present. The dermoid cysts are found chiefly in the 
ovary; the solid tumors in the testicle. 

The so-called dermoid cysts of the ovary form rather thick-walled 
cysts, varying in size from that of a pea to that of a man’s head, and are 
filled with a fatty material containing blond hair. At some point in 
the wall there will be found extending into the cyst-cavity a villus-like, 
nodular, flattened, or septum-like prominence, which is covered with hairs and 














486 TUMORS. 


strated in the case of tumors of large size. Besides the cysts, mucous 
glands may also be found. 

Of the connective-tissue substances, fibrous tissue, myxomatous tissue, 
cartilage (Fig. 357, g, h), and occasionally also muscle (Fig. 358, a), fat 
tissue, and more rarely bone, are present. 

Teratomata of the character of dermoids, containing, as in the case 
of the ovarian dermoids, such structures as skin, brain tissue, cranial 
and tracheal tissues, and more rarely teeth and structures resembling 
the eyes, are of rare occurrence in the testicles, but are found both in 
children and in adults. 

To what extent the different teratomata of the testicles are to be classed 
with the embryomata, or to what extent they can be explained by the 
assumption of tissue implantations at later stages of embryonal develop- 
ment, cannot at present be determined. When elements of all the germ- 
layers are present in the tumor, the assumption is justified that the 
growth belongs to the embryomata or embryoid tumors, and has arisen 
in the same manner as has been assumed in the case of the ovarian der- 
moids. The presence of single tissue-formations—as, for example, of 
cartilage or of muscle—in tumor-formations of a more simple character, 
may be explained by the assumption that such tissues find their way into 
the anlage of the testicle during the period of embryonal development. 


Numerous hypotheses have been advanced concerning the origin of the terato- 
mata of the sexual glands, particularly of the dermoids. Of the more recent investi- 
gations concerning this question, those of Welms are in particular worthy of consider- 
ation. This author has carried out extensive researches into the structure of these 
growths, and has emphasized with great force that the fact that these tumors contain 
elements of all germ-layers necessitates the assumption of their development from an 
ovum. Sonnet has thrown light upon the question from the standpoint of the em- 
bryologist, and likewise emphasizes the view that the complex teratomata which con- 
tain elements of all germ-layers must arise from an ovum, but that portions alone of a 
ripe and fertilized ovum, as a fertilized polar body, may develop into such an em- 
bryoma. The attempt of Bandler to refer the embryomata of the germinal organs to 
ectodermal implantations occurring accidentally during the development of the uro- 
genital system cannot be regarded as successful, inasmuch as the anlage of many 
formations contained in embryomata (teeth, thyroid, eye) cannot possibly be located in 
the region of the urogenital anlage. 


Literature. 
(Teratoid Cysts and Tumors of the Serual Glands.) 


Arnsperger: Dermoidcyste des Ovariums. Virch. Arch., 156 Bd.. 1899. 

Bandler: Die Dermoidcysten des Ovariums, Berlin, 1900; Amer. Journ. of Obstet., 
1901. 

Baumgarten: Dermoideysten d. Ovariums m. augenähnlichen Biidungen. Virch. 
Arch., 107 Bd., 1887. 

Bonnet: Giebt es bei Wirbelthieren Parthenogenesis? Ergebn. d. Anat., ix., Wies- 
baden, 1900: Aetiologie d. Embryome. Monatsschr. f. Gebh., 1900. 

Delbet: Pathogénie des tumeures heterotopiques. L’Un. méd., 1895. 

Katsurada: Zur Lehre v. d. sog. Dermoidcysten d. Eierstocks. Beitr. v. Ziegler, 
xxx,, 1901. 

Kockel: Hodenteratom. Chir. Beitr. Festschr. f. B. Schmidt, Leipzig, 1896. 

Kolaczek: Dermoid d. Ovariums m. Bauchfellmetastasen. Virch. Arch., 75 Bd., 
1879. 

Marchand: Teratom des Ovariums. Bresl. ärztl. Zeit., 1881. 

Neumann: Dermoid d. Ovariums m. centraler Nervensubstanz. Virch. Arch., 104 
Bd., 1886. 

Pilliet et Costes: Les epitheliomes du testicule. Rev. de chir., 1895. 

Sabbe: Tumeurs dermoides de l’ovaire. Ann. de la Soc. de med. d. Gand, 1898. 

Scheiber: Solides Ovarialteratom. Virch. Arch., 133 Bd., 1893. 


TERATOMATA OF THE SEXUAL GLANDS. 457 


Tauffer: Carcinomatöse Degen. v. Ovarialcysten. Virch. Arch., 142 Bd., 1896. 

Waldeyer: Die epithelialen Eierstocksgeschwülste. Arch. f. Gyn., i., 1870. 

Wilms: Dermoidcysten u. Teratome. Deut. Arch. f. klin. Med., 55 Bd., 1895 (Lit.); 
Die soliden Teratume d. Ovariums. Beitr. v. Ziegler, xix.; Die teratoiden Gesch- 
wülste d. Hodens. Ib., xix., 1896 (Lit.): Embryome u. embryoide Tumoren d. 
Hodens. Deut. Zeit. f. Chir., 49 Bd., 1898; Multiple Embryome d. Ovariums. 
Monatsschr. f. Gebh., 1899. 

Yamagiva: Dermoidcyste d. Ovariums m. krebsiger Degeneration. Virch. Arch., 147 

.. 1897. 
See also && 127 and 128, 


CHAPTER IX. 


Disturbances of Development and the Resulting 
Malformations. 


I. General Considerations Regarding Disturbances of Development 
and the Origin of Malformations. 


§ 130. After the copulation of the sexual nuclei has taken place, the 
development of the embryo proceeds by a progressive division of nuclei 
and cells, associated with which there arise in an orderly manner especial 
groupings of cell-complexes and differentiation of the same into especial 
tissues and organs. The multiplication of the cells, as well as the devel- 
opment of individual cell-groups into especial organs and parts of the 
body, depends upon intrinsic causes, and is controlled by the character- 
istics which the embryo has received through the transfer of the inherit- 
able paternal or maternal characteristics at the moment of the union of 
the sexual nuclei, which are to be regarded as the carriers of inheritable 
characteristics. It follows, therefore, that the characteristics of the 
Species as well as the especial peculiarities of the given individual are in 
general already predetermined in the germ, and the development of the 
embryo proceeds essentially under the control of innate moulding forces. 
Nevertheless, this development is not accomplished without the influence 
of environment, in that the embryo of necessity receives its nourishment 
from the maternal organism, and at the same time is exposed to mechani- 
cal influences on the part of its membranes and of the uterus. These 
influences may therefore operate to modify the development of the foetus. 

In every species of animal, man included, both the bodily form and 
the configuration of the organs present a particular type, which experience 
has shown constantly to recur, and which is therefore looked upon as 
normal. If more or less marked departures from this type occur, which 
can be referred to a more or less marked abnormal course of the intra- 
uterine development, the condition is designated as a congenital mal- 
formation. When the departure from the normal structure is very 
marked, so that the affected individual is grossly malformed, it is spoken 
of as a monster. 

According to common usage, the term malformation is usually ap- 
plied only to anomalies in the form of the body as a whole, or to single 
parts of it which present to external inspection rather striking departures 
from the normal. It is nevertheless entirely correct to use this term for 
pathological conditions of intrauterine origin, which consist not so much 
in an abnormal change in form, but rather in an incomplete or faulty 
organization of the affected part or organ. 

A malformation affecting a single individual is known as a single 
malformation or single monster; one made up from two individuals is 
termed a double malformation or double monster. 

Malformations may ove their origin to either intrinsic or extrinsic causes. 

4838 








CAUSES OF MALFORMATIONS. 491 


The period at which the injurious influence is active varies greatly, 
and consequently so does the extent of the damage done by it. The 
earlier the damage occurs, the greater the extent of the injury. Mal- 
formations in the narrower sense of the term arise chiefly during the first 
three months, during the period when the body and its individual parts 
are developing their proper forms. Damage to the foetus at a later 
period oceasions changes which are more closely allied to those acquired after 
birth. 

Some malformations are typical—that is, they always appear in the 
same form; while others again are wholly atypical, so that the most 
astonishing anomalies of form may arise. The latter are for the greater 
part the result of extrinsic harmful influences operating secondarily, 
while the former may be regarded as owing their origin chiefly to in- 
trinsic causes, although external influences may also cause typical mal- 
formations, 


Geoffroy St.-Hilaire (* Hist. gen. et partic. des anomalies de l'organization chez 
Vhomme et les animaux,” Paris, 1832-87) discards entirely the teaching of a primary 
abnormality of the germ (If«ller and Winslow), and attributes arrests of development 

urely to mechanical influences. Panum (“Untersuch. über die Entstehung der Miss- 
ildungen,” Berlin, 1860) agrees with him on the whole, although he admits the possi- 
bility of a primary ubnormality, He produced malformations in hens’ en by means 
of temperature variations and by varnishing the shells. Dareste (“Recherches sur ia 








Fra. 361. Fra, 38. 


F1o, 361,—Hand stunted by amniotic adbesions; ring-finger snared uff; middle and index fingers grown 
together and distorted. Reduced one-sixth. u 

Fıa. 382.--Hand stunted and deformed by pressure; thumb absent; hand flattened; great bending 
and shortening of the forearm. Reduced one-fifth. 


production artificielle des monstruosités,” Paris, 1877) made similar experiments and 

ced malformations due to arrested development by keeping the eggs in a vertical 
ın, by varnishing the shells, by raising the temperature above 45° C., and also by 
lar warming of the e 


BRS. 
Very recently L. Gerlach, Fol, Waryneky. Richter, Rouz, and Schultee have in par- 
ticular carried on experiments in this line, and have attempted, with partial success, to 






492 DISTURBANCES OF DEVELOPMENT. 


produce malformations in chicken-embryos through the localized influence of radiant 
heat, variations of temperature, varnishing the eggs, changes of position, injuries, 
removal of a portion of the white of the egg, and by agitation. Rouz, experimenting 
on frogs’ eggs, found that, after destruction of one of the first segmentation-spheres, 
the other continued to develop and formed the half of an embryo, thus demonstrating 
that each of the first two segmentation-cells, corresponding in their position to the right 
and left body-halves, contains within itself the anlage material for the corresponding 
half of the body. But since the body-half which is wanting may later be replaced b 
subsequent development from the undestroyed half, and a whole structure be produced, 
each half must also possess the power of producing also the other half. According to 
investigations by Herlitzka, Driesch, Morgan, Wilson, and others, the first two or even 
the first four segmentation-cells in tritons, teleosts, ascidians, and echinoderms possess 
the power of forming an entire embryo. 

Schultze experimented on the eggs of amphibia; these normally always assume 
such a position that the darkly pigmented protoplasmic substance of lighter specific 
gravity lies above, the heavier clear protoplasm rich in yolk granules lies below. By 
placing the eggs in an abnormal position and preventing their return to the normal 
position malformations may be produced, the degree of malformation standing in direct 
relation to the size of the angle formed by the line of gravity and the abnormally- 
placed axis of the egg. By turning the egg through an angle of 180° in the two-cell 
stage a double monster is regularly produced. The same turning in the eight-cell 
stage causes a complete cessation of development. These disturbances arise from dis- 
placements consequent upon the sinking of the heavier and a rising of the lighter con- 
stituents of the egg. 

According to investigations by O. Hertwig, the eggs of axolotl, when kept in a 0.7- 
per-cent. solution of sodium chloride, undergo a pathological development, which is 
confined to the central nervous system in the region of the head and trunk. The so- 
dium-chloride solution acts only upon those portions of the ectoderm which are in the 
process of changing into ganglion-cells; and asa result, with otherwise normal devel- 
opment, portions of the central nervous system may be lost. 


Literature. 


(Malformations and Their Origin.) 


Ahlfeld: Berichte und Arbeiten aus der geburtshülfl. Klinik zu Marburg, 1885-86; Die 
Missbildungen des Menschen, Leipzig, 1880, 1882. 

Ballantyne: The Diseases and Deformities of the Foetus, i. and ii., Edinb., 1893, 1895. 

Barfurth: Ueber organbildende Keimbezirke u. künstliche Missbildungen d. Amphi- 
bieneies. Anat. Hefte, Wiesbaden, 1893. 

Braun, C.: Neue Beitr. z. Lehre v. d. amniotischen Bändern, Wien, 1862. 

Charrin ct Gley: L'influence tératogéne des prod. microbiens. Arch. de phys., 1896. 

Davaine: Monstre, Monstruosité. Dictionn. encyclop., abgedr. in L’®@uvre de Da- 
vaine, Paris, 1889. 

Dareste: Rech. sur la production artif. des monstruosités, fi. éd., Paris, 1894. 

Delage: Structure du protoplasma et les théories de l’heredite, Paris, 1895. 

Driesch: Entwickelungsmechan. Studien. Zeitschr. f. wiss. Zool., 58, 55 Bd., 1891, 
1892; Anat. Anz., vii., 1892. 

Duval: Tératogénie. Path. gén. publ. p. Bouchard, i., Paris, 1895. 

Endres: Entwickelungsmechanik. Eulenburg’s Jahrb., vii., 1897. 

Endres u. Walter: Anstichversuche an Eiern von Rana. Arch. f. Entwickelungs- 
mech., ii., 1895. 

Fol ct Warynsky: Rech. exp. sur la cause de quelques monstruosités. Recueil zool. 
Suisse, i., 1883. 

Förster: Die Missbildungen des Menschen, Jena, 1865. 

Gerlach: Production v. Zwergbildungen im Hühnerei. Biol. Cbl., if., 1883; Neue 
Methoden auf dem Gebiete der experimentellen Embryologie. Ib., vii., 1889; Anat. 
Anz., 1887. 

Giaccomini: Anomalies de développ. de l’embryon humain. Arch. ital. de biol., ix., 
1888; xviii. and xix., 1892; xx., 1893; xxiv., 1895: Influence de l’air raréfié. Ib., 
xxii., 1894. 

Guinard: Précis de tératologie, Paris, 1893. 

Gurlt: Literatur über Missgeburten. Virch. Arch., 74 Bd., 1878. 

Hertwig: Exper. Erzeug. thier. Missbildungen. Festschr. f. Gegenbaur, Leipzig, 
1896; Mechanik und Biologie, Jena, 1897. 

Hirst and Piersol: Human Monstrosities, Philadelphia, 1891. 


SINGLE MONSTERS. 498 


His: aoe mechanische Grundvorgänge thierischer Formbildung. Arch. f. Anat., 


Israel: Angeb. Spalten d. Ohrläppchens, ein. Beitr. z. Vererbungslehre. Virch. 
Arch., 119 Bd., 1891. 

Kirmisson: Chir. Krankheiten angeb. Ursprungs, Stuttgart, 1899. 

Kollmann: Die Körperform mensch]. normaler u. pathol. Embryonen. Arch. f. An., 
1889. 

Küstner: Ueber eine noch nicht bekannte Entwickelungsursache amputirender 
amniotischer Fäden. Zeitschr. f. Geb., xx., 1891; Die Pathologie des Fodtus, 
Stuttgart, 1888. 

Lanneolongue et Ménard: Affections congénitales. I. Téte et cou, Paris, 1891. 

Marchand: Missbildungen. Eulenburg’s Realencyklop., xv., 1897 (Lit.). 

Mitrophanow: Teratogenet. Studien. Arch. f. Entwickelungsmech., i., 1895. 

Morian: Die schräge Gesichtsspalte Arch. f. klin. Chir., 1887. 

Moser: Missbild. durch amniotische Bänder. Prag. med. Woch., 1894. 

Otto: Monstrorum sexcentorum descriptio anatomica, 1844. 

Panum: Zur Kenntniss d. physiol. Bedeutung d. angeb. Missbildungen. Virch. 
Arch., 72 Bd., 1878. 

Piersol: Teratology. Ref. Handbook of Med. Sc., 2d ed., 1908. 

Richter: Ueber die experimentelle Darstellung der Spina bifida. Anat. Anz., iii., 
1888. 

Roux: Zur Entwickelungsmechanik des Embryo. Zeitschr. f. Biol., xxi., 1886; 
Künstliche Hervorbringung halber Embryonen durch Entfernung einer der beiden 
ersten Furchungskugeln, u. Wachsthumsentwickelung der fehlenden Kérperhalfte. 
Virch. Arch., 114 Bd., 1888; Die Entwickelungsmechanik der Organismen, Wien, 
1890: Ueb. das entwickelungsmechanische Vermögen jeder der beiden ersten 
Furchungszellen des Eies. Verh. d. Anat. Ges., vi., 1892; Ueber die Specification 
der Furchungszellen und über die bei der Postgeneration und Regeneration 
anzunehmenden Vorgänge. Biol. Cbl., xiii., 1898; Die Methoden zur Erzeugung 
halber Froschembryonen. Anat. Anz., ix., 1894; Einleitung zum Archiv für 
Entwickelunsgmechanik der Organismen. Arch. f. Entwickelungsmechanik, i., 
1894. 

Schultze: Die Bedeutung der Schwerkraft für die organische Gestaltung, sowie über 
die mit Hülfe der Schwerkraft mögliche Künstliche Erzeugung von Doppelmiss- 
bildungen. Verh. d. Phys.-med. Ges., 28 Bd., 1894; Entwickelungsgeschichte, 
Leipzig, 1896. 

Taruffi: Storia della teratologia, i.-vili., Bologna, 1881-96: Sull’ ordinamento della 
teratologia. R. Accad. delle Sc. dell’ Ist. di Bologna, 1896, 1898. 

Virchow: Descendenz u. Pathologie. Virch. Arch., 103 Bd., 1886. 

Wiedersheim: Der Bau des Menschen, Freiburg, 1898. . 

Ziegler: Können erworbene patholog. Eigenschaften vererbt werden u. wie entstehen 
erbliche Krankheiten u. Missbildungen. Beitr. z. pathol. Anat., i., 1886; Die 
neuesten Arb. über Vererbung u. Abstammungslehre, u. ihre Bedeutung für die 
Pathologie. Ib., iv., 1889. 

For literature of Malformations, see Anat. Anz., i.-xix., 1886-1901; and Cbl. f. 
allg. Path., i.-xii., 1890-1901. 


$ 131. Single malformations may be conveniently divided into five 
groups, according to the kind of change which characterizes them. 

As arrests of development or monsters due to defective develop- 
ment (monstra per defectum) may be classed in the first place all those 
malformations in which the whole or a part of the body is abnormally 
small and imperfectly developed (hypoplasia), and also those malfor- 
mations characterized by the complete absence or very great stunting 
(agenesia or aplasia) of individual organs or parts of the body. In this 
elass belong, for example, the absence of the brain or of parts of it, or 
abnormal smallness of the brain, defects in the septa of the heart, defects 
and stunting of the extremities, etc. 

If, in the case of parts or organs of the body which are normally 
formed by the union of anlage which are originally separated, such 
union should fail to take place as the result of a primary or secondary 
disturbance of growth, the arrest of development may show itself in the 
form of clefts and reduplications. Thus, for example, imperfect develop- 


494 DISTURBANCES OF DEVELOPMENT. 


ment of the plates forming the anterior body-wall gives rise to clefts in 
the median line of the thorax and abdomen; a failure of union of the 
maxillary processes of the first branchial arch with each other or with 
the nasal process of the frontal bone gives rise to clefts in the face. 
Defective union of the bilateral portions of the female genital tract 
results in a more or less extensive reduplication of the uterus or vagina. 

When the anlage of two organs lie near to each other, these may 
under certain conditions become united so as to produce a coalescence or 
adhesion between two organs or parts which should normally be sepa- 
rated. For example, the kidneys at times may be more or less united, 
and the eyes may be more or less completely merged into a single organ. 

Malformations due to excessive growth (monstra per excessum) 
are characterized in part by abnormal size of individual parts, and in part 
by an increase in number of the same. For example, an extremity or a 
portion of one, as a finger, may reach an abnormal size (partial giant 
growth), or the whole body may be involved in the abnormal growth 
(general giant growth). An increase in number occurs particularly in the 
case of the mammary gland, spleen, adrenals, and fingers. Additional 
glandular organs are designated accessory or supernumerary organs. 

As malformations due to an abnormal disposition of organs (mon- 
stra per fabricam alienam) are designated by Forster certain anomalies 
of the internal organs of the thorax and abdomen, which are character- 
ized by an abnormal position of the organs, and in part also by changes 
in the relation of individual parts to each other. In this class belongs 
the condition known as situs transversus—that is, the transposition of the 
thoracic or abdominal organs, or of both. Further, various defects in 
the heart and great vessels may also be classed here, though it should be 
noted that these are more properly regarded as arrests of development. 

A fourth group of malformations ineludes those characterized by 
displacement of tissues and by the persistence of foetal formations, as 
already mentioned in SS 127 and 128. 

Finally, as a fifth group may be classed those malformations ex- 
hibiting a mixture of the sexual characteristics, known as true and 
false hermaphroditism. True hermaphrodites possess both male and female 
sexual glands; false hermaphrodites are unisexual, but the remainder 
of the sexual apparatus does not correspond to the sexual gland, or there 
is a simultaneous formation of organs belonging to both the male and 
female. A part of these malformations are arrests of development ; 
others are to be regarded as cases in which from the original bisexual 
anlage the organs of both sexes have developed, whereas normally the 
anlage of one sex nndergo a retrograde change instead of developing, 
and persist only in a rudimentary form. 

§ 132. Double monsters (monstra duplica) are malformations in 
which the entire body or a part of it is duplicated. The twins are al- 
ways of the same sex, and are usually united at corresponding portions 
of the body. The duplicated parts are sometimes equally, sometimes 
unequally developed; in the latter case one of the parts is dwarfed and 
appears aS a parasitic appendage to the well-developed individual or 
is inclosed within the body of the latter. We may accordingly distin- 
guish equal and unequal forms of double monsters. 

All double monsters arise from a single egg and develop from a single 
germinal vesicle. The disturbance of development may occur during 
the course of the seementation process, but is first reeognizable when 
from the germinal vesicle there is formed a double embryonal anlage. A 


DOUBLE MONSTERS. 495 


double monster may then arise either through the two embryonic areas 
being united from the very beginning, or that, originally separated, 
they infringe upon one another in their growth and blend to a greater or 
less extent. A second possibility is the formation within a single em- 
bryonic area of two primitive streaks and then two medullary grooves, 
which may remain entirely separate from each other or only partially 
blend. A third possibility would be a single primitive streak, but a 
medullary groove which is double either in part or in the whole of its 
extent. Finally, it is possible that under certain conditions a duplica- 
tion takes place at a later period of development and then affects only 
individual parts of the axial zone or only the parietal zone. 


The causes of a duplication of the embryonal anlage in a single gerintnal resicle are not 
known. According to Fol, double and multiple monsters arise through the abnormal 
impregnation of an ovum with two, three, or more spermatozoa; but other observa- 
tions (Born) indicate that ova fertilized by two or more spermatozoa do not develop. 
According to Marchand, the doubling of the anlage is to be referred to conditions exist- 
ing before the beginning of segmentation, either to conditions within the egg before fer- 
tilization, or to the fertilization itself. Wiedemann and Wetzel hold the opinion that the 
origin of double monsters dates from the moment of impregnation, and is due to the 
fertilization of ova containing two germinal vesicles by two spermatozoa. 

Successful experiments in the artificial production of double monsters from the eggs 
of animals have been made in recent years by Gerlach, O. Schultze, and Born. Gerluch 
produced double monsters (anterior duplication) from hens’ eggs by varnishing these 
before incubating, leaving free only a Y-shaped spot in the region of the primitive 
streak. Inasmuch as he only rarely succeeded in obtaining such results, it is possible 
that these malformations, which not infrequently occur in chickens, were accidental. 
Schultze obtained double monsters by turning frogs’ eggs during the two-cell stage 
through an angie of 180° (cf. § 130). Spermann was able to produce double-headed 
embryos of tritons by constriction of the embryonal anlage before the closure of the 
medullary plate to form the medullary groove. Born succeeded in uniting together 
portions of the larve of amphibia, not only of the same kind, but also of different 
species, genera, and families (Rana esculenta with Bombinator igneus, and with 
Triton). The conditions were most favorable for union in the case of larvs of about 
3 mm. length. Not only the external coverings of the body, but also the anlage of 
organs (liver, intestine, heart-tube), were blended into a united organ, the union being 
completed through specific tissue of the same kind. From all these experiments the 
conclusion may be drawn that double monsters may be produced from a normal egg 
through secondary influences, and that neighboring embryonal anlage may grow one 
into the other. On the other hand lies the possibility that especial conditions within 
the egg before fertilization may be the cause of the duplication. According to Schultze, 
this may possibly lie in the presence of two nuclei or of two spindles, or in an over-ripe 
condition of the egg with a tendency to fragmentation into two halves, which divide 
shortly before fertilization. Therefore a normally fertilized ovum in the two-cell 
stage may be brought through some influence (as in the experiment of Schultze) to the 
formation of two individuals. 


Literature. 
(Double Monsters. ) 


Ahlfeld: Die Missbildungen des Menschen, Leipzig. 1880, 1882. 

Born: Furchungen des Eies bei Doppelbildungen. Breslauer ärztliche Zeitschr., 1887; 
Ueber Doppelbildungen beim Frosch. Ib., 1882; Ueber Verwachsungsversuche 
mit Amphibienlarven, Leipzig, 1897, ref. Deut. med. Woch., 1898, S. 126. 

Dareste: Product. des monstruosités. Compt. rend. Ac. des sc., 1861, 1868, 1864, 
1865, 1866. 

Debierre: Ia theorie de la monstruosité double. Arch. de phys., ii., 1890. 

Debierre ct Dutilleul: Monstres doubles du genre synote. Arch. de phys., ii., 1890. 

Fol: Recherches sur la fécondation, etc., 1879. 

Förster: Die Missbildungen des Menschen, Jena, 1865. 

Geoffroy Saint-Hilaire: Hist. gén. et partic. des anomalies de l’organisat. chez 
homme et les animaux, Paris, 1832-37. 

Gerlach. I... Ueber dic Entstehungsweise der vorderen Verdoppelung. Deut. Arch., 


496 DISTURBANCES OF DEVELOPMENT. 


1,Klin. Med., 42 Bd.; Die Entstehungsweise der Doppelmissbildungen, Stuttgart, 


Gachier: Thorscopagus tetrabrachius sequnlis. Prag. med. Woch., 1892 
Elaussner: Mehrfachbildungen bei Wirbelthieren, München, 1890. 
Kormann: Ueber lebende Doppelmissbildungen der Neuzeit. | Schmidt's Jahrb., cxliii, 


1869. 
Lochte: Ein Fall von Doppelmissbildungen. Beitr, v. Ziegler, xvi., 1894. 
Marchand: Missbildungen. Eulenburg’s Realencyklop., xv., 1897. 
a, Zwillingsschwangerschaft u. angeb. Missbildungen. Virch, Arch., 108 








Panum: Untersuchungen über die Entstehung der Missbildungen, Berlin, 1980; Zur 
Kenntniss.d, phys. Bedeutung d. Missbildungen, Virch. Arch, 72 Bd., 

Zauber. Die Theorle der excessiven Monstra., Virch. Arch., 71, 78. 14 Ba, 1817-78, 

Schäfer: Ueber einen Dicephalus. Beitr. v. Ziegler, xxvi 

Schultze, O.: Ueber die Bedeutung der Schwerkraft, etc. ern, der phys.-med. 
Geselisch., 28 Bd., 1864; Arch. f. Entwickelungsmech., i, 1894; Entwickelung d. 
Doppelbildungen. Cbl. f. allg. Path., x., 1 

Bobotta. Neue Anschauungen über Bniatehung von Doppelbildungen, Würzburg, 





1901. 
Spermann: Exper. Erzeug. zweiköpiger Embryonen. Sltaher. d. phys.-med. Ges., 


Wetzel: Drei abnorm gebildete Eier. Anat. Anz., xviii., 1900. 
‘Wiedemann: Entstehung d. Doppelbildungen. Virch. Arch., 188 Bd., 1894 (Lit.). 
See also x 189. 


ll. The Different Forms of Malformations in Tian. 
I. ARRESTS OF DEVELOPMENT IN A SINGLE INDIVIDUAL. 


(a) Arrest of the Development of the Entire Embryonal Anlage. 


§ 133. An arrest in the development of the entire embryonal 
anlage manifests itself in two ways. If the disturbance is very marked, 
a further development of 
the embryo is impossible, 
and it either dies at once 
or becomes stunted, and 
after a certain time per- 
ishes. If the disturbance 
is less severe there develops. 
a normally formed fetus, 
but it remains small and 
stunted—that is, a dwarf 
is formed (nanosomia or 
microsomia). 

A dead feetus is in the 
majority of cases expelled 
together with its mem- 
branes (abortion). In 
other cases in which the 
embryo for some cause or 
other remains stationary in 
development, the egg may 
remain for weeks or even 

Fig. 393.— Portion of a hydatid mole, Natural size. months in the uterus and 

increase in size, so that 
there arises a disproportion between the size of the embryo and of the 
egg. According to His, the first changes after death are shown ina marked 
swelling of the central nervous organs, leading to changes in the con- 








493 DISTURBANCES OF DEVELOPMENT. 


the maternal organism there may result the formation of a lithopeedion. 
This occurs most frequently in the abnormal situation of the ovum known 
as extrauterine pregnancy, in which the embryo lies in the peritoneal 
cavity, in a tube, or in an ovary. If the foetus dies at such an advanced 
stage of development that it cannot be absorbed, it may be carried within 
the maternal organism for years. Not infrequently its form is perfectly 
preserved (Fig. 364), and the whole foetus becomes inclosed in a connec- 
tive-tissue membrane. In other cases the foetus, in the course of time, 
becomes converted into a partially fluid mass, which contains the osseous 
remains, as well as fat, cholesterin, and pigment, and is surrounded by 
a fibrous capsule. Time-salts are usually deposited both in the newly 
formed membranes as well as in the portions of the foetus remaining, 
and for this reason the foetus is known as a “stone-child ” or “ petrified 
child.” 

According to the condition of the foetus there may be distinguished 
three chief forms of lithopsdion (Küchenmeister). In the first the 
nıumniified foetus may be easily shelled out from the calcified membranes 
(lithocelyphos). In the second form the foetus becomes adherent to the 
membranes at various points which become calcified, while the other 
portions become mummified (lithocelyphopedion). In the third form the 
foetus is discharged, through the rupture of the membranes, into the 
peritoneal cavity, and later becomes encrusted with lime-salts (lithopeedion 
in the narrower sense). 


The long retention of a ripe or even older fetus within the uterua (missed labor) is rare, 
but may occur (1) in an accessory horn of the uterus, (2) in interstitial pregnancy, (3) 
after rupture of the uterus. 


Literature. 


(Disturbances of Development of the Embryo. Lithopedion. ) 


Bandl: Die Extrauterinschwangerschaft. Handb.d. Frauenkrankheiten, ii., Stuttgart, 
1886. 

Eberth: Myxom des Chorion. Virch. Arch., 39 Bd., 1867. 

Engel: Rückbildungsvorgänge an abortiven Embryonen. Beitr. v. Ziegler, xx viii., 
1900. 

Giaccomini. Entwickelungsanomal. d. menschl. Embryo. Ergebn. d. Anat., iv., 1894 
and loc. cit § 130. 

His: Fragen d. path. Embryologic. Internat. Beitr. Festschr. f. Virchow, i., 1891. 

Kleinwächter: Missed Labor. Eulenburg’s Realencyklop., v., 1895 (Lit. ). 

Kroemer. Zur Kenntn. der Lithopädien. Münch. med. Woch., 1900. 

Küchenmeister: Ueber Lithopädion. Arch. f. Gyn., xviii., 1881. 

Mall: Pathology of Early Human Embryos. Johns Hopkins Hosp. Rep , ix., 1900. 

Marchand: Bau der Blasenmole. Zeit. f. Gebh., 38 Bd., 1895 (Lit. ). 

Martin Extrauterinschwangerschaft. Eulenb. Realencyklop., 1895 (Lit.). 

Müller, H.. Ueber den Bau der Molen, Würzburg, 1847. 

Virchow: Die krankh. Geschwülste, i., 1863. 

Wallenstein: Beitr. z. pathol. Embryologie. Inaug.-Diss., Freiburg, 1897. 


(b) Defective Closure of the Cerebrospinal Canal and the Accompanying 
Malformations of the Nervous System. 


§ 134. Defective closure of the vertebral canal leads to the mal- 
formations known as rachischisis or spina bifida. If the defect in the 
vertebral column is open so that at the bottom of the cleft the bodies of 
the vertebr covered by membrane are seen, the malformation is ordi- 
narily termed rachischisis. When, at the site of the defect, there is seen 
a protruding sac, the malformation is usually designated spina bifida, or 


RACHISCHISIS. 499 


more correctly spina bifida cystica; though to this formation the names- 
rachischisis cystica or hydrorachis cystica may also be applied. 

In rachischisis totalis (holorachischisis) (Fig. 365) the bodies of the 
vertebra form a shallow groove opening posteriorly, and usually covered 
by a thin, transparent membrane; in rare cases rudiments of the spinal 
cord are still present in the form of whitish bands and lines. In this 
mani there occurs a total or partial amyelia. The defect involves 
principally the motor tracts and centres, as well as the columns of, 











Fic, 385.—Cranlorachischisis with total absence of the brain and spinal cord. The skull is covered 
ith rugged membranous tnuees, the-open spinal furrow with a delicate membrane (pla mater). Kypho- 
Jordotie curvature and shortening of the spinal column. Reduced one-sixth. 


Clarke and the lateral cerebellar tract, while the spinal ganglia are devel- 
oped (Manz, Leonowa, K. and G. Petrén), and may send sensory fibres 
into the membranous masses of the spinal groove. 

The delicate membrane which lines the furrow and covers the dura 
mater lying beneath it upon the bones is the ventral portion of the 
spinal pia mater. A part of the nerve-roots may have undergone devel- 
opment, arising either from rudiments of the spinal cord or from spinal 
ganglia. 

Partial rachischisis ( merorachischisis) involves usually the sacrolum- 
bar or the upper cervical region, while the intervening portions of the 
vertebral column are only rarely the seat of malformations. The dorsal 
of the bodies of the vertebree whose arches remain rudimentary 
overed for the greater part by a mass of red velvety tissue, which 
upon a delicate membrane, though the amount of this tissue may be 
small or may even be wholly wanting. To the outside of this 
er, which is not everywhere equally abundant. and which dimin- 
ishes at the sides, there comes next a delicate, transparent, vascular 
membrane; and next, outside of this, a zone of epidermoidal tissue some- 
what thinner than normal skin, and often covered with many hairs, 
separating the reddened central area from the normal skin. 











500 DISTURBANCES OF DEVELOPMENT. 


The soft red tissue lying in the central area is the rudiment of the 
malformed spinal cord, and consists of an extremely vascular tissue 
containing more or less numerous portions of the spinal cord, as nerve- 
fibres, ganglion-cells, and glia-cells, and is designated the area medullo- 
vasculosa (von Recklinghausen). It is sometimes a continuous tissue, at 
other times it is scattered in bands and patches, and forms only a deli- 
cate veil-like net. Both the cranial and the caudal extremities of this 
median area may end in a distinct furrow, designated respectively as 
the cranial and caudal polar furrow (“Polgrube,” von Recklinghausen), 
to which the spinal cord is connected anteriorly and in lumbosacral 
rachischisis the filum terminale caudally. The membrane on which the 
area lies is the pia mater, which also continues into the red marginal 
zone above mentioned, which, being covered with epithelium, is desig- 
nated as the zona epitheloserosa (von Recklinghausen). The prominent 
zone bordering this and covering the rudiments of the vertebral arches 
is formed of skin and is known as the zona dermatica. 

On the ventral side of the pia mater forming the covering of the 
defect is a space which is bounded below by the dura mater and the ex- 
ternal layer of the arachnoid, so that it is in reality the ventral portion 
of the subarachnoidal space. 

Spina bifida cystica or rachicele (rachischisis cystica) occurs in three 
chief forms: myelomeningocele, meningocele, and myelocystocele. Accord- 
ing to its site there may be further distinguished a cervical, dorsal, Jum- 
bar, lumbosacral, and a sacral spina bifida. In general, a spina bifida 
is characterized by the development of a fluctuating tumor, which is in 
most cases visible externally (Fig. 366) on the posterior aspect of the 
spinal column (spina bifida posterior); but instances also occur in which 
the sac projects anteriorly from the spinal canal (spina bifida anterior), 
and others in which it is too small to be visible externally (spina bifida 
occulta). 

Plyelomeningocele appears most frequently as a spina bifida lumbo- 
sacralis, and usually forms a tumor varying in size from that of a nut to 
that of an apple and increasing in size after birth, in the region of the 
lower lumbar and upper sacral vertebre. It is covered either by smooth 
or scar-like skin, or may be devoid of skin on its summit and there cov- 
ered by a reddish, mucosa-like tissue (area medullovasculosa). The 





Fig. 366.—Spina bifida sacralis. (After Froriep and Förster.) Girl of nineteen years, born with a tumor 
the size of a pizeon's egg over the upper sacral and lower Jumbar regions, which enlarged from the sixth 
year on, While at the same time club-feet developed. 


portion uncovered by skin may be drawn in, like a scar. In rare cases 
there may be no external tumor (spina bifida occulta), the site of the 
cleft being indicated only by a more marked growth of hair or by a 
depression. 

On opening the sac, which is composed of the arachnoid (Fig. 367, e) 
and the pia (f, f,), while the dura (g) does not extend over the dorsal 
portion of the sac, it may be seen that the lower end of the spinal cord 





502 DISTURBANCES OF DEVELOPMENT. 


Myelocystoceles occur, in the majority of cases, in lateral clefts of 
the vertebral column. They show a tendency to be combined with defects 
and asymmetries of the bodies of the vertebra, and thereby often with 
shortenings of the trunk, which at times affect only the dorsal region, at 
other times also the lumbar region. Very frequently there exists at the 
same time an exstrophy of the abdomen, bladder, and intestine. 

Myelocystoceles are inostly covered only by the outer skin, but are 
sometimes concealed deep down in the soft parts. They may further 
be combined with a meningocele, so that a myelocystomeningocele 
arises. 

In cases of rachischisis there sometimes occurs a division of the 
spinal cord into two parts (diastematomyelia), most often in the case of 
a total rachischisis, in which indeed the rudiments of the spinal cord 
are usually only indicated. In partial rachischisis such division is more 
rare, but the separated strands of spinal cord are better developed, and 
the fibrous and bony coverings may, at the beginning or end of the cleft, 
send dividing septa between them. Cases have occurred in which each 
cord-half possessed an H-shaped area of gray matter. 

The origin of rachischisis is to be referred to agenesia and hypoplasia 
of the medullary folds, which should form the medullary groove of the 
vertebral arches. The agenesia of the spinal cord is also to be dated 
from the very earliest period. Whether it is a primary agenesia pre- 
determined in the germ, or whether extrinsic injurious influences, per- 
haps toxic substances (Hertwig), pressure from without, or the inclosure 
of foetal membranes, may have secondarily checked development or have 
destroyed parts already formed, it is usually difficult to determine; but 
the symmetrical distribution of the arrested development speaks in favor 
of the former view. 

In cases of spina bifida with hernial protrusion, the local defects in the 
bony vertebral column and the defective development of the dura mater, which 
is usually wanting at the site of the protrusion, are to be regarded as 
the primary condition. The growth of the sac may be explained as due 
to congestive and inflammatory transudation, and many times the residue 
of inflammatory changes, such as thickenings and membranous adhesions, 
may be demonstrated in the pia. 


In the earliest embryonic period the medullary groove is formed by the develop- 
ment on both sides of the median line of wall-like elevations of the ectoderm which are 
designated as the medullary folds. Through the converging growth and union of the 
latter the medullary groove is closed and formed into the medullary canal. Thereupon 
the cell-masses (primitive vertebral plates) lving at the sides of the newly formed canal 
form an envelope about it, which gives rise in the first place to a membranous, non- 
articulated vertebral column. In this, at the beginning of the second month, there 
arise discrete cartilaginous areas from which, in the course of further development, the 
vertebral bodies and arches are formed, while between them the intervertebral discs 
and vertebral ligaments appear. The development of the cartilaginous vertebre is not 
completed until the fourth month, and up to this time the dorsal covering of the med- 
ullary tube consists of the united portions of the membranous vertebral column. The 
cartilaginous constituents of the vertebrie are in the course of development replaced by 
bone. 

According to ron Recklinghausen, neither the persistence of a connection between 
the medullary canal and the epiblast nor an excessive stretching of the wall of the med- 
ullary groove through bending of the axis of the embryo can be held responsible for 
the origin of ınyelocystocele and myelocystomeningocele. According to his view, the 
former is a deficient growth in the long axis of the vertebral column, characterized 
anatomically by shortness of the column, absence of vertebre or parts of vertebrie, 
separation of wedge-shaped bony pieces from the bodies of the vertebre, and by uni- 
lateral defects in the arches. The neural canal, then, in the course of normal develop- 
ment, becomes too long for the vertebral canal, and in consequence becomes curled or 


MALFORMATIONS OF VERTEBRAL COLUMN. 503 


kinked, and there isa tendency to a partial protrusion of the medullary tube at the 
point of sharpest bending. Marchand believes that this hypothesis is not applicable to 
all cases, and Arnold is aso of the opinion that the causal relations between arrests of 
development in the muscle-plates and vertebral anlage on the one hand, and those of 
the medullary canal on the other, are not constant, but that a variety of harmful influ- 
ences may give rise to one or more of these anomalies. 

According to O. Hertwig, the ordinary spina bifida is an arrest of development 
depending upon a partially prevented closure uf the blastopore (“ Urmundspalte ”). 


Literature. 


(Malformations of the Spinal Cord and Vertebral Column.) 


D’Ajutolo: Contrib. allo studio delle varietä numeriche delle vertebre, Il., Morgagni, 
Xxx., 1888. 


Albrecht, P.: Defect der drei letzten Sacral- u. simmtl. Steisswirbel. Cbl. f. Chir., 
1885. 

Arnold: Myelocyste, Transposition von Gewebskeimen u. Sympodie. Beitr. v. 
Ziegler, xvi., 1894. 

Beneke: Diastematomyelie mit Spina bifida. Beitr. z. path. An., Festschr. f. Wagner, 
Leipzig, 1887. 

Bohnstedt: Spina bifida occulta. Virch. Arch., 140 Bd., 1895. 

Borst: Geschwülste d. Sacralregion. Cbl. f. allg. Path., ix., 1898 (Lit. ) 

Braune: Die Doppelbildungen u. d. angeb. Geschwülste d. Kreuzbeingegend., Leipzig, 
1862. 

Brunner: Spina bifida occulta mit Hypertrichosis. Virch. Arch., 129 Bd., 1892. 

Curtius: Spina bifida. Langenbeck’s Arch., 47 Bd., 1894. 

Demme: Bericht über. d. Thätigk. d. Kinderspitals, Bern, 1883; Wien. med. Blätter, 
1884 

Fischer u. Marchand: Ueber d. lumbodorsale Rachischisis mit Knickung d. Wirbel- 
siiule nebst Mittheilung cines Falles v. Myelocystocele lumbosacralis. Beitr. v. 
Ziegler, v., 1889. 

Förster: Die Missbildungen des Menschen, 1865. 

Hertwig: Urmund u. Spina bifida. Arch. f. mikr. Anat., 39 Bd., 1892. 

Hildebrand: Spina bifida u. Hirnbrüche. Deut. Zeitschr. f. Chir., 36 Bd., 1893 (Lit.). 

Jacoby: Doppelbildung des embryonalen Rückenmarks. Virch. Arch., 147 Bd., 1897. 

Joachimsthal: Spina bifida mit localer Hypertrichosis. Virch. Arch., 181 Bd., 1893 
(Lit.). 

Koch, W.: Beitr. z. Lehre von der Spina bifida, Cassel, 1881. 

Kollmann: Spina bifida u. Canalis neurentericus. Verh. d. Anat. Ges., 1893. 

Kroner u. Marchand: Meningocele sacralis anterior. Arch. f. Gyn., xvii., 1881. 

Lebedeff : Ueber die Entstehung der Anencephalie u. Spina bifida. Virch. Arch., 86 
Bd., 1881. 

Leonowa: Anencephalie mit Amyelie. Neurol. Cbl., 1893. 

Manz: Das Auge hirnloser Missgeburten. Virch. Arch., 51 Bd., 1870. 

Marchand: Spina bifida. Eulenburg’s Realencyklopädie, xxii., 1899. 

Markoe and Schley: The Sacrococcygeal Dimples, Sinuses and Cysts. Am. Jour. 
of Med. Sc., 1902. 

Meckel: Handb. d. path. Anat., i., Leipzig, 1812. 

Muscatello: Die angeb. Spalten d. Schädels u. d. Wirbelsäule. Langenb. Arch., 47 
Bd., 1894. 

Petrön, K. u. G.: Nervensystem bei Anencephalie u. Amyelie. Virch. Arch., 151 
Bd., 1898. 

Pick: Zur Agenesie des Rückenmarks. Arch. f. Psych., viii., 1878. 

v. Recklinghausen: Untersuchungen über Spina bifida. Virch. Arch., 105 Bd., 1886. 

Rex: Eigeuthümliche Umbildungen des normalen Wirbeltypus. Prag. Zeitschr. f. 
Heilk., vii., 1835. 

Ribbert: Spina bifida occulta. Virch. Arch., 132 Bd., 1893. 

de Ruyter: Schädel- u. Rückgratsspalten. Langenbeck’s Arch., 40 Bd., 1890. 

Saalfeld: Spina bifida occulta mit Hypertrichosis. Virch. Arch., 137 Bd., 1894. 

Sulzer: Spina bifida mit Verdoppelung des Rückenmarks. . Beitr. v. Ziegler, xii., 
1893. 

Taruffi: Della rachischisi. Bologna, 1890. 

Virchow: Virch. Arch., 27 Bd.; Die krankh. Geschwöülste, i., 1863. 

Wiedersheim: Der Bau des Menschen, Freiburg, i. B., 1898. 

Wieting: Ueber Spina bifida u. Zweitheilung d. Rückenm. Beitr. v. Bruns, xxv., 
1899. 











DEFECTS OF THE CRANIUM. 507 


vening space is filled by fluid distending the subarachnoidal space (A). 
In the less marked forms only individual portions of the brain are 
undeveloped, those parts chiefly affected being the olfactory lobes and 
nerves, the corpus callosum, a part of the convolutions, ete. The optic 
thalami are often blended together. The chiasm and the optic tract may 
be absent or present. The corpora quadrigemina (k), pons, medulla 
oblongata, and cerebellum (2) are usually unaffected. 


The spinal cord and brain arise from the medullary canal. In that portion that is 
to become the brain, the neural canal changes very early into three vesicles. The most 
anterior of these, the furebrain, throws out from its lateral portions the primary optic 
vesicles, while the middle portion grows forward and upward and divides into the 
telencephalon or forebrain, and the diencephalon (thalamencephalon) or tweenbrain. From 
the former are developed the cerebral hemispheres, corpora striata, corpus callosum, 
and the fornix. From the tweenbrain are formed the optic thalami and the floor of 
the third ventricle. The second vesicle or midbrain forms the corpora quadrigemina, 
while the third vesicle divides into the isthmus, metencephalon, and myelencephalon, 
from which there are developed the pons, cerebellum, and medulla oblongata. 

The cerebral portion of the meaullary canal becomes inclosed by the primitive 
vertebral plates of the head, which form the membranous primitive skull, the basal 
portions of which become cartilaginous in the second month of fetal life. In the third 
month the basal cartilage and the membranous vault begin to ossify. 

According to @. St.-Hilaire, Förster, and Panum, acrania and anencephalus are to 
be referred to anabnormal accumulation of fluid in the cerebral vesicles, a hydrocephalus, 
occurring before the fourth month. Dareste and Perls oppose this view, and point out 
that in acrania the base of the skull is usually buiged inward and not pressed outward. 
They therefore seek the cause of acrania in a pressure exerted upon the cranium from 
without (Perls), due to an abnormal tightness of the cephalic cap of the amnion, which 
retards the development of the cranium. Jbedeff seeks the cause of acrania in an 
abnormally sharp bending of the body of the embryo, which he thinks occurs when the 
cephalic end of the embryo grows abnormally in the longitudinal axis, or in case the 
cephalic covering lags behind in its development. 

By the sharp bending the change of the medullary groove into the medullary canal 
is thought to be hindered, or the canal after its formation is destroyed. From this 
could be explained the later absence of the bruin, as well as of the membranous and 
osseous cranial covering. The cystic formations in the membranes lying upon the 
base of the skull are, according to Lebedeff, formed from the folds of the medullary 
plate, which sink into the mesoderm and are then snared off. 

Hertirig thinks it possible that chemical substances circulating in the blood or 
secreted from the wall of the uterus may destroy the anlage of the brain. 

It is very probable that acrania does not always arise in the same way, and while 
in one case the influences brought forward by /’erls and Lebedeff, or also adhesions with 
the fetal membranes, may hinder the development of the skull and brain, it is probable 
that in other cases the malformation must be regarded as a primary agenesia, the 
causes of which were already present in the germ. 

According to A. and A. Petrén, the spinal ganglia in anencephalus are always nor- 
mally developed; on the other hand, the columns of Clarke, the lateral cerebellar tracts, 
and the bundles of Gowers are either wholly wanting or are imperfectly developed. 
Likewise the pyramidal tracts are wanting, while the anterior-horn ganglion-cells and 
the anterior roots are developed. K. and A. Petren, therefore, regard the malformation 
as a system-defect in which the neurones of the second order are not formed; and they 
incline to the view that the malformation is to be referred to an abnormal anlage of 
the germ. 


Literature. 
(Defects of the Cranium, Cerebral Hernia.) 


Ackermann: Die Schädeldifformität bei der Encephalocele congenita, Halle-a.-8., 
1881. 

Arnold: Gehirn, Rückenmark u. Schädel eines Hemicephalus. Beitr. v. Ziegler, xi., 
1X92. 

Beneke: Zwei Fille von multiplen Hirnhernien. Virch. Arch., 119 Bd., 1890. 

Berger: L’origine et le mode de développement de certaines encéphaloctles. Rev. de 
chir., 1890. 


508 DISTURBANCES OF DEVELOPMENT. 


Ernst: Bildungefehler d. Centralnervensystems bei Encephalocele. Beitr. v. Ziegler, 
XXV., . 

Förster: Missbildungen des Menschen, Jena, 1865. 

Fridolin: Ueber defecte Schidel. Virch. Arch., 116 Bd., 1889. 

Jacoby: Partielle Anencephalie bei einem Embryo. Virch. Arch., 147 Bd., 1897. 

Kundrat: Die Arrhinencephalie, Graz, 1882. 

Lebedeff: Entstehung d. Anencephalie u. Spina bifida. Virch. Arch., 86 Bd., 1881. 

Leonowa: Anencephalic. Arch. f. Anat., 1890. 

Manz: Das Auge hirnloser Missgeburten. Virch. Arch., 51 Bd., 1870. 

Muhr: Encephalocele anterior. Arch. f. Psych., viii., 1878. 

Mucatello: Dieangeb. Spalten des Schädels. Langenbeck’s Arch., 47 Bd., 1894 (Lit.). 

Petrén, K. u. G.: Nervensystem bei Anencephalie u. Amyelie. Virch. Arch., 151 Bd., 
1898 (Lit.). 

de Ruyter: Schädel- und Rückgratsspalten. Langenbeck’s Arch., 40 Bd., 1890. 

Schiirhoff: Anatomie d. Centralnervensystems bei Hemicephalen, Stuttgart, 1894. 

Siegenbeek van Heukelom: Encephalocele. Arch. f. Entwickelungsmech., iv., 
1896. 

Spring: Monographie de la hernie du cerveau, Bruxelles, 1858. 

Talko: Ueber angeborene Hirnhernien. Virch. Arch., 50 Bd., 1870. 

Virchow: Die krankh. Geschwülste, i., 1863. 


(c) The Malformations of the Face and Neck. 


§ 136. The development of the face not infrequently suffers disturb- 
ances leading to more or less marked facial malformations, which may 
appear alone or in association with malformations of the cranium. If 
the frontal process and the maxillary processes of the first branchial arch 
remain in a rudimentary state or are destroyed to a marked extent by 
pathological processes, there persists at the site of the face an open sinus 
giving rise to the conditions known as aprosopia (absence of the face) 
and schistoprosopia (cleft face), which may also be associated with a 
defective development of the nose and eyes. 

More frequent than these large defects are smaller clefts involving 
the lips, alveolar process of the upper jaw, the upper jaw itself, and the 
hard and soft palates (Fig. 375), which are designated as cheilo-gna- 
thopalatoschisis or ‘‘ wolf’s jaw.’’ This malformation gives rise to a 
communication between the mouth and the nasal cavity (Fig. 375). 
The hard palate is cleft in the part bordering upon the vomer; the soft 
palate in the median line. In the alveolar process of the upper jaw the 
cleft runs between the canine tooth and the outer incisor or between the 
outer and inner incisors. The malformation may be bilateral or unilat- 
eral, and is sometimes primary and inheritable, at other times acquired 
secondarily, in part as the result of amniotic adhesions (Fig. 359). 

Not infrequently the cleft involves only special portions of the regions 
mentioned, as the upper lip (harelip, labium leporinum), or, what is 
rarer, only the hard or soft palate. The lightest grades of this form of 
cleft-malformation are represented by a notch or cicatricial line in the lips, 
or by a bifurcation of the uvula. | 

Prosoposchisis or oblique facial cleft (Fig. 360) is the designation 
applied to a cleft running obliquely from the mouth to an orbit. It is 
usually associated with malformations of the brain. According to 
Morian, three forms may be distinguished. The first is a cleft beginning 
in the upper lip as a harelip, passing into the nasal cavity, thence 
around the ala nasi toward the orbit, and may extend even beyond the 
latter. The second form likewise begins in the region of a harelip, but 
extends outward from the nose toward the orbit. The third form ex- 
tends from the corner of the mouth, outward through the cheek toward 
the canthus of the eve, and divides the superior maxillary process exter- 


MALFORMATIONS OF FACE AND NECK. 509 


nally to the canine tooth. A transverse cleft of the cheek also occurs, pass- 
ing from the corner of the mouth toward the temporal region. 

Median facial clefts (nasal cleft) run in the median line involving 
the nose, upper jaw, and also the lower jaw, and may extend as far 
down asthesternum. The tongue may also be cleft (Wölfler). Further, 
the defect may extend even to the frontal bone and brain. 

All of the above-mentioned clefts may be confined to small portions 
of the regions mentioned, and moreover attain varying depths. 

If the development of the inferior maxillary process of the first 
branchial arch is retarded, the inferior maxilla also is imperfectly devel- 
oped or wholly wanting, and there arise those malformations known as 
brachygnathia or agnathia (Fig. 376). The lower portion of the face 





Fıa. 875.—Double chello-gnathopalatoschisis. Fig. 876.—Agnathia and synotia. 
(Wolf's Jaw.) (After Guardan.) 


appears as if cut away; the ears are sometimes brought so close to each 
other as to touch (synotia). Usually the superior maxillary processes 
are also imperfectly developed; not infrequently the ear is malformed. 

Abnormal largeness of the mouth (macrostomia), abnormal smallness 
(microstomia), closure (atresia oris), and duplication of the mouth (dis- 
tomia) are all rare. 

When the embryonic external branchial clefts or internal branchial 
pockets fail in part to: close, there persist fistule opening either exter- 
nally or internally, or closed cysts. The former condition is known as 
fistula colli congenita. The mouths of the external fistule are usually 
found at. the side of the neck, more rarely nearer to the median line or 
in the median line; those of the internal fistule open into the pharynx, 
trachea, or larynx. Very often the remains of the branchial pockets 
form only diverticula of the last-named organs. The fistule are for the 
chief part covered with mucous epithelium, sometimes ciliated, arising 
therefore from the visceral branchial pockets, according to von Kos- 
tanecki and von Mielecki usually from the second. In rare cases there 
is found a complete branchial fistula with both external and internal 
openings. 

The branchial cysts arising from the branchial pockets are some- 


510 DISTURBANCES OF DEVELOPMENT. 


times covered with mucous epithelium (ciliated epithelium) and contain 
fluid; hence they are called hydrocele colli congenita. At other times they 
possess an epidermoidal covering and inclose epidermoidal cell-masses, 
and are therefore classed with the atheromata and dermoid cysts. Dis- 
turbances of development of the anterior end of the branchial arch 
(mesobranchial field) and in the region of the third branchial pocket 
(thymus-anlage) and branchial cleft may lead to the formation of der- 
moids in the submental region, in the root of the tongue, and in the medias- 
tinum. 


The face and neck are developed in part from a single anlage, and in part from 
paired anlage. The latter are represented in the branchial or visceral arches growing 
from the lateral portions of the base of the skull ventrally in the primitive throat-wall. 
The single anlage, designated the frontal process, is a prolongation downward of the 
base and vault of the cranium, and is, in fact, nothing more than the anterior end of 
the skull. Between the individual branchial arches there are at a certain period cleft- 
like depressions known as the branchial pockets. 

The frontal process and the first branchial arch form the boundaries of the great 
primitive mouth-opening, which has a diamond shape. In the course of development 
the first branchial arch sends out two processes, the shorter of which applies itself to 
the under surface of the anterior portion of the head and forms the upper jaw, while 
from the longer one the lower jaw is developed. The frontal process, which forms the 
anterior boundary, gives rise to a broad prolongation of the forehead, and then pushes 
on two lateral processes which are known as the lateral nasal processes. By further 
differentiation of the central portion of the frontal process proper, the septum narium 
is formed, which by means of two spurs, the inner nasal processes, produces the borders 
of the external nasal opening and the nasal furrow. The lateral nasal processes are the 
lateral portions of the skull, and later develop within themselves the ethmoid labyrinth, 
the cartilaginous roof, and the sides of the anterior portion of the nares. At a certain 
stage they form with the superior maxillary process a furrow running from the nasal 
furrow to the eye, the lachrymal fissure. 

In the beginning the mouth is simply a large sinus, but is soon separated into a 
lower and larger digestive and an upper and smaller respiratory portion. This separa- 
tion is brought about by the development, from the superior maxillary processes of the 
first branchial arch, of the palatal plates, which from the eighth week on blend into 
each other and at the same time unite with the lower border of the nasal septum. The 
union of the anterior portions of the palatal plates takes place earlier than that of the 
posterior portions. 

Through the union of the contiguous portions of the frontal and nasal processes 
with the superior maxillary processes the check is formed and a continuous superior 
maxillary border, from which are developed later the lip and the alveolar process of 
the upper jaw and intermaxillary bones, while the external portion of the nose devel- 
ops from the frontal process. The intermaxillary bones are developed as independent 
bones, but unite very early with each other and with the upper jaw. 


Literature. 


(Wolf's Jaw; Harelip; Oblique Facial Clefts.) 


Albrecht: Arch. f. Chir.. xxxi.; Fortschr. d. Med., iii., 1885: Biol. Cbl., v., 1886. 

Bartels: Ueber vernarbte Lippenspalten. Arch. f. Anat. u Phys., 1872. 

Biondi: Lippenspalte und deren Complicationen. Virch. Arch., 111 Bd.. 1888. 

Förster: Die Missbildungen des Menschen. Jena, 1865. 

His: Anatomie menschlicher Embryonen, iii., 1885. 

Kindler Linksscit. Nasenspalte verbunden mit Defect d. Stirnbeins. Beitr. v. Ziegler, 
vi. 1889. 

Kölliker, Th.: Ueber glas Os intermaxillare u. d. Anatomie d. Hasenscharte u d. 
Wolfsrachens, Halle, 1882; Die einfache Anlage des Zwischenkiefers. Anat. Anz., 


iii... 1890. 
v. Kostanecki: Missbildungen in der Kopf- u. Halsgegend. Virch. Arch., 113 Bd., 
1891. 


Kredel: Angeb. Nasenspalten. Deut. Zeitschr. f. Chir., 47 Bd., 1898 (Lit.). 
Lannelongue: Du developpement de lintermaxillaire externe et de son incisive; 
pathogenie des fissures osseuses de la face. Arch. de med. exp., ii., 1890. 


CLEFTS OF THORACIC AND ABDOMINAL WALLS. 511 


Lexer: Angeb. mediane Spaltung der Nase. Arch. f. klin. Chir., 62 Bd., 1900. 

Madelung: Unterlippentistel u. seitl. Nasenspalte. Langenbeck’s Arch., 37 Bd., 
1889. 

Marwedel: Mediane Spalte der oberen Gesichtshälfte. Virch. Arch., 163 Bd., 1901. 

Merkel: Gesichtsspalte. Topograph. Anatomie, ii. Heft, 1887. 

Morian: Die schräge Gesichtsspalte Arch. f. Chir., xxxv., 1887. 

Müller: Die Hasenscharten d. Tübinger chir. Klinik i. d. J., 1843-85, Tübingen, 1885. 

Nasse: Mediane Nasenspalte. Langenbeck’s Arch., 49 Bd., 1895. 

Schmidt: Spaltbildung im Bereiche d. mittl. Stirnfortsatzes. Virch. Arch., 162 Bd., 
1900. 

Stöhr: Zur Zwischenkieferfrage. Arch. f. klin. Chir., xxxi., 1885. 

Taruffi: Casi di meso-rino-schisi. Mem. della R. Acc. delle Sc. dell’ Istit. di Bologna, 
1890. 

Warynski. Bec de liévre simple et complexe. Virch. Arch., 112 Bd., 1888. 

Wolfler: Zur Casuistik der medianen Gesichtsspalte. Langenbeck’s Arch., 40 Bd., 
1890. 

Wolff: Hasenscharte. Eulenburg’s Realencyklop., 1896 (Lit.). 


(Branchial-cleft Fistula and Cysts. ) 


Baumgarten u. Neumann: Fistula colli congenita. Arch. f. klin. Chir., xx., 1870. 

Bidder: Knorpelgeschwulst am Halse. Virch. Arch., 120 Bd., 1890. 

Franke: Blutcysten d. seitl. Halsgegend. Deut. Zeitschr. f. Chir., 28 Bd., 1888 (Lit. ). 

Frobenius: Ueber einige angeb. Cystengeschwülste des Halses. Beitr. v. Ziegler, vi., 
1889. 

Heusinger: Virch. Arch., 29 and 33 Bd.; Deut. Zeitschr. f. Thiermed., ii., 1875. 

König: Fistula colli congenita. Langenbeck’s Arch., 51 Bd., 1896. 

v. Kostanecki: Zur Kenntn. d. Pharynxdivertikel des Menschen. Virch. Arch., 117 
Bd., 1889. 

v. Kostanecki u. v. Mielecki: Die angeb. Halskiemenfisteln. Virch. Arch., 120 u. 
121 Bd., 1890. 

Nieny: Halskiemenfisteln. Beitr. v. Bruns, 23 Bd., 1899. 

Richard: Geschwülste der Kiemenspalten. Beitr. v. Bruns, iii., 1888 (Lit.). 

Schlange: Fistula colli congenita. Langenbeck’s Arch., 46 Bd., 1893. 

Schmidt: Halskiemenfisteln beim Kalbe. Zeitschr. f. Thiermed., i., 1897. 

Strübing: Zur Lehre v. d. congen. Hals-Luftrdhrenfisteln. Deut. med. Woch., 1892. 

Virchow: Halskiemenfistel. Virch. Arch., 32 Bd.; Tiefes auriculares Dermoid. Ib., 
35 Bd., 1866. 

Zahn: Kiemengangsfisteln. Zeitschr. f. Chir., xxii., 1885. 


(d) Faulty Closure of the Abdominal and Thoracic Cavities, and the Accom- 
panying Malformations. 


& 137. Arrests of development in the formation of the ventral 
body-wall may take place at different points and exhibit different grades 
of severity. They occur most frequently in the region of the umbilicus, 
where the closure of the abdominal cavity takes place latest. In the 
case of imperfect development of the abdominal wall at this point, so 
that a more or less extensive area of the abdominal cavity is closed in 
only by the peritoneum and the sheath of the umbilical cord—that is, 
the amnion— which are pushed forward by the abdominal organs (Fig. 
377), there is produced the condition known as omphalocele, or hernia 
funiculi umbilicalis, or umbilical hernia. The umbilical cord is at- 
tached either to the summit or at one side of the hernial sac, and is more 
or less shortened. 

If the anterior abdominal walls either wholly or in part fail to unite, 
there arise those conditions which are designated fissura abdominalis, 
or gastroschisis completa and thoracogastroschisis. These are char- 
acterized by the undeveloped abdominal coverings not having been sepa- 
rated from the amnion, but passing into it. The greater part of the 
abdominal organs lies in a sac formed by the amnion and peritoneum 





CLEFTS OF THORACIC AND ABDOMINAL WALLS. 513 


adenoma umbilicale). In very rare cases a cyst lined with mucous mem- , 
brane may be formed in the abdominal wall (omphalomesenteric cyst). 
Umbilical hernia and clefts of the upper portion of the abdominal 
wall are frequently combined with craniorachischisis, while exstrophy of 
the bladder and intestine is often associated with myelocystocele. Ac- 





FiG. 378.—Fissura abdominis et vesic@ urinarie in a girl eighteen days old. a, Border of the skin: 
>, peritoneum : ¢, bladder; d, small bladder-cavity corresponding to the trigonum : €, trough-like urethra ; 
’ Inbia minora, 


cording to von Recklinghausen, the two malformations are to be regarded. 
as coördinated to each other. Further, large abdominal clefts are often 
associated with lordotic and scoliotic curvatures of the spinal column. 


The development of the body-form from the flat embryonic anlage begins by a 
snaring-off of the individual germ: layers from the outer embryonal area, and their fold- 
ing to form two tubes, the body-wall and the alimentary canal. 

The infolding of these layers takes place at the cephalic and caudal ends, as well as 
at the lateral portions of the embryonal anlage, and as the summits of the folds gradu- 
ally grow together from all directions, those which form the body-wall produce a tube 
whose cavity finally communicates only at the parietal umbilicus, by means of a 
peduncle-like prolongation, with the cavity of the extra-embryonic portion of the 
blastoderm known at this time as the vitelline membrane. While the lateral and ven- 
tral walls of the embryo are being thus formed, within the body the intestinal furrow 
also closes to form a’ tube, which is in communication at only one point lying within 
the parietal umbilicus, known as the visceral umbilicus, with the cavity of the umbili- 
cal vesicle, by means of a channel known as the omphalomesenteric duct. 


Literature. 


Clefts of Thoracic and Abdominal Walls; Meckel’s Diverticulum ; Ectopia 
Intestini.) 


Aschoff: Verhältniss d. Leber u. d. Zwerchfells z. Nabelschnurbrüchen. Virch. 
Arch., 144 Bd., 1896 (Lit.). 

Chaudelux: Observation pour servir a V'histolre de V’exomphale. Arch. d. phys. 

Die Rückbildung des Nabels u. der Nabelgefässe, München, 1892. 

Klautsch: Bauchspalten. Cbl. allg. Path., vi., 1885. 





514 DISTURBANCES OF DEVELOPMENT. 


Küstner: Das Adenom und die Granulationsgeschwulst am Nabel. Arch. f. Gyn., 
ix., 1877; Virch. Arch., 1877. 

Praia: Ueb. d. sog. Nabeladenom. Juhrb. f. Kinderheilk., 88 Bd., 1891. 

v. Recklinghausen: Spina bifida. Virch. Arch., 105 Bd., 1886, 
Rischpler: Drei Falle von Eventration. Arch. f. Entwickelunsgmech., vi., 1898 (Lit.). 
Bauer: Prolaps eines offenen Meckel’schen Divertikels. Deut. Zeitschr. f. Chir., 44 
1 
Schild: Congen. Ektopie der Harnblase. Arb. a. d. path. Institute in München, 1886. 
ibeek van Heukelom: Die Genese der Ektopia ventriculi am Nabel. Virch. 

‘Arch., 111 Bd., 1888. 

Tillmanns: Angeb. Prolaps der Magenschleimhaut durch den Nabelring und über 
sonstige Geschwülste und Fisteln des Nabels. Deut. Zeitschr. f. Chir., xviii., 1883. 

Vejas: Eine seltene Missbildung. Virch. Arch., 104 Bd.. 1886. 

Zumwinkel: Subcutane Dottergangscyste. Langenbeck’s Arch., 40 Bd., 1890. 


(e) Malformations of the External Genitalia and Anus, due to Arrested 
Development. 


§ 138. Malformations of varying degree of the external genitals may 
be associated with malformations of the abdominal wall, bladder, and 
the internal genital organs, or may occur independently of these. Com- 
plete absence of the external genitalia occurs most frequently in con- 
nection with other malformations of this region, particularly in the case 
of sirenomelia, yet the region may in general present also a normal 
structure (Fig. 381). The internal genitals are usually also malformed. 

A stunted condition of the penis is not rare, the organ in conse- 
quence coming to resemble more or less the clitoris, This condition is 
usually associated with a hypospadias—that is, the urethra opens on 
the under side of the organ, either beneath the glans, the body or the 
root of the penis (Fig. 379), or finally even behind the scrotum (Aypo- 





FIG. 379.—Hypospadias with stunting of the penis. Fi. 30,—Epispadias. 
*Piteduced one-fourth. pe (afer anlteld.) 


spadias perineoscrotalis). These malformations may exist in penises 
otherwise normally developed, and depend upon a partial failure of the 
sexual furrow to close. 

Epispadias (Fig. 380) is that condition in which the urethral opening 
is found upon the dorsum of the penis. It is more rare than hypo- 
spadias, and is dependent upon a defective or delayed closure of the 
pelvis, so that the cloaca, before the closure, becomes divided into an 
intestinal (anal) and a genital opening (Thiersch). Under certain con- 


. MALFORMATIONS OF EXTERNAL GENITALIA. 515 


ditions the penis remains cleft throughout its entire length; at the same 
time a fissure of the bladder and abdomen may be present. 

Hypertrophy of the prepuce is not rare. If the preputial opening 
is narrowed so that the prepuce cannot be drawn back over the glans, 
the condition is designated a hypertro- 
phic phimosis. Total absence of the 
prepuce is rare; an abnormal shortness 
is more frequent. 

Defective development of the scro- 
tum is usually associated with retention 
of the testicles in the abdominal cav- 
ity or in the inguinal canal, and leads 
to appearances whereby the external 
genital organs of the male come to re- 
semble those of the female, especially so 
when the penis is also stunted. 

In the female the clitoris as well as 
the labia majora and minora may show 
a stunted development. Epispadias 
and hypospadias occur also in the fe- 
male sex, the former coincidently with 
a fissure of the abdominal and bladder 
walls (Fig. 378). In hypospadias a 
portion of the posterior wall of the ure- 
th s lacking, and the urethral open- 
ing may be found at a greater or less oF 
distance within the vagina. a “ 

Absence of the rethra occurs in and caternal wenliale ih extreme dir 
both sexes (Fig. 381). le ne 
bladder may open directly into the stunting of the e ower extremities. (Kn tha 
vagina. portions of the tubes and ovaries were 

Closure (atresia) of the urethra fund) 
occurs likewise in both sexes, and re- 
sults either from a partial defect of the same or from obliteration of 
the orifice. An accumulation of urine in the bladder may lead to a 
marked dilatation of the same (Fig. 381). 

An abnomal narrowness of the urethra may exist in a portion of 
its course or throughout its entire length. Further, its lumen may be 
narrowed as the result of a hypertrophic development of the colliculus 
lis. 

In rare cases multiple orifices of the urethra have been observed. 
Further, in men there may be found in the glans penis a blind tube 
lying beside the urethra. 

Atresia ani simplex is a closure of the anus, the intestine being at 
the same time well developed. It may arise from a failure of the ecto- 
derm to fold in at the anal site, or a cloaca already existing and open- 
ing outward may again become closed through subsequent adhesions 
(Frank). If the rectum does not end immediately above the anal mem- 
brane but higher up, there exists in addition to the atresia ani also an 
atresia recti, a malformation which may occur even when the anus is 
well developed. 

When, with absence of the anus, there is also an arrested development 
of the v: nal wall, which grows downward, between the sinus urogeni- 
talis and intestine, to unite with the perineum, there remains a cloaca 


























516 DISTURBANCES OF DEVELOPMENT. 


in which the sinus urogenitalis and the end of the bowel unite. In 
other cases there are found fistulous communications between the 
rectum and the bladder or urethra (in boys) on the one hand, or be- 
tween the rectum and the vagina or uterus on the other (atresia ant 
vesicalis, urethralis, vaginalis, uterina). 

In rare cases the intestine, in the case of anal atresia, may open 
outward by means of external fistule in the perineum, scrotum, or 
sacrum. 


Literature. 
(Disturbances of Development of the External Genitalia and of the Anus.) 


Bergh: Epispadie. Virch. Arch., 61 Bd., 1867. 

Dienst: Atresia ani congenita. Virch. Arch., 154 Bd., 1898 (Lit.). 

Eppinger: Atresia ani. Prag. med. Woch., 1880. 

Frank: Die angeborene Verschliessung des Mastdarms, Wien, 1892. 

Fürst: Weibliche Epispadie mit Nabel-Urachusfistel. Arch. f. Kinderheilk., xiv., 

Gärtner: Atresie des Darms. Jalırb. f. Kinderheilk., xx., 1883. 

Goldmann: Hypospadie. Beitr. v. Bruns, xii., 1894 (Lit.). 

Keibel: Entwickelung v. Harnblase, Harnröhre u. Damm. Verh.d. Anat. Ges., 1895. 

Loewy: Cong. Dilatation d. Harnblase. Prag. med. Woch., 1893. 

Mayr: Kloakenbildung bei Hausthieren. Ergebn. d. allg. Path., iv., 1899. 

Rasch: Weibliche Epispadie u. Fissura vesice. Beitr. v. Bruns, xviii., 1897. 

Reichel: Entstehung d. Missbild. v. Harnblase u. Harnrdhre. Langenb. Arch., 46 

., 1893. 

Roth seh ungen im Bereiche des Ductus omphalomesentericus. Virch. Arch., 
6 Bd., 1881. 

Scherer: Imperforation des Anus. Arch. f. Kinderheilk., xiv., 1892. 

Schneider: Atresia ani uterina et vesicalis. Arb. her. v. Baumgarten, i., 1892. 

Schwyzer: Atresie der Harnröhre. Arch. f. Gyn., 43 Bd., 1892. 

Seidler: Anus vaginalis. Arb. a. d. pathol. Inst. zu Göttingen, Berlin, 1898. 

Thiersch: Entstehung u. Behandlung d. Epispadie. Arch. d. Heilk., x., 1869. 


(f) Malformations of the Extremities due to Arrested Development. 


§ 139. Defective development of the extremities is not rare, and is 
to be referred in part to a primary defect of the anlage of an extremity, 
in part to a disturbance in the later development of the limbs or the. 
bones, and in part to constrictions caused by strands of the fatal mem- 
branes or by loops of the umbilical cord. Further, such defective devel- 
opment of the extremities may also follow malformations of the central 
nervous system. According to the degree of malformation, the following 
different forms may be distinguished : 

(1) Amelus. The extremities are completely absent; in their place 
are found only warty or stump-like rudiments. The trunk is usually 
well formed (Fig. 382). 

(2) Peromelus. Stunting of all the extremities. 

(3) Phocomelus. The hands and feet are alone developed and are 
attached directly to the shoulder and pelvis respectively. 

(4) Mieromelus (microbrachius, micropus), The extremities are devel- 
oped, but are abnormally small (Fig. 383). 

(5) Abrachius and Apus, Absence of upper extremities with well- 
developed lower ones, or rice versa, 

(6) Perobrachius and Peropus. Stunting of the upper or lower ex- 
tremities. 

(7) Monobrachius or Monopus.  Absence of one of the upper or 
lower extremities. 








MALFORMATIONS OF THE EXTREMITIES. 519 


(9) Absence of individual bones may occur in any part of the extremi- 
ties (Fig. 388). 

(10) Perodactylism —stunting of the fingers or toes—appears in a great 
variety of forms, but in general is seen as a defective development 
(brachyphalangism) or complete absence of individual phalanges (Figs. 
386, 388, 390, c), or as membranous (Figs. 387, 389) or bony (Figs. 
388, 390, d, e) connections between the fingers (syndactylism). 

If only the outer fingers or toes are developed while the middle ones 
are lacking, there arise those formations (Figs. 391, 392) designated as 
cleft-hand and cleft-foot (Kümmel). In more extensive malformations 





Fig. 391. Fic. 392. 


Fic. 391.—Peropus or cleft-foot. (After Otto.) Right foot. a, Great toe; J), little toe. 


Fig. 392.—Skeleton of the foot in Fig. 391, seen from the dorsal side. a, Great toe; h, little toe: c, 
rudiment of third toe; d, tibia: e, fibula; J, talus; 2, calcaneus; 3, og naviculare ; 4, 08 cuneiforme majus; 
>, os cuneifurme minus; 6, os cunelforme tertium; 7, os cubiforme. 


of the fingers there occur in part also malformations and defects in the 
region of the tarsal and metatarsal bones (Fig. 392) or carpal and meta- 
carpal bones respectively. These malformations are designated respec- 
tively as peropus and perochirus. Absence of the hand or foot is known 
as achirus Or apus. 


Literature. 


(Malformations of the Extremities. ) 


Abelin u. Blix: Ueber Abschnürung von Gliedern. Jahresber. d. ges. Med., 1863. 

Arnold: Myelocyste, Transposition v. Gewebskeimen u. Sympodie. Beitr. v. Ziegler, 
xvi., 1894. 

Bambeke: Ueber Abschnürungen von Gliedern. Annal. de la Soc. de med. de Gand, 
1861. 

Basch: Ueb. d. sog. Flughautbildung in d. Kniekehle. Zeitschr. f. Heilk., xii., 1891. 

Billroth: Durch Knochendefecte bedingte Verkrümmungen d. Fusses. Arch. f. klin. 
Chir., i., 1861. 

Börner: Anat. Unters. eines Kindes mit Phokomelie. Inaug.-Diss., Marburg, 1887. 

Brunner: Genese, congen. Mangel u. rudim. Bildung d. Patella. Virch. Arch., 124 
Bd,, 1891. 

Burckhardt: Knochendefecte am Vorderarm u. Unterschenkel. Jahrb. f. Kinder- 
heilk., 31 Bd., 1890. 

Dareste, C.: Mém. sur les anomalies des membres. Journ. de l’anat. et de la phys., 
1382. 


520 DISTURBANCES OF DEVELOPMENT. 


Ehrlich: Congen. Defecte u. Hemmungsbildungen d. Extremitäten. Virch. Arch., 
100 Bd., 1885. ; 

Fischer: Congen. Defectbildung an d. Unterextremität eines siebenj. Knaben, Rostock, 
1886 


Fricke: Ueber congen. Defect der Fibula, Bonn, 1887. 
Gebhardt: Ein Beitrag zur Anatomie der Sirenenbildungnen (contains anatomical 
study of Figs. 384 and 885). Arch. f. Anat. u. Phys., 1888. 
1 : Beitr. z. Lehre v. d. Missbild. d. Extremitäten. Beitr. v. Bruns, vii., 
1891. 


Grisson: Defect d. Oberschenkeldiaphyse. Langenbeck’s Arch., 49 Bd., 1894. 

Gruber: Defecte d. Hand. Arch. f. Anat., 1868; Defect des Radius. Virch. Arch., 
32, 40 Bd., 1861. 

Hlavaceck: Extremitätenmissbildungen. Deut. Zeitschr. f. Chir., 48 Bd., 1896. 

Joachimsthal: Defecte langer Röhrenknochen. Deut. med. Woch., 1895; Brachy- 
dactylie u. Hyperphalangie. Virch. Arch., 151 Bd., 1898; Die angeb. Verbildung 
d. ob. Extremitäten, Hamburg, 1900. 

Klaussner: Die Missbildungen der menschl. Gliedmaassen, Wiesbaden, 1900. 

Kümmel: Die Missbildungen d. Extremitäten, Kassel, 1895. 

Lotheissen: Mangel d. Oberschenkelknochen. Beitr. v. Bruns, xxiii., 1899. 

Mayer: Spalthand u. Spaltfuss. Beitr. v. Ziegler, xxiii., 1898. 

Melde: Defect der Tibia u. Polydaktylie. Inaug.-Diss., Marburg, 1892. 

Mies: ope Mangel des V. Fingers u. Mittelhandknochens. irch. Arch., 121 Bd., 
18 


Otto: L. c., 8 130. 


e 


Paster: Missbildung der Hände und Füsse. Virch. Arch., 104 Bd., 1886. 

Pauly : Mangel der Diaphyse u. der unteren Epiphyse d. Tibia. Langenb. Arch., 
xxiv., 1879. 

Pfitzner: Brachyphalangie. Verh. d. anat. Ges., 1898. 

Poelchau: Ein Fall von Perodaktylie. Inaug.-Diss., Königsberg, 1891. 

Rasch: Syndactylie und Polydactylie. Beitr. v. Bruns, xviii., 1897. 

Bennert: Beitr. zur Kenntniss v. d. Missbildungen der Extremitäten, Leipzig, 1882. 

Ruge: Sirenenbildung. Virch. Arch., 129 Bd., 1892. 

Schäfer: Congen. Defecte von Händen und Füssen. Beitr. v. Bruns, vii., 1891. 

Steinhaus: Congenitaler Tibiadefect. Virch. Arch., 163 Bd., 1901. 

Steinthal: Ueber angeb. Mangel einzelner Zehen. Virch. Arch., 109 Bd., 1887. 

Stricker: Ueber angeb. Defect des Radius. Virch. Arch., 31 Bd., 1864. 

Teacher and Coats: Siren-malformation. Journ. of Path., iii., 1895. 

Tschudi: Vollst. Verwachsung aller 5 Finger. Zeitschr. f. Chir., 85 Bd., 1893. 

Voigt: Ueber congenitalen Radiusdefect. Arch. d. Heilk., 1863. 


2. ABNORMAL POSITION OF THE INTERNAL ORGANS AND OF THE 
EXTREMITIES. 


§ 140. Of the abnormal positions of the internal organs, the most im- 
portant is the one known as situs inversus viscerum—i.e., a lateral 
transposition of the internal organs, so that the position of the thoracic and 
abdominal organs forms a mirror-image of the normal position. This 
condition has been observed both in double monsters and in single indi- 
viduals. It may be restricted to the heart alone, or to the abdominal 
organs, or more rarely to a part of the latter (situs irregularis), but the 
last is rare. In general, abnormal positions occur especially in the case 
of the abdominal organs. For example, the kidney is not infrequently 
found in an abnormal position (dystopia renis), usually abnormally low, 
so that it approaches the sacral promontory or lies in front of the same. 
The testis is not rarely retained within the abdominal cavity (ectopia in- 
terna, or abdominalis testis, or cryptorchismus), or within the inguinal canal 
(ectopia inguinalis), or at the external ring (ectopia pubica), or in the 
fold between the thigh and scrotum (ectopia cruroscrotalis), or in the peri- 
neal region (ectopia perinealis), or in the fold of the groin (ectopia cru- 
ralis). Abnormal positions of the intestines, particularly of the colon, are 
not rare. 


ABNORMAL POSITION OF ORGANS AND PARTS. 521 


Among the abnormal positions of the extremities congenital luxa- 
tions (slipping of the articular heads from their sockets) are of especial 
interest. They are most common at the hip-joint, more rare at the 
elbow-, shoulder- and knee-joints. According to von Ammon, Grawitz, 
Kronlein, and Holtzmann, the congenital luxations are in part due to 
local arrests of development, but may also be the result of mechanical in- 
fluences. In the case of the hip-joint the disturbance of development 
results in a small and imperfect acetabular socket, and the head of the 
femur is usually more or less imperfectly developed. The small acetab- 
ulum lies in the normal position, ‘but the head of the femur is displaced, 
most often backward (luxatio iliaca). At birth the ligamentum teres is 
always intact, and the capsule of the joint covers both the head of the 
femur and the acetabulum. After much use of the leg the ligamentum 
teres becomes stretched and may tear, the capsule becomes dilated and 
bag-like, and at the point where it is pressed against the bone may be- 
come perforated. A new joint may then be formed through the prolif- 
eration of the surrounding tissues. 

Abnormal positions of the feet and hands are to be referred partly 
to disturbances of development and partly to mechanical influences 
exerted upon the extremities during their growth. The most important 
is congenital club-foot (pes equinovarus), which, according to Esch- 
richt, is to be referred to an arrest of development, by which the foot is 
left in the foetal position, with accompanying abnormal development of 
the bones and their articular surfaces. The inner border of the foot is 
sharply elevated, and the foot at the same time brought into plantar 
flexion. The collum tali is elongated in an anterior and inferior direc- 
tion (Hüter, Adams). If the children thus afflicted learn to walk, they 
tread upon the outer side of the foot, which thereby becomes flattened, 
while the foot becomes still more sharply turned inward. 

Congenital club-foot, though usually to be regarded as a primary dis- 
turbance of development of the affected joint, may also under certain 
conditions be caused by an abnormal pressure due to a relatively small 
uterus (Volkmann). Under these conditions develop also those patho- 
logical positions of the foot known as pes calcaneus and pes valgus, 
which are characterized partly by strong dorsal flexion and partly by 
an outward twisting of the foot. Frequently the evidences of the press- 
ure to which the feet have been subjected are seen in an atrophic con- 
dition of the skin and portions of the bones. 

The position of the hand known as clubbed-hand or talipomanus is 
caused by a rudimentary development of the radius, and is usually asso- 
ciated with other malformations. 


Literature. 
(Malformations of the Extremities and Internal Organs, due to Change of 
Position. ) 


v. Ammon: Die congen. chir. Krankh. d. Menschen, Berlin. 1842. 

Arneill: Transposition of the Viscera. Amer. Jour. of Med. Sc., 1902. 

Bessel-Hagen: Pathologie u. Therapie des Klumpfusses, Heidelberg, 1889. 

Buhl: Transposition d. Eingeweide. Mittheil. a. d. pathol. Inst. zu München, 1878. 

Debersaques: Pathogénie du pied bot congen. Ann. de la Soc. de méd. de Gand , 
1891. 

Dollinger: Congenitale luxation. Langenbeck’s Arch , xx., 1877. 

Geipel: Situs transversus. Festschr. z. 50-jähr. Besteh. d. Krankenhauses, Dresden, 


29 


5223 DISTTRBANCES OF DEVELOPMENT. 


Grawitz: Urescten d anzeb. Hiftgeienkverrenkungen. Virch Arch. 74 Bd. 15%. 

Hirsch: Die Eotet-husg i. angeb. Hüftverrenkung. Virch. Arc. 148 Bd. 1% 

Holl- Plattfum. Langeoteck > Arch.. axv.. 199. 

Holtzmann: Die Entsschung d. cousen. Luxationen Virch Ara. 10 Bd. Mn. 

Koller. Situs viscerusm inverkus. Virch. Amb. 156 Bd. 1569. 

Kipper: Situs transversuse Inaug.-Die.. Martoirg. 1796. 

Kirmiseon: Chirurg. Krankbeiten angeb. Ursprungs. Stuttgart. 19. 

Kocher Klumpfu=. Deut. Zeit«chr. 1. Chir . ix.. 1770. 

Krönlein- Luxationen. Deut. Chir.. 26 Lief.. 12. 

Küchenmeister. Die anget. voll-t Verksgerung d. Einge werde «L Menschen. Leipzig. 
1053. 

Lochte. Zur Keuntn. d Situs transversus partialis Beitr. v. Ziegler. xvi. 194: 
Situs Vieerum irregularir. Ib . xxiv.. 182. 

Lorenz: Pathologie u. Therapie der angeb. Hüftverrenkung. Wien. 1685. 

Martinotti: Deils traspesizione laterale dei visceri. Bologna. DO 

Messner: Kuschenveränd. bei Pes calcanens congen. Arch. ft. klin Chir., 42 Bd., 12. 

Michaud: Piel bot congenital. Arch. de phys . iii. 1X70. 

Müller: Congen. Luxation im Knie. Arb. a. d. chir. Universitätspolikl. in Leipzig. 


10385, 
Pauly. Plattfuss. Langenbeck’s Arch.. xxiv., 1879. 
Sonnenburg: Klumpfuss. Beslenevklop. d. med. Wissensch.. 1296 «Lit. ). 
Wehn: Zur Frage d. Situs transversus Virch Arch.. 98 Bd,. Iss. 


3. MALFORMATIONS DUE TO EXCESSIVE GROWTH OR MULTIPLICA- 
TIONS OF ORGANS OR BODY-PARTS. 


£141. The malformation known as general giant growth occurs as 
the result of an excessive growth of the entire body, either during intra- 
uterine life or later. During extra-uterine life such an abuormal growth 
may occur that the size of the affected individual may far exceed the 
maximum normal limits. 

Partial giant growth may also take place during intra-uterine life or 
after birth. The head and portions of the extremities are usually at- 
fected. A unilateral giant growth is usually restricted to the half of the 
face or to one extremity, but in very rare cases the hypertrophy may in- 
volve all the parts of one side: face, trunk, and extremities. In extra- 
uterine life trauma sometimes gives the impulse to a pathologieal excess 
of growth. 

In the pathological hypertrophy of an extremity, or of a portion of 
the same, asa finger, the structure of the part may in general preserve 
its normal relations, in that all the constituent tissues participate in the 
increased growth. Im other cases the tissues are not equally involved, 
so that, for example, the soft parts, particularly the fat tissue, may be- 
come especially increased in amount. Further, the enlarged soft parts 
of the extremities often show a pathological structure, containing, for 
example, abnormally developed blood- and Iymph-vessels. When the 
extremities are distigured as the result of such an increase of tissue, the 
condition is usually called elephantiasis. If the thickened areas are 
sharply circumscribed, the formations are regarded as tumors, and, ac- 
cording to their structure, are classed with the angiomata, lymphangio- 
inata, and fibromata (see 88 103, 108, 109). On the trunk the local 
excesses Of tissue-growth oceur most frequently in the form of elephan- 
tiasis-like formations, or as tumors, The same is true of such growths 
of the soft parts of the face; the lips, cheeks, and tongue not infre- 
quently being more or less enlarged and disfigured through the forma- 
tion of connective-tissue hyperplasias richly supplied with lymphatic 
vessels, 

Cireumseribed hypertrophies of the bones oeeur in various portions 


MALFORMATIONS DUE TO EXCESSIVE GROWTH. 523 


of the skeleton, and are sometimes multiple. The bones of the skull 
aS well as those of the face may be thus affected, and there occur cases 
in which the hypertrophy of the bone may be so extensive that one or 
both of these regions may show marked disfiguration, and there are pro- 
duced conditions which are known under the general term of Teontiasis 
ossea (Fig. 126). Cireumscribed hypertrophies of the bones lead to the 
formation of osteomata or exostoses, which are often multiple. On the 
trunk and extremities local growths of bone may lead to the enlargement 
of single bones as well as to the formation of atypical excrescences 
known as osteomata and exostoses, which are not infrequently multiple. 


Literature. 
(Giantism.) 


Andersen: Rtiesenwuchs der Extremitäten. St. Thom. Hosp. Rep., London, 1882. 

Arnheim: Congenitale halbseitige Hypertrophie. Virch. Arch., 156 Bd., 1898 (Lit.). 

Bessel- Hagen: Part. Riesenwuchs u. multiple Exostosen. Langenbeck’s Arch., 41 
$d... 1891. 

Buhl: Ein Riese mit Hyperostose. Mitth. a. d. path. Inst. München, 1878. 

Busch: Riesenwuchs der Extremitäten. Arch. f. klin. Chir., vii., 1866. 

Curling: Riesenwuchs der Finger. Med.-Chir. Trans , xxviii., 1845. 

Ewald: Hypertrophie der Hand = Virch. Arch.. 36 Bd , 1873. 

Fischer: Kiesenwuchs der Extremitäten. Deut. Zeitschr. f. Chir., xii., 1880. 

Fränkel: Makrosomia. Virch. Arch , 46 Bd., 1869. 

Friedberg: Riesenwuchs der Extremitäten. Ib.. 40 Bd., 1867. 

Friedrich: Halbseitige congenitale Kopfhypertrophie. Ib , 28 Bd., 1863. 

Gruber: Makrodaktylie Ib., 36 Bd., 1872 

Kessler: Ucber einen Fall von Makropodia lipomatosa. Inaug.-Diss , Halle, 1869. 

Little: Riesenwuchs der Extremitäten. Trans. Path. Soc., 1866. 

Trelat et Monod: De !’hypertrophie unilatérale. Arch. gen. de méd., 1869. 

Vierordt, H.: Anatom., physiol. u. physikal. Daten u. Tabellen, Jena, 1893. 


See also § 77. 


S 142. The occurrence of supernumerary organs, or of a multipli- 
cation of parts of the skeleton, and of the muscular system, is relatively 
frequent. Such phenomena are to be attributed in part to a cleavage or 
multiple appearance of the given anlage, and in part to a more marked 
development or persistence of organs which normally remain in a rudi- 
mentary state, or undergo retrogression during the period of growth. 
Further, certain of the conditions included under this head may be re- 
garded as reversions. 

1. Duplications of the extremities. A duplication of an entire ex- 
tremity without the duplication of the pelvic or shoulder bones has not 
been observed in man. Duplication of the hands and feet is very rare 
(Fig. 393), but a number of cases are reported in the literature. The 
number of fingers may reach nine or ten. 

Much more frequent is a multiplication of the fingers (polydactyl- 
ism ) on a single hand (or foot respectively ), in which condition the super- 
numerary fingers (or toes) are attached in part at the ulnar or radial side 
(or tibial and fibular sides respectively), or in part intercalated between 
the others (Figs. 390, a; 394). Often the fingers are duplicated only in 
part—that is, by the cleavage of the first or the first and second terminal 
joints (Figs. 395, 396). Those attached at the margin of the hand may 
he well developed (Fig. 394) or rudimentary. Occasionally they appear 
as sınall peduneulated fibrous tumors. In the fully developed super- 
numerary fingers or toes the phalanges (Fig. 394) may articulate with 
the metacarpal or metatarsal bones of a neighboring finger or toe, or with 


524 DISTURBANCES OF DEVELOPMENT. 


their own (supernumerary ) carpal or tarsal bones (Fig. 390, 5a). Poly- 
dactylism in certain cases is inherited and is therefore dependent upon 
intrinsic causes. A duplication of 
& finger may also occur through 
cleavage of the anlage under the in- 
fluence of intra-uterine influences, 
and is consequently not inheritable. 





Fic. 383, Fra. 304. 
Fig. 383.—Polydactylism with forking of the hand. (After Lancereaux.) 
Fig. 364.—Polydactylism in a new-born child. Skeleton. Duplication of the phalanges of the fourth 
and Afth Angers. Natural size. 





Fig. 395, Fig. 396. 


Fig, 305.—Polydactylism and syndactylism of the left hand. Reduced one-fifth. 
Fig. 396.—Polydactylism and syndactylism of the right foot. Reduced one-fifth. 


SUPERNUMERARY ORGANS OR PARTS. 525 


2. Supernumerary nipples and breasts (hyperthelia, hyper. 
_mastia) are not uncommon malformations in both sexes, and are prob- 
ably to be regarded as a reversion to polymastic racial ancestors. The 
supernumerary organs are usually situated on the thorax, along two lines 
converging from the axillary to the inguinal regions, but in rare cases 
they may be found elsewhere—in the axilla, on the shoulder, on the 
abdomen, back or thigh. They are usually small, but in the event of 
pregnancy may take on functional activity. The number of the nipples 
may reach as high as ten. 

3. The formation in men of breasts resembling those of women 
(gynzcomastia) is rarely seen in well-developed men with normal sex- 
ual apparatus (see Hermaphrodism, $ 143), but it not infrequently hap- 
pens that the male breast: undergoes a moderate enlargement at the time 
of puberty. 

4. Duplication of the penis is of very rare occurrence, and may be 
associated with the formation of two urethre having independent open- 
ings into the bladder, and with two scrota, the two penises being typi- 
cally developed (Lange). 

5. Supernumerary bones and muscles are of frequent occurrence. 
Supernumerary vertebre may be found in any part of the spinal column; 
and at its lower end may in rare cases cause a lengthening of the column, 
resulting in the formation of a tail. According to Virchow, three forms 
of tails may be distinguished: true tails containing bones; false or im- 
perfect. tails which represent an elongation of the vertebral column, 
but contain neither cartilage nor bones (so-called pig’s-tail) ; and tail-like 
appendages of skin which consist of different forms of tissue, and in part 
are to be classed with the teratomata. The true tails are very rare; ac- 
cording to Bartels, they are more often the result of a separation or 
elongation of the vertebra than of an Increase in their number. 

Supernumerary ribs in the neck or lumbar region, as well as a forking 
of the ribs, are not rare. 

Supernumerary teeth also occur. 

6. Duplication or cleavage of the anlage of the thoracic and ab- 
dominal organs occurs most frequently in the case of the spleen, pan- 
creas, adrenals, ureters, pelvis of the kidneys, and lungs, more rarely in 
case of the ovary, liver, kidney, testicle, and bladder. 


Literature. 


(Supernumerary Organs or Parts.) 


D’Ajutolo: Contrib. allo studio delle varieta numeriche delle vertebre. Il Morgagni, 
XNX., 1888. 

Ammon: Die angeb. chirurg. Krankheiten, Berlin, 1842. 

Bartels. Schwanzbildung. Arch. f. Anthrop., 15 Bd., 1884. 

Beer: Beitr. z. d. Lehre v. d. Missgeburten. Inaug. Diss., Zurich, 1850. 

Boinet: Polydactylie et atavisme. Rev. de méd., xviii., 1898. 

Bonnet: Die Mammaorgane. Ergebn. d. Anat., ii., Wiesbaden, 1893. 

Buschan: Polymastie. Eulenburg’s Realencyklop., xix.. 1898 (Lit.). 

Ecker: Schwanzbildung. Arch. f. Anthrop., xi.; Arch. f. Anat., 1880. 

Freund: Schwanzbildung beim Menschen. Virch. Arch., 104 Bd., 1886. 

Gegenbaur: Krit. Bemerkungen über Polydaktylie als Atavismus. Morph. Jahrb., 
TSS(). 

Gerlach: Schwanzbildung. Morph. Jahrb., vi. 

Habs. Makrodaktvlie. Deut. Zeitschr. f. Chir., 37 Bd , 1898. 

Hennig u. Rauber: Ein Fall von geschwänztem Menschen. Virch. Arch., 105 Bd., 
1886. 


~ 


526 DISTURBANCES OF DEVELOPMENT. 


Joachimsthal: Hyperphalangie Virch. Arch., 151 Bd.; Die angeb. Verbild. d. ob. 
Extremität, Hamburg, 1900. 

Jolly: Polydaktylie m. Missbild. d. Arms. Int. Beitr., Festschr f. Virch., i., Berlin, 
1891. 


Klaussner: Ueber Missbildungen d. menschl. Glicdmaassen, Wiesbaden, 1900. 

Kohlbrugge: Schwanzbildung u. Steissdrüse. Natunrk. Tijdschr. voor Ned. Ind., 
1897. 

Kollmann: Handskelet u. Hyperdaktylie. Anat. Anz., iii, 1888. 

Küttner: Verdoppelung des Penis. Beitr. v. Bruns, xv., 1896. 

Lange: Complete Verdoppelung des Penis. Beitr. v. Ziegler, xxiv., 1898 (Lit.). 

Laurent: Les bisexués, gynecomastes et hermaphrodites, Paris, 1894. 

Leichtenstern: Supernumeräre Brüste u. Brustwarzen. Virch. Arch., 73 Bd., 1878 
(Lit.). 

Levin: Ueberzähl. kleine Finger. Virch. Arch., 142 Bd., 1895. 

Lissner: Schwanzbildung beim Menschen. Virch. Arch., 99 Bd., 1887. 

Neu bauer: Polymastie mit 10 Brustwarzen. Chl. f. Gyn, 1886; 35 Fälle v. Ver- 

opp. d. duss. Genitalien. Monatsschr. f. Gebh., vii.. 1897. 

Otto: Monstrorum sexcentorum descriptio anatomica, 1844, 

Pfitener: Doppelbildung d. 5 Zehe. Morph. Arb., 1895; Verdoppelung d. Zeigefingers. 
Ib., vii., 1897: Missbild. d. Extremitätenskelets. Ib., viii., 1898. 

Piatnisky: Bau des menschlichen Schwanzes. Inaug.-Diss., Petersburg; Anat. Anz., 
viii., 1893. 

Schmidt: Normale Hyperthelie menschl. Embryonen. Anat. Anz., xi., 1896. 

Sell: Hyperthelie, Hypermastie u. Gynäkomastie. Ber. d. Naturf. Ges. Freiburg. 
ix., 1894 (Lit.). 

Stieda: Gynäkomastie. Beitr. v. Bruns, xiv., 1895. 

Stahr: Congen. Tumor am kl. Finger. Virch. Arch., 151 Bd., Suppl, 1898. 

Virchow: Schwanzbildung. Deut. med. Woch., 1884. 

Wiedersheim: Der Bau des Menschen, Freiburg i. B.. 1893. 

Zander: Ist die Polydaktylie theromorphe Varietät oder Missbildung? Virch. Arch., 
125 Bad., 1891. 


4. TRUE AND FALSE HERMAPHRODISM. 


§ 143. The fact that the sexual organs, both the sexual glands and 
the external genitals, of both sexes, develop from originally similar 
anlage which contain the beginnings of all the sexual organs of both 
sexes, makes it a priori probable that malformations might result through 
unequal development of the anlage of the right and left sides, or through 
a simultaneous development of organs peculiar to both sexes, or finally 
through a lack of harmonious development of the external and internal 
genitals. 

Those malformations which are to be referred to some one of the factors 
named, and which are characterized by the fact that thesexual apparatus 
of a single individual contains parts belonging to both the male and 
female, are grouped under the designation hermaphrodismus (Fig. 
397). When both sexual glands ( testis and ovary) are present the con- 
dition is called hermaphrodismus verus (hermaphrodismus glandularis, 
Siegenbeek van Heukelom). If the mixing of sexual characteristics 
consists merely of a combination of male and female genital passages 
with the external genitalia of the opposite sex, the condition is known as 
pseudohermaphrodismus. The true sex is determined by the nature of 
the sexual glands. 

The body build of hermaphrodites frequently shows a curious mix- 
ture of male and female characteristics. Forexample, the breasts, neck, 
and shoulders may correspond to the female type, while the develop- 
ment of the beard, face, Jarynx, and voice may correspond to the male 
type. In false hermaphrodites the body characteristics do not always 
correspond to the true nature of the sexual glands; a male may resem- 
ble a female, and tice versa, 


HERMAPHRODISM. 527 


The following chief types of hermaphrodism may be distinguished: 

I, Hermaphrodismus verus or androgynes.—1. Hermaphrodismus 
verus bilateralis, or double-sided hermaphrodism, is characterized by the 
presence on both sides of both ovary and testis, or the presence on 
both sides of an organ containing both ovarian and testicular tissue. 
Heppner asserts that in a nine months’ old child, having hermaphroditie 
external genitals, with vagina, uter d tubes, both ovary and testis 
were found in the broad ligament; epididymis and vas deferens were 
wanting. 

Hermaphrodismus verus unilateralis, or one-sided hermaphrodism, is 
that condition in which upon one side there exists but one sexual gland, 
while on the other both testis and ovary are present. Salen has reported 
a case of awoman of forty-three years of age, who had menstruated since 
her seventeenth year, in whom there was found upon the right side (cas- 
tration on account of uterine myoma) a hermaphroditie gland, the 














Hermaphrodismus verus lateralis. (After Qbolonsky.) a; Urethra: b, prostate: oliculun 
hymen €. canalis urogenltalle: f, Udder: g. vagina: h, uterus: hy left uterine born: & 
infundibulum of left tube: k, left ‘ora vt ligamentum dvarit ligamentum teres sin 
istrum: 1. right tube: 0. right testicle: p. epididymis: q. right van deferens: r. ligamentum teres dextrum. 
‘Shout one-half nataral size, Spectinen ta the eellecion of the Pathological Institute of the German Cok 
versity in 5) 





nature of which was confirmed by accurate microscopical examination. 
The ovarian portion of the gland was typically developed; the epithe- 
lium of the seminiferous tubules of the testicular portion consisted of 
follicular cells and cells of Sertoli, but lacked spermatogonia and seminal 
cells. Blacker and Lawrence have also described a case of hermaphro- 
ditie gland occurring in a child still-born at eight and a half months, 

3. Hermaphrodismus verus lateralis is that condition in which there is 
an ovary on one side and a testis on the other. It has been many times 
observed in man (Rudolph, Stark, Berthold, Barkow, H. Meyers, Klebs, 
Messner, and others), though in the majority of cases no careful micro- 
scopical examination was made, and when carried out, ovarian tissue 
could not with certainty be demonstrated. Several years ago Obolonsky 
reported a case (a twelve-year-old girl) from the collection of the German 





528 DISTURBANCES OF DEVELOPMENT. 


University in Prague, in which the histological examination showed on 
the right side a testicle (Fig. 397, 0), and on the left side an ovary (k), 
but it is to be noted that ova were not seen in the latter. The right 
broad ligament contained a testis (0), an epididymis (p), a vas deferens 
(q), # rudimentary tube (x), a round ligament (r); the left broad liga- 
ment, on the other hand, contained an ovary (k), with an ovarian liga- 
ment (1), and a well-developed tube (i). Moreover, a uterus (h), 
vagina (g), and also a prostate (b) were present. According to the re- 
ported observations, the corresponding sexual passages may be wholly or 
in part wanting. The external genitals are malformed, and combine 
structures belonging to both sexes. 

II. Hermaphrodismus spurius, or pseudohermaphrodismus, is 
characterized by a bisexual development of the sexual passages and ex- 
ternal sexual organs in association with a unisexual development of the 
essential sexual gland. The most. 
pronounced cases occur in males, 
who, in addition to their proper 
sexual organs, possess a more or 
less well-developed vagina, uterus, 
and tubes. It is much more 
rare to find in females a develop- 
ment of a portion of the Wolffian 
duet. 

In male false hermaphrodites 
the external genitals are frequent- 
ly malformed and approach the 
female type, while in female false 
hermaphrodites the external geni- 
tals resemble those of the male 
(Fig. 398). 

The resemblance of the male 
external genitals to those of the 
female is brought about by a 

Fic. 308, External genitals of a female false ner- Stunting of the penis and a total or 
muphrodite, with stenowis of the vaginal orice. a, partial failure of the sexual fur- 
Penis-ike eiltoris; I, labia tuajora, row in the penis to close (hypos- 

padias), so that the two halves of 
the scrotum are separated, leaving a depression beneath the root of the 
which represents the remains of the sinus urogenitalis, The serotal 
come, therefore, to resemble the labia majora, particularly in the 
case of non-descent of the testicles. The external genitals of the female 
approach in appearance those of the male through the development of 
the clitoris into a sort of penis (Fig. 398, a), while the vaginal opening 
is narrowed or closed through the union of the labia. The vagina and 
urethra h a common opening, or open separately beneath the penis- 
like clitori 

The atypical development of the external genitals may or may not 
be associated with malformations of the sexual passages; and is, there- 
fore, not dependent upon malformations in other portions of the sexual 
apparatus, 

1. Pseudohermaphrodismus masculinus occurs in three varieties: 

First, pseudohermaphrodismus maseulinus internus, in which condition 
genitals are of the male type, and the prostate is developed, 
uly pierced at the colliculus seminalis by a canal opening into 




























but is 





HERMAPHRODISM. 529 


the urethra, the former being continued above into a rudimentary or 
ınore or less well-developed vagina, often also into a more or less well- 
formed uterus, and even tubes. The male organs may be well developed 
or more or less malformed. 

Second, pseudohermaphrodismus masculinus completus, or externus et in- 
ternus, in which form the vagina, uterus, and tubes are present in a state of 
rudimentary or more or less complete development, while the external 
genitals resemble more or less completely the female type. The penis 
presents the condition of hypospadiasand resembles the clitoris; beneath 
it lies a furrow at whose posterior end there is usually an orifice leading 
into a short vestibule which divides at once into a urethra and a vagina. 
Sometimes the vagina and vestibule are separate. In rare cases the ex- 
ternal genitals appear normal, but the penis contains a double canal, the 
upper one representing the urethra, the other the sexual passage. In 
the case of a more marked development of the ducts of Müller the vasa 
deferentia are frequently defective, and the seminal vesicles are some- 
times wanting. 

Third, pseudohermaphrodismus masculinus externus, in which only the 
external genitals depart from the male tyne, and resemble more or less 
closely the female. As in these cases the bodily habitus often simulates 
that of the female, the true sex of the individual may easily be mis- 
taken. 

2. Pseudohermaphrodismus femininus also occurs in three similar varie- 
ties, but is of much rarer occurrence. 

In pseudohermaphrodismus femininus internus rudiments of the Wolffian 
duets, lying in the broad ligament or in the uterovaginal wall. and some- 
times extending to the clitoris, are found in association with well-devel- 
oped external genitals. 

Pseudohermuphrodismus femininus externus is characterized by external 
genitalia resembling those of the male (Fig. 398). 

Pseudohermaphrodismus femininus externus et internus, in which the ex- 
ternal genitals resemble those of the male and there is a persistence of 
parts of the Wolffian ducts, is very rare. Of the internal male genitalia, 
there was found in one case a prostate, and in another case a prostate 
pierced by the vagina, an ejaculatory duct, and a sac resembling a semi- 
nal vesicle, which opened into the vagina. 


The internal sexual organs develop from the same undifferentiated anlage in both 
males and females. These anlage consist of a sexual gland lying on the medial ante- 
rior side of the Wolffian body, and a serual puasage known as the duct of Müller. The 
latter develops beside the Wolfian duct, and, like it, empties into the lower end of the 
bladder or into the sinus urogenitalis. 

In the male the duct of Miller disappears, only slight traces in the form of the 
uterus masculinus or vesicula prostatica remaining; the primitive sexual gland unites 
with a small part of the Wolffian body, which becomes the head of the epididymis, 
another small portion forming the vasa aberrantia testis (organ of Giraldes), the re- 
mainder disappears, while the Wolffian duct becomes the vas deferens and vesicula 
seminalis. 

In the female the Wolffian body and its duct disappear, leaving only a trace in the 
form of the gland-tubules known as the parovarium, but remains of the duct are not 
infrequently found preserved in the uterine wall. From the ducts of Müller, which in 
part coalesce at their lower ends, develop the vagina, uterus, and tubes. The extreme 
upper end of the duct of Miller not infrequently persists in the form of a little pedicled 
sac attached to the abdominal end of the tube, the hydatid of Morgagnti. 

The anlage of the serval glands appear in the fifth week. In mammalia (probably 
also in man) they develop through a localized thickening of the peritoneal epithelium, 
which becomes the germinal epithelium (Waldeyer), while at the same time the meso- 
derm also proliferates. Whether the seminal tubules arise from peritoneal epithelium 


530 DISTURBANCES OF DEVELOPMENT. 


(Bornhaupt Egli), or whether they are derived from an ingrowth of the Wolffian body 
into the testis-anlage ( Waddeyer), is still an undecided question (Kadliker). The ova 
arise from germinal epithelium. The environing cells of the Graatian follicle are 
regarded by Waldeyer as also derived from the germinal epithelium; while Adliker 
believes that they probably arise from the Wolffian body. 

The significance of the peduncucited and non-pedunculated hydatids, found in vary - 
ing numbers near the globus major of the epididymis, is not yet determined (Aölliker). 
The non-pedunculated cyst known as the hydatid of Morgagni is regarded by Waldeyer 
as a remnant of the duct of Miller. According to Ruth, it may also stand in a close 
relation to the Wolflun body, inasmuch as there is occasionally found a vas aberrans 
of the epididymis communicating with it. 

In the development of the vagina and uterus the ducts of Mäller and the Wolfian 
ducts unite at their lower portion to form a rounded quadrangular cord, the genital 
cord. At the end of the second month the ducts of Waller blend to form a single canal, 
which then develops into the vagina and uterus. This union takes place first near the 
middle of the genital cord. The Wolffian ducts play no réle, though remains of these 
are found at birth in the broad ligament (Aölliker) and in the wall of the uterus (Biege/). 
According to observations of Riedel, remains of the Wolffian duct are found in about a 
third of adult females, in the form of a tube lined by cylindrical epithelium surrounded 
by muscle, or as a muscle-bundle without epithelium, lying anteriorly and to the side 
of the uterus and vagina. 

The external genitals begin to develop, even before the cloaca has separated into 
the intestinal and genito-urinary orifices, by the formation, in the sixth week, of a me- 
dian genital tubercle in front of the cloaca, and further, of two lateral folds, the genital 
folds. Toward the end of the second month the tubercle becomes more prominent, and 
shows on its lower surface a furrow, the genital furrow. Inthe third month the cloaca 
becomes divided to form the anal and genito-urinary openings. In the male embryo 
the genital tubercle becomes the penis, the glans being recognizable as early as the 
third month. In the fourth month the furrow closes to form a tube; at the same time 
the two genital folds unite to form the scrotum. 

The prepuce is formed in the fourth month. The prostate arises in the third month 
as a thickening of the tissues at the junction of the urethra and the genital cord. The 
glands of the prostate develop in the fourth month from the epithelium of the canal 
and grow out into the surrounding connective tissue. 

In the female embryo the closure of the genital furrow and the genital folds does 
not take place, so that the sinus urogenitalis remains short. The genital eminence 
becomes the clitoris, the folds become the labia majora, and the edges of the genital 
furrow the labia minora. 


Literature. 


(True and False Hermaphrodism. ) 


Abel: Pseudohermaphrodismus masculinus. Virch. Arch.. 126 Bd., 1891. 

Arnold, J.: Uterus masculinus. Virch. Arch., 47 Bd., 1869. 

Becker: Ücber Zwitterbildung. Würzburger Verh., 1896. 

Benda: Hermaphrodismus. Ergebn. d. allg. Path., ii.. 1897. 

Blacker and Lawrence: Case of Truc Unilateral Hermaphrodismus with Ovotestis in 
Man. Trans. of the Obstetr. Soc. of London, xxx viii. 

Brühl: Ueber Hermaphrodismus. Inaug.-Diss., Freiburg, 1894. 

Crecchio: Hermaphrodismus fem. extern. ct intern. Wien. med. Presse, 1866. 

Debierre: |,’ hermaphrodisme, Paris, 1891. 

Geoffroy St.-Hilaire: Traité de tératologie zool., Bruxelles, 1857. 

Henrichsen: Pseudohermaphr. mascul. extern. completus. Virch. Arch., 94 Bd., 
1883. 

Heppner: Hermaphrodismus verus. Du Bois-Reymond’s Arch., 1870; ref. Cbl. f. d. 
med. Wiss., 1871. 

Keibel: Entwickelungsgesch. d. Urogenitalapparatus. Arch. f. Anat., 1896. 

Klebs: Handb. d. pathol. Anat., i., Bd., 2 Abth., Berlin, 1876. 

Kopsch: Hermaphrodismus verus beim Schweine. Anat. Anz., xii., 1896. 

Laurent: Les bisexués, gynécomastes et hermaphrodites, Paris, 1894. 

Lucksch: Hermaphrodismus spur. masc. int. Zeit. f. Heilk., xxi., 1900. 

Marchand: Hermaphrodismus spurius masculinus’ Virch. Arch., 92 Bd., 1883. 

Messner: Hermaphrodismus verus. Virch. Arch., 129 Bd., 1892. 

Nagel: Entwickelungefehler weibl. Genitalien. Handb. d. Gyn., i.. 1897. 

Nonne: Pseudohermaphrodismus mascul. Jahrb. d. Hamb. Krankenanst., ii., Leipzig, 
1893. 


DOUBLE MONSTERS. 531 


Obolonsky: Zur pathol. Anat. d. Hermaphrodismus hominis. Zeitschr. f. Heilk., ix 
1888. 

Putz: ; Hermaphrodismus verus unilateralis b. Schweine. Deut. Zeitschr. f. Thiermed., 

‚ 1889. 

Raake: Hermaphradismus spur. masc. int. Würzburger Verh., 1896. (Lit.). 

Salen: Hermaphrodismus verus unilateralis. Verh. d. Deut. path. Ges., ii., Berlin, 
1900. 

Schmorl: Ein Fall von Hermaphrodismus. Virch. Arch., 113 Bd., 1888. 

Siegenbeek van Heukelom: Tubulärer und gländularer Hermaphrodismus. Beitr. 
v. Ziegler, xxiii., 1898. 

Stroebe: Pseudohermaphrodismus masc. int. Beitr. v. Ziegler, xxii., 1897. 

Taruffi: I,’ Ermafrodismo. Mem. della Acc. delle Sc. dell’ Ist. di Bologna, 1899 (Lit. ). 

Virchow: Würzburger Verh. Ill. Berl. klin. Woch., 1872; Ges. Abh , Frankfurt, 
1856. 

Wermann: Pseudohermaphrodismus masculinus completus. Virch. Arch., 104 Bd., 
1886. 

Winkler: Pseudohermaphrodismus masculinus internus. Inaug. Diss., Zurich, 1893. 

Zweifel: Krankh. d. äuss. weibl. Genitalien. Hanbd. d. Frauenkraukh., iii., Stutt- 
gart, 1886. 


5. DOUBLE MONSTERS. 
(a) Classification of Double Monsters. 


8 144. Twin-formations lying within a single chorion may be divided 
into two large groups: ficins completely separated from one another, and 
ticins united by some portion of their bodies. 

Of the twins completely separated from one another there may be 
distinguished two types; one in which both tivins are fully developed, and 
one in which one tein is stunted. 

Twins joined together by portions of their bodies may likewise be 
also divided into two groups: twins showing uniform development and twins 
showing an unequal development. 

According to the situation of the duplicated portions of the body, 
there may be distinguished (Foerster) : 

1. Moustra duplicia katadidyma or duplicitas anterior. 

2. Monstra duplicia anadidyma or duplicitas posterior. 

3. Monstra duplicia anakatadidy ma or duplicitas paralleta. 

In general, these may also be conveniently divided into three classes 
(Taruffi): 

I. Twins united chiefly by the epigastrium and thorax. 

Twins united chiefly by the heads. 

2 Twins united chiefly by the pelves. 

Ahlfeld divides the double monsters into two chief groups, those with 
complete aud those with partial doubling of the axial structures. 

In very rare instances triple monsters occur. 


Literature. 


( Double Monsters.) 


Ahlfeld: Die Missbildungen des Menschen, Leipzig. 1880. 1882. 

Foerster: Die Missbildungen des Menschen, Jena, 1865. 

Marchand: Missbildungen. Eulenburg’s Realencyklopadie, xv., 1897. 

Tarufü: Sull’ ordinamento della teratologin. Mem. della R. Acc. delle Scienze dell’ 
Istituto di Bologna, v., 1886; vii., 1898. 
See also S 130. 


(b) The Chief Forms of Double Monsters. 


x 145. Twins separated from each other and lying within a single 
chorion are designated homologous twins. They are always of the same 


532 DISTURBANCES OF DEVELOPMENT. 


sex, have usually a common placenta, and resemble each other very 
closely. If from any cause one of the twins should die after its body has 
been developed, it may be pressed flat by the continued growth of its 
fellow, giving rise to the condition known as foetus papyraceus. 

When twins possess a common placenta within which the blood- 
vessels have abundant anastomoses, the heart of the stronger foetus 
may control the circulation and thereby cause changes in the direction of 
the blood-stream in the weaker twin. Asa result of this the latter suf- 
fers severe disturbances of development, and becomes changed into an 
acardiacus, a monster without a heart, either developing no heart at all or 
only a rudimentary one. In the .ma- 
jority of such cases the head also failx 
to develop (acardiacus acephalus) or re- 
mains rudimentary (acardiacus paraceph- 
alus), and likewise there is usually no 
development, or only a rudimentary 
one, of the upper extremities, thorax 
walls, lungs, and liver, while the ab- 
domen, pelvis, and lower extremities 
are more or less perfectly formed (Fig. 








Fig. 30.- Acardt 


8 acephalus, showing a rudimentary development of the lower extremities (acardi- 
‘cus amorphus). 


FIG. 400.--Acardiacus pseudoacorinus, (After Barkow.) a, Head; b, rudiment of the left upper ex- 
tremity; ¢, rudimentary Intestine; d, artery; ¢, vein, 


399). According to the development of the extremities the following 
varieties may be distinguished: acardiacus paracephalus (or acephalus) 
aympus, monopus, dipus, monobrachius, dibrachius, 

In rarer cases there is no recognizable development of any part of the 
body, and there is formed an acardiacus amorphus, consisting of a shape- 
less mass covered with skin, usually without any indications of extremi- 
ties, and possessing internally only rudiments of organs. 

Of very rare occurrence is the formation known as an acardiacus 
preudodcormus (Fig. 400)—that is, a monster in which the head (a) only 
is developed, while the other parts of the body are represented only by 
small rudiments (b, ¢). 

















DOUBLE MONSTERS. 533 


Literature. 
(Acardiacus.) 


Barkow: Pseudoacormus, Breslau, 1854. 

Claudius: Die Entwickelung der herzlosen Missgeburten. Kiel, 1859. 

Dareste: Compt. rent. de l’Äcad. des sciences, 1865, 1878. 

Heller: Acardiacus amorphus. Virch. Arch., 129 Bd., 1890. 

Hirschbruch: Das Problem der herzlosen Missgeburten. Inaug.-Diss., Berlin, 1895. 

: Acardiacus anceps. Prag. med. Woch., 1892. 

Mulder: Leber cine herelose Misegeburt.Inaug--Diss. Freiburg, 1891. 

Orth: Drei menschl. Missgeburten. Virch. Arch., 34 Bd.. 1872. 

Panum: Zur Kenntn. d. phys. Bedeutung d. angeb. Missbildungen. Virch. Arch., 
72 Bd. 

Perls: Lehrb. d. allgem. Pathologie, ii., Stuttgart, 1879, 1886. 
See also § 147. 


§ 146. Twins equally developed and united to each other occur in 
the following principal types: 

1. Duplicitas anterior (monstra duplicia katadidyma). Anterior du- 
Plication with union of posterior portions of the body. 

Pygopagus (Fig. 401). Union of the twins in the region of the 














Fig. 401 Arete (After Marchand.) A, B, The two twins: a, b, 

blended’ umbitical ; 4,0Ommon placenia. ‘There is a single coccyx and mcrum (from the 
ertebra downward). and tbe lower end of the medullary canal 1 si ‘The 
mfnate in one anal opening. Vestibule of vagina single, the remaining portions of 


Fig, 402.-Ischlopagus. (After Levy.) 


coccyx or of the sacrum. According as the union is more or less exten- 
sive, the sacrum, coccyx, lower end of the medullary canal, anus, lower 


534 DISTURBANCES OF DEVELOPMENT. 


end of the bowel, and the sexual apparatus are either doubled or are in 
part single. 

Ischiopagus (Fig. 402). Union of the twins in the pelvis which 
thereby forms a wide ring, the two sacra being placed opposite each 
other. The anus, lower end of the bowel, and the sexual organs may 
be single or double, and the number of the lower extremities two to 
four. 

Dicephalus (Fig. 403) and diprosopus ( Fig. 404). The duplication 
is limited to the upper part of the trunk and head, or only to the neck 
and head, or the head alone, or, finally, only to portions of the head. 
As the external blending increases in extent, there occurs also a blending 








Fig, 48, Dicephutus dibrachius dipus, Fic. 401 biprosopus distomus tetrophthalmus die- 
tus dibrachius, 


of the internal organs, the intestine, liver, lungs, heart, spinal cord, 
brain, et According to the number of the lower and upper extremi- 
ties there may be distinguished dicephalus tetrapus, dipus, tetrabrachius, 
tribrachius, dibrachius (Fig. 403). When the heads have blended there 
may be distinguished diprosopus, tetrophthalmus, triophthalmus, diophthalm us, 
tetrotun, triotus, diotus, distomus, monostomus, tribrachius and dibrachius (Fig. 
404). 

The mildest. grades of duplicitas anterior are represented by the rare 
cases of duplication of the jac, mouth, or nose. 

2. Duplicitas posterior (monstra duplicia anadidyma). Union of the 

5 the head and thence farther downward with duplication of the 
parts of the body. 
Craniopagus (Fig. 405). Union of the twins in the eranial region. 















DOUBLE MONSTERS. 535 


According to the site of union there may be distinguished craniopagus 
parietalis, frontalis, occipitalis, When the union is more extensive por- 
tions of the brain are also single. 

Cephalothoracopagus or syncephalus (Fig. 
406). Blending of the twins in the region of 
the forehead and face, and in part also of the 
abdomen. In the region of the united heads 
there is an anterior and a posterior face (janus, 
Janiceps). The two faces may be equally ( janus 
aymmetros) or unequally developed (janus asym- 
metros), one face being well developed, the 
other imperfectly. The internal organs present 
different degrees of blending and union into 
single organs, 

Dipygus. The duplication is limited to the 





Fla. 406. Fic. 408. 


iG. 405.—Crantopagus parietalis. 
. 405.—-Cephalothoracopagus with Janus bead. anteriorand 


Fic. N syncephalus, posterior faces are 
matforied, ‘and ome Dut one eyes wello he hows I repreoented by a provesciolike orga alunıcd above 
the 


lower half of the body and the lower extremities, while the upper 
parts are either wholly single or only partly cleft. The duplication 
of the spinal cord may begin at different heights. According to the 
number of extremities different forms may be distinguished. The 
mildest grades of duplication are confined to the lower end of the spinal 
column, the anus, and the external genitla.ı .' 


536 DISTURBANCES OF DEVELOPMENT. 


3. Duplicitas parallela 
(monstra duplicia anakatadidy- 
ma). Duplication of the ante- 
rior and posterior ends of the 
body with parallel positions of 
the trunk. 

Thoracopagus (Fig. 407). 
Union of the twins by the 
thorax. According to the site 
and extent of the union, as well 
as the number of extremities 
present, there may be distin- 
guished different forms, partic- 
ularly the following: ziphopagus 
(union at the xiphoid process), 
sternopagus (union at the ster- 
num), thoracopagus tetrabrachius, 
tribrachius, dibrachius, tetrapus, 
tripus, and dipus. When por- 
tions of the faces have blended 
there results a prosopothoraco- 
pagus. Blending and union of 
the internal organs into single 
organs vary with the degree of 
external blending. The heart 
may be double or single, in 





of the third arm. omens 

two dorsal surfaces. and the laterally. distorten stor the latter case malformed. 

Bosse nailson bot sides, The common tbind toot han Thoracopagus is relatively fre- 
quent. 


Rachipagus Blending of the twins in the region of the spinal col- 
umn is very rare. : 
Literature. 


(Double Monsters.) 


Ahlfeld: Die Missbildungen des Menschen, Leipzig. 1880. 

Barkow: Monstra animalium duplicia per anatomen indagata, Lipsiw, 1828. 
Burckhard: Zwei Doppelmissbildungen. Zeit. f. Geh xl., 1898. 
Lochte: Doppelmissbildung. Beitr. v. Ziegle xvi. . 
Marchand: Pygopagus. Beitr. v. Ziegler, 
Martinotti e 8perino: Diprosopus tetrophithaln 


Rune: J Janiceps asymmetros. Inaug.- Marburg, 1895. 

Schaefer: Ueber einen Dicephalus. Bei Ziegler, xxvii., 1900. 

Biegenbeek van Heukelom: Monstr. double. Rec. de trav. du Lab. Boerhaave, i., 
189! 

Taruffi: Syucephalus dilecanus (Verdopp v. Penis, Scrotum, Anus). Mem. R. Acc. 
Bologna, ix., 1889; Feto umano con due mandibole. Ib..l.. 1895. 

Virchow: Pygopagus. Berl. klin. Woch., 1873. 
See also &§ 132 and 147. 


$ 147. Twins joined together but unequally developed may occur 
in any of the double forms described in § 146. If the development of 
one of the twins remains rudimentary and if its heart does not develop, 
its nourishment can come only through its well-developed fellow. The 
better developed of the two is then known as the autosite, the other as 
the parasite. If the parasite is of only very rudimentary development, 
it may be classed with the bigeminal teratomata (cf. §§ 128 and 129). 








Internat. Monatsschr. f. An., v., 














528 DISTURBANCES OF DEVELOPMEST. 


mation may be regarded as a dipygus parasiticus. Further. there not 
infrequently occur euerygeal teratomala iu which the presence of radimen- 
tary extrem: » (Fig. 410, a, b,c) or of various body elements leaves no 
doubt that the tamor-like formation covered by the skiu of the autosite 
is to be regarded as a double monster, a rudimentary pygopagus. or else as 
4 dipygus parasitieus. Such a parasite is designated as an epipygux. 

Supernumerary estremities (Fig. 411) may also be found upon the 
trunk, or there may occur a headless trunk with extremities (Fig. 412... or a 
rudimentary thorac without extremities, or, finally, teratomata which may be 
interpreted as thoracopagns parasiticus and 
as dipygus parasiticus. The malformation 
is also often called epigastrius. 

The inclusion of such teratomata be- 
neath the skin of the abdomen or thorax, 











Fin, 412. Fro. 413. 
Fig. 412.—Thorarpagus parasiticus. (After Schenk von Grifenberg.) Parasite attached to chat of 
autenite, 


Fic, 413.—Epignathus. (After Lancereaux.) 


or within the abdominal or thoracic cavities of the autosite, gives rise 
to the condition known as inclusio fetalis subcutanea, or abdominalis, or 
mediastinalis, The abdominal inclusion is also designated engastrius. 

In the region of the head rudimentary twin-formations appear most 
often in the mouth cavity, forming usually an amorphous mass, firmly 
attached to the base of the skull, and consisting of skin, connective tis- 
sue, cartilage, bone, brain-tissue, teeth, intestinal elements and muscle, 
and rarely developed extremities. Such malformations are included 
under the designation of epignathus (Fig. 413). 

On other parts of the head rudimentary twin-formations or bigemi- 
nal teratomata are very rare (ef. $$ 128, 129). 





Literature. 


(Unequal Double Monsters.) 


Böhm: Sucralteratom. Berl. klin. Woch., 1872. 
Braune: Die Doppelbildungen u. angeb. Geschwülste d. Kreuzbeingegend, Leipzig, 


1802. 
Breslau u. Rindfleisch: Foctus in foetu. _Virch. Arch., 80 Bd., 1864. 
i n. d'origine parasitaire de la région sacro- 





Calbet: Contrib, A 1ét. des tumeurs cor 
coceygienne, Paris, 1893, 





DOUBLE MONSTERS. 539 


Foederl: Dipygus parasiticus. Langenbeck’s Arch., 58 Bd., 1899. 
Freyer: Kreuzbeingeschwulst. Virch. Arch., 58 Bd., 1873. 
Gross: I,es monstres doubles parasitaires, Nancy, 1877 
Hennig: Congenitale echte Sacraltumoren. Beitr. v. Ziegler, xxviii., 1900. 
Israel: Ein Fall von Verdoppelung der 1. Unterkieferhälfte. Inaug. -Diss., Berlin, 
1867. 
Moussaud: Des inclusions foetales. These de Paris, 1861. 
Otto: Zusammenstellung d. bestbeschrieb. Fälle v. Epignathus. Arch. f. Gyn., viii. 
Schwarz: Beitr. z. Geschichte d. Foetus in foetu, Marburg, 1860. 
Taruffi: Caso d’engastro amorfo extraperitoneale. Mem. R. Acc. Bologna, iii., 1893. 
Wright and Wylie: Included Fatus. Brit. Med. Journ., ii., 1900 
See also SS 128, 129, 132, and 144. 


CHAPTER X. 


The Parasitic Fission-fungi and the Diseases Caused 
by Them. 


I. General Considerations Regarding the Schizomycetes or Fission- 
fungi. 


1. GENERAL MORPHOLOGY AND BIOLOGY OF THE FISSION-FUNGI. 


§ 148. The Schizomycetes or fission-fungi, often also designated 
collectively as bacteria, belong to the protophytes—that is, to the smallest 
simplest forms of plant-life. Many of them are so small that they stand 
upon the very border-line of invisibility even with the use of the highest- 
power objectives and eye-pieces. When occurring in animal tissues, it 
is often very difficult to distinguish them from the products of cell-dis- 
integration; and often this can be accomplished only through the em- 
ployment of specific reagents or staining-methods, and occasionally only 
through culture experiments. 

The Schizomycetes throughout are non-chlorophyllaceous, unicellular or- 
ganisms, but as a result of their growth and multiplication they often 
form colonies made up of numerous cells. 

The form and character of the single cells, as well as their manner of 
growth, division, and multiplication, vary greatly, and at present these 
differences are used as a basis for the classification of bacteria. In the 
first class are placed the Cocci, often designated as Micrococci or as Sphero- 
bacteria (Cohn), that form of bacteria which constantly occurs in the 
form of spherical or oval cells. According to the grouping of the cells 
during their division, there may be distinguished six forms of cocci: 
double-cocci or Diplococei, chain-cocei or Streptococci, clustered cocci or Staph- 
ylococci, tablet-cocet or Merismopedia, packet-shaped cocci or Sarcine, and 
tube-cocei or Ascococci. 

The second class constitutes the Bacilli (rod-shaped bacteria) which 
formerly were divided by Cohn into Microbacteria and Desmobacteria, ac- 
cording to the length of the rods. These may also be designated as short 
rods and long rods. In association with the designation bacillus many 
authors use the term Clostridium, particularly for bacilli which during 
spore-formation assuine spindle or club shapes. Long threads are often 
also called Leptothrix. 

To the third class belong the Spirilla (screw-shaped bacteria). 
Serew-shaped forms with short, wide turns are known as Spirilla, those 
with drawn-out turns as Vibrios, those with a long, closely wound screw as 
Spirochates. According to their length the spirilla may also be divided 
into short screws and long screics. 

All of the bacteria thus far referred to occur either in one single form 
or in a very limited cycle of forms of growth, and they may therefore be 
grouped together as monomorphous or oligomorphous bacteria. Cohn, 

540 


GENERAL MORPHOLOGY AND BIOLOGY. 541 


to whom we are indebted for the fundamental investigations regard- 
ing bacteria, united under the term bacteria only the oligomorphic 
forins. 

Many writers, however, classify also as bacteria those organisms which 
during their development pass through a whole series of forms: spherical 
cells, as well as rods and simple and branching threads. These may be 
collected into a second group—the polymorphous bacteria—to which 
belong in particular the fungi known as Streptothrir, Cladothrix, Beg- 
giatoa, and Crenothrix. Other authors (Lehmann, Neumann, Levy, Lu- 
barsch) classify these forms with the Hyphomycetes or regard them as 
transition forms between the latter and the Schizomycetes. 

All of the Schizomycetes consist of a plasmatic cell-contents and a 
cell-membrane, both of which, according to Nencki, consist essentially 
of an albuminoid body, mycoprotein, which varies with the species. 
Many bacilli contain fat within their cell-bodies, at times so abundantly 
that it may be demonstrated by staining with Sudan III. Some of 
these bacteria (tubercle-bacillus, lepra-bacillus, and actinomyces) show 
the presenee of fat both when growing in living tissues and when culti- 
vated upon artificial media; others (staphylococcus aureus, anthrax- 
bacillus, bacillus of glanders) show the presence of fat only when grown 
upon certain media (Sata). According to A. Fischer the cell-contents 
consist of a protoplasmic tube without a nucleus, but containing a cen- 
tral collection of fluid. Bütschli, Schottelius, and others regard the cen- 
tral bodies, recognizable in certain bacteria, as nuclei. Aceording to 
investigations by Ziemann, Zettnow, and Feinberg, it is possible by 
staining with a mixture of methylene-blue and eosin (Romanowski-stain ) 
to demonstrate in the cells of the majority of bacteria a ‘nuclear sub- 
stance,” or “chromatin” (Ziemann, Zettnow), or “nucleus ” (Feinberg) 
—that is, bodies of varying size lying within the bacteria, which stain red 
as do the nuclei of malarial plasmodia (Romanowski) or of other proto- 
zon or of tissue-cells, while the protoplasm takes a blue color. Accord- 
ing to Naegeli, Zopf, and others, many schizomycetes possess a membrane 
of cellulose or of a carbohydrate closely related to cellulose. In many 
forms of bacteria the membrane swells under certain conditions of 
growth, and forms a capsule having a hyaline appearance. Certain bac- 
teria (rel sulphur-baeteria) contain coloring matter within their cell- 
bodies, others (Bacillus amylobacter, Spirillum amyloferum ) give at certain 
stages of their growth a marked reaction with iodine. 

In all forms of bacteria, with the exception of the coeci, there have 
been observed swarming movements whieh are brought about by means 
of tine thread-like flagella attached singly at the ends or scattered over 
the entire bacterial cell. In addition there also occur slow oseillatory 
or gliding and creeping movements which are dependent upon the con- 
tractile and flexible qualities of the plasma. Both forms of motion oecur 
only under certain conditions of nutrition and growth, and only in cer- 
tain species, 

Multiplication of bacteria takes place through a transverse division 
of cells whieh have previously become elongated. In some forms divi- 
sion ean also take place in two or even three dimensions. After division 
the cells separate immediately or remain for a time attached to each 
other. When the cells remain attached after dividing transversely, 
threads are formed (Streptococcus, Leptothrix); after dividing both trans- 
versely and longitudinally, flat, tablet-like colonies (Merismopedia) ; 
after dividing in all three dimensions, colonies resembling a solid body 


542 THE PARASITIC FISSION-FUNGI. 


(Sareina) are produced. Long threads may become segmented inte 
shorter pieces. 

According to the investigations of Buchner, Longard, and Riedlin, the 
period of reproduction—that is, the time from one cell-division to the 
next—is, in the case of the cholera-spirillum under favorable conditions 
of nutrition, about fifteen to forty minutes. 

If resting bacterial cells, as the result of a constantly progressing re- 
production or through the accumulation of neighboring cells, heap them- 
selves anywhere in great masses, there are often formed jelly-like colo- 
nies, which are called zoéglea. The jelly-like substance is formed from 
the ınembranes of the bacteria and, according to Nencki, consists of 
mycoprotein. The jelly masses may assume the most varied form, and 
occasionally reach a large size, so that the clumps, or lobulated masses, 
or strands may attain a diameter of one to three or more centimetres. 

Under certain conditions many of the bacteria form spores. These 
are cells which are distinguished by the fact that they remain alive under 
conditions in which the ordinary forms of vegetation die; and, when 
brought into fresh nutrient solutions, are able to produce a new gener- 
ation. Spo'e-formation is most frequently endogenous—that is, the spore 
arises inside the cells (particularly in bacilli), and is developed out of 
the cell-protoplasm, in which there appears a small granule which grows 
into an oblong or round, highly refractive, sharply-contoured body 
always remaining smaller than the mother-cell. After the death of the 
latter the spore is set free. Arthrogenous spore-formation, as observed in 
micrococci, is said to occur through the direct assumption of spore-quali- 
ties by individual members of acolony or of aseries of generations, which 
at the same time remain externally unaltered or take on other morpho- 
logical peculiarities. 

In old eultures bacteria nearly always show degeneration-forms, 
which are swollen and distorted, and stain poorly and irregularly. 

As non-chlorophyllaceous plants, the schizomycetes are restricted in 
their nutrition entirely to ready-formed organic substances which are 
soluble in water, and which are also supplied to them in an abundance 
of water. In addition they need also various mineral substances, 
especially sulphur, phosphorus, potassium or rubidium, or cesium and 
calcium (or magnesium, barium, or strontium ). 

The carbon necessary to their growth they are able to take from most 
of the carbon compounds which are soluble in water. They can also 
derive their carbon from dilute solutions of substances which in greater 
concentration are injurious to them—as, for example, from benzoic aeid, 
alcohol, salicylic acid, phenol, ete. 

Their nitrogen is derived from albuminous matter ; further, from those 
compounds designated as amins (methy]-, ethyl-, propylamin ), amido-acids 
(asparagin, leucin) and amides (oxamide, urea), as well from the am- 
monia-salts and in part also from nitrates. The albumiuates, previous to 
their assimilation, are changed into peptone by means of a ferment. given 
off froin the bacteria. Free nitrogen cannot) be assimilated as such. 
Nitrogenous and non-nitrogenous compounds are not only assimilable as 
such, but also in combination. The fission-fungi are able to take nitro- 
gen from ammonia and nitrie acid only in the presence of organic carbon 
eompounds. 

Sulphur, according to Naegeli, is essential to the schizomyeetes, and 
they take it from sulphates, sulphites, and hyposulphites. The other 
mineral substances mentioned above are derived from various salts. If in 


GENERAL MORPHOLOGY AND BIOLOGY. 543 


the case of an abundance of nutrient material there is too little water 
present, all further growth ceases; yet many of the fission-fungi are able 
to dispense with water temporarily. Spores suffer little from drying. 

Some of the fission-fungi are either chiefly or wholly restricted for 
their food-supply to dead organisms or to solutions of organic matter, 
and are, therefore, classed as saprophytes ; others are able to take their 
nutrition also from living animals or plants, and live as parasites. 

If bacteria get into water which contains no food-material, many of 
them die in time. The spores survive the longest. 

Free oxygen is necessary for the development of many bacteria; 
others can dispense with it as long as they are under favorable conditions 
of nutrition in other respects; others develop only in the absence of oxy- 
gen. The first are designated obligate aérobes, the second facultative 
anaérobes, the third obligate anaérobes. 

The facultative anaérobes produce in part fermentation through their 
multiplication in the absence of oxygen; but according to the investiga- 
tions of Flügge and Liborius, the phenomena of fermentation appear 
often to be absent. The pathogenic bacteria are, according to Liborius, 
facultative or obligate anaérobes. 

Carbon dioxide has no influence upon the development of many 
bacteria, as, for example, upon the typhoid-bacillus and Friedländer’s 
pneumobacillus. Upon others, on the contrary, it has an inhibitory 
action, as, for example, upon Bacillus indicus, Proteus vulgaris, Bacillus 
phosphorescens, the bacilli of anthrax and cholera, the pus-cocei, and 
others (C. Frankel). The bacilli of anthrax, Asiatic cholera, and of 
rabbit septicemia die out in a few hours in artificial Seltzer water, but 
anthrax-spores remain alive in it indefinitely (Hochstetter). 

Intense light has an injurious or destructive influence upon the de- 
velopment of many forms of bacteria, and it is therefore possible to dis- 
infect by means of strong light water which is infected (Buchner). The 
virulence of the bacillus of anthrax may be lessened by exposure to sun- 
light (Arnold, Gaillard). When exposed to the direct rays of the sun 
anthrax bacilli die in twenty-four to thirty hours, the spores survive as 
long as six to eight weeks (Arloing, Duclaux). According to Geisler 
the green, violet, and ultra-violet rays are particularly active. Accord- 
ing to Rieder bacteria may be destroyed by the Roentgen-rays. 

According to Naegeli, Hauser, Buchner, Zopf, and others, different 
conditions of nutrition act in modifying the form and dimensions of the fission- 
Sungi. Thus, for example, bacilli cultivated in different nutrient solu- 
tions assume different lengths and thicknesses. Further, many varieties 
form in one medium spherical cells and short rods, while in another, on 
the other hand, they form long threads (Zopf). Finally, the physiological 
properties may also change with the different conditions of nutrition. 

The temperature of the surrounding medium acts in general upon the 
bacteria in such a way that when it falls the life-processes of the organ- 
isms become weaker and slower, and finally cease entirely, whereas with 
an elevation of the temperature they rise to a certain maximum, and at 
a slight increase above this suddenly cease; still higher temperatures 
kill the fungi. The maximum of permissible teniperature lies at a dif- 
ferent height for different fungi, and is in part dependent. also upon the 
character of the nutrient substance. There are forms of bacteria which 
grow well at a temperature of 55° C. or higher. 

A low temperature checks development in all varieties; they fall into 
a state of immobility, but do not die even at great degrees of cold. The 








544 THE PARASITIC FISSION-FUNGI. 


immobility due to cold occurs at different temperatures with different 
varieties. The most favorable temperature for development lies between 
30° and 40° C. for the anthrax bacillus; at temperatures above 44° and 
below 15° C. its development ceases. Many bacilli form spores only at 
high temperatures. 

Boiling water and steam at 100° C. kill all bacteria and bacterial 
spores if allowed to act for sometime. In dry air bacteria and their 
spores withstand higher temperatures, so that a temperature of 140° C. 
for three hours is necessary to kill the latter. Many bacteria are killed 
at a temperature of 60° to 70° C., provided it is kept up for a very long 
time. 

Anthrax-spores die in boiling water in two hours, in confined steam 
in ten minutes. The action of steam at 105° C. for ten minutes kills all 
spores. Live steam kills all spores in ten to fifteen minutes, and pene- 
trates very well into the objects to be disinfected (Koch, Gaffky, Löfller ). 

If fission-fungi find themselves in a suitable medium, their multiplica- 
tion can still be brought to a standstill, since the fluid may contain sub- 
stances which hinder the growth of the bacteria or even kill them. 
This effect is produced by many substances (sublimate, lysol, carbolic 
acid, iodine, formaldehyde, etc. )—even in comparatively great dilution. 
Other substances act injuriously upon the bacteria only when in stronger 
concentration. The point at which the multiplication is hindered is 
always reached at a much greater dilution than that at which the bacteria 
are killed. Spores are much more resistant than the vegetative forms. 

Many bacteria are very sensitive to acids, so that even aslight degree 
of acidity hinders their growth (for example, anthrax bacilli and the 
Fränkel- Weichselbaum pneumococeus). Others are able to grow with a 
moderate amount of acid in the nutrient fluid. Asa general rule they 
are especially sensitive to mineral acids, but the presence of a large 
amount of citric, butyrie, acetic, and lactic acids hinders also their mul- 
tiplication. In this connection belongs the fact that the products of 
decomposition caused by the fermentative action of the fungi are at a 
eertain degree of concentration harmful to the development. of the fun- 
gus, and finally stop its growth entirely. Thus, for example, in butyric- 
acid and lactice-acid fermentation the amount of butyric or lactie acid 
gradually formed finally checks the multiplication of the fungus. A 
similar result occurs in the bacterial putrefaction of albumin, since the 
products of the same, such as phenol, indol, skatol, phenylacetic acid. 
phenylpropionic acid, ete., hinder the further development of the bac- 
teria. To alkalies the fission-fungi are less sensitive, and many can 
bear a rather high degree of alkalinity in the nutrient fluid, but there 
also exist forms which do not thrive in alkaline fluids (acetic-acid 
fungus). 

The growth and multiplication of bacteria also cease in the presence 
of a superabundance of nutrient material—that is, in the case of insuf- 
ficient amount of water. The fact that fruits preserved in sugar do not 
ferment and that salted and dried meats do not putrefy depends upon 
this fact. Food-stuffs can also be preserved through the removal of 
water and by the addition of substances which are dissolved in the 
tissue-fluids and in this way inerease the proportion of the same in solid 
contents. The limit at which the fission-fungi and yeast-fungi cease to 
develop is reached at a much higher degree of humidity than for the 
moulds, 

According to the investigations of Pfeffer and Ali-Cohen many motile 


GENERAL MORPHOLOGY AND BIOLOGY. 545 


bacteria show chemotactic properties—that is, they are attracted or 
repelled by certain chemical substances dissolved in water. Bacteria 
Swimming about in fluids collect, therefore, at places where there are 
chemicc! substances which attract. For example, typhoid-bacilli and 
cholera-spirilla are attracted by potato-juice (Ali-Cohen). Potassium 
salts, peptone, and dextrin likewise attract, but the individual forms of 
bacteria behave very differently toward these substances. Free acids, 
alkalies, and alcohol have a repelling action. 

If a nutrient fluid contains other lower fungi besides the bacteria 
there often takes place a competition between the different micro-or- 
ganisms; and fission-fungi, yeasts, and moulds may crowd one another 
out. Likewise a reciprocal crowding between the bacteria themselves 
may occur. For example, cocci may be crowded out and destroyed by 
bacilli, or one form of bacillus by another. This would happen when 
either the composition or the temperature of the nutrient medium is 
more favorable to one form than to the other; or also when one form of 
bacteria produces products which act injuriously upon the other, or 
when one form grows more rapidly than the other, and thereby deprives 
its competitor of the necessary food-supply. 

Aceording to investigations by Pasteur, Emmerich, Bouchard, Wood- 
head, Blagovestchensky, and others, the antagonism between many forms 
of bacteria is shown also in inoculation experiments on animals. By 
simultaneous inoculation with different bacteria the development of a 
pathogenic bacterium in the body of a susceptible animal may be hin- 
dered. For example, the development of anthrax bacilli may be hin- 
dered by simultaneous inoculation with erysipelas-cocci (Emmerich) or 
with the Bacillus pyocyaneus (Bouchard ). 


Babes and Ernst, by means of especial staining methods with Léffer’s methylene- 
blue, hematoxylin, and Platner’s nuclear black, have demonstrated the presence of 
granites within different forıns of bacteria, which according to their behavior probably 
stand in some relation to the processes of division and spore-formation. Hruat desig- 
nated the appearances seen by him as sporogenous granules, since he was able in certain 
bacteria to demonstrate their transition into spores; he is inclined to regard them as of 
the nature of cell-nuclei, a view which Bütschli also favors. Bunge regards the gran- 
ules described by Zrnst as cell-granules which have nothing to do with spore-forma- 
tion, and describes other granules, which stain with Zöfler's methylene-bluc, as the 
forerunners of spores. Marr and Woithe regard the Bubes- Ernst granules as not being 
nuclei in the ordinary sense of the word, but as representing products of the maximal 
condensation of the euchromatic substance of the cells, which are a sign of the highest 
intensity of vitality on the part of the cell. Wagner, on the contrary, holds that cer- 
tain bodies. which he has observed in ty phoid- and colon-bacilli, are nuclei. 

According to Nakanish?, the spores form (in anthrax- and hay-bacilli) by a concen- 
tration of the chromophile substance about the nucleus, while the remaining portion of 
the protoplasm becomes clear; a membrane is then formed about the chromatin body, 
it takes on a fat-like shine. and loses its power to take stains (methylene-blue BB). 

The Romanowski stain isa mixture of methylene-blue and eosin, whereby a red 
dye contained in methylene-blue (Rorin. Berl. klin. Wochen., 1899; Nocht, Cot. f. 
Bakt., 1899) is precipitated. Zettnow’s formula is as follows: 50 c.c. of a one-per-cent. 
solution of methylene-blue (Höchst) is mixed with 3-4 c.c. of a five-per-cent. soda solu- 
tion. To 2 e.c. there is added drop by drop while shaking 1 c.c. of a one-per-cent. 
solution of eosin (Höchst BA). Stain on cover-glass for five minutes. Examine in 
Water. 


516 THE PARASITIC FISSION-FUNGL 


Literature. 
( Bacteria. ) 
1. TertIumks aud Mowrpraphs 


Vergl. Morphol. u. Bio 
Vorlen. über Bakterien warb. 





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1190. 

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berg Bakterislog. Diagnostik. Leipzig. 1006. 
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Fraenkel, C.: Grundriss d. Bakterienkunde, Berlin. 1499. 
Fraenkel u. Pfeiffer: Mikrophotographischer Atlas der Bakterienkunde, Berlin, 1994 
Flagge: Die Mikroorganismen, Leipzig. 1996. 
Gamaleia: Les poisons bacteriens. Paris, 1892. 
Günther: Einführung in d. Studium der Bakteriologie. Leipzig. 189. 

Ueber Fäulnissbakterien. Leipzig. 1885. 
Hueppe: Naturwissenschaftl. Einführung in d. Studium d. Bakteriologie, Wiesbaden, 


Kite! Bakterienkunde, Wi ien, 1999. 
Lehmann u. Neumann: Atlas u. Grundriss d. Bakteriologie, München, 1899. 
Löffler: Vorles. tib. d. geschichtl. Entwickelung der Lehre von d. Bakterien, Leipzig. 
1837. 

Migula: System der Bakterien, i. and 

eli- Die nied. Pilze. München, 1877; U: . niedere Pilze, München, 1832. 

: Elementos de microbiologia, Madrid, 1899. 

logy in Medicine and Surgery, 1899. 

Unters. ib. die Entwickelungsgesch. einig. Bakterien, Leipzig. 1280. 
shes patlogenes. Path. gen, publ. par Bouchard, ii, Paris 1896. 
ris and their Products, London, 1891. 

Zopf: Die Spaltpilze. Breslau, 1885. 

Zurn: Die Schmurotzer auf und in dem Körper der Haussäugethiere, Weimar. 1882-29, 























uruuals and Yearbooks. 





v. Baumgarten: Jabresber. über die Fortschritte in d. Lehre von den pathogenen 
Mikroorganismen, umfassend Bakterien, Pilze und Protozoen, since 1886. 

Duclaux. Ann. de ’Inst. Pasteur, Paris, since 1897. 

hresber. über die Fortschritte ind. Lehre von d. Gährungsorganismen, since 











Koch u. Flügge. Zeitschr. f. Hygiene. Leipzig, since 1888. 
Uhlworm: (bl. f. Baki Parssitenkunde, Jens, since 1887. 
Ziegler u. Kahlden: Cl. f. allg. Path. und path. Anatomie, since 1890. 








‚rtielen in Journals, 


Ali-Cohen Die Chemotaxis als Hülfsmittel bakt. Forschung. Cbl. f. Bakt., vii 
1890. 











du bacill 
s. Bakterien 
hromttnue Amn, de Ih 
chromat. Ki vache Sporen, 

Lt 


Bakterien. Zeitse 








nfectionsmittel u. Desinfectionsmethode. Zeitschr. f. 





Hya.. ix. 

Blagov. tchonsy Sur Tantagonisme entre les hucilles du charbon et ceux de pus 
bleu Pasteur, iv. WM). 

r Le istianes fühigkeit mehrerer chem. Desinfectionsmittel. Zeitschr. f. 








par les microbes pathogenes, Paris, 1890. 


Bouchard. Action ies produits seer 
; Einfluss des Lichtes auf 


Buchner In Niigeli, Untersuch. über niedere Pilze, 189 





GENERAL MORPHOLOGY AND BIOLOGY. 547 


Bakterien. Cbl. f. Bakt., xi. and xii., 1892; xv., 1894; Ursache d. Sporenbildung. 
Bakt. Cbl., viii., 1890. 

Bütschli: Ueb. d. Bau d. Bakterien u. verwandter Or anismen, Heidelberg, 1890. 

Bunge: Sporenbildung bei Bakterien. Fortschr d. Med., xiii.. 1895. 

Cheyne-Kammerer: Die antiseptische Chirurgie, Leipzig. 1883. 

v. are eran ee ack Holmfeld: Das Terpentinöl als Antisepticum. Fortschr. 
( et 1887 

Cohn: Untersuch. über Bakterien. Beitr. z. Biol. d. Pflanzen, i., ji., and iii. 

Cornil, M.: Lecons professées pend. le I sem. de Vannée 1883-84, Paris, 1884. 

Cramer: Zusammensetzung d. Bakterien in ihrer Abängigkeit vom Nährmaterial. 
Arch. f. Hyg., xvi.; ref. Cbl. f. Bakt., xiv., 1893. 

Duclaux: Action de la lJumiere sur les microbes. Ann. de l’Inst. Pasteur, iv., 1890. 

v. Dungern: IIemmung d. Milzbrandinfection durch Friedländ. Bakt. Zeitschr. f. 

. Hyg., xviii., 1894. 

Eidam: In Cohn. Beitr. z. Biol. der Pflanzen, i. and ii. 

Emmerich u. di Mattei: Vernichtung der Milzbrandbacillen im Organismus durch 
Erysipelkokken. Fortschr. d. Med., v., 1887; Arch. f. Hyg., vi.; Heilung des 
Milzbrandes durch Erysipelserum. Münch. med. Woch., 1894. 

Ernst: Ucber den Bacillus xerosis und seine Sporenbildung. Zeitschr. f. Hyg., 
1888; Ueber Kern- und Sporenbildung in Bakterien. Ib., 1889. 

Feinberg: Ueber den Bau d. Bakterien. Anat. Anz., xvii, > Cbl. f. Bakt., xxvii., 


1900. 
Fränkel, C-: Die Einwirkung d. Kohlensäure auf d. Mikroorganismen. Zeitschr. f. 
lIvg., 1888. 


Frankel u. " Pfeiffer: Mikrophotogr. Atlas d. Bakterienkunde, ii. Aufl., Berlin, 1894. 
de Freudenreich: De l’antagonisme des bactéries. Ann. de l’Inst. Pasteur, ii., 1888. 
Gärtner: Desinfection. Handb. d..spec. Therapie, i., Jena, 1894. 

Gaillard: De Vinftluence de la lumiere sur les microorganismes, Lyon, 1888. 

Garre: Antagonisten unter den Bakterien. Corresphl. f. Schweizer Aerzte. 1887. 

Geisler: Wirkung des Lichtes auf Bakterien. Cbl. f. Bakt., xi., 1892. 

Geppert: Ueber Desinfection. Zeitschr. f. Hyg., ix.; Deut. med. Woch., 1891. 

Gerlach: Ueber Lysol. Zeitschr. f. Hyg., x., 1891. 

Globig: Ueber Bakterienwachsthum bei 50-70°. Zeitschr. f. Hyg., iii., 1888. 

Haegler: .Die Hindereinigung, Basel, 1900. 

Heim: Dic Neuerungen auf dem gebiet der bakteriologischen Untersuchungsmethoden 
seit dem Jahre 1887. Cbl. f. Bakt., 1891. 

Hochstetter: Mikroorganismen im künstl. Selterswasser. Arb.a. d. K. G. -A.,ii.. 1887. 

Hoppe-Seyler: Ueber den Eintluss des Sauerstoffs auf Gährungen, Strassbute. 1881. 

Kitasato: Ueber das Verhalten d. Cholerabakterien zu anderen pathogenen u. nicht 
pathogenen Mikroorganismen in künstlichen Nährsubstanzen. Zeitschr. f. Hyg., 
vi., 1889. 

Klein, L.: Botan. Bakterienstudien. Cbl. f. Bakt., vi., 1889; vii., 1890. 

Koch: Mittheil. a. d. Kais. Gesundheitsamte, Berlin, 1881. 

Koch, Wolffhügel, Gaffky, u. Löfller: Desinfection mit heissen Wasserdampf. 
Mittheil. a. d. Kais. Gesundheitsamte, Berlin, 1881. 

Krönig u. Paul: Chemische Grundlage d. Giftwirkung u. Desinfection. Zeitschr. f. 
Hy, xxv., 1897 (Liät.). 

Lachowicz u. v. Nencki: Anatrobiose. Pflüger’s Arch., xxxiii., 1884. 

Lewek: Wachsthumseinfluss nicht pathogener Spaltpilze auf pathogene. Beitr. v. 
Ziewler, vi., 1889. 

Löfller: Die Beizung u. Färbung d. Geisseln. Cbl. f. Bakt., vi., 1889; vii., 1890. 

Löwit: Zur Morphologie d. Bakterien. Cbl. f. Bakt., xix.. 1896. 

Lüderitz: Zur Kenntniss der ana@roben Bakterien. Zeitschr. f. Hyg.. 1888. 

Marx u. Woithe: Morphol. Unters. z. Biologie d. Bakterien. Cbl. f. Bakt., xxvii,, 
1900. 

Metschnikoff: Note sur le pléomorphisme des bactéries. Ann. de l’Inst. Past., iii., 
1889, 

Nakanishi: Neue Färbungsmethode v. Leukocyten u. Bakteriensporen. Münch. 
med. Woch., 1900. 

Nencki: Journ. f. prakt. Chem., N. F., xix., xx.; Beitr. z. Biol. d. Spaltpilze, 1880; 
Ber. d. Chem. Ges., xvii., 1884; Arch. f. d. ges. Physiol., xxxiii.; Arch. f. exp. 
Path., xx., xxi., 1886. 

Noetzel: Nachweis d. Kapseln d. Mikroorganismen. Fortschr. d. Med., xiv., 1896. 

Pfeffer: Ucber chemotaktische Bewegungen d. Bakterien, Untersuch. a. d. Botan. 
Institute zu Tübingen, 1886-88. 

Raum: Der gegenwärtige Stand unserer Kenntnisse über den Einfluss des Lichtes auf 
Bakterien und auf den thierischen Organismus. Zeitschr. f. IIyg., 1889. 


| ee ee [Ti A 


og == 


344 THE FARANTSH. FisesoS-FUSGL 


Rieder Wrı.ır : Wreirewraiet 2.’ Bekvors 2 Wiwi nei Work. I 

Romasowski Z.: Fraz- or Preis ze — Tiere 2 Maar <1 

de Rossi Ws. wu. per como na ai ur OA per eS. Mei. oxiiv.. 
99 

Roux ik wise m a: en ia Aca ie 1 Iek Pax i. lw. 

Saelkowski 1. mes te Win nr. ren fr waere Im mei Wc | 1m. 

Sames Ke wastes T-:;et2r or. ewes Beitvrsa | Zeiehr ? Are. sııi. 


‘on Lr: 
Bete Foil ong ott ee Lint: Bas br it), £ ate Pak Is 
Schottrlius K-rzriz- Kexqer im ese vo Su püzn Ua f Bakt. iv. ives, 


In wine Werk „nz einiger Terni “te Mie. u zei Weak. io 
Giretinin Erntsiie. fnew SB wet iewipee: ote i Besteren Zeituhr £ 
Hyg. iv Im 
Veter Kerr. Toeii.zmeuth 4 Bekteren. Chi § Bakt.. xi. 192 
ka. Bandler Die Ei aukeinz vıc geil retest Spaltpilzer unber Wew-bse ixeiti- 
gem Boe see ihrer Doceigunreprad ue. Futter. Meu 1. 
Tausche itr. 7 Deen ferting mit Waseriamr! Zrizechr. f Hez. ix.. 19m. 
Wagner (..i ı Toph tain -irei vinkernize Zien Chl f. Bakt.. xxiti . [ie 
Wernich Twinfetzin. Pulentburz s Reaseoet kip. 194 Lit. 
Wesbrook Fierce of “ur izht on Tetanus Carr Je um of Path. iL. 1098 
Zettnow: Iunnamımaki- Farpurg tei Bak’erien. Zitsbr. f. Hye... 3» Bi. iv 
foe ot el Worn . Som. 
Ziemann. leiser Maaris . andere Bi parasiten. 19&. 


“14%. The growth and multiplication of the fission-fungi give 
rise always to chemical transformations of the nutrient material, 
which are brought abont in part through the intluence of ferments pora- 
Aurel by the bueteria. and in part directly through the metabslic prorescx x 
occurring within the barteral cells themsy- lees, 

Among the ferments or enzymes are to be meutioned first the prot - 
Aytic or alhumin-disgdcing enzymes (hacteriotrypsins» which bring about a 
wolution of the albuminous bodies and cause the disintegration of the 
peptone molecule, Further, bacteria give rise to diastatic ferments which 
convert starch into sugar, also to incerting ferments which transform cane. 
sugar (disaccharid ) into grape-sugar (monosaccharid ). 

The chemical results of bacterial metabolism, which are brought 
about by the vital activities of the fission-fungi aided by the enzymes 
produced by them, consist in the first place of a decomposition of com- 
lex organic compounds. By many authors all these processes are desisr- 
nated) as fermentations, while others : Lehmann ı speak of fermentation 
only when a fission-fungus breaks down a given food-material with espe- 
Cial ease, thereby giving rise to one or more especial products in marked 
Quantity, in association with or in place of its other metabolic products. 
Other authors still narrow the term fermentation to the decomposition of 
arbohvdraten. 

In the decompositions caused by the fission-fungi very differeiit 
products are formed, which vary according to the composition of the 
nutrient material and the character of the fission-fungus. For the pro- 
duction of fermentation. a proper fermentable material is necessary. 
Many fungi are able to cause fermentation In the presence as well as in 
the absence of oxygen, while to some of them a lack of oxygen is neces- 
NY. 

Among the products of bacteria of especial importance to the physi- 
Chinare those which have a poisonous action and cause tissue-changes, 
to which belong particularly those substances which are described as 
plomaina, toring, and torabumins. 

The ptomains are basie, crystallizable, nitrogenous products of the 
bacterial decomposition of albuming they are also known as putrefaetire 


PRODUCTS OF THE VITAL ACTIVITY OF BACTERIA. 549 


alkaloids or cadaveric alkaloids. Whien these display poisonous properties 
they are classed with the toxins. The best known are sepsin, putrescin 
(dimethylethylendiamin), cadaverin (pentamethylendiamin), collidin 
(pyridine derivative), peptotoxin, neuridin, neurin, cholin, gadinin, and 
substances resembling muscarin. 

The toxalbumins are amorphous poisons, which may be precipitated 
from bouillon cultures containing many bacteria by the same methods 
that cause the precipitation of albumins. They are, therefore, regarded 
by most investigators as albuminous bodies. It should be noted, however, 
that they are, possibly, in part, only bodies which are carried down with 
the precipitated albumin; and in proof of such a conception speaks the 
fact that the specific poisons of tetanus and diphtheria have been shown 
(Brieger) to be free from albumin. It appears, therefore, more correct 
to designate these specific poisons as toxins. They constitute those 
poisons which determine the special form of intoxication in the various 
infectious diseases. 

Among other decompositions produced by bacteria the following are 
worthy of note: the formation of lactic acid, formic acid, acetic acid, 
propionic acid, butyrie acid, often also the formation of alcohol and car- 
bonie acid from sugar; the formation of acids (acetic, butyric, pro- 
pionic, valerianic, succinic, formic, and carbonic) from alcohol and 
organic acids; the formation of indol, skatol, phenol, cresol, pyrocat- 
echin, hydrochinon, hydroparacumarie acid, and paroxyphenylacetic 
acid (von Nencki, Salkowski, Brieger), and finally hydrogen sulphide, 
ammonia, carbonic acid, and water from albumin; the formation of am- 
monium earbonate from urea; the transformation of nitrous and nitric 
acids into free nitrogen; the reduction of nitrates to nitrites and to am- 
monia, ete. Finally, there are also bacteria living in the soil—the nitro- 
bacteria--which are able to form nitrous and nitrie acids from ammonia 
( Winogradsky ). 

Along with the nitrification of nitrogen there occurs simultaneously 
a decomposition of earthy alkali carbonates, as shown by the fact that 
the nitrobacteria are able in the presence of organic carbon compounds 
to derive from the carbonates the carbon necessary to the building-up of the 
cells. There takes place, therefore, through the vital activity of these 
organisms, a synthesis of organic material out of inorganic substances. 

Under the influence of the fission-fungi there are formed bitter, sharp, 
nauseating substances (bitter milk). Further, bacteria occasionally pro- 
duce pigments of a red, yellow, green, blue, or violet color. For exam- 
ple, Bacillus prodigiosus produces a blood-red coating upon bread (bleed- 
ing bread); bandages and pus take on a bluish-green color as the result 
of the presence of the Bacillus pyocyaneus. In many cultures there is also 
formed a fluorescent coloring matter. 

The phosphorescence not infrequently seen upon decomposing sea-fish 
depends also upon bacterial products of decomposition, as has been 
shown by Pflüger, and appears when there is an active multiplication of 
the bacteria. 


The first investigations to establish the nature of the processes of putrefaction were 
made by Th. Schwann and Franz Schulze (Pooggend. Annl., 29 Bd., ref. in Schmidt's 
Juhrb., 1866), in the middle of the fifties, and upon the results of their experiments 
was based the view that fermentation and decomposition are dependent upon the pres. 
ence of very small organisms. Almost at the same time (1857) Cagnard- Latour observed 
the increase of yeast-cells in the course of alcoholic fermentation. The observations 
made by Schwann were later confirmed by Helmholtz. H. Schroeder and von Dusch 


550 THE PARASITIC FISSION-FUNGI. 


then showed that by filtering through cotton-wool the air admitted to a fluid capable 
of fermentation, as well as by the action of higher temperatures, the appearance uf fer- 
mentation may be hindered. 

Since the investigations of Schicann, many different hypotheses as to the cause 
of fermentation, alcoholic fermentation in particular, have been advanced. Certain 
writers have endeavored to bring these processes into immediate relationship with the 
life of the cells causing the fermentation; others have sought to separate them from the 
latter. According to Liebig, the process is due to a molecular movement which an un- 
formed ferment or body in a state of chemical activity—that is, decomposing—imparts 
to other bodies whose elements are not closely held together. According to /lvpmpe- 
Seyler and Traube (cf. Hoppe-Seyler, Pflüger’s Arch., Bd. xii., 1875; Physiologische Che nite). 
the cells produce certain substances, the so-called unformed ferments, which cause 
decomposition by contact action—that is, merely through their presence, without tak- 
ing part chemically or entering themselves into combination. 

According to Pasteur (cf. Pusteur, Ann. de chim. et de Phys., tome 58, 1860, and 64, 
1862; Comptes rend. de U Acad. des Sciences, tomes 45, 46, 47, 52, 56, 80: aud Duchenne, 
“Ferments et maladies,” Paris, 1882), fermentation is directly dependent upon the life 
of the cells causing fermentation. It occurs only when free oxygen is lacking to the 
cells, so that the latter must take oxygen from the chemical compounds in the nutrient 
fluid. In this way the molecular balance of the latter is destroyed. Acording to cron 
Nencki, anaerobiosis is to be regarded as the cause of the different kinds of fermentation. 

According to Nägeli’s moleeular-physical theory (Abhandl. der Bayr. Akad. Math. 
physik., Kl. iii., Ser. 76, 1879), fermentation is a transfer of conditions of motion (which 
are present in all substances) from the molecules, atom-groups, and atoms of the differ- 
ent, chemically unchanged combinations constituting the living protoplasm to the 
material undergoing fermentation, whereby the molecular balance of the latter is dis- 
turbed and the molecules become disintegrated. 

According to E. and JI, Buchner, there can be obtained from yeast, by a pressure 
of 400-500 atmospheres, a cell-juice which causes at once fermentation of sugar-solu- 
tions. Fermentation is, therefore, not bound up with the life of the cells, but is caused 
by a cell-substance “zymase,” which is probably secreted by the cell. This experi- 
ment has, indeed. been confirmed from other quarters, but the possibility that living 
protoplasm still remains in the expressed juice has not yet been excluded. 

The power to produce fermentation—1.e., decomposition—in a nutrient fluid is very 
likely a property, not only of the schizomycetes and blastomycetes, but also of the 
cells of more highly organized beings, even also of man. According to Voit (* Physi- 
ologie des Sauerstoffwechsels,” Leipzig, 1881), the decomposition of the dissolved albu- 
min circulating in the organism is to be referred to a fermentative activity of the cells. 
Pasteur has shown that fruit and leaves also possess fermentative properties under suit- 
able conditions. 

Besides the fermentation and decomposition caused by fungi, there are other de- 
compositions of organic substances in the production of which the fungi have no part. 
These consist chiefly in a slow oxidation or burning, in which carbonic acid and water 
ure formed, and, in the case of nitrogenous substances, also ammonia. This form of 
decomposition takes place under conditions in which atmospheric air and moisture are 
in contact with organic matter. Moreover, it also takes place in the living organism. 
In the case of dead organic-matter, this burning corresponds in part to the process 
commonly called mouldering. 


Literature. 


(Chemical Changes Produced by Schizomycetes. ) 


Baumann u. v. Udranszky: Vorkommen von Diaminen (Ptomainen) bei Cystinurie. 
Zeitschr. f. phys. Chem., xiii., 1889. 

Bocklisch. Fäulnissbasen aus Fischen. Ber. d. Deut. chem. Ges., xviii., 1885. 

Brieger: Ueber Ptomaine, Berlin, 1885, 1886; Berl. klin. Woch., 1886; Zusammenset- 
zung des Mytilotoxins, nebst einer Uebersicht der bisher in ihren Haupteigenschaf- 
ten bekannten Ptomaine und Toxine. Virch. Arch., 115 Bd., 1889; Bakteriengifte. 
Zeitschr. f. IIyg.. xix., 1895. 

Buchner: Active lösliche Zellproductee. Münch. med. Woch., 1897. 

Cahen: Ucb. d. Reduetionsvermögen d. Bakterien. Zeitschr. f. Hyg., ii., 1887. 

van Ermengem: Anatrob. Bacillus u. seine Bez. z. Botulismus. Zeitschr. f. Hyg., 26 
Bd., 1897. 

Fermi: Die Leim und Fibrin lösenden u. die diastatischen Fermente der Mikroorgan- 
ismen. Cbl. f. Bakt.. vii.. 1890. 

Forster: Ueb. einige Eigenschaften leuchtender Bakterien. Chbl. f. Bakt., ii., 1887, 


INFECTION BY BACTERIA. 551 


Gamaleia: Les poisons bactériens, Paris, 1892. 

Gautier: Sur les alcalotdes dérivés de la destruction bactérienne ou physiologique des 
tissus animaux, ptomaines, et leucomafnes, Paris, 1886. 

Hueppe: Ueb. die Zersetzungen der Milch und die biologischen Grundlagen der 
Gährungsphysiologie. Deut. med. Woch., 1884, p. 777; Mittbeil. a. d. Kais. 
Gesundheitsamte, ii., Berlin, 1884. 

Ingenkamp: Unsere Kenntnisse v. Fäulniss u. Gährung. Zeitschr. f. klin. Med., x., 


1885. 

Krannhals: Ueb. Kephir u. üb. den Kephirpilz. Deut. Arch. f. klin. Med., XXXV., 
1884. 

Lassar: Die Mikrokokken der Phosphorescenz. Pflüger’s Arch., xxi., 1880. 

Ludwig: Die bish. Unters. über pathogene Bakterien. Cbl. f. Bake. ii., 1887. 

Lüderitz: Zur Kenntn. d. anatroben Bakt. Zeitschr. f. Hyg., 1888. 

v. Nencki: Zersetzung d. Gelatine u. d. Eiweisses bei d. Filulnise mit Pankreas, Bern, 
1874; verschied. Arb. im Journ. f. prakt. Chem., im Journ. f. phys. Chem. u. ind. 
Ber. d. Deutsch. chem. Ges. a. d. J.. , 1876-91; Die Anatrobien u. d. Gährungen. 
Arch. f. exp. Path., xxi., 1886. 

Pflüger: Piltiger’s Arch., 1875: Phophorescenz der lebendigen Organismen. Arch. f. 
d. ges. Phys., x., 1875: Phosphorescenz verwesender Organismen. Ib., xi., 1875. 

Podwyssozki: Kephir, Petersburg, 1894. 

Salkowski: Zahlr. Arb. i. d. Ber. d. Deut. chem. Ges. ; Zeitschr. f. phys. Chem. aus 
den letzten Jahren. 

Vaughan and Novy: Cellular Toxins, 1902. 

Winogradsky: Rech. sur les organismes de la nitrification. Ann. de l’Inst. Pasteur, 
1890, 1891. 

Wortmann: Ueb. d. diastatische Ferment d. Bakt. Zeitschr. f. phys. Chem., vi. ; 
Pflanzl. Verdauungsprocesse Biol. Cbl., iii.; Organismen d. Nitrification u. ihre 
physiol. Bedeutung, Landwirthsch. Jahrb., xx., 1891; ref. Bakt. Cbl., x., 1891. 
See also SS 148 anc 150. 


2. GENERAL CONSIDERATIONS CONCERNING THE PATHOGENIC SCHIZO- 
MYCETES AND THEIR BEHAVIOR IN THE HUMAN ORGANISM. 


§ 150. As has already been explained in §§ 11 and 12 there are among 
the schizomycetes numerous species which are capable of causing disease- 
processes in the human organism, and are therefore called pathogenic 
schizomycetes. The first condition of such action is evidently that the 
bacteria concerned must possess properties enabling them to multiply in 
the tissues of the living human body. They must therefore find in the 
tissues the suitable nutrient material, and in the body-temperature the 
warmth necessary to their growth. The tissues, moreover, must not 
contain substances which are a hindrance to their growth (cf. 88 30 
and 32). 

If pathogenic fission-fungi succeed in growing in the tissues of the 
body, if infection takes place (ef. § 12), their action is in general char- 
acterized by the production, at the point of multiplication, of tissue-degener- 
ations, necrosis, inflammation, and new-growths of tissue, while at the same 
time the fo.rins produced by them cause manifestations of poisoning. 

In individual cases the pathological processes vary greatly, in that 
the distribution of the bacteria in the organism, and their local action, 
as well as the production of the poisons, differ greatly with the different 
forms of bacteria. 

With many the local action upon the tissue is the most prominent 
characteristic, with others the general intoxication. Many bacteria confine 
themselves to the region in which they have gained entrance ; others advance 
uninterruptedly upon the surrounding tissues ; others still are carried by the 
blood and lymph streams and lead to the formation of metastatic foci, and, 
finally, others increase within the blood. 

If a spread of the bacteria takes place through the blood, the bacte- 


552 THE PARASITIC FISSION-FUNGI. 


ria may pass from the mother to the fetus during pregnancy, since the pla- 
centa forms no certain filter against: pathogenic bacteria. This has 
been demonstrated, for example, in the case of anthrax-bacilli, bacilli 
of symptomatic anthrax, glanders-bacilli, spirilla of relapsing fever, 
typhoid-bacilli, and the pneumococcus. According to observations of 
Malvoz, Birch-Hirschfeld, and Latis, changes in the placenta, such as 
hzmorrhages, loss of epithelium, and alterations of the vessel-walls, 
favor the passage of bacteria. Moreover, bacteria—as, for example, 
anthrax-bacilli—can grow through the tissue-spaces. In general the pas- 
sage of bacteria from the mother to the foetus presupposes that after the 
entrance of these organisms into the circulating blood of the mother, the 
latter shall remain alive, at least long enough to allow of the passage of 
the bacteria into the foetus. 

The bacteria which succeed in multiplying within the human organ- 
ism die out again in many cases within a short time; and the disease pro- 
duced by them may proceed to recovery (cf. § 31). Nevertheless, it not 
infrequently happens that they are preserved for a long time within the body, 
and either excite a continuous disease process, or at times remain in 3 con- 
dition of inactivity, so that no pathological processes are recognizable 
until after alonger or shorter period of latency, an active reproduction again 
takes place and manifestations of disease show themselves anew. 

Not infrequently a secondary infection associates itself with an infee- 
tion already existing. The relation between the two infections is either 
that the second infection follows the first accidentally, or that through the 
first infection the soil is prepared for the second (ef. § 12). 

Finally, there not infrequently occur double infections, iu that two 
or more forms of bacteria develop coincidently in the tissues, and pro- 
duce their characteristic injurious influence upon the tissues. 

Each pathogenic fission-fungus has a specific action upon the tissues 
of the human organism; but, nevertheless, different species may exert a simi- 
lar action. For example, thereare various bacteria capable of producing 
suppuration. Only in a certain proportion of cases do the pathological 
tissue-changes show such specific characteristics that from these the spe- 
cies of the pathogenic fission-fungus can be recognized with certainty. 

Further, it has been demonstrated that pathogenic properties of 
bacteria are by no means constant; that, on the contrary, their viru- 
lence varies, so that bacteria, which cause severe—that is, fatal—infec- 
tions may become ckanged (weakened) through external influences, so 
that they either wholly lose their power of causing disease-processes in 
the organism, or at least cause only mild forms of disease. This pecu- 
liarity is not alone of theoretical interest, but is also of great practical 
importance. It explains to a certain extent, on the one hand, why a 
certain infection does not always run the same course, and, moreover, 
why along with severe attacks light ones also oceur. On the other hand, 
it affords us the possibility of obtaining material for inoculation from 
attenuated cultures of bacteria, by means of which mild grades of infee- 
tion or intoxication can be produced, which are able to protect the organ- 
ism from severe infections or to bring about the cure of an infection 
already acquired (ef. § 32). 

Weakening of the pathogenic properties of a fission-fungus can be 
brought about through the suitable action upon cultures of the same, by 
high temperatures, oxygen, light, or chemical antiseptic substances, as 
well as by the cultivation of the fungus in the body of a less susceptible 
animal. In some forms it is only necessary to cultivate the bacteria in 


ATTENUATION. METHODS OF BACTERIOLOGICAL INVESTIGATION. 553 


question for some time upon artificial media (diplococcus of pneumonia), 
or to expose the culture to the air for some time (bacillus of chicken- 
cholera), in order to bring about an attenuation. If it is desired to pre- 
serve the virulence of the pneumococcus for some time, it is necessary, 
from time to time, to pass the bacteria cultivated upon artificial media 
through rabbits, which are very susceptible. The glanders-bacilli, tu- 
bercle-bacilli, and the cholera-spirilla lose virulence when cultivated 
uninterruptedly upon artificial media for some time. The streptococcus 
of erysipelas (Emmerich) becomes so attenuated through continued cul- 
tivation in bouillon or nutrient jelly that it is no longer capable of kill- 
ing even mice. 

As tothe nature of the attenuation of virulence of bacteria by the 
methods mentioned above, it is possible to give only hypotheses. If the 
bacteria cultivated for a long time upon artificial media change in viru- 
lence, this may perhaps be explained in part by assuming that in a series 
of generations the less virulent varieties, which surely often arise, grad- 
ually gain the upper hand. For the attenuation of virulence by heat, 
chemical agents, etc., such an explanation is not adequate. In this case 
there is very probably a general weakening or degeneration of the proto- 
plasm, and in harmony with this theory is the fact that such bacteria 
show a diminution in energy of growth. 


If the presence of bacteria be suspected in any tissue-tluid or in the tissue-paren- 
chyma, their demonstration may first be attempted by means of a microscopicai 
investigation. Occasionally this is successful by the mere examination of a drop of 
the suspected fluid or of a smear-preparation of the tissue-juice diluted with salt-solu- 
tion or distilled water. In other cases it is necessary to employ staining methods, in 
which case cover-glass smears of the fluid are made and allowed to dry. The smeared 
cover-glass is then fixed by passing through the flame, and after cooling is stained. 
For this purpose methylene-blue is preferably employed, in a preparation of a one- 
per-cent. methylene-blue solution in a 1-to-10,000 solution of caustic potash. Water 
solutions of fuchsin and methyl-violet are also frequently used. For many bacteria 
there are employed especial staining methods, in which ordinarily the preparations are 
heavily overstained with a solution of gentian-violet or fuchsin in aniline water, or with 
a water solution of methyl-violet, the excess of stain then being removed by means of 
weak acids or by iodine and alcohol (Gram’s method). In this way it is often brought 
about that the bactcria alone remain stained, often certain forms of bacteria only. 

When it is desired to demonstrate the presence of bacteria in tissues, small portions 
of the tissue are hardened in absolute alcohol, and are then cut into the thinnest possible 
sections which are stained by appropriate methods. Here again the methods most fre- 
quently employed are those mentioned above: gentian-violet, methyl-violet, and fuchsin. 
Good objectives are necessary for the microscopic examination; if possible, oil-immersion 
lenses and illumination with substage condenser should be employed. 

If through any method the presence of bacteria in the tissue has been demon- 
strated, the attempt is next made to cultivate them. For this purpose the methods 
developed by Hoch are usually employed. These, in principle, consist in obtaining 
first a fluid containing the bacteria, by means of scraping the tissue or by rubbing up 
pieces of tissue in sterilized salt-solution. This fluid is then evenly distributed in a 
solution of gelatin or agar which has been liquefied by warming; and the mixture is 
then poured upon horizontal glass plates, solidifying as it cools. The individual bac- 
teria, or spores, thus separated from each other develop in the firm nutrient medium. 

By a proper application of this method there are obtained in the layer of gelatin 
various colonies (Fig. 414), which differ in appearance so that they may often be differ- 
entiated from each other by the naked eye alone. When suffic ently separated from 
one another, the individual colonies may be taken up by means of a fine platinum 
needle, and transferred either to a boiled potato, or to a sterile gelatin plate, or streaked 
upon the surface of the solidified nutrient fluid in a test-tube. Very often the infected 
necdle is stuck into the solidified transparent medium contained in a test-tube. 

If the culture on the gelatin plate is pure, and if the entire procedure is carried out 
with the necessary care and the avoidance of contamination, pure cultures may be ob- 
tained by this method. In stab-cultures, as well as in smear-cultures on potatoes or any 
other nutrient medium, special peculiarities often show themselves which make it pos- 


554 THE PATHOGENIC FISSION-FUNGL 


sible for the experienced observer to recognize the form of bacteria. At times, how- 
ever, itis necessary to make u therough microscopic examination of the colonies. 

It is evident ‘that ull the above mauipulutions must be carried out with care, and 
that absolute cleanliness of the instruments used—glass-plates and test-tubes—as well 
sterilization of the nutrient medium are necessary. The proper methrds of 
ization in which a lonz-eontinued heating or an exposure to high temperatures 
in important rie, are bent learned in properiy equipped laboratories. The neces 

anew is furnished in the: varivus be -ks va bacterfological methods of examina- 





























a3 peptone and gelatin is eommoaly empl 
atery infusion of choppel meat, to which a 
further neutralized with carbe1 



















mount of pep 
oda, abd enor 
For streak and same fe 
ily made of a mi, Stract Of Mint. pepte 
blal-serum which has bea evaruived by warmize 

Por stab-cultur i 
dicular positi 
the jelly 

Sterilized benilien is often used for cultures, The in 
kept either at root-temperature or at higher 


at other times a 
ie. and azar-agur; or again 
















tube in a_perpen- 
kept in an oblique position ur! 








culated nutrient media are 
rs in an incubating even 

















wal, wh 


ante 


‚Audate uf a purus 





taeitı. and small. sp 











Reduced one-third. 








"rient medium te be u: 
shown th: 


proper 

Exp 
preis 
ium then 





Th 





the ind Tincteria behave very 
others upon another medium. 
ge stich substances as sugar, 












iat the prrecesses bri above may be modified accord. 
the case. Par example cases in Which it is necessary 
igh tenperatures, Uh in should be avoided and 
plates shen le made instead. Occasionally membranes or exudates from 
mucous surlaces Gtiphtheriay or small bits of excisl ti-sae are placed directly into thy 
Wien it is desired t the cultures directly under the mier 
may be made upen slassalides, In the cuse of many bacteria, as 
the ase of drop cultures is advised. In this method a drop of 
steritized beuilion hans de m the under surfac glass, and is inocu- 
ed from a previously cultivated pure culture of the fungus. _ The cover-glass is then 
ever tne exe Evaporation is prevented 
exclusion of the by a rim of oil or vaseline 
Placed beneath the « glass. By this method the multiplication of bac- 
teria can be observed 
When bacthrinare songht in water a definite amount of the suspected water is dis- 








aut 





























zent the coy 








TISSUE CHANGES CAUSED BY BACTERIA. 555 


tributed in gelatin, and plate-cultures are made. arth is rubbed up with sterilized 
salt-solution; air is made to pass in definite amount through a sterilized salt-solution; 
and the salt-solutions thus infected are then mixed with gelatin, and from this gelatin 
plates are made. 

The culture of bacteria on and in different media, accompanied by the microscopic 
examination of the different stages of development, serves fur a more exact characteriza- 
tion, and thereby for the differentsation of the species of the bacteria tn question. After its 
properties have been thoroughly studied in this way, the influence of the bacterium 
upon the animal organism is tested. As experimental animals, rabbits, dogs, guinea- 
pigs, rats, mice, and small birds are most frequently employed. The bacteria to be 
tested are introduced, sometimes under the skin, sometimes directly into the blood- 
current, sometimes by inoculation into the internal organs, sometimes by inhalation 
into the lungs, or sometimes by administration with the food into the intestinal canal. 
Bacteria can be regarded as pathogenic for a given animal when they multiply within 
the tissues and excite disease processes. If relatively large amounts are inoculated, the 
animal experimented upon may die under certain conditions, even if the bacteria do 
not increase at all in its body, since the poisonous substances formed in the culture and 
introduced by inoculation often suffice to kill the animal. 

Experience has taught that only some of the bacterial infections which occur in 
man, when inoculated into animals, run the same course as in man, and, indeed, only 
those which also occur otherwise in animals. In other cases the pathogenic fission- 
fungi occurring in man or in certain animals are, it is true, pathogenic for the experi- 
mental animal, but the pathological process shows another localization and another 
course. Ina third case the experimental animals are in part or wholly immune. 

Inversely, fission-tungi that are often extremely pathogenic for the experimental 
animals are harmless for other animals or for man. 


Literature. 
. (Local Tissue-changes in Bacterial Infections. ) 


Bard: Charactéres anat.-pathol. généraux des lésions microbiennes. Arch. de phys., 
ix., 1887. 

Baumgarten: Zur Kritik der Metschnikoff'schen Phagocytentheorie. Zeitschr. f. klin. 
Med., xv., 1888; Das Experimentum crucis d. Phagocytenlehre. Beitr. v. Ziegler, 
vii., 1890. 

Birch-Hirschfeld: D. Eindringen v. Darmbakt. in d. Innere d. Organe. Beitr. v. 
Ziegler, xxiv., 1898 (Lit.). 

Buchner: Die chem. Reizbarkeit d. Leukocyten und deren Beziehung z. Entzündung 
u. Eiterung. Berl. klin. Woch., 1890; Cbl. f. Bakt., ix., 1891. 

Cattani: Ueb. d. Reaction d. Gewebe auf specif. Reize. Beitr..v. Ziegler, vii., 1890. 

Faulhaber: Bakterien in d. Nieren b. acuten Infectionskrankheiten. Beitr. v. Ziegler, 


x., 1891. 

Flexner: The Pathologic Changes Caused by Certain Toxalbumins. The Med. News, 
1894. 

Gamaleia: Sur la lésion locale dans les maladies microbiennes. Arch. de méd. exp., 
iii., 1891. 


Goldscheider u. Müller: Phagocytose. Fortschr. d. Med., xiii., 1895. 

Hess: Unters z. Phagocytenlehre. Virch. Arch., 109, 110 Bd., 1889. 

Janowski: Die Ursachen d. Eiterung. Beitr. v. Ziegler, xv., 1894. 

Leber: Entsteh. d. Entzündung. Fortschr. d. Med., vi., 1888. 

Lewin: Histol. d. acut. bakt. Entzündungen. Arb. a. d. path. Inst. zu Tübingen, i., 
1891. 

Massarl ct Rodet: Le chimiotaxisme des leucocytes et l’infect. microb. Ann. de 
l’Inst. Pasteur, 1891. 

Metschnikoff: Sprosspilzkrankheit d. Daphnien. Virch. Arch., 96 Bd., 1884; Be- 
ziehung d. Milzbrandbacillen z. d. Phagocyten. Ib., 97 Bd., 1884; Pathol. Bedeu- 
tung d. intracellulären Verdauung. Fortschr. d. Med., iii, 1884; Kampf d. 
Zellen geg. Erysipelkokken. Virch. Arch., 107 Bd., 1887; Phagocytenkampf beim 
Rückfalltyphus. Ib., 109 Bd., 1887; Sur la lutte des cellules de l’organisme contre 
l'invasion des microbes. Ann. de !’Inst. Pasteur, i., 1887: Offener Brief an Weigert. 
Fortschr. d. Med.. vi., p. 81; Phagocytäre Rolle der Tuberkelriesenzellen. Virch. 
Arch., 113 Bd., 1888; Verhalten der Milzbrandbakterien im Organismus. Ib., 114 
Bd., 1888; Destruction des bactéries. Ann. de l’Inst.Pasteur, 1895. 

Netschajeff: Bedeutung der Leukocyten bei der Infection. Virch. Arch., 125 Bd., 
1891. 








556 THE PATHOGENIC FISSION-FUNGI. 





Pernice et Alesst: Le alterazioni del sangue nelle infeziont sperimentali. La Si 
i 

Prudden and Hodenpyl: Action of Dead Bacteria in the Living Body. New Yori 
Med. Journ., 1891. 

Ribbert: Schicksal pathogener Pilze im Organismus. Deut. med. Woch., 1885; De: 
Untergang pathogeuer Schimmelpilze im Körper, Bonn, 1887; Ueber wiederholt 
Infectionen mit pathogenen Schimmelpilzen. Deut. med. Woch., 1888; Verlau 
der durch Staphylococcus aureus in der Haut von Kaninchen hervorgerufener 
Entzündungen. Ib., 1889; Die patholog. Anatomie und die Heilung der durct 
den Staphylococcus pyogenes aureus hervorgerufenen Erkrankungen, Bonn, 1801 

ch: Wirkung "Rauschbrandbacillus auf d. thier. Organs Beitr. v 





Star sa, Beziehungen der Tuberkelbacillen zu den Zellen. Virch. Arch., 11: 


Tschistovitsch: Etude sur la pneumonie fibrineuse. Ann. del’Inst. Pasteur, v.. 1891 

Virchow: Der Kampf der Zellen und der Bakterien. Virch. Arch., 101 Bd., 1885. 

Weiger ‘a : Leber Metschnikoff’s Theorie der tuberculdsen Riesenzellen. Fortschr. d 

Wraokwitch: Schicksal ins Blut injieirter Mikroorganismen. Zeitschr. f. Hyg. 
1 


Ziegler: Die Ursachen u. das Wesen der Immunität des menschl. Organismus geger 

Infectionskrankheiten. Beitr. v. Ziegler, v., 1889; Ursachen d. Gewebsneubildun 

n. Intern. Beitr. z. wiss. Med., Festschr. f. Virchow, ii., Berlin, 1891; Entzün 

ung. Eulenb Reuleneyklop Ueber die Zweckmassigkeit d. pathol. Lebensvor 
gänge. Münch. med. Woch., 1896. 


(Ptomains and Toxins, and their Relations to the Infectious Diseases. ) 


Arloing: Les virus, Paris, 1893. 

Backlisch: Ptomatne aus Fischen. Ber. d. chem. Ges., x’ 1885. 

Beck: Unters. in d. Geb. d. Anatomie, Phys. u. Chir.. Karls ihe, 1852. 

v. Bergmann: Das putride Gift u. d. putride Intoxication, Dorpat, 1868; bl. f.d. 
me Wiss., 1868. 

Billroth: Unters. üb. die Vegetationsformen d. Coccobacteria septica, Berlin, 1874. 

Blumberg: Putride Intoxication. Virch. Arch., 1 85. 
Bouchard: Action des produits söer&t£s par les inicrobes pathog., Paris, 1890; Théorie 
de l'infection. Verh. d. X. intern. med. Congr., i., Berlin, 1891; Les microbes 
pathogines, Paris, 1892. 

Brieger: Aetiol. d. Wundstarrkrampfs. Biol. Centralbl., vii., 1887; Tetanin u. My- 
tilotoxin. Virch. Arch., 112 Bd.; Zusammensetzung d. Mytilotoxins nebst 
Uebersicht d. bisher in ihren Haupteigenschaften gekannten Ptomaine und Toxine. 
Virch. Arch., 115 Bd.; Ueber Ptomaine, i.-iii., Berlin, 1885-86; Bakterien u. 
Krankheitsgifte. Biol. Centralbl., x., 1890; Beziehungen d. Fäulnissproducte zu 
Krankheiten. Zeitschr. f. klin. Med., iii. Bd. 

Brieger u. Fraenkel, C.: Unters. üb. Bakteriengifte. Berl. klin. Woch., 1890. 

Brieger u. ‚Wassermann: Auftreten v. Toxalbuminen b. Menschen. Char.-Ann., 
xvii., 1892. 

Charrin: La maladie pyocyanique, Paris, 1889. 

Charrin ct Gley: L’uction des produits s 
téme nerveux. Arch, de phys., iv., 1890, v., 

Debierre: Les maladies infeetieuses, microbes, tometines, leucomafnes, Paris, 1888. 

Duclaux: Ferments et maladie: s, Paris, 189! Le microbe et les maladies, Paris, T886; 

oménes généraux de la vie des microbes, Ann. de l’Inst. Pasteur, 1., 

albuminoides. Ib. „1892. 

natrobe Bac. u. s, Bezich. z. Botulismus. Zeitschr. f. Hyg., 26 


























Par le bncille pyocyanique sur te sys- 




















Gaffky u “Pan Warst- und ‚Fleischvergiftung. Arb. a.d. K. Gesundheitsamte, vi. ; 
f. Bakt.. 130K 

es poi 
Hiller: Die Lehre von der 
Hoffa: Zur Lehre der Sepsi 
Husemann: Ueber Ptomai 
Jacquemart: Les ptomaine 
Koch: Untersuchungen über Wundinfectionskrankheiten, Leipzig, 1878. 
Leber: Die Entstehung «der Entzündung, Leipzig, 1801. 








Langenbeck’s Arch., 89 Bd., 1889. 
ie, 1880-83. 











DOUBLE AND SECONDARY INFECTION. 557 


Otto: Anleit. z. Ausmittelung d. Gifte, Braunschweig, 1883. 
Paltauf ot Heider: Der Bacillus maidis u. seine Beziehungen z. Pellagra. Med. 
ahrb., . 

Panum: Das putride Gift, die Bakterien, putride Intoxication u. Septikämie. Virch. 
Arch., 60 Bd., 1874. 

Pouchet: Matiéres extractives, ptomalnes et leucomalnes. Revue de méd., vii., 1887. 

Sahli: Moderne Gesichtspunkte in d. Path. d. Infectionskrankh. Kl. Vortr., Nos. 
319-320, 1888. 

Schmiedeberg u. Harnack: Bildung von Muscarinaus Neurin. Arch. f. exp. Path., 
XVi., . 

Selmi: Berichte d. Deutsch. chem. Ges., vi., vii., and xii.; Ptomalne o. Alcaloidi 
cadaverici, 1881. 

Trambusti: Physiol. Wirkung v. Hydrophilus fuscus. Beitr. v. Ziegler, xiv., 1898. 

Vaughan and Novy: The Cellular Toxins, Philadelphia, 1902. 
See also §§ 12 and 149. 


(Transmission of Bacteria from the Mother to the Fetus.) 


Ahlfeld : Milzbrand des Neugeb. nach Infection d. Mutter. Ber. u. Arb., iii., Leipzig, 

1886. 

Birch-Hirschfeld: Pforten der placentaren Infection des Fötus. Beitr. v. Ziegler, 
ix., 1891. 

Bollinger: Uebergang path. Organismen v. d. Mutter auf d. Kind. Münch. med. 
Woch., 1887. 

Eberth: Geht der Typhusorganismus auf den Fötus über? Fortschr. d. Med., vii., 
1889. 

Ernst: Intrauterine Typhusinfection einer lebensfähigen Frucht. Beitr. v. Ziegler, 
viii., 1890. 

Hildebrant: Zur Casuistik d. placentaren Tebergangs d. Typhusbacillen. Fortschr., 
vii., 1889. 

Kockel u. Lungwitz: Placentartuberculose beim Rind. Beitr. v. Ziegler, xvi., 1894. 

Latis: Uebergang d. Milzbrandes v. d. Mutter auf d. Fötus. Beitr. v. Ziegler, viii., 
1890 


Löffler: Die Aetiologie der Rotzkrankheit. Arb. a.d. Kais. Gesundheitsamte, i., 1886. 
Lubarsch: Intrauterine Uebertragung pathogener Bakterien. Virch. Arch., 124 Bd., 
1891. 

Malvoz: Sur la transmission intraplacentaire des micre-organismes. Ann. de l’Inst. 
Pasteur, ii., 1888; Le passage des micro-organismes au fetus. Ib., iii., 1889. 
Marchand: Milzbrand b. einer Schwangeren m. Infection d. Kindes. Virch. Arch., 

104 Bd., 1887. 
Netter: Transmission intra-utérine de la pneumonie. Arch. de biol., 1889. 
Perroncito e Carita: De la transmission de la rage. Ann. de l’Inst. Pasteur, i., 1887. 
Schmorl u. Kockel: Tuberculose der menschl. Placenta. Beitr. v. Ziegler, xvi., 1894. 
Straus et Chamberland: Rech. exper. sur la transmission de quelques maladies viru- 
lentes, en particulier du charbon, de la mére au fetus. Arch. de phys., i., 1883. 
Rosenblath: Uebergangsfähigkeit d. Milzbrandbacillen v. d. Mutter auf d. Kind. 
Virch. Arch., 115 Bd. 1889. 
Wolff: Vererbung von Infectionskrankheiten. Virch. Arch., 112 Bd., 1888. 


(Double Infection and Secondary Infection. ) 


Babes: Recherches sur les associations bactériennes du bacille de la tuberculose. Le 
Progrés méd., Roumain, 1888; ref. Cbl. f. Bakt., v., 1888; Bakteriol. Unters. über 
septische Processe d. Kindesalters, Leipzig, 1889; Les associations bactériennes. 
Verh. d. X. internat. med. Congr., ii., Berlin, 1891; Ueber einige bei Influenza 
gefundene Bakterien. Cbl. f. Bakt.. vii., 1890; Associat. bacter. du bac. de la 
tuberculose avec des microbes hémorrhagiques. La Roumaine méd., xv., 1898. 

Barbier: De quelques associat. microbiennes dans la diphthérie. Arch. de med. exp., 
iii., 1891. 

Bein: Bakteriolog. Unters. über Influenza. Zeitschr. f. klin. Med., xvii., 1890. 

Buchner: Bakteriolog. Befunde bei d. letzten Influenzaepidemie. Münch. med. 
Woch., 1889. 

v. Dungern: Mischinfection bei Diphtherie. Beitr. v. Ziegler, xxi., 1897. 

Hericourt: Les associations microbiennes. Revue de méd., vii., 1887. 

Heubner: Ueber die Scharlachdiphtherie. Samml. klin. Vortr., No. 322, 1888. 

Lenhartz: Secundärinfectionen bei Scharlach. Jahrb. f. Kinderheilk., xxvii., 1888. 








558 THE PATHOGENIC FISSION-FUNGI. 


Polguére: Les infections secondaires, leurs localisations secondaires au cours de la 
tievre typholde et de la pneumonie, Paris, 1888. 

Raskin: Unters. über Secondärinfectionen bei Scharlach. Chbl. f. Bakt., v., 1889. 

Ribbert: Bakt. Mittheil. über Influenza. Deut. med. Woch., 1890. 

Romberg: Beobacht. üb. Leberabscesse b. Typhus abdominalis. Berl. klin. Woch., 

). 

Rosenbach: Mikroorganismen bei den Wundinfectionskrankheiten, Wiesbaden, 1884. 

Bata: Leber die Bedeutung der Mischinfection bei der Lungenschwindsucht, Jena, 
1899. 

Weichselbaum: Bakteriolog. und anat. Unters. über Influenza. Wien. klin. Woch., 
1890. 


(Changes in the Physiological Properties (Attenuation) of Bacteria. ) 


Adami: On the Variability of Bacteria. Med. Chronicle, September, 1891. 

Arloing, Thomas, Cornevin: Du charbon symptomatique, Paris, 1887. 

Buchner: Die Nägeli'sche Theorie der Infectionskrankheiten, Leipzig, 1878; several 
articles in Nägeli's Unters. üb. nied. Pilze, 1882; Immunität u. Immunisirung. 
Münch. med. Woch., 1889. 

Chauveau: Rech. sur le transformisme en microbiologie pathogéne; des limites, des 
conditions et des conséquences de la variabilité du bacillus anthracis. Arch. de 
med. exp., 1889. 

Flü Be: Abschwächung virulenter Bakterien u. erworbene Immunität. Zeitschr. f. 

yg., iv., 1888. 

Gaffky: Mittheil. a. d. K. Gesundheitsamte, i., 1881. 

Hueppe: Die Formen der Bakterien, Wiesbaden, 1886. 

Koch: Wundinfectionskrankheiten, 1878. Mittheil. a. d. K. Gesundheitsamte, i., 1881; 
Ueber die Milzbrandimpfung, Berlin, 1882. 

Koch, Gaffky-Löfller: Abschwächung d. Milzbrandbacillen. Mitth. a. d. K. Ges.- 
Amt., ii., Berlin, 1884. 

Lubarsch : Abschwächung d. Milzbrandbacillen im Froschkörper. Fortschr. d. Med., 
vi., 1888. 

Nägeli: Die niederen Pilze, 1877; Untersuchungen über niedere Pilze, München, 1882. 

Pasteur: Sur les maladies virulentes et en particulier sur la maladie appelée vulgaire- 
ment choléra des poules. Acad. de méd., 19 févr., 1880; Sur le choléra des poules, 
étude des conditions de la non-récidive de la maladie. Acad. de méd., 27 avr., 
1880; Atténuation du virus du choléra des poules. Acad. des sciences, 26 oct., 
1880; De l’attenuation du virus. Congrés internat. d’hyg. & Genéve, 1883; zahl- 
reiche Mittheilungen in den Berichten der Acad. de med. aus den Jahren, 1880-89 
(cf. Rodet). 

Pasteur ct Throllier: Abschwächung des Giftes des Rothlaufes der Schweine durch 
Impfung auf Kaninchen. Compt. rend., xcvii., 1883. 

Rodet: L’atténuation des virus. Revue de méd., vii., 1887, viii., 1888; De la varia- 
bilité dans les microbes, Paris, 1895. 

Schottelius: Untersuch. üb. Micrococcus prodigiosus. Festsch. f. v. Kölliker, Leip- 
zig, 1887. 

Viala: Sur les causes de l’attenuation des moélles rabiques. Ann. de l’Inst. Pasteur, 
v., 1891. 

Wasserzug: Variations de la forme et de la fonction chez les bactéries. Ann. de 
l’Inst. Pasteur, 1888. 


(Methods of Bacteriological Investigation. ) 


Abel: Taschenbuch f. bakteriologische Praktikanten, Würzburg, 1900. 
Crookshank: An Introduction to Practical Bacteriology, London, 1886. 
Fischer: Vorlesungen über Bakterien, Jena, 1897. 
Flügge: Die Mikroorganismen, Leipzig, 1896. 
Fraenkel, C.: Grundriss der Bakterienkunde, Berlin, 1890. 
Günther: Einführung in das Studium der Bakteriologie, Leipzig, 1898. 
Hueppe: Die Methoden der Bakterienforschung, Wiesbaden, 1891. 
v. Kahlden: Technik der pathol.-anat. Untersuchungen, Jena, 1900. 
Migula: Bakteriologisches Praktikum, Karlsruhe, 1892. 
Novy: Laboratory Work in Bacteriology, 1899. 
Numerous articles on the investigation of bacteria are found in the Centralblatt f. 
Bakteriologie. 


THE COCCI. 559 


Il. The Different Forms of Bacteria and the Infectious Diseases 
Caused by Them. 


I. THE Coccl, OR SPHAROBACTERIA, AND THE MORBID PROCESSES 
CAUSED BY THEM. 


(a) General Considerations Regarding the Cocei. 


§ 151. The cocci or coccacese (Zopf) are bacteria that occur exclu- 
sively in the form of round or oval or lanceolate cells. In their multi- 
plication by division they often form peculiar aggregations of cells, 
which are commonly designated by special names according to the char- 
acter of the different forms appearing. Since certain forms of cocci are 
especially likely to develop in definitely shaped aggregations, advantage 
has been taken of this fact, to classify them in different species. It 
should be noted, however, that a given species does not always appear in 
the same form, but may vary according to the nutrient conditions. 

Many of the cocci multiply by division in one plane only—at right 
angles to the length of the elongated spherical cell. If the spheres re- 
sulting from division remain together for some time in the form of double 
spheres, and if this 
form appears with 
especial frequency in 
the of any one 
speci it is desig- 
nated as a diplococcus 






wen 
.- 
tees 
Nez 
Fia. 415. Fia. 416. Fig. 418. 
Fra. 5. Streptococcus from a, purulent peritoneal exudate of a case of puerperal peritonitis. a, 
Single coccl; I, diplococel ; c, streptococe! or torula-chalns. X 500. 


Fic. 418, “Colonies of micrococe! In DIood-capillartes of the liver, causing metastatic ubecens formation. 
From a case of pyamia. Necrosis of liver-cells. x 400. 


Fig. 417.—Cocet grouped in tetrads (merismopedia), from a softening tnfarct of the lung. X 500. 
Fig. 415.- Sareina ventricull, x 400. 











(Fig. 415, 6). If, from a further continued division of the cells in one 
plane, rows of cocci (torula chains) result, these are known as strepto- 
cocci (Fig. 415, e), and this term is used also as the name for a group. 
If the division of the cells takes place irregularly, and the cells remain 
together in small collections or heaps, the bacteria are usually desig- 
nated as micrococci (Zopf) (Fig. 416). By Ogston and Rosenbach 
the name staphylococcus or grape-coccus has been used to indicate some 
of these forms. Larger collections of cells, which are held together by 
a gelatinous substance derived from the cell-membranes, have been 
designated as zoöglea masses. If the masses of cocci are united into 
larger collections by means of a gelatinous envelope, they are spoken of 
as ascococci or tube-cocci. 

To those cocei which remain united for a long time in a four-celled 
tablet (Fig. 417), the name of merismopedia, tetracoccus or tablet-coccus 





560 THE PATHOGENIC FISSION-FUNGI. 


was applied by Zopf. Others class such bacteria with the micrococ 
The cocci that go by the name sarcinse are characterized by division 
three directions of space, so that compound cubical packets of spheri 
cells are formed from tetrads (Fig. 418). 

The cocci not infrequently show a tremulous molecular motion 
fluids; swarming movements have not been observed with certain 
Spore-formation has not been demonstrated in fhe majority of forı 
According to Cienkowski, Van Tieghem, and Zopf, the Coccus (leucon 
toc) mesenterioides, that produces a frog-spawn-like culture on sugar 
parsnips, forms arthrogenic spores, in that some particular cell in 
torula chain becomes larger and glistening. According to Prazmows 
the Micrococcus uree also forms spores. 

The saprophytic cocci grow upon very different nutrient substré 
and cause by their growth in suitable media various processes of ¢ 
composition. Many also form pigments. Micrococcus uree (Paste 
Van Tieghem, Leube) causes fermentations in urine by means of whi 
ammonium carbonate is formed from the urea. Micrococcus viscosus 
the cause of the slimy fermentation of wine. The cause of the phosph« 
escence of decomposing meat was found by Pflüger to be a micrococcus th 
forms slimy coatings on the surface of the meat. 

Of the pigment-producers the best known are Micrococcus luteus, A 
crococcus aurantiacus, Sarcina lutea, Micrococcus cyaneus and Micrococe 
violaceus, which, when grown upon boiled eggs or potatoes, produce y« 
low, blue, and violet pigment respectively. 

Saprophytic cocci are found in the mouth cavity and intestine, 
well as on the surface of the skin, and occasionally also in the lung 
Micrococcus hematodes (Babes) is said to be the cause of red sweat, aı 
forms red zodgloea masses. 

Sarcina ventriculi (Fig. 418) occurs not infrequently in the stoma 
of man and animals, especially when abnormal fermentations are goiı 
on. According to Falkenheim the stomach sarcines can be cultivate 
upon gelatin, and form in this medium round, yellow colonies, whic 
contain colorless monococci, diplococei, and tetrads, but never cubic 
packets. They form these, however, in neutralized hay-infusion, ar 
their growth causes a souring of the infusion. The membrane of tl 
sarcing is said to consist of cellulose. 

Microcococcus tetragenus (merismopedia) is not infrequently four 
in human sputum, and in the mouth and throat; it may be preseı 
further in the wall of tuberculous cavities, or in hemorrhagic or gai 
grenous foci of the lungs. It forms tetrads (Fig. 417) whose cells a: 
held together by a gelatinous membrane. On gelatin-plates it forn 
round or oval, lemon-yellow colonies. It is pathogenic for white mi 
and guinea-pigs, to a less extent for rabbits, and, when injected subeut 
neously, excites purulent inflammations, in the mouse often also a se 
ticemia. Intratracheal injections may give rise to inflammations of tl 
respiratory passages and the lungs. 

The pathogenic cocci cause acute inflammations which usually he 
after the death of the bacteria; but it not infrequently happens th 
cocci may remain in the body for a long time and give rise to chron 
processes. 





THE PATHOGENIC COCCI. 561 


Literature. 
(The Cocci.) 


Babes: Rother Schweiss. Biol. CLl., ii., 1882. 

Bancel et Hasson: Sur la phosphorescence de la viande de homard. Compt. rend.. 
t. 88, 1879. 

Bienstock: Bakterien d. Darmes. Fortschr. d. Med., i.; Zeitschr. f. klin. Med., v 
1384. 

Bosc et Galavielle: Sur le micrococ. tetragenus. Arch de med. exp., 1899. 

Brieger: Bakterien des Darmes. Berl. klin. Woch., 

Chauffard et Raymond: Septicemie tetragenique. Arch. de med. exp., 1896. 

Cohn: Beiträge z. Biologie d. Pflanzen, i.-iv. 

Ebarth: Blauer Eiter. Virch. Arch., 73 Bd., 1878. 

Escherich: Bakterien d. Darmes. Fortschr. d. Med., iii., 1885; Münch. med. Woch., 
1886. 

Falkenheim: Ueber Sarcine. Arch. f. exp. Path., xix., 1885. 

Gessard: De la pyocyanine et de son microbe. These de Paris, 1882. 

Lücke: Blauer Eiter. Arch. f. klin. Chir., 1892. 

Ludwig: Micrococus Pflügeri (Phosphorescenz), Hedwigia. 1884. 

Miller: Die Mikroorganismen der Mundhöhle, Leipzig, 1892. 

Prazmowsky: Ueber Sporenbildung bei den Bakterien. Biol. Cbl., viii., 1888. 

Prove: Micrococcus.ochroleucus. Beitr. z. Biol. d. Pflanzen v. Cohn, iv., 1887. 

Schröter: Pigmentbildende Bakterien. Beitr. z. Biol. d. Pflanzen, v., Cohn, i. 

Stubenrath: Das Genus sarcina, München, 1897. 

Vignal: Rech. s. ). microorganismes de la bouche. Arch. de phys., viii., 1886; Rech. 
s. 1. microorg. des maticres fecales. Ib., x., 1887. 
See also S 148. 


(b) The Pathogenic Cocci. 


x 152. The Streptococcus pyogenes (Rosenbach) is a eoceus which, 
in multiplying, forms double spheres and chains of spheres (Fig. 415) of 
different lengths, containing from four to twelve or more cells. This 
chain-formation comes to an especially full development when the strep- 
tocoecus is growing in Auids--in nutrient. bouillon or fluid exudates—but 
is also usually seen when it is growing within the tissues. 

The coeci stain well by Gram’s method, are facultative anaérobes, 
grow best at 37° C., and form small whitish colonies on gelatin and agar. 

The streptococcus pyogenes is especially pathogenic for mice and 

abbits (much less so for dogs and rats); but its virulence varies greatly, 
and rapidly decreases In cultures grown on ordinary media. Its v irulence 
is retained for a relatively long time (Marmorek ) in cultures of the cocci 
in human- or in horse-serum (serum two parts, bouillon one part), or in 
a mixture of bouillon and ascitic fluid. 

Streptococcus pyogencs causes in man inflammations, thich usually, 
though not alırays, assume a purulent character. Occasionally it is found 
also upon normal mucous membranes, for example, in the upper air-pas- 
sages, or in the vagina aud cervix uteri; it may therefore be assumed in 
such cases that its virulence is very slight, or that the mucous membranes 
offer a successful resistance to its entrance into their tissues. 

An infection with streptococci may occur either in healthy indi- 
viduals, or in those who have received some injury, or finally as an ac- 
companiment and sequela of other infections, particularly of scarlet 
fever, diphtheria, and pulmonary tuberculosis. 

If the streptococcus multiplies upon the surface of mucous membranes— 
for example, of the respiratory tract. (Fig. 419)—it excites an inflamme- 
tion, Which may bear the character of a desquamative or purulent catarrh 








eee tee len mon.) ee, BT OO Te LF" 
oe ° « - — - e - = Pan - =" * - u 
- u m. e nd : . - - 7 ... 
. . ° .o Pe _ ne - . _ 
“ww. - Lat wt - - _™ - — - - 2 EEE 
. .- ° : oe = - = "eo a7 ~ =~ _ 
- — = 
« ‘a. 
> -__ Pa) 
._ ~ wer’ a. u 
- - - ws N) er - 
u. 


an oty > nn. - 
ow 2 
oa~ - . = »4*. N wT 
a ee een = 
Bu» > . - =. 
. m . = Ya . - _ 
te . bd 2 v2 “> x 5 = N - 
~ eye tk rt: ar 
stg? Fw he - . . ur i . 
- . a Ir ae A amt. om 


la. 1 Been the pte lege on fhe risk. after phleszmen ef the arm !form.acır, 
una moat Wo etna weed an The she Satechs 0 DBes tive: Csethe ood begins zz 


od ail zanztene of the eorium 17,7, ervsipelas gangrenosuin a1 
Nppunation ol the tissue, 

In Ihe zubenteneons tissue the spread and multiplication of the ec 
Pie. 100 lead ton progressive seropurnlent GA) and Ahrinopurul 
in llananatio. olten With subsequent THissue-suppuration. Such forms 
tnleetion cater Know ses phlequons, 

I the une chen become turolre cl inca plleqmonous process, the streptoce 
nee ane spread: ehietiv in the connective tissue of the perimysi 
termin bet tay penetiate also dite the sarcolemma-tubes. Here: 
Ihe con eqgnenee- af the rifeetion are more or less severe inflaaimiati 
IE lin leo soppiralton. 

Doren reves rar mitochon of the Iunys ec: :TUSeS purulent, or CTOU pos, 
bometihaere essuelattons inte: the pulmonary alveoli 

Shell bene become involved Chant the skin or from a NUCOUS mie 
Piste a. bor example, from the middle ear the coce: may Inerease 














STREPTOCOCCUS PYOGENES. 569 


ess consists of a progressive proliferation of granulation tissue and a new- 
formation of connective tissue due to streptococci (or staphylococci), 
while suppuration is absent or confined to circumscribed areas. 


The biological characteristics of the Streptococcus pyogenes are very variable, and 
this is well shown both in its behavior as a disease-producing agent and in the cultures 
of streptococci taken from different cases. Consequently an effort has been made to 
divide the streptococci into different species, and in particular has the streptococcus 
which causes erysipelas been regarded as a distinot form—the Streptococcus erysipela tts. 
Further, according to the place in which the streptococcus was found, it was formerly 
customary to speak of a Streptococcus pverperalis (.Arloing), Str. articulorum (Flägge). 
Str. scarlatinoaus (Klein); or, according to the manner of growth, of a Sr. longus and 
Str. breris, etc. (von Lingelsheim). These characteristics are, however, not sufficient to 
form a basis for the separation of the streptococci into different species; and it appears 
more correct, or at least more expedient, to consider all the chain-forming streptococci 
as One species, which appears in many varietics. 

In diphtheria and scarlet fever, streptococcus infections of the throat and air-pas- 
sages ure extremely common, particularly in the case of the first named, so that many 
authors (Baumgarten, Dahmer) are inclined to assign to the streptococcus a co-ordinate 
position with the diphtheria-bacillus in the causation of diphtheria—the diphthetia- 
bacilli predominating in the lighter forms of infection, the streptococci in the more 
severe. Pure streptococcus infections may present the same picture as that produced 
by the Zöfler’s bacillus. If both forms of bacteria are present, their effects may be 
combined; perhaps also the presence of streptococci increases the virulence of the 
diphtheria-bacilli. 


Literature. 


(Streptococcus Pyogenes. ) 


Babes: Sur les streptocoques. Ann. de l’Inst. d. path. de Bucarest, vi., 1898. 

Bender: Ueber den Erysipelcoccus. Cbl. f. Bakt., iv., 1888 (Lit.). 

Bonome ct Bombicci: Proteine degli streptococchi. Rif. Med., 1899. 

Bordet: Serum antistreptococcique. Ann. de l’Inst. Pasteur, 1897. 

Brunner: Die Begriffe Pyämie u. Septhimie, Frauenfeld, 1899. 

Bumm: Die puerperale Wundinfection. Cbl. f. Bakt., ii., 1887. 

Chiari: Ilolzphlegmone. Beitr. z. Dermat., Festschr. f. Neumann, Wien, 1900. 

Dahmer: Streptokokken bei Diphtherie. Arb. her. v. Baumgarten, ii., 1896. 

Dennig: Septische Infection. Münch. med. Woch., 1897. 

Denys: Trav. exec. sur le streptocoque pyog. Chbl. f. Bakt., xxiv., 1898. 

v. Dungern: Mischinfection bei Diphtherie. Beitr. v. Ziegler, xxi., 1897. 

Fehleisen: Deutsch. Zeitschr. f. Chir., xvi. ; Die Aetiologie des Erysipels, Berlin, 1883. 

Fränkel, E.: Identität d. Streptococcus pyog. u. Streptoc. erysipelatis. Cbl. f. 
Bakt., vi., 1889. 

Guarnieri: Contrib. allo studio dello streptococco dell’ eresipela. Arch. p. le Sc. 
Med.. xi., 1887. 

Hajek: Ueb. d. ätiol. Verhältniss d. Erysipels zur Phlegmone. Wien. med. Jahrb., 
IN87. 

Hoffa: Erysipelkokken b. einer Kniegelenksentzündung nach Erysipel. F.d. Med., 
iv., 1886. 

Homen: Die Wirkung d. Streptokokken u. ihre Toxine. Beitr. v. Ziegler, xxv., 1899. 

Howard and Perkins: Streptococcus mucosus. Jour. of Med. Res., 1901. 

Janowsky: Die Ursachen der Eiterung. Beitr. v. Ziegler, xv., 1894 (Lit.). 

Jordan: Die Aetiologie des Erysipels. Arch. f. klin. Chir., 42 Bd., 1891. 

v. Kahlden: Verhältn. d. Bakteriolog. z. Chirurg. Cbl. f. Bakt., i., 1887; Sepsis. 
Eulenburg’'s Realencyklop., 1899. 

Kusnetzoff: Holzphlegmone. Arch. f. klin. Chir., 58 Bd., 1899. 

Koch: Wundinfectionskrankheiten, Leipzig, 1878. 

Koch u. Petruschky: Erysipelimpfungen. Zeit. f. Hyg., xxiii., 1896. 

Krause: Holzart. Entzünd d. Bindegewebes. Cbl. f. Chir., 1899. 

Kurth: Unterscheidung der Streptokokken. Arb. a. d. K. Gesundheitsamt, vii., 1891. 

Laitinen: Streptococcustoxin. Cbl. f. allg. Path., vii., 1896. 

Lemoine: Angines non diphthériques. Ann. de 1’Inst. Pasteur, ix., 1895. 

v. Lingelsheim: Eigenschaften versch. Streptokokken. Zeit. f. Hyg., x., 1891. 

Longcope: Streptococcus mucosus (Howard). Jour. of. Med. Res., 1902. 

Lubarsch: Streptokokkengruppe. Ergebn. d. allg. Path., iii., 1897. 











570 THE PATHOGENIC FISSION-FUNGI. 


Lukkomsky: Unters. über Erysipel. Virch. Arch., 60 Bd., 1874. 

de Marbaix: £t. sur la virulence des streptocoques. La Cellule, viii., 1892. 

Marchand: Ta phagocy ‘ytose des streptocoques. Arch. de méd. exp., 1888. 

Marmorek: Versuch einer Theorie der septisclen Krankheiten, Stuttgart, 1604 

Metschnikoff: Ueber den Kampf der Zellen gegen dic Erysipelkokken. Virch. A 
109 Bd., 1887. 

v. Noorden: Streptokokken im Blut bei Eryeipelas. Münch. med. Woch., 1887. 

Pasquale: Vergleich. Unters. über Streptokokken. Beitr. v. Ziegler, xii. 1898. 

Pawlowsky: Aetiologie der ucuten Peritonitis. Conf. Chir, 1887; Ueber die M 
rennen des Erysipels. Berl. klin. Woch.. 

: Ueber die Specifitat des Erysipel- ‘streptococeus. Zeit. f. Hyg.. x 














“Phlegmone ligneux du cou. Rev. de Chir 
r: Contr, Al’öt. exp. du streptoroque de Verysiptle. 
roorganismen der W undinfectionskranklı 
; Actiologie u. Klinik d, aeuten Gelenkrheumtismus, 
Streptokokkenembolie im Auge. Zeit. f. Gebh., xvii 
The Vitality of Bacteria from the Throuts of Searlei-Fever Patients, 
Special Study of Streptococci. Jour. of Med. Res., 1908. 
Weiss: Actiologie d. Otitis Media im Säuglingsalter. Beitr. v. Ziegler, xxvii., 1 





Rev. de möd., 1892, 1 
iten, Wiesbaden, 


















$ 153. The Diplococcus pneumoniz (Fränkel, Weichselbaum ) 
Streptococcus lanceolatus (Gamaleia), or Diplococcus lanceolatus (| 
Bordoni-Uffreduzzi), and also known as the Preumococeus, is a pathog 
streptococcus of very frequent occurrence. It formsspherical, oval, 
lanceolate cocci (Fig. 430, a), which in the human body.are usually 
rounded by a transparent capsule, and are grouped together in pairs 
d), or more rarely in chains of such pairs (c), or in large colonies (d 

The Diplococcus pneumoniz stains well with fuchsin and with gen 
violet, and by these stains the capsule may be demonstrated in sm 
preparations. The cocci are also stained 
Gram’s method. 

The cocci are facultative anaérobes. T 
will not grow upon gelatin at ordinary ro 
temperature, but do so upon slightly alka 
blood-serum-gelatin, upon agar and in bouil 
at a temperature above 22° C., and best at 
temperature of the body. They form upon 
ener surface of the medium a delicate, translucı 
Covel without capsule; >. glistening culture, which suggests the dew-! 
a gelatinous capsil cl deposit of moisture upon a cover-glass (Friink: 
and consists of diploeocei and chain-eocei with 
capsules. The growth is, however, scanty; : 
easily dies out. Upon potatoes the cultures do not thrive. 

The Diplocoecus pnenmoniz is iu a great number of cases (accord 
to Weichselbaum in seventy-one per cent.) the cause of the affeetioı 
the lung known as croupous pneumonia, in which the lung is the seat of 
acute infl: ation which is ushered in by a congestive hyperemia (1 
431, a). In the course of the disease the alveoli r large areas of 
lung become filled with a coagulated exudate consisting of desquama 
epithelium, leucocytes, red blood-cells, serous fluid and fibrin (Fig. 1¢ 
In the normal course of the disease the exudate becomes liquefied : 
absorbed. As has been shown by numerous observations, the Diplo 
cus pheumonie the lungs other inflammatory proce: 
‘ing the character of a catarrhal bronchopneumonia, which is chai 
tion of foci of a serocellular exudate. During 
se the eoeei are found especially in the inflar 
y greatest numbers at the beginning of the inflammati 












































Hz THE PATHOGESIC FISSION-FUNGL 


When injected beneath the skin of the rabbit's ear ( Neufeld ; they al: 
produce ipelatous inflammations. Rabbits are especially susceptibl 
a» they die with symptoms of septicemia in from thirty-six to forty-cig] 
hours after subcutapeons inoculation. The injection of pure caltan 
into the pleural cavity of rabbits gives rise to a pleuritis, as weil as 
splenization of the lung, iu which the parenchyma of the organ is filk 
with a haemorrhagic serous exudate. 

ording to A. Frankel the cocei very easily lose their virulene 
particularly when cultivated upon milk; ard if it is desired to reta 
their virulence they must, from time to time, be passed through susce) 
tible animals. Cultivation of the cocci at 42° C. for one to two da! 
destroys their virulence. 





















The Diptiwroenn Jr ummia belongs to those bacteria whose physiological properti 
ka ishes, according to the principal places in which th 

are found, a me ummreun and & meningwoeeus, In cerebrospinal meningitis cocci a 
nd which ure closely related in part to the Streptococcus pyogenes (Strejtwuer 
Di «1 in part to the Diplococcus pneumonie (Lapdococens iutrıc 

Weichw tutus. Whether these represent especial forms or on 
ies of the species mentioned has not at the present time been decided with ce 
tainty. ‚Jäger is of the opinion that the Diplococcus Intracellularis meningitidis 
the cause of epidemic cerehrominal meningitix, and is entirely distinct from the pneum 
Sporadic meningitis may, on the other bund, be caused also by the pneun: 





















coveus, 
Ace ring to Emmerich, there is formed in bouillon-cultures of pneumococci 8 sed 








ns res sistant cells which remain capable of development far month 

immune (Emmerich) by repeated injections of hi 

res of increasing virulence, 90 that 30 c.c. of cultun 

ithout any striking disturbance. The injected bacter 

‘The serum of immunized rabbits can cure pneum« 
coccus infections in rabbits and mice. 








Literature. 
(Diplococcus Pneumonia. ) 


Banti: Contrib. allo studio degli pneumococchi. Lo Sperimentale, 1886; Sull“ 





olori: ‚la pneumonite Ib., 1890; Aetiolo; der Endocarditis. Dew 
ined. Woch,, 1884; Localisazzioni extrapolmonari del diplococco lanceolate. Arch 
di Anat, Firenze, 101. 

Emmerich: Infection u. Immunisirung bei croup. pneumonie. Zeit. f. Iyg.. xvii. 
101 

Faulhaber. Bukterien in d. Nieren bei cut. Infectionskrankheiten. Beit. v. Ziegler 
x., 1801 






Foa: infez. del diple 
xiv., 1898. 

Fo& u. Bordoni-Uffreduzzi: Bukterienbefunde bei Meningitis cerebrospinalis, Deut 
med, Woch.. 1846; Actiologie d. Meningitis cerebrospinalis epidemica. Zeit. f 
Hye. 1MRM, 

Frankel, A.: Verh, d. med. Congresses, Wiesbaden, 1884. Zeit. f. klin. Med.. x.. xi. 
Deut, med. Woch., 1886. 

Gabbi: Sull’ urtrite sperimentale da viro pneumonico. Lo Sperimentale, 1890 

Gamaleia + de la pneumonie fibrineuse. Ann. de I'Inst. Pasteur, 
INS 





cco lanceolato, Arch. p. le Sc. Med., xvii; Zeit. f. Hyg. 
























Haegler: Die pyogenen Eigenschaften von Pneumokokken. Fortschr. d. Med., viii. 
TNO, 

Hauser: Mucumonickokken bei Monlygitiscerebrospinalis. Münch. med. Woch., 

Herrick: Paeumococcic Arthritis, Amer. Jour. of Med. Se., 










Jäger: Act 

med, We 
Janowsky: Ur 
Koch. Mittheil 
Kruro u Pansini: Unters. ib Bine cus pneun 
Macnigne ct Chipault: Arthrites ü pneumocoques. 


gitis eerebrospin. epidemiea. Zeit. f. ive. xix., 1896; Deus 
., 1894. 


f. Tyg., xi., 1899, 
de nid. 1891. 











576 THE PATHOGENIC FISSION-FUNGL 


the first-named, less so for the last. In these animals it causes suppu- 
ration. The staphylococcus loses its virulence easily in cultures. The 
inoculation of cultures of high virulence into susceptible animals causes 
a gelatinous oedema. 

Closely related to the Staphylococcus pyogenes aureus are the Staphy- 
lococcus pyogenes albus ( Rosenbach ) and the Staphylococcus pyogenes 
citreus (Passet ); these forms probably represent modified varieties of 
the aureus. The albus forms whitish, the citreus lemon-yellow colonies. 
These bacteria occur in the same regions and produce the same effects as 
the aureus, but are more rare than the last named. 

The Staphylococcus pyogenes aureus usually occurs alone in the pus- 
foci, but not infrequently there may be associated with it other pus- 
cocci or even bacilli, as, for example, the Bacterium coli commute, or 
the typhoid. bacillus. 


Literature. 


(Staphylococcus Pyogenes Aureus. ) 


Babes: Bakt. Unters. tb. septische Processe im Kindesalter, Leipzig, 1889. 

Bockhart: Aetiol. d. Impetigo, d. Furunkels u. d. Sykosis. Monatsh. f. pr. Dermat., 
1887. ' 

Bonome: Staphylocoques pyogenes. Arch. ital. de biol., viii... 1887. 

de Christmas: Rech. exper. sur la suppuration. Ann. de I'Inst. Pasteur, ii., 1888. 

Dennig: Ueber septische Erkrankungen, Leipzig, 1891. 

Escherich: Staphylokokken in Hautabscessen v. Säuglingen. Münch. med. Woch.. 
1886. 


Gamaleia: Les poisons bacteriens, Paris, 1892. 

Garre: Zur Actiologie der acuten eiterigen Entzündung. Fortschr. d. Med., iii.. 1485. 

Heiberg: Die puerperalen septischen Processe, Leipzig, 1873. 

Hessler: Die otogene Pyämie, Jena, 1896. 

Hohnfeldt: Histugenese d. durch Staphylococcus hervorger. Abscesse. Beit. v. Ziex- 
ter. iii, 1868. 

Janowski: Die Ursachen der Eiterung. Beitr. v. Ziegler, xv., 1894 (Lit.). 

Jürgensen. Kryptogenetische Septikopyämie. Lehrb. d. spec. Path., Leipzig, 189. 

v. Kahlden: Sepsis. Eulenburg’s Realencyklop.. 1899. 

Koch: Die Wundinfectionskrankheiten, Leipzig, 1878. 

Kocher: Osteomyelitis, Periostitis. Strumitis. Langenbeck’s Arch., xxiii... 1879. 

Kraske: Actiologie dd. acuten Osteomyelitis. Werh. d. XV. Chir.-Congr.. Berlin, 1886. 

Krause: Mikrokokken der infectidsen Osteomyelitis. Fortschr. d. Med., ii., 1884. 

Lübbert: Der Staphylococcus pyogenes aureus, Würzburg, 1886. 

Neumann: Micrococcus pyog. tenuis u. Pneumoniecoceus. Chbl. f. Bakt., vii., 1890. 

Ogston: Micrococcus poisoning. Jouin. of Anat. and Phys., xvi., xvii., 1882. 

Passet: Actiologie d. acuten eiterigen Entzündung. Fortschr. d. Med.. iii., 1885. 

Petruschky: Infection mit pyogenen Kokken. Zeit. f. Hyg., xvii., 1894. 

Ribbert: Experiment. Myo- u. Endocarditis. Fortschr. d. Med., iv., 1886; Verlauf 
der durch Staphylococcus in d. Haut v. Kaninchen hervorgerufenen Entzüindun- 
gen. Deut. med. Woch., 1889; Die patholog. Anat. u. die Heilung der durch d. 
Staphylococcus pyog. aureus hervorger. Veränderungen, Bonn, 1891. 

Rodet et. Courmont: Subst. toxiques Clab. par le staphyloc. pyog. Rev. de med.. 
xiil., 1893 

Rosenbach Mikroorganismen d. Wundinfectionskrankh., Wiesbaden, 1884. 

Sahli: Actiol d Gelenkrleumatismus (Staph. citreus). Corr. f. Schweiz. Aerzte, 
1892. 

Scholtz: Paras. Natur d. Ekzems. Deut. med. Woch., 1900. 

Singer: Actiologie u. klin. d. acuten Gelenkrheumatismus, Wien, 1897. 

Steinhaus: Actiologie d. Eiterung. Zeit. f. IIyg., v., 1888. 

Struck u. Becker: Mikrok. d. infectiésen Osteomyelitis. Deut. med. Woch., 1883. 

Ullmann: Fundorte d. Staphylokokken. Zeltschr. f. Hye.. iv., 1888. 

Wyssokowitsch u. Orth: Beitr. z. Lehre v. d. Endocarditis. Virch. Arch., 103 Bd., 


ISS6, 
x 155. The Micrococcus Gonorrhee or Gonococcus (Fig. 435) is a 





578 THE PATHOGENIC FISSION-FUNGI. 


orrheea the coccus usually forms clumps, and for the greater part appears 
in the form of diplococei, the opposing surfaces of which are flattened 
(Fig. 435); but occurs also in part free (a), and in part inclosed within 
cells (b). It stains easily with aniline dyes, but is decolorized by Gram’s 
method. 

The gonococcus penetrates into the epithelial layer of the affected 
mucous membrane, and lies partly between and partly in the epithelial 
cells, and in leucocytes. Only the uppermost layers of the connective 
tissue are infiltrated. The infiltration is most marked in the case of 
cylindrical epithelium, while in the regions covered by squamous epithe- 
lium (fossa navicularis, vagina) the cocci lie more superficially. They 
cause inflammations which bear the character of purulent catarrhs, and 
are associated with a cellular infiltration of the tissue of the mucosa 
(Fig. 436, db, c, d) and with epithelial desquamation. The male and 
female urethra and the adjoining parts of the genital glands and ducts, 
and the urinary passages form the chief seats of localization. According 
to Scholz there occurs, after a three-weeks’ duration of the disease in 
the male urethra, a metaplasia of cylindrical cells into stratified squanı- 
ous cells, and the secretion decreases after this time. To what extent 
the deeper inflammations so frequently accompanying or following gonor- 
rhea ( peri-urethral abscesses, prostatitis, epididymitis, vesiculitis, cysti- 
titis, inflammation of the ducts of Bartholin’s glands, salpingitis, ovar- 
itis, pelvic peritonitis, arthritis, ete.) are to be referred to the spread of 
the gonococcus or to what extent to secondary infections by the pus-cocei 
is yet a disputed question. According to the investigations made up to 
the present time there can be no doubt that the gonococcus may become 
widely spread over the surface of the mucous membranes. It has been 
many times demonstrated in inflamed tubes, ovaries, joints, cardiac 
valves, tendon-sheaths, burs, in peri- and parametritic foci of inflam- 
mation, and in peri-urethral abscesses. In these cases it has been re- 
garded as the cause of the inflammation, yet the processes which lead to 
suppuration and even the metastases in distant organs appear to be more 
frequently dependent upon the presence of pus-cocci. 

Gonorrheeal infection is at the beginning an acute process, but may 
become chronic, and is cured only with great difficulty; since the gono- 
cocei can maintain themselves here and there in the urethra, tubes, etc., 
for years, and continue to cause inflammation. 


Literature. 
( Gonococcus. ) 


Bockhart: Actiologie u. Pathologie d. Harnröhrentrippers. Vierteljahrsschr. f. 
Derin., 1883; Secundiire Infection (Mischinfection) b. Tripper. Monatsschr. f. 
prakt. Derm., 1887. 

Bröse: Diffuse Gonorrhea! Peritonitis. Berl. klin. Woch., 1896. 

Bumm: Der Mikroorganismus d. gonorrhoischen Schleimhauterkrankungen, Wiesbad- 
en, 1886. 

de Christmas: Le gonocoque et sa toxine. Ann. de l’Inst. Past., 1897, 1900. 

Cushing: Gonococcus peritonitis. Bull. of the J. Hopkins IIosp., 1899. 

Finger: Die Blennorrhöe d. Sexualorgane u. ihre Complicationen, Leipzig, 1896: Die 
Syphilis und die venerischen Krankheiten, Wien, 1901. 

Finger, Ghon u. Schlagenhaufer: Beitr. z. Biol. d. Gonococcus. Arch. f. Derm., 
xxviii., 1894; Endocarditis, Arthritis, Prostatitis. Ib., xxxiii., 1895. 

Fritsch: Die gonorrhoischen Erkrankungen d. weibl. Sexualorgane, Berlin, 1892. 

Ghon u. Schlagenhaufer: Zur Biol. d. Gonococcus. Wien. klin. Woch., 1898. 

Haab, O.: Der Micrococcus der Blennorrh. neonat. Horner’sche Festschr., 1881. 


THE PATHOGENIC COCCI. 579 


Hartdegen: Der Gonococcus Neisser u. s. Bez. zur Gonorrhöe. Cbl.f. Bakt., i., 1887 

(Lit.). 

Heiman: Studies on the Gonococcus, i., ii., iii. series. Studies from Dept. of Path. of 
Columbia University. 

Jadassohn: Path. Anat. d. gonorrh. Processes. Verh. d. derm. Congr., 1894. 

Krause: Die Mikrokokken der Blennorhea neonatorum. Cbl. f. Augenheilk., 1882. 

Lang: Der venerische Katarrh, Wiesbaden, 1893. 

Lartigau: Gonorrheeal Ulcerative Endocarditis. Amer. Jour. of Med. Sc., 1901. 

Martin: Rech. s. l’inflamm. metastat. suppur. a la suite de la gonorrhée, Genéve, 1882. 

Neisser: Cbl. f. d. med. Wiss., 1879; Deut. med. Woch., 1882; Bresl. ärztl. Zeitschr., 
1886; Bedeut. d. Gonokokken f. d. Diagnose. Arch. f. Derm., xxi. Bd., Ergän- 
zungsh., 1889. 

Pelizari: Gonokokken in periurethralen Abscessen. Cbi. f. allg. Path., i., 1890. 

Schäffer: Gonokokken. Ergebn. d. allg. Path., iii., 1897 (Lit.). 

Scholz: Zur Biologie d. Gonococcus. Arch. f. Derm., 49 Bd., 1899. 

See: Le gonocoque, Paris, 1897. 

Steinschneider: Kultur der Gonokokken. Berl. klin. Woch., 1893. 

Thayer u. Blumer: Endocardite blennorrhagique. Arch. de med. exp., 1895. 

Thayer and Lazear: Gonorrheal Septicemia and Ulcerative Endocarditis, with Ob- 
servations upon the Cardiac Complications of Gonorrhea. Jour. of Exp. Med., 
1899 (Lit. ). 

Touton: Ucber Folliculitis preputialis et paraurethralis gonorrhoica. Vierteljschr. f. 
Derm., xxv., 1889; Der Gonococcus u. 8. Bez. z. Blennorrhöe. Berl. klin. Woch., 
1894. 

Wassermann: Gonokokkenkultur u. Gonokokkengift. Berl. klin. Woch., 1897. 

Wertheim: Die ascendirende Gonorrhöe beim Weibe. Arch. f. Gyn., 42 Bd., 1892. 


$ 156. Cocci have been demonstrated with certainty as the cause of 
disease in animals in the case of a large number of infectious diseases, 
and are regarded with probability as the cause in the case of others. 
As has already been stated, the Streptococcus pyogenes, the Diplococcus 
pneumoniae, and the Micrococcus pyogenes aureus are also pathogenic for 
different animals, and the last named in particular often causes sponta- 
neous—not caused by inoculation—suppurative inflammations in animals. 
Moreover, diseases have also been produced experimentally in animals 
by different cocci which were not pathogenic for man. Further, in 
many spontaneous diseases of animals cocci have been demonstrated, 
which are probably to be regarded as the cause. 


(1) According to Schatz (* Der Streptococcus der Druse der Pferde,” Arch. f. wiss. u. 
prakt. Thierheilk., xiv., 1888; Zeit. f. Hygiene, iii.), Sandand Jensen (“ Die Aetiologie der 
Druse,” Deutsch. Zeit. f. Thiermed., xiii.), and Poels (“Die Mikrokokken der Druse der 
Pferde,” Foriscir. «. Med., vi.) the strangles of horses is an infectious disease, in which 
the mucous membrane of the upper respiratory tract is the seat of a mucopurulent 
inflammation, in which, moreover, the lymph-glands pertaining to the region become 
swollen and in part suppurate; and is caused by a chain-forming coccus, which can be 
cultivated, and, when inoculated into horses (Schutz) again produces the disease. 

(2) According to Schütz (* Die Ursachen der Brustseuche des Pferdes,” Arch. f. wis- 
sensch. u. prakt. Thierheilk., 1887; Virch. Arch., 107 Bd., 1887) the epidemic lung-dis- 
ese of horses (infectious pneumonia) is caused by an oval coceus, which forms pairs and 
chains, and is not identical with the Diplococcus pneumonie# (Frankel) or the Bacillus 
pneumonis (Friedlander), and therefore not identical with the bacterium described by 
Perroncito (Arch. ital. de biol., vii., 1886) as occurring in the pneumonia of horses, and 
held by him to be identical with the Diplococcus pneumonie. 

(3) According to Semmer and Archangelskt (Centralbl. f. d. med. Wiss., 1883; 
Deutsch. Zeit. f. Thiermed., xi.) the microparasite of “ Rinderpest” is a micrococcus. 
According to Vetschnikof and Gamaleia (Centralbl. f. Bakt., i., p. 638) it is a bacillus. 
The disease is characterized anatomically by an inflammation of the intestinal tract, in 
part of a croupous or diphtheritic character, as well as by swelling and at times necro- 
sis of Peyer’s patches. 

(4) According to Poels and Nolen (Fortsch. der Med., iv., 1886) monococci and diplo- 
cocci, which in part possess a gelatinous capsule, are found constantly in the lungs and 
in the pleural exudate, in the contagious pleuropneumonia of cattle. On gelatin and agar- 


580 THE PATHOGENIC FISSION-FUNGI. 


agar they form chiefly white colonies which later become cream-colored. Pure cult 
injected into the lungs of rabbits. guinea-pigs, dogs, and cattle give rise to pneum 
changes. (Literature: Pasteur, Recueil de méd. vét., 1883; Cornil et Babes, Arch 





¢ Bergeaud, 
dung, gelber Galt genannt,” Schweiz. Arch. f. Thierkeilk., 80 Bd., 1888; Frank, “ Eu 
entzündungen,” Dtsch. Zeit. f. Thiermed., ii., 1876; Kitt, “ Euterentzündung,” “Lel 
uttgart, 1804; Jensen, “Mastitis,” Ergebn. d. allg. Pa 


(& According to Jolne (“Seuchenart. Cerebrospinalmeningitis d. Pferde,” Di 
Zeitschr. f. Thiermed., xxii., 1887) the cerebrospinal meningitis, which occurs epide 
cally in horses, is caused by the Diploooccus intracellularis (Weichselbaum, § 158). 

(7) Babes found in the hemoglobinuria of cattle, which occurs as an epide 
disease in Roumania, a coccus similar to the gonococcus, which he regards as the ca 
of the disease (“Sur I'hémoglobinurie bactérienne du boeuf,” Compt. rend. de I’ Acad. 
Keiences de Paris, cvii., 1888; Virch. Arch., 115 Bd.; Annal. de U Institut de patho 
Bucarest, 1890). 

(8) According to Semmer, Friedberger, and Mathis (Centralbl. f. Bakt., iii. p. ! 
the distemper of dogs is also caused by a coccus. 

(9) The foot-and-mouth disease of cate, according to Klein (CB. 1. d. med. Wi 
1896) is caused by a streptococcus. ‘Several years ago Sehotteius ("Ueber einen } 
teriologischen Befund bei Maul- und Klauenseuche,” Übl. f. Bakt., xi., 1892) and Kt 
(“Bakt. Untersuch. bei Maul- und Klauenseuche,” Arb. a. d. Reichagesundheiteamt, v 
1893), and others also found cocci in the organsof animals affected with foot-and-mo 
disease; but the bacteria described do not correspond with one another, and their 
ogenic significance is doubtful (John, Disch. Zeitschr. f. Thiermed., xix., 1908; 24 
and Frosch, Col. f. Bakt., xxii., p. 257, 1897). 

(10) According to Zivolta and Johne (Dtsch. Zeitschr. f. Thiermed., xii.; “Ber 
Aber das Veterinärwesen im Königr, Sachsen fd. J. 1885") and Rabe (Dtsch. Zeite 
J. Thiermed., xii.) there occurs in horses a peculiar tumor-like growth of connective 
aue, designated by Johne as mycofbroma or mycadermotd, which is caused by a micro. 
cus that grows in animal tissues in round or grape-like colonies which quickly bec: 
surrounded by a hyaline capsule, and are therefore to be reckoned as ascococes ( Mi 
coceus uscoformans). Bollinger designates the coccus as Botryomyces, Rabes as Mierc 
cus botryogenes, Kitt as Botryococcus ascoformans. The growths consist of connec 
tissue, resembling those of actinomycosia, and inclose small suppurating foci of 
lation tissue which contain the fungi. They appear to develop most frequently in 
spermatic cord after castration, but occur also on other parts of the body (Kitt, © 
Micrococcus uscoformans und das Mycofibrom des Pferdes,” Obl. f. Bakt., iii., 1 
Schneidemüht, ~ Botryomycosis,” Col f. Bakt., xxiv. 1898 [Lit.); 

(11) According to Eberth (Virch. Arch., 90 Bd.) and M. Wolff (Virch. Arch. 
Bd.) many of the gray parrots brought to Europe (Psittacus erithacus) die of a stre) 
coccus mycusis. The micrococel are found in almost all the organe, but especiall 
the capillaries of the liver and their neighborhood, where they cause necrosis of 
liver-cells, but no suppuration. 

(12) According to Eberth (Virch. Arch., 100 Bd.) a part of the pseudotubercu! 
processes occurring in guinea-pigs represent a chronic suppuration caused by a coc 
and sometimes lead to metastases in other organs. 








2. THE BacILLı AND THE POLYMORPHOUS BACTERIA, AND TH) 
PATHOLOGICAL PROCESSES PRODUCED BY THEM. 


(a) General Considerations Regarding Bacilli and the Polymorphous Bacte: 


$157. Under the designation bacilli or bacillacese (A. Fischer), 
Bacteriace@ (Zopf) may be classed all those bacteria which occur in 
form of straight rods or rods which are slightly bent in one plane. 
many authors (Cohn, Hüppe, Lehmann) the bacillaces are divided i 
two groups: bacterium and bacillus, the latter being characterized 
the production of endogenous spores, while spore-formation is lack 
in the former. 


THE BACILLI. 581 


The bacilli multiply by division. The rods grow in length, and 
divide into approximately equal parts through the formation of a trans- 
verse partition-wall. If the division of one of the elongating bacilli is 
delayed, or if the separation of the individual rods from one another is 
not distinctly recognizable, there arise long, unbranched rods or threads 
(Fig. 438, b). If the divided rods remain attached to each other, there 
are formed chains of rods (Figs. 437, c; 438, c). In many forms of 
bacilli the ends of the individual rods are blunt, in others rounded or 
pointed. 

In many bacilli resting as well as swarming stages are observed. 
Flagella serve as the organs of motion (Fig. 437, 5); they are situated 
sometimes at the ends, sometimes on the sides of the rods, and may occur 
in large numbers. In nrany bacilli an endogenous spore-formation is 
observed (Figs. 437, d, e; 438, d), the spores lying sometimes in the 
middle, sometimes at one end of the cell. Not infrequently the spores 
appear within jointed threads. The germination of spores results in the 
formation of new rods (Figs. 437, f'-*, 438 e'-’). 

During spore-formation the rods usually do not change their shape 


La > J; 000 
oy ha Ft Ars 


(fe J GS 


¥0 


Fig. 437. FIG. 438. 


Fic. 437.— Bacillus subtilis in various stages of development (Prazmowski). a, Single rods; h, rods 
with flagella ; Gghaln of rods; d, single cells with spores; e, chain of rods with spores; f '—* . germination 
ofaspore. X 


Fic. 438.—Clostridium butyricum (Prazmowski). a, Short rods; b, long rods; ¢, chain of rods; dd, cells 
with spores: c !—?, germination of aspore. »~ 800. 


to any marked extent. In other cases they assume a spindle-, club-, or 
pear-shape (Fig. 438, d), and these changes have been taken as the basis 
for the establishment of an especial group, clostridium. On the other 
hand, numerous authors class these forms with the bacilli. 

In the non-pathogenic bacilli spore-formation and spore-germination 
have been more carefully studied, especially in the case of Bacillus subtilis 
and Bacillus amylobacter ; and these bacilli offer good examples of the 
processes which come under consideration in this connection. 

Bacillus subtilis is a fission-fungus whose spores are widely distrib- 
uted in the ground, hay (hay-bacillus), and in the air. When cultivated 
upon potato or upon the dung of herbivorous animals, it forms whitish- 
yellow colonies; upon liquids it forms thin and thick pellicles. It re- 
quires oxygen for its development. 

The fully developed rods (Fig. 437, a) are 6 » long. The snake-like 
motions oecurring at times are produced by means of numerous lateral 
and terminal flagella. Through the growth of the rods undivided threads 
are formed which after division form chains of rods. The separate cells 
may develop in their interior glistening, sharply contoured spores (d, ¢), 
which lie either in the middle or nearer to one end of the cell. Later 


IN, THE PATHOGENIC FISSION-FUNGI. 


the cells in which the spores have been formed die. During germination 
the spores become pale (Fig. 437 '-’), lose their glistening appearance 
and their sharp contour. A shadow then appears at each pole, while the 
spore begins a tremulous motion. After a time the contents of the spore 
project from the membrane of the spore in the form of a germinal utricle, 
which later becomes elongated, divides, and produces swarming rods. 
The empty spore membrane may remain preserved for some time after 
the exit of the young cell. 

The Bacillus butyricus (Bacillus amylobacter of Van Tieghem, Vibrion 
butyrique of Pasteur, Clostridium butyricum of Prazmowski) consists of 
rods of 3to 10 » in length, and also forms threads and chains of rods. 
During spore-formation the cells become spindle-, club-, or tadpole- 
shaped (Fig. 438, d), and then produce one to two glistening spores. In 
germination, after the absorption of the spore-membrane a germinal 
utricle appears at one of the two poles (Fig. 438, e'-"); this becomes 
elongated, and produces new rods by segmentation. 

The Bacillus butyricus does not need oxygen for its development ; it 
produces butyric-acid fermentation with evolution of carbonic acid, in 
solutions of starch, dextrin, sugar or glycerin. In media containing 
starch, glycerin, or cellulose the bacilli are colored blue with iodine. 

The polymorphous bacteria are distinguished from the bacilli by the 
fact that they form, besides rods, also long threads, in part with false or 
true branching; and in individual cases a basal non-proliferating end 
and an apical proliferating end may be distinguished. In this category 
may be placed the fungi designated Streptothrir, Cladothriz, Beggiatoa, and 
Crenothric. They are here placed with the bacilli, because, on the one 
hand, their botanical position is not definitely determined, while, on the 
other, in so far as they are pathogenic, they conform most closely to the 
bacilli in their biological properties (ef. diphtheria-bacilli, tubercle- 
bacilli, and actinomyces). 

The saprophytic bacilli produce many forms of fermentation by their 
growth in nutrient fluids; many also form pigments. 

Bacillus prodigiosus grows upon potatoesand bread, as well as upon 
agar-agar, and upon nutrient gelatin, liquefying the latter. It forms a 
red coloring matter which is soluble in aleohol. The pigment is formed 
only in the presence of oxygen; in the growth in milk the coloring-mat- 
ter is contained in the fat-droplets. The bacilli themselves are always 
colorless. 

Bacillus fluorescens liquefaciens forms whitish cultures in gelatin, 
in the neighborhood of whieh the gelatin is liquefied while in the remote 
surrounding portions it gradually takes on a greenish-yellow fluorescence. 

Bacillus cyanogenes ( Neelsen, Hueppe), when cultivated in sterilized 
milk, causes a slate-gray color that changes through the addition of acid 
to an intense blue. In unsterilized milk, in which lactie-acid bacteria 
develop at the same time, a blue color appears without the addition of 
acid. On potatoes it forms vellowish, slimy cultures, in the neighbor- 
hood of which the substance of the potato is colored grayish-blue 
(Flügge ). 

Bacillus acidi lactici ferments milk-sugar into lactic acid and coagu- 
lates casein, In gelatin it produces white cultures. 

Bacillus caucasicus ( Dispora caucasica) forms one of the constituents 
of the fungus-conglomerate known as kephir-ferment, which is used by 
the inhabitants of the Caucasus in the preparation, from cow’s milk, of 
the aleoholic drink called kephir. The kephir-ferment consists of small 


SAPROPHYTIC AND IN PART PATHOGENIC BACILLI. 583 


granules containing yeast-cells and bacilli. The latter at times show 
movements, and form a round spore at the end of each rod. As the re- 
sult of their growth in milk the milk-sugar is probably converted into 
glucose, while the yeast-cells produce alcoholic fermentation. According 
to Hueppe, the kephir granules contain still other bacteria which pepto- 
nize casein. 

As Proteus vulgaris, Hauser has described a bacillus (Bacterium vul- 
gare of Lehmann) which is very frequently present in decomposing ani- 
mal substances and in human cadavers, and in gangrenous ulcers, and 
causes putrid decomposition. It forms rods of varying length, and pro- 
duces, when cultivated in meat (Carbone), zthylendiamin, gadinin, and 
trimethylamin, of which the first two bases are poisonous for animals. 
According to observations by numerous authors, it is not infrequently 
found in human tissues, chiefly in association with other bacteria, strepto- 
cocei, pneumococci, diphtheria-bacilli; and by its presence aggravates 
the course of the infection and causes putrid decomposition of the pus and 
the neerotic tissue. In rare cases it may alone, without the association 
of other bacteria, cause inflammations, particularly of the urinary bladder 
(cystitis). Several cases of hemorrhagic enteritis have also been described, 
in which a form of proteus was regarded as the causal agent. Further, 
proteus has also been found in inflammations of the female genital tract, 
serous membranes, and liver (infectious icterus), and has been considered 
to be the cause of the given inflammation. Proteus must therefore be 
Classed with the parasitic or pathogenic bacteria. Its pathogenic activity 
rests chiefly upon the formation of poisonous substances. (Literature 
given by Meyerhof, 7. c.). 

Bacillus aceticus (Mycoderma aceti) is a bacillus which converts the 
alcohol of fermented beverages into acetic acid. 

Bacillus pyocyaneus occurs occasionally in bandages upon suppurat- 
ing wounds and causes a greenish-blue discoloration of the same. The 
bacilli are small and slender. The cultures show different forms of 
growth. Gelatin is liquefied and turned green. The coloring-matter 
called pyocyanin is soluble in chloroform and crystallizes from the solution 
in long blue needles. The bacillus is pathogenic for rabbits, guinea-pigs, 
pigeons, and frogs; inoculations give rise partly to local ulcerations, partly 
to general infections. According to Kossel, Kramhals, Neumann, and 
others it may also be pathogenic for man during the age of childhood, and 
from suppurating wounds or mucous membranes (middle ear) it may 
cause septicemia with splenic tumor and enteritis. Blum observed a 
pyocvanie endocarditis in a nursing infant. 

The pathogenic bacilli and polymorphous bacteria cause partly 
acute, and partly chronic affections, the former terminating either in 
death or in healing after the destruction of the bacteria. It also hap- 
pens in the acute diseases that the bacteria may remain in the body for a 
long time. The chronic affections are characterized by the persistence 
and multiplication of the bacteria within the body, so that the disease 
assumes a progressive character, and sometimes slowly, sometimes rapidly, 
new regions are in turn invaded by the bacteria and suffer pathological 
changes. 


584 THE PATHOGENIC FISSION-FUNGI. 


Literature. 
(Saprophytic [in Part Pathogenic] Bacilli.) 
Babes: Rech. sur les bacilles du pus vert. Ann. de l’Inst. de path. de Boucareat, L, 


Banti: Sopra quatri nuove specie di Protei o Bacilli capsulati, Firenze, 1888. 

Blum: Pyocyaneusseptikämie. Cbl. f. Bakt., xxv., 1899. 

Bordoni- uzzi: Proteus hominis capsulatus. "Zeitschr. f. Hyg., iii., 1888. 

Bunge: ht aoe” Bakterien. Fortschr. d. Med., xii., 1894; Sporenbildung. 

x 

Carbone: Ueber die von Proteus vulgaris erzeugten Gifte. Cbl. f. Bakt., viii., 1890. 

Charrin: La maladie pyocyanique, Paris, 1889. 

Ernst: Bacillus des blauen Eiters. Zeitschr. f. Hyg., ii., 1887. 

. Foa et Bonome: Maladies causées par Proteus. Ärch. ital. de biol., vii., 1887. 

Fränkel: Ueber Gasphlegmone, Leipzig. 1898. 

Frick: ( Grünes Sputum u. grünen Farbstoff produc. Bacillen. Virch. Arch., 116 Bd., 
1 


Gessard: Rech. sur le microbe pyocyanique Ann. de l’Inst. Pasteur, 1890. 

Goebel: Bacillus d. Schaumorgane. Chbl. f. allg. Path., vi., 1895. 

Grethe: Keimung d. Bakteriensporen. Fortschr. d. Med., xv., 1897. 

Hauser: Ueb. Fäulnissbakterien u. deren Beziehung z. Septikämie, Leipzig, 1886. 

Heim: Versuche über blaue Milch. Arb. a. d. K. Gesundheitsamte, v., 1890. 

Jaeger: Die Aetiologie des infectiösen fieberhaften Ikterus. Zeitschr. f. Hyg., xii., 
1892. 

Jakowsky: Bakterien des blauen Eiters (B. pyocyaneus). Zeitschr. f. Hyg., xv., 
1893. 

Kossel: Zur Frage d. Pathogenität des Bac. pyocyaneus. Zeitschr. f. Hyg., xvi., 
Krai ils 


ocyaneusinfection. Deut. Zeitschr. f. Chir., 87 Bd., 1898. 

Krause: Z Zur Rechte d. Bac. pyocyaneus. Cbl. f. Bakt., xxvii., 1900. 

Lartigau: Bacillus py ocyaneus as a Pathological Factor. Phil. Med. Jour., 1898. 

Ledderhose: Ueber den blauen Eiter. Deut. Zeitschr. f. Chir., xxviii., 1888. 

Levy: Die Aktinomycesgruppe. Cbi. f. Bakt., xxvi., 1899 (Lit.). 

Meyerhof: Biologische u. thierpathogene Eigenschaft des Bacillus proteus (Hauser), 
mit eines Zusammenfassung d. wichtigsten Literatur über Proteus. Cbl. f. Bakt., 
xxiv., 189 

Miller: Die Mikroorganismen der Mundhöhle, Leipzig, 1896. 

Prazmowski: Unters. über d. Entwickelungsgeschichte einiger Bakterien, Leipzig, 
1880. 

Perkins: Report of Nine Cases of Infection with Bacillus Pyocyaneus. Jour. of Med. 
Research, 1901. 

Schedtler: Beitr. z. Morphologie der Bakterien. Virch. Arch., 108 Bd., 1887. 

Schimmelbusch: Grüner Eiter u. d. Bac. pyocyaneus. Samml. klin. Vortr., No. 62, 
1893. 


(b) The Pathogenie Baeilli and Polymorphous Bacteria. 


§ 158. The Bacillus anthracis (Bac teridie du charbon) is the cause of 
anthrax, a disease occurring chiefly in cattle and sheep, and occasionally 
transmitted to man. It is a fission-fungus which, when inoculated into 
a susceptible animal, may increase within the tissues as well as in the 
blood. 

The anthrax-bacilli (Fig. 439) are 3 to 10 » long and 1 to 1.52 
broad. In the blood of animals affected with anthrax they occur either 
singly or in thread-like jointed bands of two to ten rods, whose ends are for 
the greater part sharply cut across (Figs. 439, 440), more rarely slightly 
concave or even slightly convex (Johne). According to Pianese, Sera- 
fini, Günther, and Johne they possess a gelatinous capsule which is best 
brought out by the staining of dried preparations with methylene-blue. 
They can be cultivated upon blood-serum-gelatin, in bouillon, upon 


BACILLUS ANTHRACIS. 585 


slices of potatoes and turnips, in infusions of peas and mashed grain of 
various kinds, ete., in the presence of oxygen (according to Klett also 
in an atmosphere of nitrogen); and grow most rapidly at a temperature 
of from 30° to 40° C. At temperatures below 15° and above 43° C. 
development is impossible. 

Under suitable conditions of growth the rods increase in length, and 
may within a few hours form non-encapsulated threads of considerable 
length. These consist of short seg- 
ments whose outlines may be made 
visible by treatment with iodine or 
by stains (Fig. 440). Ten hours 
later the clear contents of the 
threads become granular, and at 
regular intervals there become ap- 
parent dull-shining bodies, which 
after a few hours enlarge into 
strongly refractive spores (Fig. 
440). Later the threads disinte- 
grate and the spores become free. 

According to Brefeld, Prazmow- 
ski, Klein, and others, the spore 
consist of a protoplasmic centre, 

Fig, 489,—Rection from a liver whose capillaries Which is inclosed by a double mem- 
quis Scien, SEES eames brane, the exosporium and the en- 
300, dosporium. During germination 

the former is ruptured, the latter 
becomes the membrane of the embryo. The liberated embryo multiplies 
by division. 

Swarming movements are not seen throughout the entire period of 
development; the bacilli are always motionless. 

The bacilli of anthrax are easily killed by high temperatures, drying, 
and through the decomposition of the nutrient fluid. The spores on the 
other hand are very resistant, and are therefore 
usually the medium of the spread of the disease. 

The colonies upon gelatin show a wavy, ir- 
regularly shaped margin, and consist of many 
interlacing strands of threads, which later grow 
out of the culture in all directions, The gelatin 
is liquefied immediately about the culture. On 
potato the bacillus forms grayish-white, slightly 
granular colonies having a sharply outlined bor- 
der. On blood-serum it forms a white coating. Fic. 440.—Spore - containing 

Stab-cultures in gelatin are white and during PT and free area: 
the process of growth they radiate at right an- culture of the bacilli grown in 
gles from the line of inoculation out intothe gel- BS jne" wit ‘undafaad eth 
atin, particularly near the surface. Afterlique-  Ylene-blue. X #00. 
faction of the gelatin they sink to the bottom. 

If the bacilli or the spores gain entrance into the blood, they increase 
and form rods as described above, which stain with different aniline 
dyes, and also by Gram’s method. Sections of hardened tissue show that 
they are present in large numbers in the capillaries (Fig. 439), particu- 
in the spleen, liver, lungs, and kidneys. The neighboring pare: 
ma for the greater part appears unchanged; still the local prolifer- 
ation of the bacilli can also cause tissue-degeneration and necrosis. If 











BACILLUS ANTHRACIS. 587 


exudate as well as by bacilli. The bacilli lie particularly in the outer 
portions of the corium (d,) and in the papillary body (c), but may also 
penetrate into the deeper layers of the corium (f). In the neighborhood 
of the papillary body (c) the exudate is sanguineous. Vesicles filled 
with bloody fluid result if the exudate extends up to the epithelial cover- 
ing, and if the deeper portions of the latter become liquetied, thereby 
permitting the lifting-up of the superficial layers by the exuded fluid. 
If the upper layers of the skin are also lost, the bloody fluid containing 
the bacilli (9) appears upon the surface. 

The cellular infiltration has its seat chiefly in the corium (4d, d,, e), 
and the impression is obtained as if the great massing of cells formed a 
certain protection against the further spread 
of the bacilli. The cells which collect belong 
for the greater part to the polynuclear leuco- 
cytes (Fig. 442). The bacilli lie sometimes 
in, sometimes between the cells. 

If an infeetion with anthrax-spores takes 
place in the intestinal canal, an event which 
occurs most frequently in the small intestine, 
less often in the stomach and large intestine,. ra, ue. 
there develop dark-red or brownish-red hem- IG. 442. Portion of the anthrax 
orrhagie fork, the size of a lentil or beau or Ponalning bectit “seas 41 
larger, with a grayish-yellow or greenish-yel- 
low, discolored slough in the centre. In other cases the crests of the 
folds of the mucosa are swollen and hemorrhagic, and show evidences 
of sloughing in the most prominent parts. The mucosa and submucosa 
filtrated with blood in the region of the foci; the surrounding tissues 
e edematous and hyperemic. Bacilli are found in the tissues both 
in and about the foci, particularly in the blood- and lymph-vessels, and 
they may also be demonstrated in the neighboring lymph- glands. 

According to observations by Eppinger and Paltauf, primary lung in- 
y also occur in man as the result of the inhalation of anthrax- 
spores, proving fatal in from two to seven days. Individuals who have to 
handle the hair of animals that have died of anthrax are especially ex- 
posed to infection; and the disease known as rag-sorter’s disease, which oc- 
in men and women employed in the sorting of rags in paper-factories, 
u part of the cases nothing more than an anthrax infection. The 
‘aken into the lungs in the respired air develop inthe bronchi and 
alveoli, in the lymph-spaces of the lungsand pleura and in the bronchial 
nds, and penetrate also into the vessels. Their growth causes inflam- 
'y processes in the lungs, as well as serous hemorrhagic exudations 
into the pleural cavity and the mediastinal tissue, and swellings of the 
Iymph-glands. It may also lead to the production of necrotic foci in the 
lungs, and in the bronchial and tracheal mucosa. 

Mice, rabbits, sheep, horses, and sparrows are very susceptible 
to anthrax; white rats, dogs, and Algerian sheep are less susceptible 
or immune. Cattle are easily infected through the taking in of the 
spores from the alimentary canal, but are less susceptible to inocu- 
lation. Formation of spores does not take place in the tissues and in 
the blood. 


‘A marked attenuation of anthrax-bacilli may be produced by keeping the bacilli for 
ten minutes at a temperature of 55° C. (Toussaint) or for fifteen minutes at 52° C., or 
for twenty minutes at 50° C. (Chanrean), or further through the influence of oxygen 
under high pressure (Chaureau). The bacilli attenuated by exposure for a short time 





















588 THE PATHOGENIC FISSION-FUNGI. 


to high temperatures quickly regain their virulence; those attenuated at lower tem- 
peratures remain weakened for many generations. 

The addition of carbolic acid to the nutrient fluid in a proportion of 1: 600 permits 
the further development of anthrax-bacilli, but destroys their virulence within twenty- 
nine days (Chamberland, Roux). Likewise, an attenuation may be produced by the 
addition of potassium bichromate (1: 2,000-1:5,000). The addition of carbolic acid up 
to 1: 800 hinders at the same time the formation of spores. 

Through cultivation of the bacilli at 42-48° C. (Toussaint, Pasteur, Koch). their 
virulence may be so weakened that they no longer kill first sheep, then rabbits and 
guinea-pigs, and finally mice. If the temperature is kept in the neighborhood of 48° C. 
this result may be obtained in six days; at 42° C. it may require about thirty days to 
decrease the virulence to this extent (Aoch). By first inoculating with bacilli which 
kill mice but are harmless for guinea-pigs, and afterward inoculating with bacilli which 
kill guinea-pigs but not strong rabbits, an immunity against anthrax may be obtained 
in sheep and cattle but not in the case of mice, guinea-pigs, and rabbits. Such protec- 
tive inoculations are, however, not of practical value, since, in order to protect against 
natural infection with spores from the intestinal canal, such virulent inoculation-mate- 
rial must be used that a large per cent. of sheep (ten to fifteen per cent.) die from the 
inoculations. Further, the protection afforded by the inoculations is of very short 
duration, and the inoculation must be repeated within a year’s time. 

According to observations by Rour and Chamberland anthrax bacilli which are 
cultivated in bouillon to which a small amount of potassium bichromate (1: 2.000) or 
carbolic acid (1 to 2: 1,000) has been added, permanently lose their power of spore-forma- 
tion while retaining their virulence. 

According to Koch, anthrax-bacilli may be cultivated in the presence of abundance 
of water upon potatoes and in an alkaline or neutral hay-infusion, cold infusions of pea- 
straw, on mashed barley and mashed wheat, in the juice of turnips, on maize, legumi- 
nous seeds, and numerous dead plants. Consequently they are able to grow and 
develop outside of the animal body—for example, in marshy regions and on river-banks 
(R. Koch). The entrance into the animal body: is to be regarded as an accidental excur- 
sion of ectogenic bacilli. According to Soyka the development of spores takes place 
very quickly in a moist medium containing the necessary nutrient material at tempera- 
tures above 15° C. According to Arté the dung of cattle forms a nutrient substratum 

or the bacilli. 


Literature. 
(Bacillus Anthracis. ) 


Behring: Beiträge zur Aetiologie des Milzbrandes. Zeitschr. f. Hyg., vi., vii., 1889. 

Bleuler: Hautmilzbrand. Correspbl. f. Schweizer Aerzte, 1884. 

Blumer: Anthrax Septicemia. Bull. of Johns Hopkins Hosp.. vi., 1895. 

Bourgeois: Traité pract. de la pustule maligne, etc., Paris, 1861. 

Brauell: Unters. betreffend den Milzbrand. Virch. Arch., 11 Bd., 1857. 

Buisson: Charbon intestinal chez l’homme. Arch. de med. exp., i., 1889. 

Czaplewski: Unters. üb. d. Immunität d. Tauben gegen Milzbrand. Zeit. f. Hyg., 
xii., 1893. 

Davaine: Compt. rend. de l’Acad. des sciences, 1863, 1864, 1865, 1868, 1870, 1873. 
Republished in L’wuvre de C. J. Davaine, Paris, 1889. 

Dittrich: Prim. Milzbrandinfection des Magendarmkanales. Wien. klin. Woch., 1891. 

Eppinger: Die Hadernkrankheit, Jena, 1394. 

Frank: Milzbrandimpfung. Zeitschr. f. Thiermed., vii., Suppl., 1884. 

Hoffa: Die Natur des Milzbrandgiftes, Wiesbaden, 1886; Zur Lehre d. Sepsis u. d. 
Milzbrandes. Langenbeck’s Arch., 39 Bd., 1889. 

Jacobi: Vier Fälle v. Milzbrand beim Menschen. Zeitschr. f. klin. Med., 17 Bd., 18%. 

Johne: Morphologie der Milzbrandbacillen. Deut. Zeitschr. f. Thiermed., xix., 1893. 

Karg: Verhalten der Milzbrandbacillen in der Pustula maligna. Fortschr. d. Med., 
vi., 1888. 

Klett: Sporenbildung d. Milzbrandb. bei Anatrobiose. Zeit. f. Hyg., 85 Bd., 1900. 

Koch, R.: Beitr. z. Biol. d. Pfl. v. F. Cohn, 2 Bd., p. 272. Mittheil. a.d. K. Gesund- 
heitsamte, Berlin, 1881, 1884; Ueber die Milzbrandimpfung, 1882. 

Koch, W.: Milzbrand und Rauschbrand. Deut. Chir.. 9 Lief.. 1886. 

Krumbholz: Darmmilzbrand. Beitr. v. Ziegler, xvi... 18994. 

Kurloff: Im Laboratorium acquirirte Milzbrandinfection. Deut. Arch. f. kl. Med., 
xliv., 1889. 

Lewin: Milzbrand beim Menschen. Cbl. f. Bakt., xvi.. 1894. 

Lodge: La maladie des trieurs de laine. Arch. de med. exp.. 1890 


BACILLUS TYPHI ABDOMINALIS. 589 


Lubarsch: Milzbrand. Ergebn. d. allg. Path., v., 1900. 
Martinotti u Barbacei: Jeb. d. Physiopathologie d. Milzbrandes. Fortschr. d. 
., iX., . 

Melnik ow A gy ünstliche Immunität d. Kaninchen geg. Milzbrand. Zeit. f. Hyg., 
XXV., . 

Müller: Der Milzbrand der Ratten. Fortschr. d. Med., 1893; Aeusserer Milzbrand 
des Menschen. Deut. med. Woch., 1894 (Lit.). 

Palm: Histologie des äusseren Milzbrandcarbunkels. Beitr. v. Ziegler, ii., 1888. 

Paltauf: Aetiologie d. Hadernkrankheit. Wien. klin. Woch., 1888. 

Parmier: La toxine charbonneuse. Ann. de l’Inst. Pasteur, 1895. 

Pasteur: La vaccination charbonneuse, Paris, 1888. 

Pawloweky: Verhalten d. Milzbrandbacillen im Organismus. Virch. Arch., 108 Bd., 
1887. 

Physalix: Nouv. rech. sur la maladie charbonneuse. Arch. de méd. exp., iii., 1891. 

Pianese: La capsula del B. anthracis. Giorn. dell’ Assoc. di Nat., 1891. 

Pollender: Casper’s Vierteljahrsschr. f. ger. u. Off. Med., 8 Bd., 1855. 

Reinbach: Zur Aetiologie d. Lungengangrän. Cbl. f. allg. Path.. v., 1894. 

Rembold: Zur Aetiologie des Milzbrandes. Zeitschr. f. Hyg., iv., 1888. 

Roloff: Der Milzbrand, Berlin, 1888. 

Roux: Bacteridie charbonneuse asporogéne. Ann. de l’Inst. Pasteur, iv., 1888. 

Straus: Cas de charbon mortel. Arch. de phys., i., 1888; Contrib. A l’anat. pathol. 
de la pustule maligne. Ann. de I'Inst. Pasteur, i., 1887. 

Toepper: Die neueren Erfahrungen fb. d. Aetiol. des Milzbrandes, Jena, 1888. 





FiG. 443. Fig, 444. 
Fru. 443.—Typhotd-bacilli from a pure culture. Streak-preparation (methylene-blue). X 1,000. 
Fic. 444..- Typhoid-bacilli with flagella. (After Bunge.) X 1,200. 


Toussaint: lech. ex périmentaies sur la maladie charbonneuse, Paris, 1889. 
Wagner: Le charbon des poules. Ann. de l’Inst. Pasteur, iv., 1890. 
Werigo: Developp. du charbon chez le lapin. Ann. de l’Inst. Pasteur, 1894. 
Zörkendorfer: Darmmilzbrand. Prag. med. Woch., 1894. 

For literature coucerning the intra-uterine transmission of the bacillus to the foetus, 
see S 150. 


x 159. The Bacillus typhi abdominalis (Fig. 443), or the Bacterium 
typhi, is a fission-fungus which occurs chiefly in the form of plump rods 
2to 3 n long, having rounded ends, and in cultures growing also in 
pseudothreads. It is regarded as the cause of typhoid fever. When exam- 
ined alive in cultures it shows lively independent movements which are 
accomplished by means of flagella (Fig. 444) attached to the sides of the 
rods as well as to their ends. The flagella may be demonstrated by pro- 
per staining-methods. The bacillus was first observed in the intestinal 
lesions by Eberth and Koch, and described by them; and was later iso- 
lated in pure cultures by Gaffky. A. Pfeiffer demonstrated its presence 
in the dejecta of typhoid patients, and his findings have been confirmed 
from many sides. According to Seitz, Hueppe, Neumann, and others 
it may also be present in the urine of typhoid patients. 

It stains well in cover-glass preparations, with gentian-violet, alka- 
line methylene-blue, and Bismarck brown. It is decolorized by Gram’s 


590 THE PATHOGENIC FISSION-FUNGI. 


method. It is difficult to demonstrate it in seetions of hardened tissues, 
‚since the cell-nuclei also take the stain, and because the bacilli are not 
uniformly distributed but are usually found lying in the tissue in clamps. 

The bacillus may be cultivated upon nutrient gelatin, agar-agar, and 
blood-serum, also in milk, and upon potato. Upon the last named it 
forms a coating which can be scarcely recognized by the naked eye; but 
when the surface is touched with a platinum wire it becomes apparent 
that it is covered with a pellicle, which on microscopic examination is 
shown to consist of bacilli. 

On gelatin and agar-agar the bacilli form grayish-white, irregularly 
shaped, flat growths. Gelatin is not liquefied. Milk in which the bacilli 
are grown is not changed externally. 

The cultures thrive at room-temperature as well as at body-temper- 
ature. Potato-cultures made in the usual manner, when kept between 
30° and 42° C., produce rods which have glistening bodies in their poles. 
Gaffky regarded these as spores, and the majority of authors formerly 
accepted this view. According to Buchner and Pfuhl, however, these 
granules at the poles are degeneration phenomena, which occur particu- 
larly when acid is present in the culture medium. The polar granules 
represent condensed protoplasm, and therefore stain in fresh preparations 
more quickly with the aniline dyes than do the other parts of the cell. 
The clear, colorless spots which are seen at the ends of the rods in dried 
and stained bacilli have been held to be identical with the polar granules 
and therefore regarded as spores; but are due, according to Buchner. 
to hollow spaces formed at the ends of the rods as the result of the 
retraction of the protoplasmic tube following the death and drying of 
the bacilli. Spore-formation has, therefore, not yet been demonstrated. 

In moist earth (Grancher, Deschamps), in pure and impure water. 
typhoid bacilli may remain alive for weeks. In artificial Seltzer water 
they do not die out for a longer period (Hochstetter). In privy vaults 
and fecal masses, or in earth saturated with fecal matter (Finkler, 
Uffelmann, Karlinski) they may under certain conditions live for weeks 
and months. 

Inoculations of the bacilli in the case of the animals ordinarily used 
for experiment do not produce a disease corresponding to typhoid fever 
in man. On the other hand, the experiments of Sirotinin, Beumer, Pei- 
per, and others have shown that the typhoid-bacilli produce active toxins 
and toxalbumins (Brieger) which in large doses kill the animals, causing 
hyperemia and swelling of the intestinal follicles, mesenteric glands, and 
the spleen. Cultures injeeted into the tissues cause a local inflammation 
of greater or less intensity. 

The bacilli or their spores gain entrance into the human organixm 
through the drinking-water and food; though infection through the lungs 
is not to be excluded. According to the results of anatomical investiga- 
tions, they develop particularly in the intestinal wall, in the solélary and 
agminated follicles of the small and large intestines, as well as in the mesen- 
terie lymph-glands and in the spleen. In the first-named. place they cause 
an inflammatory infiltration of the mucosa and submucosa (Fig. 445, a, 6,) 
which is extraordinarily rich in cells, and appears in the form of flat or 
somewhat rounded elevations projecting above the inner surface of the 
intestines. Anexudationof fibrin inthe form of threads may take place 
both on the free surface and in the deeper layers. Occasionally cellular 
inflammatory foci of limited extent also oecur in the muscularis (c, d,) 
and the serosa (e). A part of the infiltrated tissue usually sloughs and 





31 THE PATHOGENIC FISSION-FUNGL 


fever. Reher, Eberth, Chantemesse, Widal, and Ernst have reported 
similar Cases. 

Since the typhoid bacillus produces toxins and toxalbumins, the 
symptoms of the disease are for the greater part to be referred to the 
intoxication. In the course of typhoid fever there appear in the blood 
certain bactericidal substances which cause a degeneration of typhoid- 
bacilli (cf. § 31). This may be demonstrated by the fact that ( Widal- 
Gruber reaction), through the addition of serum from an individual ill 
or convalescent from typhoid fever, to a bouillon-culture of freely motile 
typhoid-baeilli, the latter become motionless, clump together (agglutina- 
tion), sink to the bottom and die. This reaction may be used asa means 
of diagnosis, but is not of absolute certainty, since agglutination may be 
produced by the serum of -individuals who have not had typhoid fever, 
and may be absent in the case of typhoid (Fischer). 


The cultures of aif phoid bacilli show but few characteristic pro ies, and are 
therefore distinguished with difficulty from other widely distributed ia. Their 
properties are very similar to those of the Bacillus coli communis (cf. § 160). Asa dif- 
ferential point may be mentioned the fact that typhoid bacilli produce no indol, while 
other similar bacilli, including the colon bacillus produce indol, so that bouillon-cul- 
tures turn red on the addition of potassium nitrite and sulphuric acid. Further, the 
typhoid-bacillus produces no gas in a two-per-cent. glucose-bouillon while the colon- 
bacillus produces gas. Finally, the typhoid-bacillus produces a faint acidity in milk 
without coagulation, while the colon-bacillus causes a strong acidity and coagulation 
of the milk within from twenty-four to forty-eight hours at 87° C. 


Literature. 
(Bacillus of Typhoid Ferer.) 


Arustamoff: Zur Frage üb. d. Entstehung d. typhösen Pneumonie. Cbl. f. Bakt., 
iv., 1889. 

Babes: Ueber Variabilität und Varietäten des Typhusbacillus. Zeitschr. f. Hyg.,-ix.. 
1890. 

Beumer: Aetiologie d. Typhus (Nachweis d. Bacillen im Trinkwasser). Deut. med. 
Woch., 1887. 

Beumer u. Peiper: Aetiolog. Bedeutung d. Typhusbacillen. Zeit. f. Hyg., i., 1886, 
ii., 1887. 

Buchner: Ucber die vermeintl. Sporen der Typhusbacillen. Cbl. f. Bakt., iv., 1888. 

Bunge: Zur Kenntniss der geisseltragenden Bakterien. Fortschr. d. Med., xii., 1894. 

Buschke: Lebensdauer d. Typhusbacillen in ostitischen Herden. Fortschr. d. Med., 
xii., 1894. 

Chantemesse et Widal: Bacilletyphique. Arch. de phys., ix., 1887; Ann. de 1’Inst. 
Past., 1892. 

Chiari: Cholecystitis typhosa. Prag. med. Woch., 1893.; Zeit. f. Heilk., xv., 1894. 

Coleman and Buxton: Paratyphoid Infections. Amer. Jour. of Med. Sc., 1902. 

Cygnäus: Studien über den Typhusbacillus. Beitr. v. Ziegler, vii., 1890. 

Dmochowski u. Janowski: Eiterung erreg. Wirkung d. Typhusbacillus. Beitr. v. 
Ziegler, xvii., 1895 (Liät.). 

Ebermaier: Knochenerkrankungen bei Typhus. Deut. Arch. f. klin. Med., 44 Bd., 
1889. 

Eberth: Virch. Arch., 81 Bd.; Samml. klin. Vortr., No. 126; Geht der Typhusbacil- 
lus auf den Fötus über? Fortschr. d. Med., vii., 1889. 

Faulhaber: Bakterien ind. Nieren bei acuten Infectionskrankheiten. Beit. v. Zieg- 
ler, x., 1891. 

Fischer: Werth der Widal’schen Reaction. Zeitschr. f. Hyg., 32 Bd., 1899. 

Flexner: (‘certain Forms of Infection in Typhoid Fever. Johns Hopkins Hosp, Rep., 
v., 1895; Unusual Forms of Infection with the Typhoid Bacillus, ete. Johns 
Hopkins Hosp. Rep., 1900. 

Förster: Baktericide Wirkung d. Blutserums v. Typhuskranken. Zeitschr. f. Hyg., 
xxiv., 1897 (Lit.). 

Fränkel, E.: Complication v. Abdominaltyphus. Jahresber. d. Hamburg. Kran- 
kenanst., i., 1890; Roseola typhosa. Zeitschr. f. Hvg., 3 Bd., 1900. 


BACILLUS COLI COMMUNIS. 593 


Frankel, E. u. Smmmonds: Die ätiologische Bedeutung d. Typhusbacillen, Leipzig, 

886. 

Gaffky: Aetiologie dl. Abdominalty phus. Mittheil. a. d. K. Gesundheitsamte, Berlin, 
884 


Gasser: Le bacille typhique. Arch. de med. exp., iii., 1891. 

Germano u. Maurea: Typhusbac. u. ähnliche Bakterien. Beitr. v. Ziegler, xii., 1898. 

Grancher et Deschamps: Le bacille typhique dans le sol. Arch. de med. exp., i., 
1889. 

Hamilton: The Fly as a Carrier of Typhoid. Jour. of Amer. Med. Ass., 1903. 

Hesse: Unsere Nahrungsmittel als Nährböden f. Typhus u. Cholera. Zeitschr. f. 

_ Hyg., v., 1889. 

Hiss: Studies in the Bacteriology of Typhoid Fever, etc. Med. News, 1901; New 
and Simple Media for the Differentiation of the Colonies of Typhoid, Colon, and 
Allied Bacilli. Jour. of Med. Res., 1902. 

Hodenpyl: On the Occurrence of Typhoid Fever without Characteristic Lesions of the 
Small Intestine. Stud. from Dept. of Path. of Columbia University, 1897-98. 
Holz: Exp. Unters. üb. d. Nachweis d. Typhusbacillen. Zeitsch. f. Hyg., viii., 1890. 

Janowski: Zur Biologie d. Typhusbacillen. Cbl. f. Bakt., viii., 1890. 

Jatta: Agglutination d. Typhusbacillus u. d. Colibacillen. Zeitschr. f. Hyg., 33 Bd., 
1900 (Lit.). 

Johnston: Paratyphoid Fever. Amer. Jour. of Med. Sc., 1902. 

Karlinski: Typhusbacillen in typhösen Dejectionen. Cbl. f. Bakt., vi., 1889. 

Kitasato: Verh. d. Typhusbacillus zu säure- u. alkalibaltigen Nährböden. Zeitschr. 
f. Hyg., iii., 1888. 

Klebs: Bacillen im Typhusdarm. Arch. f. exp. Path., xii., xiii., xv., 1880-82. 

Mallory: Histological Study of Typhoid Fever. Jour. of Exp. Med., 1898. 

Meisels: Ueber das Vorkommen von Typhusbacillen im Blute. Wien. med. Woch., 
1886. 

Muscatello: Sul potere piogeno del bacillo di Eberth. La Riforma med., 1890. 

Neuhauss: Nachweis d. Typhusbacillen am Lebenden (in Roseolaflecken). Berl. kL 
Woch., 1886. 

Neumann: Ueber Typhusbacillen im Urin. Berl. klin. Woch., 1890. 

Orloff: Actiologie der d. Typlıus abdom. complicirt. Eiterungen. Cbl. f. Bakt., viii., 
1890. 

Osler, Flexner, Blumer, Reed and Parsons: Studies in Typhoid Fever. J. Hop. 
Hosp. Itep., v., 1895. 

Petruschki: Ausscheidung d. Typhusbacillen durch Trin. Cbl. f. Bakt., xxiii., 1898. 

Pfeiffer: Nachweis d. Typhusbacillen im Darminhalt u. Stuhlgang. Deut. med. 
Woch., 1885. 

Pfeiffer u. Kolle: Spec. Immunititsreaction d. Typhusbacillen. Zeitschr. f. Hyg., 
xxi., 1896. 

Quincke: Zur Pathologie des Abdominaltyphus. Berl. klin. Woch., 1894. 

Remy ct Sugg: Rech. sur le bacille d’Eberth-Gaffky, Gand, 1898. 

Rodet: Avyzlutin. du bac. d’Eberth et du B. coli. Jour. de phys., ii., 1900. 

Sanarelli: Et. sur la fievre typhofde expérimentale. Ann. de l’Inst. Pasteur, vi., 
1892. 

Seitz: Bericht üb. die Aetiologie d. Abdominaltyphus. Cbl. f. Bakt., ii., 1887. 

Sirotinin: Die Uebertragung v. Typhusbacillen auf Versuchsthiere. Zeitschr. f. 
Hyg., i., 1886. 

Thayer: Observations on the Blood in Typhoid Fever. Johns Hopkins Hospital Re- 
port, 1901. 

Tictine: Meningitis et abcés produits par le bacille de la fievre typh. Arch. de méd. 
exp., 1894. 

Uffelmann: Lebensfähigkeit d. Typhus- u. Cholerabacillen in Fäcalmassen. Cbl. f. 
Bakt., v.. 1889. 

Widal et Sicard: Le sérodiagnostic. Ann. de l’Inst. Pasteur, 1897 (Lit.). 

Winterberg: Typhus-Agglutinin. Zeitschr. f. Hyg., 32 Bd., 1899. 


§ 160. The Bacillus coli communis or the Bacterium coli commune 
(Escherich ) is a fission-fungus which is constantly present in the intes- 
tinal tract of man as well as of the mammalia. The bacilli are rods 
2-3 » long and 0.3-0.4 » thick. They are motile and may possess as 
many as twenty flagella on one rod (Bunge, Luksch, Günther). The 
bacilli grow at room-temperature as well as at the temperature of the 
incubator. They form within the gelatin small, round, white colonies; 
upon its surface pellicle-like coatings. Upon potatoes they form moist 


594 THE PATHOGENIC FISSION-FUNGI. 


coatings of the yellow color of maize or pease (Günther). They do not 
form spores; and are not stained by Gram’s method. 

The Baeillus coli is very similar to the typhoid bacillus, but may be 
differentiated from it by proper methods of cultivation and by the em- 
ployment of suitable reactions (cf. $ 159). It was formerly regarded as 
a harmless saprophyte of the colon; but from later investigations it can- 
not be doubted that it also possesses pathogenic propertiesand may cause 
degenerations and inflammations in various tissues. Under suitable condi- 
tions (perforation or incarceration of the intestine, or impaction of faeces) 
it may pass into the peritoneal cavity and excite purulent inflammations, 
or at least take part with other bacteria in the production of inflamma- 
tion. Further, it not infrequently gains access to the bile-passages and 
gall-bladder, as well as to the descending urinary passages and the kid- 
neys, giving rise to inflammations of varying intensity. The bacillus 
has also been found in the meningeal exudate in certain cases of sepsis; 
it has been demonstrated also in pericarditis, bronchopneumonia, stru- 
mitis, angina of scarlet-fever, acute yellow atrophy of the liver (Stroebe, 
von Kahlden), and it cannot be doubted that it may be the cause of the 
affections named. 


The similarity between the colon-bacillus and the typhoid-bacillus has led various 
authors to assume that the two bacilli are only varieties of the same species, and that 
the two forms may pass over into cach other. At the present time the view prevails 
that the two bacilli are to be wholly separated from each other (§ 159.) Moreover, the 
form of bacillus which is described as colon-dacillus is not a very distinct form, but rep- 
resents rather a group of different rarictica, Three to four days after the inoculation of 
an animal with colon-bacilli the blood-serum of the infected animal produces an agglu- 
tination of colon-bacilli (Jatta), which is most marked in the case of that variety which 
was used for the inoculation. Colon-bacillus serum (‚Jatta) agglutinates typhoid-bacilli 
more markedly than does normal blood-serum. On the other hand, typhoid serum can 
agglutinate different varicties of colon-bacilli. 


Literature. 


(Bacillus Coli Communis.) 


Ackermann: Lés. ostéomy€élitiques expér. prov. par bac. colicomm. Arch. de med. 
exp., Vii, 1895. 

Adami, Abbott and Nicholson: On the Diplococcoid Form of the Colon Bacillus. 
Jour. of Exp. Med., 1899. 

Allen: Paracolon Infection. Amer. Jour. of Med. Se., 1903. 

Arloing: Rapport du bac. coli comm. avec le bac. d’Eberth. Lyon med., 1891. 

Arnaud: Rech. sur l’Ctiologie de la dysentérie. Ann. de l’Inst. Pasteur, viii., 1894. 

Bunge: Yur Kenntniss der geisseltragenden Bakterien. Fortschr. d. Med., xii., 1894. 

Buxton: A Comparative Study of the Bacilli Intermediate between B. Coli Communis 
and B. Typhosus. Jour. of Med. Res., 1902. 

Cushing: A Comparative Study of Some Members of a Pathological Group of Bacilli 
of the Hog Cholera Type, Intermediate between the Typhoid and Colon Groups. 
Johns Hopkins Hosp. Bull., 1900. ; 

Dunbar: Unters. üb. Typhusbac. u. Bact. coli. Zeitschr. f. Hyg., xii, 1892. 

Ford: Varieties of Colon Bacilli Isolated from Man. Mont. Med. Jour., 1900. 

Hofmeister: Zur Charakteristik d. Eklampsiebacillus Gerdes. Fortschr. d. Med., x., 
1392. 

Janowski: Die Ursachen der Eiterung. Beitr. v. Ziegler, xv., 1894. 

Jatta: Agglutination d. Typhusb. u. d. Organism. d. Coligruppe. Zeitschr. f. Hyg., 
32 Bd., 1900 (Lit.). 

v. Kahlden: Ueb. acute gelb. Leberatrophie u. Lebereirrhose. Münch. med. Woch., 
1897. 

Kamen: Actiologie der Winckel’schen Krankheit (Bac. coli). Beitr. v. Ziegler, xiv., 
1X93. 

Kiessling: Das Bacterium coli commune. yg. Rundschau, 1898. 

de Klecki: Pathogénie de Vappendicite. Ann. de Inst. Pasteur, 1899. 

Lartigau: The Bacillus Coli Communis in Human Infections (Lit.). Studies from the 
Dept. of Path. of Columbia University, 1901-02. 





596 THE PATHOGENIC FISSION-FUNGI. 


form upon the surface of the gelatin porcelain-white, button-shaped cul- 
tures consisting of oval and rod-shaped cells possessing no capsules. 
Stab-cultures in gelatin are nail-shaped (Fig. 447), the growth forming 
a knob-like prominence at the entrance of the stab-canal. This charac- 
teristic the pneumonia-bacilli share in common with many other bacteria. 
On blood-serum they form translucent, gray colonies; upon agar-agar 
jelly-like, grayish-white, and upon potatoes grayish-white or yellowish- 
white, creamy colonies. Spore-formation has not been observed. 

Rabbits are almost completely immune to inoculation of the lungs. 
Mice on the other hand die of pleuritis and disseminated pneumonia 
within eighteen to thirty hours after injection of the bacilli into the 
lungs; the exudate as well as the blood contains bacilli with gelatinous 
capsules, partly free and partly enclosed within céils. A typical lobar 
pneumonia cannot be produced in the ordinary experimental animals by 
inoculation. 


According to Fricke the bacterium of Friedlander is the chief representative of a 
BrouP of bacteria which are classed Log ‘ther under the name Bacillus mucosus capsn- 
tus, and represent varieties of a single species. The fission-fungus described as the 
ozena-bacillus is identical with the pneumonia-bacillus, probably also the bacillus from 
the milk-feeces of nurslings described as the Bacterium lactis aérogenes (Eschertch). It 
is possible that a greater etiological significance may be attached to it in so far as the 
origin of many diarrhwas is concerned. 


Literature. 
(Bacillus Pneamonie. ) 


Emmerich: Pneumoniekokken in der Zwischendeckfüllung. Fortschr. d. Med., ii 
1884. 

Frankel: Pneumonickokken. Zeitschr. f. klin. Med., x., xi.; Deut. med. Woch., 
1886. 

Fricke: Ueb. d. sog. Bacillus mucosus capsulatus. Zeit. f. oe xxiii., 1896 (Lit.). 

Friedländer: Pneumoniekokken. Virch. Arch., 87 Bd., 1882 Fortschr. d Med.,i., 
1883. 

Grimbert: Pneumobacille de Friedliinder. Ann. de l’Inst. Pasteur, 1896. 

Weichselbaum: L. c., § 153; Von einer Otitis media suppurativa ausgehende, durch 
den Bacillus pneumoniır bedingte Allgemeininfection. Monatsschr. f. Ohrenheilk., 


1888. 
Wilde: Ueber d. Bacillus Friedländer. Cbl. f. Bakt., xx., 1896. 


8 162. As the influenza-bacillus (Fig. 448) there was described by 
R. Pfeiffer, in the year 1892, a bacillus whose occurrence in influenza 
has been many times confirmed ; it is now regarded as the cause of influ- 
enza. In individuals suffering from influenza it is found in the catarrh- 
ally affected respiratory passages, occasionally also in the lungs ; and the 
small bronchi may contain enormous numbers of the bacilli in pure cul- 
ture. It is assumed that their multiplication in the respiratory tract 
gives rise to the inflammation, and that the bacilli produce poisons, 
which, when absorbed, cause the symptoms characteristic of influenza. 
The bacilli may also pass into the blood and become spread throughout 
the body. The inflammatory changes of internal organs occurring during 
influenza are to be referred in part to the influenza-bacillus, in part to 
the poisons produced by them, and in part to secondary infections. 

The influenza-bacilli are very small, thin rods with rounded ends 
(Fig. 448), which lie separate or joined together in twos. They stain 
with the ordinary aniline dyes, but not by Gram’s method. They may 
be cultivated at the body- -temperature upon blood-agar or upon agar that 


BACILLUS DIPHTHERLE. 597 


has been smeared with human or pigeon blood. They form upon this 
medium small, drop-like colonies as clear as water. They cannot be 
cultivated upon the other usual media. Spore- 

formation has not been observed. In apes a on 
catarrhal inflammation of the respiratory tract 32% 
may be produced by intratracheal injections 
of pure cultures. Rabbits may be poisoned 3, hp 
through the incorporation into their bodies of ‘48 
cultures; and are affected in consequence by a 
paralytic weakening of the muscles and dysp- + 
nea. According to Cantani the poison pro- 








saa . iQ. Fic. 448. — Infiuenza-bacilli 
duced by the bacilli exerts its effects partic- | us-corpuscles, from spu- 
ularly upon the central nervous system. tum (fuchsin). 1,000. 


According to investigations by Czaplewski and Hensel (“ Bakteriolog. Untersuch. über 
Keuchhusten,” Centrbl. f. Bakt., xxii., 1897) and Aoplik (“ Die Bakteriologie des Keuch- 
hustens,” Centralbl. f. Bakt., xxii., 1897), there is found in the respiratory tract in 
whooping-cough a small, non-motile bacillus similar to the influenza-bacillus, which is 
thought to be the cause of whooping-cough. Zuzzatto (“Zur Aetiol. des Keuchhustens,” 
Centralbl. f. Bakt., xxvii., 1900) found in cases of whooping-cough two bacilli, but was 
unable to determine with certainty their pathogenic significance. Jochmann and Krause 
(“ Actiol. des Keuchhustens,” Zeit. f. Ilyg., 86 Bd., 1901) found in whooping-cough a 
bacillus resembling the influenza-bacillus (Bacillus pertussis, Eppendorf); this could be 
cultivated upon media containing hemoglobin; they regard it as the cause of whooping- 
cough. Their bacillus is not identical with the one described by Czaplewskyand Ilensel. 


Literature. 
(Bacillus of Influenza.) 


Bäumler: Die Influenzaepidemie, 1893-94, in Freiburg i. Br. Münch. med. Woch., 

1894. 

Beck: Influenza. Ergebn. d. allg. Path., v., 1900 (Lit.). 
Canon: Mikroorganismen im Blute von Influenzakranken. Virch. Arch., 181 Bd., 

1893. 

Cantani: Wirkung d. Influenzabacillen a. d. Centralnervensyst. Zeitsch. f. Hyg., 

xxiii., 1896 (Lit.). 

Grasburger. Zur Bakteriologie d. Influenza. Zeitsch. f. Hyg., xxv., 1897. 

Huber: Ueber den Influenzabacillus. Zeitschr. f. Hyg. xv., 1893. 

Kitasato: Ucber den Influenzabacillus. Deut. med. Woch., 1892. 

Kruse: Aetiologie der Influenza. Deut. med. Woch., 1894. 

Kuskow: Pathol. Anatomie d. Grippe. Virch. Arch., 139 Bd., 1895 (Lit.). 
Nauwerck: Influenza u. Encephalitis. Deut. med. Woch., 1895. 

Ophüls: Infection of the Rectum with Secondary Infection of the Liver, Caused by 

the Bacillus Influenze Similis. Amer. Jour. of Med. Sc., 1901. 

Pfeiffer, A.: Die Actiologie der Influenza. Zeitschr. f. Hyg., xiii., 1893. 
Pfuhl u. Walter: Influenzabacillen im Centralnervensystem. Deut. med. Woch., 

1896. 
Weichselbaum: Actiologie u. path. Anat. d. Influenza. Wien. klin. Woch., 1892. 

$163. The Bacillus diphtheriz (Fig. 449) was first thoroughly studied 
by Löffler; it is found in the eroupous membrane occurring in diph- 
theria, and is regarded as the cause of this disease. In the internal 
organs, as the spleen and lymph-glands, it is either entirely absent or 
present in such slight numbers that it can be demonstrated only by 
methods of cultivation. 

The bacilli are 1.5-3 » long, often somewhat thickened (club-shaped ) 
or pointed at the ends. When stained the bacilli appear spotted or 
granular. They stain best in a staining-solution composed of 30 c.c. of 
concentrated aleoholie methylene-blue solution in 100 c.c. of 0.0001 per 
cent. potassium hydroxide solution, after which the sections are treated 


598 THE PARASITIC FISSION-FUNGI. 


for a few seconds in a 0.5-per-cent. solution of acetic acid and then with 
alcohol. In stained sections the bacilli often appear segmented. They 
also stain by Gram’s method, provided the treatment with Lugol’s solu- 
tion and alcohol is of brief duration. 

Diphtheria-bacilli grow best in the presence of air (Loffler) on a mix- 
ture of three parts of calf’s or sheep’s serum, and one part of neutralized 
veal-bouillon, to which one per cent. of peptone, one per cent. of grape- 
sugar, and 0.5 per cent. of common salt are added; or upon blood-serum 
and agar-agar with an addition of ten per cent. glycerin or of sugar-con- 

taining bouillon (Kolisko, Paltauf, Kitasato). 

=\ & They form grayish-white colonies. For their de- 

£.'Ne velopment they need a temperature above 20° C.; 

al > they grow best at 33°-37° C. They are resistant 

n 7 ral to drying; but may be quickly killed by moist 

‘ heat. Spore-formation has not been observed. 

[7 \ Guinea-pigs inoculated subcutaneously with cul- 

R f tures of diphtheria-bacilli die in two to three days 

%. és n 5 (Lofiler, Roux, Yersin); whitish deposits and a 

a x hemorrhagic cedema are found at the point of the 

ins. 449.— Diphtheria-ba- inoculation. The inoewation area contains baci 

Srreak a @ Pure cuture. the internal organs, on the contrary, are free. The 

fene-biue). x 10000 introduction of cultures into the opened trachea of 

rabbits, chickens, and pigeons, as well as the inoc- 

ulation of the conjunctiva of rabbits and the vagina of guinea-pigs is followed 

by an inflammation with the formation of a pseudomembrane. Sheep, 

horses, cats, dogs, cows, rabbits, and pigeons are susceptible to subeu- 
taneous inoculation. Rats and white mice are nearly immune. 

Roux, Yersin, Löffler, Spronck, and others observed the later appear- 
ance of paralysis in pigeons and guinea-pigs surviving the inoculation. 
Roux and Yersin assert that the intravenous injection of filtered bouillon- 
cultures free from bacteria will cause in guinea-pigs and rabbits after two 
to three days a severe illness characterized by paralysis and fatal termi- 
nation. 

The virulence of the cultures varies greatly. Diphtheria bacilli pro- 
duce in the human body and also in cultures toxins, which may be pre- 
cipitated by alcohol and obtained as a whitish powder. This substance 
has been classed with the toxalbumins, but according to Brieger and Boer 
it is not an albuminous body. It is also formed when the bacilli are cul- 
tivated in alkaline urine (Guinochet). According to Kossel the poison 
is formed within the bacterial cell from its food-material and then se- 
creted. 

Water-solutions of the poison injected subcutaneously into animals 
cause local tissue-necrosis, hemorrhagic oedema, and inflammation; when 
taken up into the body-juices they give rise to pleural effusions, nephri- 
tis, fatty degeneration of the liver, and paralysis. 

Diphtheria in man is characterized by an inflammation involving usu- 
ally the mucous membrane of the pharynx, palate, arch of the palate, 
and upper respiratory passages. It appears as a febrile infectious dis- 
ease associated with symptoms of intoxication and gives rise to local croupous 
erudations, in part also to diphtheritic sloughings (ef. § 92, Figs. 189, 
190). The croupous membranes constitute the most striking feature of 
the disease ; they are found in the throat and nose usually in the form of 
circumscribed flat patches, more rarely uniformly spread over larger 
areas; or, on the other hand, they may form a continuous layer lining 


nm 


BACILLUS DIPHTHERIE. 599 


the larynx and trachea, or even the bronchi. Beneath the croupous 
membrane the epithelium is for the greater part lost; and the connective 
tissue of the mucosa is hyperemic, infiltrated, and swollen (Fig. 190). 
In severe cases the superficial layers of the connective tissue are necrotic 
in places, most frequently in the tonsils, which are more or less, often 
markedly, swollen. Of the deeper tissues the neighboring cervical 
lymph-glands 1n particular are swollen, and often show, when examined 
microscopically, small foci of necrosis and degeneration. Of the inter- 
nal organs the kidneys especially are accustomed to show changes, in the 
form of a more or less severe fatty degeneration of the epithelium and 
of the cells of the capillary walls; not infrequently they also present 
swellings and focal areas of small-celled infiltration. In the spleen 
there are frequently found areas of degeneration in the white-appearing 
follicles, in which the cells are more or less necrosed, in part disinte- 
grated and have lost their nuclei. In the blood many of the leucocytes 
show fatty degeneration. Degenerative changes and areas of inflamma- 
tion are not infrequently found in the heart-muscle. Paralyses are 
caused by degeneration and necrosis (Katz) of the ganglion-cells of the 
medulla oblongata and of the spinal cord and of the corresponding 
nerves. 

The lungs are not demonstrably changed by the diphtheria poison, 
but bronchopneumonia, due to the aspiration of irritating bronchial 
contents or to an extension of the bronchial inflammation to the respi- 
ratory parenchyma, is of frequent occurrence. 

The local inflammations of the mucous membranes as well as the symp- 
toms of intorication may be caused by the diphtheria bacilli and their toxins 
alone ; but it must: be noted that streptococci are almost regularly pres- 
ent in the diseased area, and that a pure streptococcus infection may 
present the clinical and anatomical picture of a “diphtheria.” When 
both bacteria are present the injurious effect of one may be supple- 
mented by that of the other, and the presence of streptococci appears to 
increase the virulence of the bacilli. In severe forms of diphtheria 
streptococei are usually present in great numbers; yet every streptococ- 
cus infection does not warrant a bad prognosis, since the virulence of the 
cocei varies greatly. 

In the course of the infection with diphtheria bacilli there arise in the 
body antitorins, which nullify the poisonous action of the toxins, and aid 
and make possible recovery from the disease. The formation of anti- 
toxins follows the inoculation of animals with attenuated bacilli, and 
upon this rests the possibility of obtaining from animals (sheep, horses), 
that have been repeatedly inoculated with bacilli of increasing virulence, 
a serum which contains an antitoxin of value for therapeutic purposes 
(ef. § 32). 


Lehmann and Neumann call the diphtheria bacillus corynebactertum on account of 
the club-shaped appearance of the rods. Since the bacilli can also form branching 
threads in cultures, they class it with the hyphomycetes, among which the tubercle-bacil- 
lus and the fungus of actinomyces (oöspora) are also classed by them and others. 

Ehrlich (* Die Constitution des Diphtherie-Giftes,” Deut. med. Wochenschr., 1898, 
p. 597) distinguishes different kinds of poisons produced by the diphtheria-bacillus, 
namely, forins and torons, these again representing no ies of definite unity, but 
breaking up into several subdivisions (prototoxin, deuterotoxin, and tritotoxin) which 
are distinguished by the different degrees of avidity with which they unite with the 
antitoxin. He further assumes that there are present in the poison-molecule two atom- 
complexes independent of each other, one of which is of haptophorous nature and 
brings about the union with the antitoxin or with the corresponding side-chains of the 


VAN a wa aa aw XS us eo u 


qr OT WA FRNA 
LAST UBER. 


N 





i 
| 
i 
1 


600 THE PATHOGENIC FISSION-FUNGL 


cells. o atom-complex is toxopl t it cause 0! s] 
Ils. The other complex is Lorous—that is, it is the f the spi 
action of the poison (cf. ¢ 
‘According to Lifer, con Hofmann, Rouz, Yersin, Babes, and others there are 
frequently present in the mouth and throat bacilli, which are often designated pseı 
diphtheria becilll. These resemble the true bacilli of diphtberia and can be di 
fished from them only in cultures. Since the diphtheria-bacilli can lose their ı 
lence, it is not impossible (Zz, Fermin) that both bacilli represent varieties of 
same species. According to Kober and others diphtheri are also found ir 
mouths of healthy individuals. 


Literature. 
(Bacillus Diphtheria and Diphtheria.) 
Babes: Les bactéries de ladiphthérie. Ann. de I'Inst. de path. de Boucarest, i 
Virch. Arch., 119 Bd., 190. 
Baginsky: Diphtheric u. diphther. Croup, Wien, 1898. 
Barbacei; Alterut. d. Milz, Lymphdrüsen u. Leber bei Diphth. Cbl. f. allg. Pa 


Barbie; de “quelques associat. microbiennes dans la diphtherie. Arch. de med. ¢: 














ie Geschichte d. Diphtherie mit Berücksichtigung d. Immunitatslel 

Bernheim: Mischinfection bei Diphtherie. Zeitschr. f. Hyg., xvili.. 1894; Pr 
ogenese d. Wien, 1898. 

Blasi: Association buctér. dans la diplitherie. Ann. de I'Inst. Past., 1896. 

Bock: Bakt. Unters. über die Aetiologieder Diphtherie. Zeitschr. f. Hyg., viii., 18 

Brieger u. Boer: Toxine d. Diphtherie. Deut. med. Woch., 1896. 

Challlon « et Martin: Et. clin. et bacter. sur la diphtherie. Ann. de I'Inst. Paste 
1804. 

Solbet: "Pseudoliphtberia Bacillus. Journ. of Path., iv., 1896. 

‘n, Mallory and Pearce: A Study of the Bacteriology and Pathology 
oon Hundred an Twenty-five Fatal Cases of Diphtheria. Jour. of Bost. Soc 
Med. Se., 1900. 

Alter du sy 


(Li 
Denny : Morphology of B. Diphtherie, B. Pscudo-diphtherie, and B. Xerosis. Jc 
Med. Res., 1903, 
vy. Dungern: Mischinfection bei Diphtherie. Beitr. v. Ziegler, xxi., 1897. 
Ehrlich u. Wassermann: Die Gewinnung d. Diphtherieantitoxine. Zeitschr. 
y .. 1804. 

ologie u. Pathogenese der Diphtherie, Wien, 1894. 
breitungsweise der Diphtherie. Zeitschr. f. Hyg., xvii., 

Actiolog. Bedeutung der Löffler'schen Bacillen. Deut med. Wor 








. nerveux dans les paralys. diphth. Arch. de med. exp., 1 














Frosch: Verbreitung des Diphtherichac. im Körper. Zeitschr. f. Hyg. 2 Eu 1898. 
Gorham: Morphological Varieties of Bacillus Diphtherie. Jour. of 1% 
Guinochet: Contr. a de la toxine du bacille de la diphthérie. Arch. Pi méd. eı 


Diphtherie. Arb. a, d. path. Inst. zu Tübingen, ii., 1€ 
Diphtheric. Deut. Arch. f. klin. Med., 59 Bd., 18 
ing d. Giftproduction an Diphtheriebucillen durch "Symbiose m. Strep 
hr. f. Hyg., 29 Bd., 1898. 

Hin: Branching in Bacteria with Special Reference to Bacillus Diphtherie. Jour. 
Med. Res., 1902. 

tz: Diphtherische Lihmungen. Arch. f. Kinderheilk., 1897. 

i zur Actiologie der Diphtherie. Chl. f. Bakt., vii., 1890. 
pacillen auf d. Mundschleimhaut gesunder Menschen. Zeitsch. 






















1899. 
Kondievetzhy: Rech. exp. s. immunisation contre la diphthörie. Arch. de m 









Kossel: Zur Kenntniss d. Diphtheriegiftes. Cbl. f. Bakt., xix., 1896. 

N ‘eis d. Diphtheriebae. ind. Lunge. Zeitschr. f. Hyg., xvili., 189 
r Diphtherie. Deut. med. Woch.. 1890; Bedeutung der Mik 
Entstehung der Diphtherie. Mittheil. a. d. Kais. Gesundh 









i. . 
Madsen: Zur Biologie d. Diphtheriebacillen. Zeitschr. f. Hyg., xxvi.. 1897. 


BACILLUS TETANI. 601 


Millard et Regaud: Myocardite diphthérique. Ann. de l’Inst. Pasteur, 1897 (Lit.). 

Mouravieff: Infi. de la toxine diphth. sur le syst. nerveux. Arch de ıned. exp., 1897. 

Oertel: Die Pathogenese der epidem. Diphtherie, Leipzig, 1887; Das diphtherische 
Gift. Deut. med. Woch., 1890. 

Orth: Zur Geschichte der Diphtherie. Arb. a. d. path. Inst. zu Göttingen, Berlin, 
1893. 

Peters: Diphtheria u. Pseudodiphtheria Bacilli. Journ. of Path., iv., 1896. 

Proschaska: Pseudodiphtheriabacillen d. Rachens. Zeitschr. f. Hyg.. xxiv., 1897. 

Prudden: Studies on the Etiology of Diphtheria. Med. Rec., New York, 1891. 

Roux et Martin: Sérothérapie ede la diphtherie. Ann. de l’Inst. Pasteur, viii., 1894. 

Roux ct Yersin: Diphthérie. Ann. de l’Inst. Past., ii., 1888; iv., 1890. 

Schottelius: Wachsthum d. Diphtheriebac. in d. Milch. Cbl. f. Bakt., xx., 1896. 

Schlesinger: Diphtherie d. Conjunctiva. Münch. med. Woch., 1901. 

Slawyk u. Manicatide: Variabilität d. Diphtheriebacillen. Zeitschr. f. Hyg., 29 
Bd., 1898. 
Spronck: Pathogene Bedeutung d. Diphtheriebacillus. Cb). f. allg. Path., i., 1890; 
Invasion des Diphtheriebacil us i ind. Unterhaut d. Menschen. Ib., iii., 1892. 
Wassermann u. Proskauer: Vom Diphtheriebac. erzeugte Toxalbumine. Deut. 
med. Woch., 1891. 

Welch: The Histological Changes in Exp. Diphtheria. Bull. of the Johns Hopk. 
Hosp., ii., 1891. 

Welch and Abbot: The Etiology of Diphtheria. Bull. of the Johns Hopk. Hosp., ii., 
1891. 

Williams: Persistence of Varieties of B. Diphtheri® and of Diphtheria-like Bacilli. 
Jour. of Med. Res., 1902. 

Zarniko: Zur Kenntniss d. Diphtheriebacillus. Cbl. f. Bakt., vi., 1889. 
See also § 32. 


§ 164. The Bacillus tetani (Kitasato) is a fine, slender bacillus (Fig. 
450) which is widely distributed throughout the superficial layers of the 
earth, and is to be regarded as the cause of tetanus. According to ob- 
servations made by Nicolaier in 1885, it is often possible to produce in 
mice, guinea-pigs, and rabbits, by means of subcutaneous inoculation of 
surface-earth, a typical tetanus with fatal termination, 


due to this bacillus. ~ 

It was first demonstrated by Rosenbach in 1886 that l 1// 4 / 
this same form of bacillus is present in the seat of in- Qo & 
jury in cases of tetanus in man following trauma or freez- o ‘eo 
ing; and that when inoculated into guinea-pigs and mice = \- 
it again produces tetanus. Since that time this discovery c= w 
has been many times corroborated. The bacillus is not = pig. 450.-Tete- 
present in an isolated condition in either the earth or in pc with ter. 
the infected wound; and consequently the inoculations 1,000. 
were made with a mixture of bacteria. Attempts to 
isolate by cultures the bacillus that was regarded as the cause of tetanus 
were unsuccessfully made by many investigators. In 1889, in Koch’s 
laboratory, Kitasato succeeded in isolating the tetanus-bacillus by allow- 
ing the mixed cultures to remain in the incubator for several days and 
heating upon a water-bath at 80° C. for a half-hour or an hour, and then 
subsequently keeping plate-cultures in an atmosphere of hydrogen. The 
bacteria growing in association with the tetanus-bacillus are killed, while 
the tetanus-bacillus is preserved. 

The tetanus-bacillus is anaerobic and thrives very well in an atmos- 
phere of hydrogen, but not in carbonic-acid gas. It grows on ordinary 
peptone-agar that is slightly alkaline, on blood-serum, and in nutrient 
gelatin. The latter is liquefied with evolution of gas. The addition of 
from 1.5 to 2 per cent. grape-sugar to agar-agar accelerates the growth ; 
a temperature of 36°-38° C. is most favorable for its development. It 
forms long, thin, bristle-shaped rods which form terminal spores (Fig. 

32 


2 THE PATHOGENIC FISSION-FUNGI. 


450, giving rise to a spherical swelling at the end of the rod (kn 
bacilli, In cultures it may form long pseudothreads The cu 
give off an offeusive odor; gelatin is slowly liquefied. The bacilli 
by Grams method. They are motile except during the time of : 
formation, and possess peritrichous flagella. Pure cultures inocı 
into horses, asses, guinea-pigs, mice. rats, and rabbits cause tetanu 
in the case of rabbits larger amounts must be injected. The tetani 
tractures begin in the neighburhood of the point of inoculation. 
puration does not occur at the point of inoculation. The bacilli ¢ 
be demonstrated after the death of the animal, and are never fou 
the tissues except at the seat of inoculation. 

According to experimental investigations by Kitasato, the filtn 
bouillon-cultures of the bacilli, which does not contain bacilli, acts 
cultures containing the bacilli, and guinea-pigs are 
N eto it. The blood or transudate from the thoracic ¢ 
of an animal infected with tetanus, although free from bacilli, will 
tetanus when injected into inice. It may therefore be assumed th 
tetanus there is an intoxication with a poison (tetanolorin) which is dif 
throughout the blood. This poison is ı Kitasato) destroyed by he: 
a temperature of 65° C. and over, within a few minutes), and by ¢ 
sunlight (in fifteen to eighteen hours), and in diffuse daylight los 
virulence within a few weeks. According to investigations of Bı 
and Cohn the purified poison gives no reaction for albumin, and t 
fore is not a toxalbumin. 

The infection—intoxication—of man takes place usually throug 
medinm of small wounds; idiopathic or rheumatic tetanus, which 
not start from wounds, may arise through infection of the mouth-c 
and the respiratory tract (Carbone, Perrero, Thalmann). A preexi 
eatarrh favors the infection (Thalmann). The tetanus-toxin a 
chiefly the nervous system. 

The Bacillus eedemat: 


























(Vibrion septique of Pasteur) 
aörobie bacillus first refully studied by R. Koch. It is prese 
rious putrefying substances, and is almost never absent from 
fertilized by decomposing fluids or liquid manure. The bacill 
5 Jong, and 1-1.1 + broad; they often form long pseudothr 
ey resemble the anthrax-bacilli, though somewhat more slende 
rounded at the ends, and not sharply cut across. In spore-format 
swelling of the rod takes place, as in the of the Bacillus buty. 
so that spindle- and tadpole-shaped forms ai 

The bacillus is motile, and possesses flagella on the ends as well 
the sides, It is not stained by Gram’s method. 

It grows in nutrient gelatin as well as in agar and coagulated b 
seruin, but must be introduced deeply into the medium and protected 
the air. Nutrient gelatin to which one to two per cent. of grape- 
ulded is an especially favorable medium (Flügge). Nui 
nd blood-serum are liquefied, the latter with evolution of ; 

The bacillus can be y obtained by sewing up garden-earth 1 
the skin of a guinea-pig, care being taken to prevent the access of : 
the point of inoculation, The ensuing multiplication of the bac 
sa progressive cedematous swelling of the subcutaneous t: 
Ata later stage the bacilli spread over the serous membranes, an 
volve the spleen and other organs, 

Mice, guinea-pigs, horses, sheep, and swine are susceptible te 
bacilli; cattle are not. 






































BACILLUS PHLEGMONES EMPHYSEMATOSZE. 603 


According to observations by Brieger, Ehrlich, Chauveau, Arloing, 
and others, the bacilli of malignant cedema may also occasionally develop 
in the human body, particularly when the tissues are poorly nourished 
and the bacilli through any accident—puneture of a hypodermic syringe 
—gret into the deeper tissues. They excite gangrenous processes asso- 
ciated with hemorrhagic edema and gas-production. 

As the Bacillus phlegmones emphysematosz R. Fraenkel in 1892 
deseribed an anacrobie bacillus which in many cases is to be regarded as 
the cause of phlegmonous inflammation associated with gas-formation. 
Aceording to Fraenkel the bacillus is motile and only exceptionaily 
forms spores. It occurs in the external world (by Fraenkel it was 
demonstrated upon a splinter of wood with which a man dying of gas- 
phlegmon had been wounded); and when injected subcutaneously into 
guinea-pigs or sparrows produces a progressive gangrenous process with 
disintegration of the subeutaneous tissues and muscle, as well as free 
collections of fluid and gas. Intravenous injection into rabbits and 
guinea-pigs is followed by the formation of gas in the internal organs. 

It is probable that this baeillus is identical with one described by 
Ernst, Welch, and Nuttall (by the latter as Bacillus aérogenes capsulatus ) 
as the cause of “foamy liver” (“Sehaunleber”) (Ernst )—that is, with a 
bacillus which is regarded as the cause of gas-formation in the human 
liver (Ernst). The condition of “foamy organs ” (Schaumorgane) prob- 
ably arises (Fraenkel) from the fact that the bacillus in question gains 
an entrance before death into the tissues, into the liver in particular. 


According to Vadllard and Vincent tetanus does not follow the inoculation of teta- 
nus-bacilli deprived of poison. Consequently it must be assumed that the bacilli can 
increase in the tissues of man and animals and lead to poisoning only under certain con- 
ditions, When at the same time the poison of tetanus or of other bacteria (for example, 
Baeillas prodiqioxus) gain access tothe tissues. Blumenthal holds that the bacilli secrete 
a ferment which produces, within the organism, the tetanus poison. 

According to investigations by Avtaaato, Tizzoni, Cattani, Baquis, Behring, and 
others, susceptible animals may be made immune against tetanus, or, more correctly, 
mav be made poison-proof against the tetanus-poison. The blood of animals thus made 
poison: proof, possesses the power of destroying the tetanus-poison, and consequentl 
it. is possible to immunize susceptible animals with the curative serum derived from this 
blood, or to cure an attack of tetanus after the disease has already been acquired (cf. § 
32). 

As regards the bacteria of hemorrhagic infection, see § 44. 


Literature. 
(Bacillus Tetani.) 


Achard: Lésions des nerfs dans le tétanos. Arch. de med. exp., iv., 1892. 

Babes: Rech. sur le tétanus. Ann. d. l’Inst. de path. de Boucarest, iv., 1893. 

Beumer: Zur Actiologie des Trismus sive Tetanus neonatorum. Zeitsch. f. Hyg., iii., 
ISS7. 

Blumenthal: Tetanusgift. Zeitschr. f. klin. Med., 32 Bd., 1897. 

Bonome: Ueber die Actiologie des Tetanus. Fortschr. d. Med., 1887. 

Bassano: Origine tellurique du tetanos. Revue de méd., ix., 1889. 

Brieger: Actiologie d. Wundtetanus. Deut. med. Woch., 1887; Biol. Cbl., vii., 1887. 

Brieger . Boer: Toxine d. Diphtherie u. d. Tetanus. Deut. med. Woch., 1896. 

Brieger u. Cohn: Unters. üb. d. Tetanusgift. Zeitschr. f. Hyg., xvi., 1898. 

Carbone « Perrero: Actiol. d. rheumat. Tetanus. Cbl. f. Bakt., xviii., 1896. 

Danysz: Toxine tétanique et subst. nerveux. Ann. de l’Inst. Pasteur, 1899. 

Engelmann: Serumtherapie des Tetanus. Münch. med. Woch., 1897 (Lit.). 

Fermi u. Pernossi: Ucb. das Tetanusgift. Zeitschr. f. Hyg., xvi., 1894. 

Hochsinger: Zur Actiologie des menschl. Wundstarrkrampfes. Cbl. f. Bakt., ff, 
1887. 





604 THE PATHOGENIC FISSION-FUNGI. 


Kitasato: Der Tetanuserreger. Verh. d. XVIII. Congr. d. Deut. Ges. f. Chi: 
Deut. med. Woch., 1890; Tetanusbuciline, Zeitschr. f. Hyg., vil., 1889; 1 
gift. Ib., x., 1897. 

Kitt: Ueber Tetanusimpfungen bei Hausthieren. Cbl. f. Bakt., vii., 1890. 

Kohler: Stand d. Serumtherapie d. Tetanus. Münch. med. Woch., 1898 

Marie: La toxine tétanique. Ann. de I'Inst. Pasteur, 1897. 

Moschcowitz: Tetanus, a Study, ete. (Lit.). Studies from Dept. of Path. of 
bia University, 1899-1901. 

Rosenbach: Zur Aetiol. d. Wundstarrkrampfs. Langenbeck’s Arch., xxxiv., 

Roux ct Vaillard: Contr. a 1'ét. du tötanos. Ann. de l’Inst. Pasteur, 1898. 

Thalmann: Actiologie d. Tetanus. Zeitschr. f. Hyg., 88 Bd., 1900 (Lit.). 

Tizeoni: Bieroterapia nel Tetano. Mem. della R. Acc. dell” Ist. di Bologne 


Tizzoni u. Oattani: Tetanusgift. Cbl. f. Bakt., viii., 1890; Arch. f. exper. I 
27 Bd., 1890; Widerstandsfahigkeit der Tetanusbacillen. Arch. f. exper. A 
Bd., 1890; Ueber die Arts einem Thiere die Immunität gegen Tetanus zı 
trigen. Chl. f. Bakt., ix.; Eigenschaften des Tetanus-Antitoxins. 1b., 

1 


Tizzoni, Cattani u. Baquis: Bukteriol. Unters. üb. d. Tetanus, Beitr. v. i 

vii., 1890, 

Vaillard: Immunit contre le tétanos. Ann. de I'Inst. Pasteur, v., 1891. 

Wellner: Tetanus. Ergebn. d. allg. Path., iii., 1897. 

Wiedenmann. Beitrag zur Actiologie des Wundstarrkrampfs, Zeitschr. £. 11 
1889. 














(Bacillus Cödematis Maligni. Bacillus Phlegmones Emphysematosa 


Brieger u. Ehrlich: Malignes Ocdem bei Typhus abdom. Berl. klin. Woch., 
Cornevin : Gangréne foudroyante ct son inoculation préventive. Rev. de méd 


1888. 
Ernst: Gasbildende Anatroben u. ihre Bez. z. Schaumleber. Vireh. Arch., 1 
1893, 





Frankel: Ueber die Gasphlegmone, Hamburg, 1898; Ueber die Erreger der Ga 
mone, Monch, med. Woch., 1899. 

Harris, Welch: Morbid Cond 
‘of Johns Hopkins Hosp., 1900. 

Hesse, W. u. B.: Züchtung der Oedembacillen. Deut, med. Woch., 1885. 

Hibler: Durch wma@robe Spaltpilze beilingte Infectionserscheinungen. Chl. f. 








s caused by Bacillus Atrogencs Capsulatus. 





XX . 

Howard: A Contribution to the Knowledge of Bacillus Aerogenes Capsulatus. 
Festschrift, 1900; The Origin of Gas and Gas Cysts in the Central Nervous £ 
Jour. of Med. Res., 1901. 

Jensen u. Sand: Ueber maligues Oedem bei Pferden. Deut. Zeit. f. Thiermed 
1887. 






Koch, Zur Aetiologie d. Milzbrandes, Mittheil. a. d. K. Gesundheitsaı 
188 
Norris: Infection with Bacillus Atrogenes Capsulatus. Amer. Jour. of Med. St 


1899. 
Pasteur: Vibrion septique. Bull. de Acad, de méd., 1877, 1881. 
Welch u. Nuttall: Johns Hopkins Hospital Bull., 1892. 


§ 165. The bacillus of bubonic plague (Bacillus pestis) was d 
ered in 1894 by Kitasato and Yersin, of the Japanese and Frenct 
mission, while investigating an epidemic which had broken out in 
Kong. The pest. bacillus is a small rod with rounded ends (resen 
the bacillus of chicken-cholera). It stains easily with aniline dyes. 
cially well with methylene-blue, and in part shows an exquisite 
staining (Fig. 451). It is decolorized by Gram’s method. It is 
in all cases of plague, in especial abundance in the swollen lymph-g 
but also in the spleen and blood. Tt may be cultivated upon the v 
media, and forms bluish-gray colonies, which contain rods of v 
lengths. It multiplies abundantly in bouillon containing sugaı 
forms toxins. Independent movements have not been observed. | 














BACILLUS PESTIS. 605 


are not formed. The bacilli are easily killed by warming, but are able 
to withstand drying well. 

The bubonie plague, which destroyed great numbers of the inhabitants 
of Europe, at the close of the seventeenth and beginning of the eigh- 
teenth centuries (“Black Death”), has since 1720 almost disappeared 
from Europe and has shown itself only here and therein Eastern Europe. 
In different countries of Asia (Yunnan in China, Arabia, Mesopotamia), 
and in the interior of Africa (Koch) the disease seems to be endemie, 
and spreads from time to time in the same manner as cholera. 

Man is infected usually through the skin, more rarely from the mu- 
cous membrane of the mouth, nose, throat, and conjunctiva, still more 
rarely from the deeper parts of the respiratory tract, although cases of 
primary pest-bronchitis and pest-pneumonia occur. Small wounds usu- 
ally form the avenne of entrance in the skin, but it appears (Albrecht 
and Ghon) that a violent rubbing of an area of the skin with infected 
fingers or clothing may be sufficient to bring about an infection. 

The bacilh are taken up by the lymph-vessels and taken to the 
regional lymph-glands, where they cause a very marked swelling of the 
infected gland or group of glands—the primary bubo. Through the in- 
fection of Iymph-glands situated farther 
along the Ivmph-system there arise pri- Yoo pe ® 


1, 
mary buboes of the second class, and by cee” I 7S 
° , we os o§ fd é ol, ji} 
metastasis through the blood-stream 8 „wu. Sues 4 
secondary buboes are formed. The plague % a u Pe PS 
is thus characterized in the first placeby 9 g>,) = g= N 
an acute polyadenitis. Since the poisons oe ~~ N N“ 
AG . mor . . 3 “2 ° ra 
Which are in association with the bodies - 27h tn dt 
of the pest-bacilli exert a degenerative 3% ~ * & %  °* aly 
and necrotic effect upon the vessel- walls, > oog <a wo EN 
numerous hemorrhages are also caused, +», * ere » 
_ ae “er SS 3 


and these are absent only in rare cases. 
To these changes there are also added Fis. #1.—Plague bacilli (fuchsin). x ISO. 
circumscribed foci in the spleen, liver, 

kidneys, lungs, skin, ete. With the exception, therefore, of those cases 
in which the pest-infection is confined to the primary bubo, the disease 
is to be regarded as a general infection (Albrecht and Ghon), which arises 
from the taking-up of bacteria from a primary focus of infection, and 
runs ifs course with the clinical picture of a polyadenitis and a severe 
hemorrhagic septicemia, 

The individual foei are characterized by tissue-necroses of the nature 
of coagulation-neerosis (Albrecht and Ghon), as well as by severe eruda- 
tions, inflammation, and hemorrhage, and are eaused by the presence of 
extraordinarily large numbers of bacilli. The lymph-glands of the pri- 
mary bubo show either wholly or for the chief part the appearance of 
hemorrhagic infaretion, and are swollen and of a medullary consistence. 
After the course of a few days they also show yellow necrotic areas which 
later undergo liquefaction. When the disease has lasted longer than six 
days, the liquefaction of the lymph-glands may take on the character of 
a suppuration. 

The tissues in the neighborhood of the lymph-gland are always more 
or less cedematously swollen, infiltrated with blood; and hamorrhages 
are also found in the walls of the neighboring large veins. 

The secondary inflammations of the lymph-glands and of the lvmph- 
adenoid tissue of the mouth and throat do not usually cause such a 


606 THE PATHOGENIC FISSION-FUNGI. 


marked degree of swelling as do the primary; they resemble the medul- 
lary swelling occurring in typhoid fever. The surrounding tissues are 
also less changed, but if the process be prolonged the picture comes to 
resemble that of the primary buboes. 

The spleen of plague-patients is somewhat swollen, dark red, finely 
granular, shagreened (Albrecht and Ghon), and often contains small 
necrotic foci, which are caused by the development of the bacilli in great 
numbers. 

In the glandular organs and in the skin, there occur, besides hemor. 
rhages, also necrotic areas and exudative inflammations, all due to the 
presence of bacilli. In the lungs there may occur, in addition to the 
primary pest-bronchopneumonia, secondary metastatic focal inflamma- 
tions and aspiration-bronchopneumonias. 

The majority of individuals infected with pest die within the first 
eight days, but others may live several weeks and then die of marasmus. 

Not infrequently secondary infections, particularly of streptococci and 
diplocvcei, are associated with the pest-infection. They arise chiefly in 
the tonsils and follicular glands of the tongue following the chauges 
caused by the pest-bacilli (Albrecht and Ghon). 

Among animals, rats, mice, apes, and cats are especially susceptible to 
pest ; and in these, particularly in rats, spontaneous infections occur, so 
that they may aid in the spread of epidemics. Swine and dogs are less 
susceptible, birds still Jess so. 

The changes in infeeted animals agree in general with those observed 
in man. The infection may remain local or become general. After the 
lymphadenitis and the multiple hsmorrhages there arise also miliary, 
tubercle-like foci in the spleen, liver, and lungs. The course is usually 
acute, rarely chronic. In the latter case the larger necrotic foci may be 
encapsulated by connective tissue. The animals are easily infected from 
the skin, as well as from the mucous membranes of the intestinal and 
respiratory tracts; and such infection may take place from an uninjured 
mueous membrane. The inoculation of one mouse confined in a cage 
with other mice may give rise to a cage-epidemic (Schottelius). 


Attempts toimmuntze animals and man against pest by means of dead and attenuated 
peat-hacillé have been many times carried out, especially by Yersın, Haffkin, and Lus- 
tig; and have been successful in so far that rodents, horses, and apes have been ren- 
dered immune against inoculations otherwise fatal. According to the reports of such 
attempts in man, a smaller per cent. of inoculated individuals acquire the disease than 
of those not inoculated; but doubt is thrown upon the results of these inoculations by 
other authors (Bitter). Further, attempts at tmmunization and healing have been made 
in man, with the serum of animals which hare been rendered immune, particularly of 
horses (Yersin, Lustig); and different authors ascribe to such serum a favorable influ- 
ence. 

During the last several vears, as the result of the spread of Plague in India and its 
appearance in Europe, numerous erticles upon pest have appeared. he most thorough 
pathological anatomical and experimental investigations are those carried out by .Al- 
hrecht and Ghou, whose articles have been used chiefly in the preparation of the text as 
given above. 

Slicker differentiates the following forms of pest according to the first localization 
of the bacilli: (1) Bubonic plague (the most common form); (2) the cutaneous form 
(formation of vesicles and ulcers or furuncle-like inflammations); (3) the pulmonary 
form: (4) the intestinal form. 

Some years ago Senarelli (“Sur la fiévre jaune,” Ann. de UInst. Pastenr, 1897: 
Cent. f. Bakt., xii.) described as the cause of yellow fever a bacillus whose properties 
he sought to determine by means of culture-experiments and animal-inoculations. He 
is still of the opinion that his Baeillue jeteroides is the cause of yellow fever (“ Zur Lehre 
vom gelben Fieber,” Ch. f. Bakt., xxvii., 1900), and reports favorably of the protective 
and curative effects (“Exper. sur l'emploi du serum curatif et preventif de la fiévre 


BACILLUS PESTIS. 607 


jaune,” Ann. de U’Inst. Pasteur, 1898) cf his serum obtained from vaccinated animals 
(dogs, horses, cattle). Freire(“ Man. sur la bactériologie, pathogénie et traitement de 
la fi¢vre jaune,” Rio de Janeiro, 1898, Cdl. f. Bakt., xxvi.) on the other hand opposes 
energetically the correctness of Sanarelli’s views, and maintains that the cause of yellow 
fever is a coccus earlier described by him, which he calls the Micrococcus ranthogenicue. 
By inoculations of the same into dogs, guinea-pigs, and rabbits he was able to produce 
a disease resembling yellow fever, and likewise reports successful protective inocula- 
tions with attenuated cultures. 

Through the investigations of Ducrey, Krefting, and Petersen (cf. Petersen, * Ulcus 
Molle,” Arch. f. Derm., xxix., 1894; xxx., 189.) it is probable that the ulcus molle or 
soft chancre is caused by a bacillus. This view is, however, opposed by competent 
authors (Finger, “ Die Syphilis und die venerischen Krankheiten,” Leipzig, 1896); and 
the opinion is advanced that there is no single specific virus of soft chancre. It must 
also be remarked that attempts to cultivate the chancre bacillus have not been success- 
ful. (See also “ Observations on the Distribution and Culture of tle Chancroid Bacillus, 
by Dacis, Jour. of Med. Res., 1902.) 


Literature. 
( Plague.) 


Abel: Geschichtliches über die Rattenpest. Zeitschr. f. IIyg., 36 Bd., 1901. 

Albrecht u. Ghon: Ueber die Beulenpest in Bombay im J., 1897, Wien, 1898, 1900. 

Aoyama: Die Pestepidemie im Jahre 1894 in Hong-Kong, Tokio, 1895. 

Babes: Durch Pestbacillen verursachte Veränderungen. Virch. Arch., 150 Bd., 1897. 

Bitter: Schutzimpfungen gegen Pest. Zeitschr. f. Hyg., 30 Bd., 1899. 

Däubler: Grundzüge der Tropenhygiene, Berlin, 1900. 

Dewel: Empfänglichkeit d. Frösche f. Beulenpest. Cbl. f. Bakt., xxii., 1897. 

Flexner: The Pathology of Bubonic Plague. Univ. of Penn. Med. Bull., 1901. 

Gaffky, Pfeiffer, Sticker u. Dieudonné: Pest. Arb. a. d. K. Gesundheitsamte, 
xvi., 1899. 

Kitasato: Preliminary Note of the Bacillus of Bubonic Plague, Hong-Kong, 1894. 

Koch: Verbreitung d. Beulenpest. Deut. med. Woch., 1898. 

Kolle: Bakteriologie der Beulenpest. Deut. med. Woch., 1897. 

Lustig: Gewebsveränderungen bei Beulenpest. Cbl. f. allg. Path., viii., 1897; Siero- 
terapia e vaccinazioni preventive contro la peste bubonica, 1897. 

Markl: Pesttoxine. Cbl. f. Bakt., xxiv., 1898. 

Metschnikoff: La peste bubonique. Ann. de l’Inst. Pasteur, 1897. 

Müller u. Pöch: Die Pest, Wien, 1900. 

Netter: Le microbe de la peste. Arch. de med. exp., 1% 0 (Lit.). 

Nuttall u. Kolle: Die Insekten bei der Pest. Cbl. f. Bakt., xxii., 1897. 

Sata: Actiologie u. Anat. d. Pest. Arch. f. Hyg., 37. 89 Bd., 1900, 1901. 

Scheube: Pest. Eulenb. Itealencyklop., 1897; Die Krankheiten d. warmen Länder, 
Jena, 1900. 

Schottelius: Die Bubonenpest in Bombay. Hygien. Rundschau, 1901. 

Simond: La propagation de la peste. Ann. de l'Inst. Pasteur, 1898. 

Sticker: Die Pest nach Erfahr. in Bombay. Münch. med. Woch., 1898. 

Wyssokowitz et Zabolotny: Rech. sur la peste. Ann. de l'Inst. Pasteur, 1897. 

Yamagiva: Die Bubonenpest. Virch. Arch., 149 Bd., Suppl., 1897. 

Yersin: Sur la peste bubonique. Ann. de !’Inst. Pasteur, 1894, 1897. 

Zettnow: Bacillus der Bubonenpest. Zeitschr. f. Hyg., xxi., 1896. 


§ 166. The Bacillus tuberculosis is the cause of the infectious disease 
occurring so frequently In man and the domestic animals which is known 
ordinarily as tuberculosis, but is also sometimes called pearl disease 
( Perlsucht) in animals. 

The tuberele-bacillus was discovered and thoroughly studied by Koch 
in 1882. It isa slender rod (Fig. 452), of 1.5-4 » in length, and is 
usually slightly curved. It may be stained by aniline-dyes (fuchsin, 
gentian-violet) to an aqueous solution of which an alkali, or carbolic 
acid, or aniline oil is added. The bacilli when once stained retain the 
stain, even when the preparation is decolorized in dilute sulphuric acid, 
or nitrie acid, or hydrochloric acid and alcohol. 

The stained bacilli not infrequently show in their interior clear, shin- 


608 THE PATHOGENIC FISSION-FUNGI. 


ing, unstained areas, or are composed of little stained spherules. Koch 
formerly regarded these clear spots as spores, and this view was generally 
accepted for a long time. Nevertheless, a germination of these struc- 
tures could not be demonstrated, and at the present time they are no 
longer regarded as spores. Consequently, the tubercle-bacilli form no 
special resistant forms, but on the other hand the bacilli are more resist- 
ant against external influences, for example, against drying, than are 
many other bacteria. 

The tubercle-bacilli may be cultivated at the body temperature and 
in the presence of oxygen upon coagulated blood-serum, blood-serum- 
gelatin, nutrient agar, and in bouillon. They increase, however, very 
slowly, so that only on the seventh to tenth day or even later, do the cul- 
tures become visible in the form of dull-white flakes resembling little 
scales. Larger cultures form, on the surface of coagulated blood-serum, 
whitish, irregularly shaped, lustreless deposits. According to Noeard, 
Roux, and Bischoff the growth of the bacilli is greatly aided by the 
addition of glycerin (four to eight per cent.). Pawlowski succeeded in 

cultivating them upon potato in sealed 

-@ ~ a glass-tubes. In cultures the tuberele- 

}, » oa | \ . bacilli also form threads, which in part 
8% \\t, show branching. 


\ iQ At temperatures below 28° C. and 

Ve ON SU above 42° C. the growth of the bacilli 

* "er  -_@ . “= ceases. Sunlight kills the bacilli in a 
€ \S \ ‘@ _- Short time (Koeh). 

& Ny If the bacilli from pure cultures are 


Inoculated into experimental animals, 
emmy NY ax % .~ \. tuberculosis is produced in these; and 
cig, 442._Tahervtechactil, & tum from the infection is transmitted as well by 

a lan suffering with pulmonary tubereu. INoeulation under the skin, or into the 

a un seupieaetne, Peritoneal cavity, or the anterior cham- 
x 400, ber of the eye, as also by inhalation of 

an atomized suspension of the culture, 
by teeding, and by injection of bacilli into the veins. Guinea-pigs, 
rabbits, cats and gray field mice are especially susceptible; dogs, rats, 
and white mice less so. 

Infection of man and of animals occurs from the taking up of tuber- 
cle-bacilli from the lungs, respiratory passages, and the intestinal tract, 
or from wounds and tissue-uleerations. In the alimentary tract the 
Ivmphadenoid apparatus, tonsils, and the intestinal lIymph-follieles form 
the most frequent avenue of entrance. Further, a direct transmission of 
the bacilli from the mother to the fetus in utero, may oceur, but this is 
rare. 

The bacilli are spread throughout the external world chiefly by the 
sputa, under certain conditions also by the feces and urine, farther from 
tubereulous ulcers, or from tubere lous organs which are taken from liv- 
ing or dead persons. Since the bacilli are rather resistant, they may be 
preserved outside of the animal body for a long time under certain con- 
ditions, and may become mixed with the respired air, as well as with the 
food and drink. The milk of tuberculous cows contains the bacilli es- 
pecially when the udder is diseased ; but the bacilli may also pass into 
the milk when no disease of the udder can be demonstrated (Hirschberg, 
Ernst, Leuch). 

If the bacilli sueceed in developing and multiplying in any tissue of 














TUBERCULOSIS. 613 


necrobiosis of the cells, and on the other upon the deposit of coagulated sub- 
stances in the spaces between the cells. The cell-necrosis is characterized 
by a loss of the nuclei and a transformation of the cells into lumpy 
masses which later disintegrate and become granular (Fig. 458 «a. a). 
The deposit between the cells consists either of a network of fibrin ( Fig. 
457, a) or of a granular or hyaline reticulated fibrinoid substance resem- 
bling fibrin but which does not take the Weigert's fibrin stain and is 
stained yellow by Van Gieson’s. In the further course of the process of 
caseation the fibrin and fibrinoid substanee disintegrate into a granular 
mass which fuses with the cell-detritus, so that the central part of the 
tubercle consists of a lumpy granular mass (Figs. 459, a, 460, a) which 
takes a weak diffuse stain with nuclear stains. 

The caseation affects at first the central portion of the tubercle, and 
is usually confined to this, while connective tissue is formed at the per- 
iphery, so that the tubercle comes to consist of a caseous centre (Fig. 
459, a) and a fibrocellular periphery (b) which usually contains giant-cells, 
Under certain conditions the caseation may involve the entire tubercle. 
If the caseation does not affect the periphery, the fibrocellular tissue of 
the peripheral zone, sooner or later, becomes transformed into a pure 
fibrous tissue, so that a fibrocaseous tubercle (Fig. 460, a, 6) is formed, 
the connective tissue of which is coarsely fibrillar or hyaline and poor in 
cells (8), and in the course of time usually becomes sharply defined from 
the caseous centre (a), So that the latter appears to be encapsulated by 
connective tissue. If the tuberculosis runs a favorable course the cen- 
tre instead of caseating may undergo a connective-tissue metamorphosis 
(Fig. 461, 6, c, d), so that the tubercle becomes changed into a fibrous 
nodule. 


The infectious nature of the disease known as tuberenlosin had already been deter- 
mined by the experimental transmission of tuberculosis to animals (Villemtu, Lebert, 
Wysxe, Cohnheim, Klebs, Langhans, and others), before the discovery of the tubercle- 
bacillus. Nevertheless, it was a long time before the view that tuberculosis was au 
infectious disease received general acceptance, and opposition to this view has even to- 
day not wholly disappeared (Widdendorp). 

The peculiar behavior of the tubercle-bacillus toward stains—that is, its property 
of retaining the stain after treatment of the preparation with acids and alcohol, the so- 
called acid- and alcohol-resistance—makes it possible to demonstrate with relative case 
the presence of tubercle-bacilli in the sputum or in the tissues, and to differentiate it 
from other bacteria. It should be noted, however, that other bacteria show these prop- 
erties; the bacillus of leproay, the amegma-dacillus (a bacillus very frequently found on 
the corona glandis, between the scrotum and thigh and in the folds between the labia 
majora and minora), further two different bacillé found tn butter (one described by L. [ub- 
inmeitsch and Petri, the other by Korn), and finally also different bacilli cultivated by 
Moeller from grasses (timothy-grass) and from core-dung. All these acid-resisting bacilli 
may under certain conditions lead to errors of diagnosis; for example, the smegma- 
bacillus in the examination of urine, the butter-bacilli in the examination of butter, the 
latter particularly, since the bacillus described by Ftabinorritsch, when injected into the 
peritoneal cavity of guinea-pigs, causes a disease of the abdomen similar to true inocu- 
lation-tuberculosis, while the bacillus described by Aorn causes a pseudotuberculosis in 
white mice (these animals showing but slight susceptibility to true tuberculosis). 

Since the tubercle-bacillus in cultures forms simple and branching threads (Alein, 
Fischel, Coppen-Jones, Nocard, Maffucci, and others) and bud- and club-like swellings, 
many authors are inclined to group it with the thread-fungi. Lehmann and Neumann 
designate it as Uyobaucterium tuberculosta, Coppen-Jones as Tuberculomyces. 

Since the tubercle-bacillus in caseous pulmonary foci (Coppen-Jones), and after 
direct injection into the parenchyma of the brain, kidneys, mammary glands, and testi- 
cles, as well as after the intra-arterial injection of large numbers of bacilli (Z3ubea, Leou- 
ditt, Schulze, Lubsersch, Friedrich, and Nösske) forms, in addition to the ordinary colonies 
of bacilfi, fungus-masses also resembling those of actinomyces, on the outer surface of 
which ray-lixe clubs radiate into the surrounding tissne, Lubarach and others, in the 
assumption that the fungus-masses consist of branching threads, have classed the 


614 THE PATHOGENIC FISSION-FUNGI. 


tubercle-bacillus with the actinomyces or ray-fungi. Zubarsch regards the ray-fungi 
as a sub-class of the Streptothrices, an intermediate group lying between the Schizo- 
mycetes and the //yphomycetes, and characterized by the formation of clubs; and to this 
class he assigns also the butter- and dung-fungi mentioned above. According to Fried- 
rich and Nösske the fungus-masses regarded as resembling those of actinomyces consist 
Oun.y OT rods. 

Y Kecordin to the investigations of Z/ammerschlag, Ruppel, Sata; and others. the 
tubercle-bacilli contain an abundance of fat, which under proper conditions may be 
demonstrated by staining with sudan (Sata). According to Hammerschlag the tubercle- 
bacilli contain twenty-seven per cent. of substances soluble in alcohol and ether (fats, 
lecithin, poisonous substances), while other bacteria contain only 1.7-10 per cent. of the 
same. The remaining substance insoluble in alcohol contains albumin and cellulose. 

. According to the investigations of Prudden, IHodenpyl, Kostenitsch, Vissmann. Ma- 
sur, Kockel,.and others, dead tubercle-bacilli, when introduced into the tissues of an 
animal by inoculation, or injection into the blood-stream, or through introduction into 
the respiratory passages, excite, at the point of deposit, inflammation and tissue-pro- 
liferation similar to that caused by living bacilli, and in the case of a large inoculation 
may lead also to suppuration. These changes differ, however, from those produced by 
living bacilli, in that the bacilli are destroved after a few wecks and the nodules of 

ranulation tissue heal through a transformation into fibrous tissue; and further, by the 
act that the severity of the local tissue-proliferation is dependent wholly upon the 
amount of dead bacilli introduced, and that there is no spread of the process throughout 
the body. The dead bacilli must therefore contain substances (proteins) which cause 
inflamination and later also tissue-proliferation. 

In addition to the local effects, the substance contained in the cell-bodies of the 
bacilli may also cause emaciation of the animal. 

The actire substance of the bodies of the bacilli—tuberculin—was first produced by Auch 
(1890) from six- to eight-weeks-old cultures in a weak alkaline veal-infusion, to which 
one per cent. of peptone and four to five per cent. of glycerin were added, by evapor- 
ation upon a water-bath to one-tenth of the original volume and filtering through a 
filter of earthenware and silicious marl. Later (1897) he dried highly virulent cultures 
of tubercle-bacilli in a vacuum-exsiccator, then triturated the dry substance, mixed it 
with distilled water and centrifugated it. The active principle is contained in the 
muddy precipitate thus obtained, which is again dried and triturated and dissolved in 
water to which twenty per cent. of glycerin is added for the purpose of preservation. 
This tuberculin (designated by Koch as T. R.) is said to contain 10 mgm. of solid sub- 
stance in 1 c.c. (prepared by Meister, Lucius, and Drünning). 

Yabe, by treating tubercle-bacilli killed by heating, with alcohol, ether, potassium 
hydroxide, and the Schweizer reagent (copper oxide-ammonia, solvent of cellulose), 
obtained three substances: ‚fat, an albuminous body which he called tuberenlo-mycopro- 
tein, and a substance whose chemical nature was not definitely determined, which be 
called tuberculo-bactericidin. 

Mycoprotein, when injected subcutaneously, causes a collection of leucocytes; 
large doses kill guinea-pigs in two to four days. Tuberculo-bactericidin also causes 
. local inflammation; but is less poisonous for the organism as a whole. 


Literature. 
(Tubercle-bacilli and Formation of Tubercles. ) 


de Aquilar: Fibriubildung in Producten d. Tuberk. Arb. v. Baumgarten, ii., 1897. 

Arnold: Anatomie d. miliaren Tuberkels. Virch. Arch., 82 Bd., 1880. 

Auclair: J.ecs poisons du bac. tuberculeux. Arch. de med. exp., 1899. 

Babes u. Proca: Wirkung d. Tuberkelbacillen. Zeitschr. f. Hyg., xxiii., 1896. 

Baumgarten: Tuberkelbakterien. Cbl. f. d. med. Wiss., 1882, 1883: Tuberkel u. 
Tuberkulose. Zeitschr. f. klin. Med., xi., 1885; Diagn. tuberk. u. syph. Processe. 
Wien. med. Woch., 1900. 

Buhl: I,ungenentzündung, Tuberkulose u. Schwindsucht, München, 1872. 

Bunge u. Trantenroth: Smegma- u. Tuberkelbacillen. Fortschr. d. Med., xiv., 1896. 

Carriere: Altérat. du foie et des reins prod. p. 1. toxines tub, Rev. de méd. exp.. 


1897. 
Cohnheim u. Frankel: Uebertragbarkeit d. Tuberkulose. Virch. Arch., 45 Bd.. 
1869. 


Cornet: Die Tuberkulose, Wien. 1899. . 
Czaplewski: Nachweis der Tuberkelbacillen im Sputum. Cbl. f. Bakt., vili., 1890. 
Dobroklonski: Développ. de la tuberculose eyperim. Arch. de med. exp., ii., 1890. 


TUBERCULOSIS. 615 


Ernst: How Far may a Cow be Tuberculous before her Milk becomes Dangerous as 
an Article of Food? Amer. Journ. of Med. Sc., 1889. 

Falk: Exudative Vorgänge bei d. Tuberkelbildung. Virch. Arch., 139 B«l., 1895. 

Ferrän: Neue Entdeck. bezügl. d. Bac. d. Tuberkulose. Wien. klin. Woch., 1898. 

Fischel: Ueber die Morphol. u. Biol. d. Tuberkulose-Erregers. Fortschr., x., 1892, 
Wien, 1898. 

Fischer: Uebertrag. d. Tub. durch die Nahrung. Arch. f. exp. Path., xx., 1886. 

Flügge: Die Verbreitung der Phthise. Zeitschr. f. Hyg., 30 Bd., 1899. 

Fraenkel: Smegmabacillen. Cbl. f. Bakt.. xxix., 1901. 

Friedrich u. Nösske: Localisirung der 'Tuberkelbacillen. Beitr. v. Ziegler, xxvi., 
1899. 

Ginther: Bakteriologie, Leipzig, 1898. 

Hammerschlag: Bakteriolog.-chem. Unters. über Tuberkelbacillen. Cbl. f. klin. 
Med., 1891. ' 

Hering: Studien über Tuberkulose, Berlin, 1873. 

Hirschberger: Infectiosität d. Milch tuberkulöser Kühe. Deut. Arch. f. klin. Med., 
44 Bd., 1889. 

Jani: Tuberkelbacillen in gesunden Geweben bei Lungeuschwindsucht. Virch. Arch., 
103 Bd., 1886. 

Johne: Die Geschichte der Tuberkulose, Leipzig, 1883. 

Jones: Morphologie u. system. Stellung d. Tuberkelpilzes. Cbl. f. Bakt., xvii., 1895. 

Kastner: Beitr. z. Infectiosität des Fleisches tuberkul. Rinder. Münch. med. Woch., 
1889. 

Klebs: Impfversuche. Virch. Arch., 44, 49 Bd.; Arch. f. exp. Path., i., x., xvii.; 
Prag. med. Woch., 1877. 

Koch: Die Aetiologie der Tuberkulose. Berl. klin. Woch., 1882, No. 16; 1883, No. 
10. Verh. d. Congresses f. inn. Med., Wiesbaden, 1882; Mittheil. a. d. Kais. 
Gesundheitsamte, ii., Berlin. 1884: Mittheil. üb. ein Heilmittel geg. d. Tuberku- 
lose. Deut. med. Woch., 1890; Mittheil. über das Tuberkulin. Ib., 1891; Neue 
Tuberkulinpräparate. Ib., 1897. 

Kockel: Histogenese des Miliartuberkels. Virch. Arch., 143 Bd., 1896 (Lit.). 

Korn: Säurefeste Bakterien. Cbl. f. Bakt., xxv.. 1899, xxvii., 1900; Bacillenbefunde 
in der Marktbutter. Arch. f. Hyg., 66 Bd., 1899. 

Kostenitsch: De l’&volution de la tuberculose par les bacilles morts. Arch. de med. 
exp.. v., 1893. 

Kostenitsch et Wolkow: Rech. sur le developp. du tubercule. Arch. de med.exp., 
iv., 1892. j 

Köster: Ueber fungöse Gelenkentzündung. Virch. Arch., 48 Bd., 1869. 

Langhans: Die Uebertragung der Tuberkulose auf Kaninchen, 1868; Riesenzellen 
mit wandständigen Kernen in Tuberkeln. Virch. Arch., 42 Bd., 1868. 

Lebert u. Wyss: Uebertrugung d. Tuberkulose. Virch. Arch., 40 Bd., 1867. 

Leuch: Hygien. Milchcontrole. Correspbl. f. Schweizer Aerzte, 1896. 

Levene: Biochemical Studies on tlıe Bacillus Tuberculosis. Jour. of Med. Res., 1901. 

Lubarsch: Zur Kenntn. d. Strahlenpilze. Zeitschr. f. Hyg., xxxi., 1899. 

Maffucci: Prod. tossici del Bac. tuberculare. Policlinico, ii., Roma, 1895; Die MNüh- 
nertuberkulose. Zeitschr. f. Hyg., xi., 1892. 

Masur u. Kockel: Wirkung todter Tuberkelbacillen. Beitr. v. Ziegler, xvi., 1894. 

Metschnikoff: Die phagocytäre Rolle der Tuberkelriesenzellen. Virch. Arch., 113 
Bd., 1888. 

Middendorp: La cause de la tuberculose, Groningen, 1897. 

Milchner: Uebertragung d. Tub. durch Milch u. Milchproducte. Zeitschr. f. Tub., 
i., 1900. 

Nocard et Roux: Bacille de la tuberculose. Arm, de l’Inst. Pasteur, xi., 1897. 

Orth: Exp. Unters. über Fütterungstuberkulose Virch. Arch., 76 Bd., 1876. 

Pawlowsky: Culture des bac. de la tub. sur la pomme de terre. Ann. de l’Inst. Pas- 
teur, ii.. 1888; Entwickelungsgeschichte der Gelenktuberkulose. Cbi. f. Bakt., 
vii., 1890. 

Predöhl: Die Geschichte der Tuberkulose, Hamburg, 1888. 

Prudden: A Study of Experimental Pneumonitis in the Rabbit Induced by the In- 
fection of Dead Tubercle Bacilli. New York Med. Journ., 1891. 

Prudden and Hodenpyl: Action of Dead Bacteria in Living Body. New York Med. 
Jour., 1891. 

Pütz: Die Beziehungen d. Tuberkulose d. Menschen zur Tuberkulose d. Thiere, 
Stuttg., 1883. 

Rabinowitsch: Zur Frage d. Vork. v. Tuberkelbac. in d. Marktbutter. Zeitschr. f. 
Hyg., xxvi., 1897; Deut. med. Woch., 1899; Säurefeste Bacillen bei Lungengan- 
gran. Ib., 1900; Uebertragung d. Tuberkulose durch Milch. Ib., 1900. 


616 THE PATHOGENIC FISSION-FUNGI. 


Rabinowitech u. Kempner: Infectiosität d. Milch tuberk. Kühe. Zeitschr. f. Hyg., 

xxxi., 1899. 

Raymond et Arthaud: Rech. exper. sur l’etiol. de la tub. Arch. gen. de meéd., 
1883 


Reissmann: Schädlichk. d. Fleisches tuberkul. Thiere. Hyg. Rundschau, 1896, ref. 
Chol. f. Bakt., xxi. 

Ruppel: Chemie d. Tuberkelbacillen. Zeitschr. f. phys. Chem., xxvi., 1898. 

Sata: Fettbildung durch verschiedene Bakterien. ast f. allg. Path., 1900. 

Schieck: Exper. Tuberkulose d. Kaninchencornes. Beitr. v. Ziegler, xx., 1896. 

Schmaus u. Albrecht: Die käsige Nekrose tuberkul. Gewebes. Virch. Arch., 144 
Bd., Suppl., 1896. 

Schüppel: Untersuchungen über die Lymphdrüsentuberkulose, Tübingen, 1871. 

Sibeley: The Nature of the Giant-cells of Tubercle. Journ. of Anatomy, xxiv., 1890. 

Straus: La tuberculose et son bacille, Paris, 1895; Tuberculose par ingestion. Ann. 
de med. exp., viii., 1896. 

Straus et Gamaleia: Contrib. a l’Et. du poison tuberculeux. Arch. de med. exp., iii., 
1891. 

Stroebe: Die Wirkung des neuen Tuberkulins T. R., Jena, 1898. 

Stschastny: Formation des cellules geantes, etc. Ann. de l’Inst. Pasteur, 1888; 
Virch. Arch., 115 Bd. 

Tappeiner: Inhalationstuberkulose. Virch. Arch., 74, 82 Bd. 

Tripier: Ueber den Bau der Miliartuberkel. Cbl. f. allg. Path., i., 1890. 

Veraguth: Exp. Unters. üb. Inhalationstuberkulose. Arch. f. exp. Path., xvii., 1888. 

Verneuil: Etudes sur la tuberculose, i.-iii., 1887-91. Rev. de la tub., i.-v., 1898-9. 

Villemin: Gaz. hebdom., 1865, No. 50. Compt. rend., Ixi., 1866; Etudes sur la tuber- 
culose, Paris, 1886; Etudes expér. sur la tuberculose, Paris, 1887-89. 

Virchow: Die krankh. Geschwülste, iii., 1865. 

Vissmann: Wirkung todter Tuberkelbacillen. Virch. Arch., 129 Bd., 1892. 

Wagner: Das tuberkelähnliche Lymphadenom, Leipzig, 1871. 

Waldenburg: Die Tuberkulose, 1869. 

Walther: Ueber das Vork. v. Tuberkelbacillen im gesunden Genitalapparat bei Lun- 
genschwindsucht. Beitr. v. Ziegler, xvi., 1894. 

Wechsberg: Primäre Wirkung der Tuberkelbacillen. Beitr. v. Ziegler, xxix., 1901. 

Weichselbaum: Bacillen im Blute bei allgemeiner Miliartuberkulose. Deut. med. 
Woch., 1884; Zusammenfass. Bericht üb. d. Aetiologie der Tuberkulose CDl. f. 
Bact., iii., 1888. 

Welcker: Phagocytire Rolle d. Riesenzellen. Beitr. v. Ziegler, xviii., 1895. 

Wesener: Beitr. z. Lehre v. dd. Fütterungstuberkulose. Freiburg, 1884. 

Yabe: Etude de l’immunite de la tuberculose, Paris, 1900. 

Yersin: Etude sur le développement du tubercule exper. Ann. de l’Inst. Pasteur. ii., 
1888. 

Ziegler: Ueber die Herkunft der Tuberkelelemente, Würzburg, 1875; Ueber patholog. 
Bindegewebs- u. Gefässneubildung, Würzburg, 1876; Tuberkulose. Eulenburg’s 
Realencyklop., xxiv., 1900 (Lit.). 


$ 167. Tuberculosis is at the beginning a local disease, which occurs 
most frequently in the lungs, intestinal tract, and skin; that is, in places 
accessible from without. Cases of cryptogenic infection are by no means 
rare; in these the first demonstrable disease-changes appear in tissues 
concealed in the deeper portions of the body-parenchyma—as, for exam- 
ple, in the lymph-glands, adrenals, bones, joints, brain, tubes—and it is 
to be assumed that under certain conditions the bacilli enter the body 
withont causing lasting changes at the point of entrance, so that they 
develop first in some distant organ to which they are carried by the blood 
or lymph, and through multiplication give rise to tissue-proliferation and 
to emigration of white blood-cells. 

The local disease usually begins with the formation of miliary tu- 
bercles—that is, cellular nodules of the kind deseribed above— which 
arise in the tissue either singly or (in case of multiple infection) in great 
numbers simultaneously, or one after another (secondary dissemination 
of the multiplying bacteria). The tissue in the neighborhood of the 
individual tubercles, as well as that between the tubereles, shows some 

















TUBERCULOSIS. ; 627 


serous or serofibrinous, or pure fibrinous, or fibrinopurulent exudates 
may collect in large quantities in the tissues (in the pulmonary alveoli, 
on the pleura, and in the subarachnoideal space, ete.). A high (septic) 
fever, rapid destruction of tissues with a tendency to suppuration, and 
an unusually severe intlammation, in part of a hemorrhagic character, 
point to a secondary infection. Nevertheless, it is often impossible to 
determine, without a special investigation directed to this point, whether 
a pure tuberculosis or a mixed infection is present. 

For the treatment of tuberculosis with bacterial extracts and curative 
serum see § 32. 


The question as to how often tubercuiosis is transmitted by the passage of 
bacilii from the mother to the chiid is still an open one. It has, however, been 
shown by Schmorl, Birch-Hirsehfeld, and Landouzy that in cases of miliary tuberculosis 
in pregnant women, tubercle-bacilli are present both in the intervillous spaces and in 
the blood of the chorionic vessels, and that the liver of the fatus may contain bacilli. 
Further, cases of tuberculosis of the placenta also occur (Schmorl, Kockel, Lungiritz), 
which may be regarded as stages on the way of the tubercle-bacillus froin the mother 
to the foetus. 

Cases of tuberculosis occurring at an carly period of life, reported by Demme, 
Baumgarten, Rilliet, Charrin, and others, as well as the statements of Armanni, Lan- 
douzy, and Martin, that the inoculation of portions of the organs of human fectuses 
obtained from tuberculous mothers produced tuberculosis in guinea-pigs, speak in favor 
of a passage of tubercle-bacilli from the mother to the fetus. Still more important are 
the experimental investigations of de Renzi and Gärtner, who succeeded through the in- 
oculation of pregnant guinea-pigs, white mice, and rabbits in producing tuberculosis in 
a part of the young born of these animals. Gdrtneris consequently of the opinion that 
under certain conditions tubercle-bacilli may pass from the mother to the foetus in the 
case of both animalsand man. Finally, Wagfucct and Baumgarten succeeded in effecting 
a transfer of tubercle-bacilli to impregnated hen’s eggs, and discovered that the infec- 
tion did not disturb the development of the chick, but, on the contrary, the bacilli that 
were taken up by the embryo remained in the tissue of the latter without multiplying 
to any extent, later to cause a tuberculosis in the body of the hatched-out chick. Ac- 
cording to the investigations of Friedmann tubercle-bacilli deposited at the same time 
with semen, in the vagina of rabbits, gained entrance into the embryo and could still 
be demonstrated on the sixth day. 

The experiments cited above pot only justify the assumption that bacilli may be 
transferred from the mother through the placenta to the child, but also that they may 
remain in the body of the embryo for a long time without causing specific changes. 
The occurrence of a conceptional tuberculosis through the transmission of bacilli in the 
semen is still a question. It must be noted, however, that the semen and the contents 
of the seminal vesicles often contain tubercle-bacilli, not only in cases of tuberculosis of 
testicle and epididymis, but also in cases in which no tuberculous affection of the sex- 
ual apparatus could be demonstrated. In general, the following principles may be 
summed up: Tuberceulosis ie uanally to be referred lo an ertra-uterine infection ; and the 
children of tuberculous parents suffer so frequently from this disease, because they are 
more exposed to infeclion with tuberele-bacilli than are the children of healthy individuals. 
A special predisposition of the children of tuberculous parents to tuberculosis has not 
been demonstrated. 

In animals a transmission of tuberculosis to the foetus seems occasionally to occur, 
according to the reports of Zippelius, Jessen, Pütz, Grothans, Malvoz, Lydtin, Broutier, 
Adams, and others. Johne was not only able to demonstrate in a fatal calf the pres- 
ence of miliary nodes and larger nodules in the lungs, liver, and various lymph-glands, 
but also to show the presence of characteristic bacilli in the lesions. 

From the side of clinicians and physicians the so-called scrofula has been many 
times regarded as an especial pathological condition of the organism of the child, pre- 
disposing it in an especial degree to tuberculosis. As scrofulous are regarded those 
children who permanently or at least very frequently suffer from inflammations of the 
mucous membranes (nose and its accessory cavities, conjunctiva, middle ear), as well as 
of the skin, also from swelling of the lymph-glands leading occasionally to necrosis and 
suppuration, finally also from chronic inflammations of the bones and joints, and who 
present a flabby, pale, often bloated appearance. In many cases these symptoms are 
due to tuberculosis; in other cases they are caused by an infection with streptococci or 
staphylococci, or are the results of syphilis. Scrofula is not a disease entity, but is only 
an especial sy mptom-complex belonging to different diseases. Whether the affected 


628 THE PATHOGENIC FISSION-FUNGI. 


children possess an eapecial predisposition to all these infections which may be designated 
as scroful ie difficult of proof. ‘The organism of ita is In general easily infected 
by these agents, and the frequent illness of certain children due to these infections may 
be referred to a lack of cleanliness, or to especial conditions of the environment of the 
chil, or to frequent injuries, ete., as well as to an especial predisposition of the child 
itself. . 
Tuberculosis of mammals is observed most frequently in the case of cattle, and 
preseuts in general a course similar to that of the disease in man, though the granula- 
tion-areas develop more frequently into larger tumor-like nodules, particularly so in 
cattle, and the tendency to a generalization of the disease is less. The tuberculosis of 
the serous membranes which is often designated as pearl disease (“ Perlancht ”) begins 
with the formation of small nodules, leading then to a more marked proliferation of the 
connective tissue, giving rise to the formation in the thickened serusa of nodules of the 
size of a pea or bean or even as large as a hen’s egg or man’s fist (Fig. 477). which in 
the beginning are soft and sarcoma-like, but later become firmer and denser and often 
enclose calcified areas of cascation. The form of the proliferation is sometimes villous- 
like and warty, at other times of 
& mulberry- or grape-like form, 
cauliflower-like or even polypoid. 

Next to cattle the dog is most 
frequently affected with tubereu- 
losis, more rarely the horse, goat, 
sheep, cat, and still more rarely 
the dog. 

Of wild animals in captivity, 
the ape, lion, tiger, bear, jackal, 
panther, jaguar, giraffe, and drom 
edary easily ‘acquire tubereu- 
losis. Of the small animals used 
for experiment the guinea-pig is 
the most susceptible. After sub- 
cutaneous inoculations there re- 
sults a progressive tuberculosis 
which kills the animal in from 
about four to eleven weeks. In 
rabbits an inoculation tuberculosis 
may heal. 
mice are 

Tuberculosis. of fi 
occurrence in birds (chickens, 
pigeons, pheasants, and parrots), 
but the bacillus of avian tuber- 
culosis is not identical with that 
of mammalian tuberculosis (Magfuce’, Rirolta, Straus, Gamaleia, Baumgarten, Reger, 
and others); the tuberculosis of parrots alone is in great part caused by the bacillus 
of mammalian tuberculos 

The cultures of tubercle-bacilli from man are dry, warty, or scaly and lustreless; 
those of avian tuberculosis moist, wrinkled, and soft, and moreover grow best at 43° C. 
Dogs are wholly immune to avian tuberculosis, but not to human tuberculosis. The 
intraperitoneal inoculation of mammalian tuberculosis ( Zeray) causes in rabbits numer- 
ous ci 3 foci in the liverand spleen with few giant-cells and scanty bacilli, and in the 
lungs numerous caseous nodules containing numerous bacilli, Inoculations into these 
animals of chicken-tuberculosis, on the other hand, cause a scanty production of non- 
caseating cellular proliferations containing giant-cells and great numbers of bacilli. 
prding to Mapneei, Martin, and Gärtner, the inoculation of human tuberculosis 
into chickens does not produce tuberculosis, but the bacilli remain alive for weeks 
ly of thechieken. Pigcons (.Ivehrir) die after intraperitoneal inoculation, 
are found in the tissues; the liver and lungs may contain living bacilli 
fourteen ys after the inoculation. In guinea-pigs (Straus) the bacilli of human 
tuberculosis cause much more severe changes than do the bacilli of chicken-tubercu- 
losis. Whether man is susceptible to avian tuberculosis is still an open question. 

As pseudotuberculosis may be classed all those affections characterized by the 
formation of cellular and fibrous nodules, and in part also undergoing necrosis, and which 
are similar to tubercles, but which are not caused by Aoch’s bacillus. According to 
the etiology the following forms may be d ished: 

1. Pseudotubereulusis due to dead foreign budies, This may be caused by the experi- 
mental injection of lycopodium-sporcs, vlive-oil, aud mercury into the blood-vessels, 





















«pleut ina case of bovine tubers 
ulosts (= Perisueht ©). 





























































“ TUBERCULOSIS. 629 


the inhalation of irritating material into the lungs, the injection of large quantities of 
milk into the peritoneal cavity, etc. The presence in the tissue of caterpillar hairs, 
pieces of wadding, silk threads, etc., cholesterin tablets from ruptured ovarian cysts, 
and stomach-contents which have gained entrance into the peritoneal cavity, etc., may 
also lead to the formation of fibrocellular nodules. 

2. Pseudotuberculosis caused by monomorphous and polymorphous bacteria. Eppinger, 
Bucholz, and Flerner have described forms of Cladothriz and Streptothriz obtained from 
apparently tuberculous lungs and bronchial glands which they are inclined to regard 
as the cause of the disease. Courmont found in an apparently tuberculous elbow-joint 
a bacillus which was not identical with Avck’s bacillus. An affection of the peritoneum 
resembling tuberculosis may be produced in guinea-pigs by the injection of the butter- 
bacillus of Rabtnowttech (which probably comes from cow-dung) as well as by the grass- 
bacillus of Moéller; and in white mice by the inoculation of the butter-bacillusof Korn. 

In the rodents a disease resembling tuberculosis is not infrequently produced by & 
plump. thick bacillus with rounded ends (Pfeiffer, Preisz, Zagari, Nocard, Bonome, Del- 
banco, and others). Other forms of bacillary pseudotuberculosis have been observed in 
rabbits (A4erth), in birds (Muir), in the cow (Courmont), etc. 

3. Pxeudotuberculosia due to hyphomycetes occurs in the lungs and may be produced 
artificially by the injection of different forms of aspergillus and mucor; but the affec- 
tions so produced show peculiarities which make possible a differentiation from true 
tuberculosis. 

4. Preudotuberculosis caused by animal parasites occurs particularly in the sheep, 
hog, goat, cat, hare, roe, stag, and chamois, and is caused by different forms of Stron- 
gylus and by Pseudalius capillaris (Miller); it is therefore a vermian pseudotuberculosis. 


Literature. 
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d’Arrigo: Uebertragung der Tuberk. durch die Placenta. Cbl. f. Bakt., xxvii., 1900. 

Barié: Rech. zur la tuberculose sénile. Rev. de méd., 1895. 

Baumgarten: Samml. klin. Vorträge v. Volkmann, No. 218. Berliner klin. Woch., 
1883; Experimentelle congen. Tuberkulose. Arb. a. d. path. Inst. zu Tübingen, 
i., 1892, 

Benda: Acute Miliartuberkulose. Berl. klin. Woch., 1899. 

Brehmer: Die Aetiologie der chron. Lungenschwindsucht, Berlin, 1885. 

Bugge: Augeborene Tuberkulose. Beitr. v. Ziegler, xix., 1896. 

Buhl: Lungenentzündung, Tuberkulose u. Schwindsucht, München, 1872. 

Cobnheim: Die Tuberkulose vom Standpunkt der Infectionskrankheiten, 1880. 

Cornil et Leloir: Lupus. Arch. de phys., iii., 1884. 

Demme: Bacillen in lupösen Herden. Berl. klin. Woch., 1893: Ueber tuberkulöse 
Ekzeme, xx., xxi. Jahresber. d. Jennerschen Kinderspitals, Bern, 1883, 1884. 

Dennig: Tuberkulose im Kindesalter, Leipzig, 1896. 

Doutrelepont: Lupus u. Miliartuberkulose. Deut. med. Woch., 1885. 

Dürck: Tuberkulose. Ergebn. d. allg. Path., ii., Wiesbaden, 1897 (Lit.). 

v. Düring: Lupus. Eulenburg's Realencyklop., 1897. 

Fraenkel u. Troje: Pneumonische Form d. Lungentuberkulose. Zeitschr. f. klin. 
Med., xxiv., 1898. 

Friedländer: Loc. Tub. Klin. Vortr. v. Volkmann, No. 64; Lupus. Virch. Arch., 
60 Bd., 1874. 

Friedmann: Gaumentonsille als Eingangspforte. Beitr. v. Ziegler, xxviii., 1900; 
Studien über die Erblichkeit der Tuberkulose. Deut. med. Woch., 1901. 

Garré: Actiologie der kalten Abscesse. Deut. med. Woch., 1886. 

Gärtner: Ueber die Erblichkeit der Tuberkulose. Zeitschr. f. Hyg., xiii., 1893. 

Gatti: Sul proc. di regress. della peritonite tub. per la laparotomia. Arch. per le Se. 
Med., xxi., 1897 (Lit.). 

Hahn: Tuberculose congen. et héréd. Rev. de la tub., 1895. 

Hauser: Die Vererbung der Tuberkulose. Deut. Arch. f. Klin. Med., 61 Bd., 1898. 

Henke: Intra-uterine Infection. Arb. her. v. Baumgarten, ii., 1897. 

Hering: Studien über Tuberkulose, Berlin, 1873. 

Jakowski: Mischinfectionen d. Phthisiker. Cbl. f. Bakt., xiv., 1893. 

Jäckh: Bucillengehalt d. Geschlechtsdrüsen Tuberkulöser. Virch. Arch., 142 Bd., 
1895. 

Jobne: Geschichte d. Tuberkulose, Leipzig. 1888; Congen. Tub. Fortschr. d. Med., 
iii., 1885. 

Jousset: Transmission de la tuberculose. Et. sur la tub. publ. par Verneuil, iii., 1892. 


630 THE PATHOGENIC FISSION-FUNGI. 


Kockel u. Lungwitz: Placentartuberkulose beim Rind. Beitr. v. Ziegier, xvi , 1x9. 

v. Koranyi: Lungenschwindsucht. Eulenburg’s Itealenceyklop.. 1897. 

Kossel: Tuberkulose im frühen Kindesalter. itschr. f. IIyg.. xxi., 1895. 

König: Die Tuberkulose der Knochen und Gelenke, Berlin. 1884. 

Küttner: Lupus d. Finger u. Zehen. Beitr. v. Bruns, xviii., 1897 (Lit.). 

Landouzy: Heredite tuberculeuse. Rev. de med., xi., 1891. 

Langerhans: Zur Actiologie der Phthise. Virch. Arch., 97 Bd., 1884. 

Lartigau: Chronic Hyperplastie Tuberculosis of the Intestine. Studies from Dept 
of Patlı. of Columbia University, 1901-2. 

Maffucci: Sulla infezione tubercolare degli embrioni di pollo. Ref. Cbl. f. Bakt.. v.. 
1889. 

Malvoz et Brouvier: Deux cas de tuberculose congen. Ann. de l'Inst. Pasteur, iii.. 
1888. 

Meyer: Ausscheidungstuberkulose d. Nieren. Virch. Arch., 141 Bd., 1895. 

Mögling: Ueberchir. Tuberkulos. Mittheil. a. d. chir. Klinik v. Bruns, i.. Tfibingen, 
1884 


Ortner: Die Lungentuberkulose als Mischinfection, Leipzig, 1893. 

Pasquale: Die Streptokokken bei der Tuberkelinfection. Cbl. f. Bakt.. xvi.. 189. 

Petruschky: Tuberkulose u. Septikämie. Deut. med. Woch., 1893. 

Predöhl: Die Geschichte der Tuberkulose, Hamburg, 1888. 

Ribbert: Ucber die Ausbreitung der Tuberkulose in Körper, Marburg, 1900. 

Sanchez-Toledo: Transmission de la tubereul. de la mere au foetus. Arch. de med. 
exp., i., 1889. 

Sata: Die Bedeutung d. Mischinfeetion bei Lungenschwindsucht. Beitr. v. Ziegler 
Suppl., 1899. 

Schlenker: Menschl. Tuberkulose (Statistik). Virch. Arch.. 184 Bd., 1893. 

Schmorl u. Birch-Hirschfeld: Uebergang von Tuberkelbacillen aus dem mütter- 
lichen Blut auf die Frucht. Beitr. v. Ziegler, ix., 1891. 

Schmorl u. Kockel: Tuberkulose der mensch. Placenta. Beitr. v. Ziegler, xvi.. 1894. 

Schottländer: Ucber Eierstockstuberkulose, Jena, 1897. 

Schüppel: Unters. tiber Lymphdrisentuberkulose, Tübingen, 1871. 

- Schürhoff: Pathogenese der allgem. Miliartuberkulose. Cbl. f. alle. Path.. iv., 1883. 

See, G.: La phthise bacillaire, Paris, 1884 

Straus: La tuberculose et son bacille, Paris, 1895. 

Verneuil: Etudes sur la tuberculose, Paris, 1887-93; Rev. de la tub., 1893-99. 

Virchow: Die krankhaften Geschwülste, H., Berlin, 1865. 

Wagner: Das tuberkelähnliche Lymphadenom, Leipzig, 1871. 

Weigert: Die Entstehung d. acuten Miliartuberkulose. Deut. med. Woch., 1897. 

Wild: Entstehung der Miliartuberkulose. Virch. Arch., 149 Bd., 1897. 

Ziegler: Veber Tuberkulose u. Schwindsucht. Samm. klin. Vortr. v. Volkmann, No. 
151, 1878; Tuberkulose. Eulenbure’s Realeneyklop., xxiv., 1900 (Löt.). 
See also S 166. 


(Tuberculosis of Animals.  Pseudotubereulosis. ) 


Apostopulos: Ilistologie d. Pseudotuberkulose. Arb. her. v. Banumyarten, ii., 1896. 

Auclair: La tub. humaine chez le pigeon. Arch. de med. exp., 1897. 

Bang: Eutertuberkulose u. tuberkulése Milch. Deut. Zeitschr. f. Thiermed., xi., 1885. 

Baumgarten: Ucbertragung d. Tuberkulose dureli die Nahrung. Cbl. f. klin. Med., 
1884. 

Bollinger: Identität dd. Perlsucht mit menschl. Tuberkulose. Münch. med. Woch., 
1895. 

Bonome: Sulla pseudotubereulosi mierobien. Arch. per. le Se. Med., xxi.. 1897 (Lit.). 

Chantemesse: [La tuberculose zoogleique. Ann. de VInst. Pasteur, 1887. 

Courmont: Tuberc. bacillaire dorigine bovine, Ft. sur la tub. publ par Verneuil. ii., 
1890. 

Delbanco: Pseudotuberkulose d. Nagethiere. Beitr. v. Ziegler, xx., 1896 (Lit. ). 

Eberth: Pseudotuberkulose d. Kaninehens, Fortschr. d. Med., 1885: Virch. Arch., 
102 Bd., 1885. ; 

Frothingham: Impfversuche an Kälbern. Zeitschr. f. Thiermed.. i., Jena, 1897, 

Gadiot, Gilbert et Roger: Inocul. aux gallinaees de la tuberculose des mammiferes. 
Mem. de la Soc. de biol., 1891. 

Gilbert et Roger: Inocul. de la tuberenlose aviaire au cobaye. Mém. de la Soc. de 
biol., 1891. 

- Grancher «t Ledoux-Lebard: Tuberculose zoogléique, Arch. de med. exp.. 1889, 

1890. 


SYPHILIS. 631 


Jeanmaire. Hist. Veränd. bei d. verminösen Pneumonie d. Katzen u. Hasen. Inaug.- 
Diss., Freiburg, 1900. 

Jensen: Tuberkulose beim Hund und bei der Katze. Deut. Zeitsch. f. Thiermed., xvii., 
1891. 

Johne: Die Geschichte der Tuberkulose, Leipzig, 1893; Hithnertuberkulose. Deut. 
Zeitschr. f. Thiermed., x.; Uebertragung der Tuberkulose v. Mensch auf Hund. 
Ib., xiv., 1889. 

Kastner: Infectiosität des Fleisches perlsüchtiger Thiere. Münch. med. Woch., 1892. 

Kostenitsch ct Wolkow: Tuberculose aviaire chez le lapin. Arch. de med. exp., 
v., 1898. 

Kruse: llühnertuberkulose beim Menschen u. Säugethier. Beitr. v. Ziegler, xii., 1893. 

Leray: Tub. de ’homine et tub. avinire Arch. de med. exp., vii., 1895. 

Maffucci: Aetiologie d. Tub. Cl. f. a. Path., i., 1890; Hülinertuberkulose. Zeitsch. 
f. Hye., xi., 1892. 

Mair: On Pseudotuberculosis. Journ. of Path., v., 1898. 

Malassez et Vignal: Tuberculose zoogleique. Arch. de phys., iv., 1884. 

Müller: Die Nematoden d. Säugethierlungen. Deut. Zeitschr. f. Thiermed., iv., 1889. 

Pfeiffer, A.: Ueber die bacilläre Pseudotuberkulose bei Nagethieren, Leipzig, 1888. 

Pütz: Ueber die Bezieh. d. Tuberkulose des Menschen zur Tub. d. Thiere, Stuttgart, 


1883. 
Ribbert: Verbreitung der Bacillen bei IHühnern. Deut. med. Woch., 1888. 
Straus et Gamaleia: Rech. exp. sur la tuberculose. Arch. de med. exp., , 1891. 


Wehmer: Perlsucht. Eulenburg’s Realencyklop., xviii., 1888 (Lit. ). 

Zagari: Tuberculosis zoogloeica oder Psetidotuberkulose. Fortschr. d. Med. , Vii., 
1890. 

Ziegler: Tuberkulose. Eulenburg’ s Realencyklop., xxiv., 1900 (Lit.). 
See also § 166. 


x 168. Syphilis is, like tuberculosis, an infectious disease, which, 
proceeding from a local infection, spreads throughout the organism by 
means of the blood- and lymph-channels, and leads to the formation of 
localized inflammations and proliferations of granulation tissue, which, 
however, do not present so characteristic astructure as does the tubercle. 

As the cause of syphilis there was described by Lustgarten, in 1884, 
a bacillus which, it is possible, may have pathogenic significance and 
may represent the contagium of syphilis. The only point in favor of this 
assumption is the fact that the bacilli have been demonstrated in all 
stages of the most varied forms of syphilitic foci. The bacilli have not 
yet been cultivated. 

The bacillus is similar to the tubercle bacillus, 3 to 7 long, often 
curved, and somewhat swollen at the ends. According to Lustgarten it 
may be made visible by a complicated staining-process, by which the 
sections are stained in aniline-gentian-violet solution, then decolorized 
in potassium permanganate, and washed in sulphurous acid. Other 
authors have more recently published other methods. 

The bacilli are found in syphilitic foci only in small numbers, and lie 
for the greater part from one to four in a single cell (Lustgarten’, but 
also between the cells, and are at times also present in the blood (Dou- 
trelepont). The Lustgarten bacillus can hardly be used, at the present 
time, as an aid to differential diagnosis, since the smegma-bacillus found 
in the preputial secretion and in the smegma between the labia majora’ 
and the labia minora stains also by the method described by Lustgarten. 
According to Doutrelepont, Klemperer, and Lewy, it is possible to dis- 
tinguish these bacilli from one another by proper staining methods (car- 
bol fuchsin). 

The poison through whose inoculation syphilis is produced occurs 
only within the human organism, where it is alone reproduced; and is 
communicated to other individuals only by direct: or indirect. transfer. 
When implanted in an organism it excites inflammatory processes of 











636 THE PATHOGENIC FISSION-FUNGI. 


opment of the gumma, but also the infiltrated tissue itself, in that the 
latter also undergoes necrosis and becomes caseated. 

The cause of the frequent disintegration and necrosis occurring in 
syphilitic inflammations lies in the peculiar character of the exciting 
cause of the disease. A second factor may also be largely responsible 
for this manner of termination—namely, the extensive participation of 
the blood-vessels, particularly of the arteries, in the inflammation. 
When a syphilitic inflammation leads to the formation of granulation 
tissue or to a connective-tissue hyperplasia, the vessel-walls also become 
thickened, particularly the intima (Fig. 481, e), so that the vessel-lumen 
is narrowed and not infrequently completely closed. Occasionally the 
syphilitic process is localized chietly in 
the vessels. 

Besides the peculiar foci of inflam- 
mation ich point to a localization of 
the exciting cause of syphilis, there not 
infrequently oceur in individuals who 
have suffered a syphilitic infeetion 
specific degenerations of the central nerrous 
system (tabes, progressive paralysis), 
which are associated with proliferations 
of neuroglia. Nevertheless, these atfec- 
tions, though regarded as the sequela of 
ayphilis, present histologically no peculi- 
arities characteristic of syphilis, and 
occur in the same form in other individ- 
uals who have never had a syphilitic 
fection. 

Hereditary syphilis is character feel 
chiefly by peculiar tissue-changes, w! 
differ considerably from the manitesta- 
tions of acquired syphilis, but changes 
also oc vhich correspond to the latter. 
In the skin hereditary syphilis may cause 
macular, papular, and pustular syphil- 
ides which may lead to ulceration. The 
spleen. ally more or less enlarged, 
and in individual cases may attain ten 
times its normal volume. In the liver 
there occur intravascular and perivas- 
cular collections of round cells which 
often collect in small closely packed foc’ ated with these there 
is a periportal new-formation of connective tissue. There is also a 
diffuse hyperpla ive ti roughout the entire liver 
(Fig. 484, a. b), giving to the or consistence and a peculiar 
yellowish-brown color. Further, so a proliferation of connee- 
tive tissue limited to the pe The lungs may present. 
throughout or in part, a dense gray or grayish-white structure resem- 
bling that of ‘coma. tissue, TI appearance is due to the formation 
in the altered area of a cellular connective tissue (Fig. 485, a, 6) which 
contains only imperfectly developed alveoli ce, ¢,) and bronchi (d, d,) 
or none at all. In of slight severity there exists only a thiek- 
ening of the peribronchial and perivascular tissue and interalveolar 
septa, in part associated with an accumulation of desquamated epithe- 





































Papiliary proliferations 
thickenings and papillary proliferati 
the left wall of the larynx and the s 
rior thyruarytenold Iygainent, Natural 




































t 











638 THE PATHOGENIC FISSION-FUNGI. 


tilage, and lead to disturbances in the structure of the subchor 
spongy bone-substance. Through the formation of granulation-t 
proliferations which undergo caseous necrosis, larger defects may 
in the bone substance. 


Syphilis can be transmitted to the fatus by the sperm as well as by the ¢ 
Paternal transınission is more common. After conception a transmission of sy 
from the mother to the fatus may take place. The transmission occurs most fregı 
in the second stage of syphilis. If infection and conception take place at the same 
the disease appears in the child in its most severe form; but even freshly infecte: 
ents may produce healthy children (Neumann). Syphilis transmitted by the n 
during the eatly months of preguaney kills the fetus. In the later months of 
nancy philis is as a rule not transferred to the child (Neumann). 

Teultby women impregnated by syphilitic men may bear syphilitic childrei 
remain fret themselves from syphilis throughout their lives Women who. are 
nant with a syphilitic fertus infected from the father, but who have themselves es 
contact-infection, acquire through such a pregnancy a certain, though very var 
degree of immunity (Hochsinger). The immunity of the mother is the result of the 
sage of immunizing substances to the mother from the fartus infected through the 9] 
and is therefore not un absolute immunity (Hockeinger). 

Hügel and Holzhauaer affirm that syphilis can be transmitted to swine. 














Literature. 
(Syphitie.) 










, Naumburg. 1898. 
Deut. Arch, f. klin. Med., 12 


Heller: Die Lunzenerkrunkung be 
1898 (Lit.). 


Hochsinger; Stilien Aber die hereditäre § i 
Hügel u. Holzhauser: Syphilisimpfun; Arch. 
Hutinel ct Hudelo: ft. sur les I¢sions syphilitiques du foie chez les foetus et les 1 
: 1890 
in her cine ın Mikroorgunismus In den Geweben hered 
Syphlitischer Kinder Wien, med. Bl ba 
Lang: Vorl. üb. Pathol. u, Ther. d. 
Lang u. Ullmann: Syphilis. Ergebi 
U - u. Smegmabaci 























1900 (hit. ). 
Diss., Bonn, 1888. Ref. Cbi 






en Toa, 


Bakt 
Lustgarien: Sr ‘philishac illen. Wien. med. Woch., 1884; Die Syphilisbacillen, Wir 





is- u. Smegmubacillen, Vierteljahrssehr. f. Derm., > 








SNK, 
Matterstock: Syphilishacill Sitz berd. Phys.-med, Ges. zu Würzburg, 18 
Veber Bacillen bei Syphilis. Mitth. a. d. med. Klinik zu Würzburg, i, W 
baden, 1886. 
Mauriac: Lecons sur les maladies 








iennes, Paris. 1890. 


LEPROSY. 639 


Meyer: Syphilis d. Centralnervensystems. Chl, f. allg. Path., ix., 1898 (Lit.). 

Müncheimer: Die extragenitale Syphilis. Arch. f. Derm., 40 Bd., 1607 (Liv). 
Vererbung der Syphilis. Arch. f. Derm., xxiv., 1898. 

itr. zur Syphilisforschung, Wiesbaden, 1900. 

ie Literatur Ober die venerischen Krankheiten, Bonn, 1889-91. 

Rumpf: Die syphilitischen Erkrankungen des Nervensystems, Wiesbaden, 1887. 

Stroebe: Zur Histologie d. congen. Nieren- u. Lungensyphilis. Cbl. f. allg. Path., ii.. 

1891. 

Burico: Ta Sifilide congenita. Giorn. Ital. della Mal., Ven., 1900. 

Virchow: Die krankhaften Geschwülste, 

Zeissl: Syphilis. Eulenburg’s Realencyklop., x 
















, 1900. 


$ 169. The Bacillus leprs (described by Neisser in 1879 and 1881, 
and by Armauer Hansen in 1880) is a small slender bacillus, from 4 to 6 # 
long. It is regarded as the cause of leprosy—also called elephantiasis 
Grecorum. It is found constantly and in great numbers in the diseased 
tissues (Figs. 486, 487, 488). 

The foci of disease in leprosy are in general characterized by a pro- 
liferation (Fig. 486) which consists of cells of different sizes and of a 
fibrous ground tissue. The bacilli lie sometimes between (e), sometimes 
in the cells (c, d), and in the latter appear usually in such great numbers 
that the cells may become greatly swollen (d) and in part become 
changed into mono- and multinuclear giant-cells (Fig. 487). The latter 
occasionally enclose large vacuoles which contain great numbers of bacilli 
as well as the granular, thready detritus of the liquefied protoplasm. 
The nuclei remain preserved for a long time, and are pressed to the pe- 





Mia. 487. 


Fıa. 488. Tissue from & leprous nodule (alcohol, fuchsin, methylene-blue). a, Fibrocellular tissue: 
b, round-cella; c, medium-sized tells: d, very large colis Alled with bacilil: ¢, free Uecill. "> 00. 


Fia. 487,—Glant-cells, with vacuoles containing bacilli, from proliferations of the nasal mucosa 
‘alcotiol, Gabbet's stain). X 400. ne a ™ 


riphery by the vacuoles containing the bacilli. Later they are destroyed, 
so that the entire cell becomes changed into a vacuole containing bacilli 
(Fig. 486, d). The cells in which the bacilli lie are in part the original 
cells of the tissue, and in part newly formed cells. 

The bacilli are surrounded by a slimy envelope (Neisser), and react, 
to stains in much the same manner as do tubercle-bacilli. The same 
staining methods may therefore be used for the former as for the latter. 
The stained bacilli often show clear spots or appear as if made up of 
stained granules. 

According to Bordoni-Uffreduzzi the bacilli may be cultivated upon 
peptone-glycerin-blood-serum, upon gelatinized blood-serum, and upon 
builed eggs. Upon these media they form threads of four times their 
original length, which are often swollen into a club shape at the ends. 
Czaplewski cultivated bacilli, showing a moderate acid-resisting power, 








642 THE PATHOGENIC FISSION-FUNGI. 





tion of the arterial walls causes a proliferating arteritis, by which the 
walls become greatly thickened and the lumina narrowed. In the ner- 
yous system the bacilli are found both in the connective tissue and in the 
nervous elements, particularly in the ganglion cells (Sudakewitsch }. 
The cells occupied by them undergo degeneration in the course of time, 
occasionally with hydropic swelling and the formation of vacuoles. 

The tissue-proliferations caused by the growth of the bacilli may 
almost wholly disappear through the disintegration and absorption of the 
cells after the condition has lasted for years; but there always remain 
indurations rich in cells and pigmentations in the skin. Caseation never 
takes place. 

Leprosy of the skin occurs especially in the face, on the extensor sur- 
face of the knees and elbows, as well as on the back of the hands and 
feet. It begins with the formation of red spots which either vanish, le: 
ing pigmented spots behind, or become elevated into nodules of a brown- 
ish-red color (lepra tuberosa sive tuberculosa sire nodosa). In the region 
of the red spots the tissue contains large numbers of bacilli (Philipson), 
which for the most part lie within the vessels, and already at this stage 
the proliferation of the tissue can be demonstrated. According to the 
investigations of Müller the vesicular eruptions which occur in leprosy, 
and were formerly regarded as the sequel of the leprous disease of the 
nerves, are caused by the presence of the bacilli. 

The nodules may remain unchanged for months, or they may increase 
in size and become confluent, so that very large protuberances may be 
formed, which, because of the distortion of the face thereby occasioned, 
have given occasion for the designation facies leontina (Fig. 489). 

Through external influences ulcers may be produced which show no 
tendency to healing. New nodules appear occasionally following er 
sipelatous reddenings and swellings of the skin. The glands of the sub- 
maxillary and inguinal region swell to form very large nodules. 

Leprosy of the nerves (lepra nervorum sive anesthetica) leads first to 
hypervesthesia and pain, later to anesthesia, more rarely to motor paraly- 
ses in the region of the affected nerves. The further consequences of the 
disease of the nerves are disturbances which express themselves in the 
skin by the formation of white and brown spots (lepra maculosa, morphea 





















FIG. 490, -Lepra amesthetica uleerosa of the leg and foot. (After G, Münch.) 


nigra et alba), and in the bones and muscles by atrophy. Since those 
suffering from the dis « likely to injure themselves after the ap- 
pearance of anesthesia, ulcers are often formed at a later period (Figs. 
490, 491) which cause deep erosions and may lead to the loss of entire 
phalanges (lepra mutilans. 

























644 THE PATHOGENIC FISSION-FUNGI. 


Bergmann: Die Lepra in Livland, Stuttgart, 1897. 

Blaschko: Die Lepra im Kreise Memel, Berlin, 1897. 

Bonome: Sulla lepra dei polmoni. Arch. per le Sc. Med.. xii., 1888. 

Bordoni-Uffreduzzi: [La coltivazione del bacillo della lepra. Arch. p. 1. Sc. 
xii., 1888, 

Campana: (Impfungen). Arch. ital. de biol., ; Arch. per le Sc. Med., 
1883; Vierteljahrsschr. f. Derm., xiv., 1887, 

Czaplewski: Aus einem Leprafall gezüchtete Bacillen. Cbl. f. Bakt., xxiii., 18 

Damsch: Ucbertragungsversuche v. Lepra auf Thiere. Virch. Arch., 92 Bd., 

Doutrelepont u. Wolters: Viscerale Lepra. Arch. f. Derm., 34 Bd., 1896. 

Ehlers: Actiol. Studien über Lepra, Berlin, 1896. 

Gerlach: Die Beziehungen zwischen Hautflecken u. d. Nervenerkrankung bei 
anwsthetica. Virch. Arch., 125 Bd., 1891. 

Hansen, Armauer: Bacillus lepre. Virch, Arch., 79, 80, 114, 120 Bd., 1880-9 

Joseph: Viscerale lepra.. Arch. f. Derm., 43 Bd., 1898. 

Kühne: Zur pathol. Anat. d. Lepra. Monatsh. 'f. prakt. Derm., Ergänzungst 
1887. 

Leloir: Traité pratique et théorique de la lépre, Paris, 1886. 

Lie: Zur pathol. Anat. der Lepra. Arch. f. Derm., 29 Bd., 1894. 

Melcher u. Orthmann: Experiment. Darm- u. Lymphdrisenlepra der Kanii 
Berl. klin. Woch., 1885. 

Müller: Lepra. Deut. Arch. f. klin. Med., xxxiv., 1884. 

Münch: Lepra u. Vitiligo im Süden Russlands, Kiew, 1884-86. 

Neisser: Bacillus lepr&®. Bresl. ärztl. Zeitschr., 1879, Virch. Arch., 84, 108 B 
Ziemssen’s Handb. d. spec. Path., xiv.; Structur d. Lepra-bacillen u.-Zellen. 
f. a. Path., i., 1890. 

Philippson: lHistologie d. hyperäm. Flecke d. L. tuberosa. Virch. Arch., 13% 
Symbiose d. Tuberkelbacillen mit Leprabacillen. Ib., 182 Bd., 1898. 

Prus: Verhalten d. Morvan’schen Krankh. zur Lepra. Ärch. f. Psych., 27 Bd., 

Ramon y Cajal: Sobre las celulas gigantes de la lepra. Caceta Sanit. de Barc 

1890. 

Ricki: Zur pathol. Anatomie d. Lepra. Virch. Arch., 129 Bd., 1892. 

Scheube: Die Krankheiten der warmen Linder, Jena, 1900. 

Sokolowsky: Zur pathol. Anat. d. Lepra. Virch. Arch., 159 Bd., 1900. 

Sticker: Lepra. Münch. med. Woch., 1897; Arb. a. d. K. Gesundheitsamte, 
1899. 

Sudakewitsch: Zur pathol. Anatomie d. Lepra. Beitr. v. Ziegler, ii., 1887. 

Teich: Kultur d. Leprabacillus. Cbl. f. Bakt., xxv., 1899. 

Thoma: Anatomisches üb. Lepra. Virch. Arch., 75 Bd., 1871; Deut. Arch. f. 
Med., 47 Bd., 1891. 

Touton: Toporraphie d. Leprabactllen in d. Maut. WVirch. Arch., 104 Bd.. 1886 

Uhlenhut u. Westphal: Histol. d. Lepra tuberoso-anwsthetica. Cbl. f. Bakt., x 
1901. 

Unna: Leprastudicn. Monatsh. f. prakt. Derm., Ergänzungsh., 1885; Dermat. 
dien, i., Hamburg, 1886. Deut. med. Woch., 1886; Virch. Arch., 103 Bd., 18 

Virchow: Die krankh. Geschwülste, ii.; Lepra d. Milz. Berl. klin. Woch., 1885 

Vossius: Tebertragburkeit d. Lepra auf Kaninchen. Ber. d. Ophthal. Ges. in He 
berg, xvi., 1894. Zeitschr. f. vergl. Augenheilk., vi., 1889; Beitr. v. Ziegler, 
1890. 

Wesener: Zur Ucbertragbarkeit d. Lepra. Beitr. v. Ziegler, vii., 1890. 

Wolters: Der Bacillus lepre (zusammenfassender Bericht). Cbl. f. Bakt., xiii., 
See also the Mittheil. u. Verhandl. d. Le praconferenz, Berlin, 1897; and the Zeit: 

“Lepra.” edited by von Ehlers, appearing since 1900, in Leipzig. 


$ 170. The Bacillus mallei is a bacillus discovered by Löffler, Sch 
and. Israel in glanders foci; and later coutirmed and studied by Weich 
baum, Kitt, and others. It is to be regarded as the cause of glanc 
(malleus, maliasmus) and of farcy (skin glanders, malleus farciminosus 
contagious disease of horses, which occurs in man chiefly through tr 
mission from horses. 

The glanders bacilli are very small, slender rods, which oecur in 
diseased foci, sometimes scattered, sometimes lying together in sı 
clumps. Alkaline metbylene-blue or gentian-violet are employed e 
cially for their staining. 








646 THE PATHOGENIC FISSION-FUNGI. 


In chronic farcy of the skin larger nodules are developed which j 
gether in rows, forming worm-like cords. 

The nodules of the mucous membrane break down easily. TI 
of which they are composed bear precisely the character of pus-¢ 
cles. Through the disintegration, softening, and suppuration 
nodules ulcers with yellowish infiltrated bases are formed. Thi 
large through a progressive, nodular or more diffuse infiltrati« 
subsequent disintegration of the edges of the ulcer, as well as throu 
confluence of neighboring ulcers. Horses dying of glanders often | 
in the mucosa of the nasal septum very extensive irregularly s 
sinuate ulcers, with eroded edges and floors covered with gray a 
lowish material. In addition to these there are numerous small, I 
lar ulcerations and gray or yellowish nodular foci which are on thi 
of breaking down. The whole process is closely related to purul 
flammation. The healing of the ulcer is characterized by the for 
of radiating scars. 

The cervical lymph-glands are constantly swollen and inflame: 
the internal organs the lungs especially are involved. They ¢ 
either nodules having a caseated and disintegrated centre and ag 
eellular periphery, or foci of lobular pneumonia, which present e' 
clear gray or a more hemorrhagic appearance, or through fatt 
cheesy metamorphosis become opaque and yellowish-white. Occasi 
the mucosa of the alimentary tract contains nodules of varying s 
part clear gray and consisting of cellular tissue, in part opaque y 
ish-white, undergoing caseation or approaching suppuration. 
spleen, liver, kidneys, and bone-marrow may also contain nodules. 

In farcy, which runs a more chronic course than glanders, the 
formed in the skin and muscles nodules consisting of a small-celled 
which later undergoes retrogressive metamorphoses, caseates and 
tegrates. 

In man an infection with glanders takes place usually th 
small] wounds of the skin, but may also occur primarily in the m 
membranes adjacent to the skin. In the skin and subcutaneous tie 
gives rise to nodular, pustular exanthemata, carbuncular and phle; 
ous inflammations which may result in suppuration, and to purule 
flammations of the lymph-vessels and lymph-glands. In the mue 
the respiratory tract catarrhs are produced and suppurating nodule 
nodes are formed, leaving ulcers behind. In the internal organs me 
tic small-celled nodules are formed, showing a tendency to suppuri 
also extensive abscesses and purulent infiltrations, especially in the 
cles. In chronic farey which may last for years, large nodules are 
sionally formed in the skin and muscles which through disintegı 
give to ulcers which heal with difficulty. For the diagnosis o 
condition the bacteriological examination and inoculation experimen. 
necessary. 

















According to the investigations of Aalning, Preusse, and others, an active 5 
mallein, may be extracted from cultures of glanders bacilli which, when injec 
small doses into horses sick of glanders, causes a febrile rise of temperature, an 
be used us a diagnostic aid. 


GLANDERS. RHINOSCLEROMA. 647 


Literature. 
(Glanders and the nes» 
Babes: Observations sur la morve. Arch. de med. exp.. iii.. 1891. Ann. de l’Inst. de 


path. de Boucarest, ii., 1893, vi., 1898. 

v. Baracz. Chron. Rotz beim Menschen. Virch. Arch., 159 Bd., 1900. 

Bass: Die Rotzkrankheit der Pferde. Deut. Zeitschr. f. Thiermed., xix., 1893 (Lit.) 

Baumgarten: Zur Frage der Sporenbildung bei Rotzbacillen. Cbl. f. Bakt., iii., 1888. 

Bollinger: v. Ziemssen's Handb. d. spec. Path., 3 Bd. 

Bordoni-Uffreduzzi: Ucber die Kultur der Rotzbacillen. Zeitschr. f. Hyg., iii , 1888. 

Buschke: Chron. Rotz d. Haut d. Menschen Arch. f. Derm., 36 Bd., 18 606. 

Cadéac ct Malet Et. expér. de la transmission de la morve. Rev. de méd., vii., 1887. 

Coleman and Ewing: Septicemic Glanders in the Human Subject. Jour. of Med. 
Res., 1903. 

Duval: Morve humaine. Arch. de med exp., 1896. 

Eber: Ueber Rotzlymphe (Malletn). Cbl. f. Bakt., xi., 1892. 

Ehrich: Rotz beim Menschen. Beitr. v. Bruns, xvii., 1896. 

Finger: Zur Frage der immunität u. der Phagocytose beim Rotz. Beitr. v. Ziegler, 
vi.. 1889 

Foth: Das Mallein. Fortschr. d. Med., xiii., 1895. 

Frothingham The Diagnosis of Glanders by the Straus Method. Jour. of Med. Res., 
1901. 

Galli-Valerio. La morphologie du B. mallei. Cbl. f. Bakt., xxviii., 1900. 

Glaser: Ueber die Rotzkrankheit beim Menschen, I.-D., Breslau, 1876. 

Hartge: Ein Fall von Malleus humidus beim Menschen. St. Petersb. med. Woch., 
1890. 

Jakowski: Chron. Rotz beim Menschen. Zeitschr. f. klin. Med., xvii., 1891. 

Johne: Mallein-Rotzimpfungen bie Pferden. Deut. Zeitschr. f. Thiermed , xix., 1898. 

v. Kahlden. Rotz. Eulenburgs Realencyklop.. xx., 1889 (Lit.). 

Kernig: Fin Fall v. chronischem Rotz beim Pferde. Zeitschr. f. klin. Med . xiii., 1887. 

Kitt: Tmpfrotz bei Waldmaüsen. Chi. f. Bakt., ii.. 1887. 

Kranzfeld: Zur Kenntniss des Rotzbacillus. Cbl. f. Bakt., ii., 1887. 

Küttner: Rotz beim Menschen. Virch. Arch., 39 Bd., 1867. 

Leclainche et Montané: Anat. Path. de la morve pulmonaire. Arch. de V’Inst. P., 
vii., 1893. , 

Löfller: Die Aetivlogie der Rotzkrankheit. "Arb. a. d. Kais. Gesundheitsamte, i., 1886. 

Marx: Morphologie d. Rotzbacillus. Cbl. f. Bakt., xxv., 1899. 

Mayer: Rotzbacillus u. Rotzknötchen. Cbl. f. Bakt., Xx vil, 1900. 

Pflug: Zur pathol. Zootomie d. Lungenrotzes, Leipzig. 1877. 

Rémy: Morve chronique de l’'homme. Arch. de med. exp., ix., 1897. 

Straus. Essais de vaccination contre la morve. Arch. de méd. ex p., i., 1889. 

Tedeschi: Rotzmeningitis. Virch. Arch., 130 Bd., 1892; Wirkung ‘d Einimpfung d. 
Roztes in die Nervencentra. Beitr. v. "Ziegler, xiii. 1893. 


$171. As the Bacillus of rhinoscleroma, Frisch, Pellizari, Chiari, 
Cornil, Alvarez, Köbner, Paltauf, von Eiselsberg, Dittrich, and others 
have described a bacillus with rounded ends, which is constantly present 
in the diseased condition known as rhinoscleroma or scleroma respiratorium 
(Bornhaupt, Wolkowitsch), and is therefore regarded asthe cause of the 
same. It stains best with methyl-violet, the sections being left in the 
stain for twenty-four to forty-eight hours. After staining, the sections 
are treated with iodine water, or left in absolute alcohol for one to three 
days. 

The bacilli for the chief part have a hyaline capsule. According to 
Paltauf, von Eiselsberg, Dittrich, Wolkowitsch, and others they may be 
cultivated upon blood-serum, gelatin, agar-agar, and potatoes, and also 
form capsules in the cultures. When grown in bouillon they show on 
the contrary no capsules (Dittrich). Stab-cultures in gelatin resemble 
closely the nail-cultures of the Friedlander pneumonia-bacillus, but are 
of a translucent grayish-white and not dead white. The bacilli stain 








648 THE PATHOGENIC FISSION-FUNGI. 


more easily than the pneumonia bacilli, and also stain by Gram’sm 
Stepanow observed, in inoculations into the eyes of guinea-pigs, pi 
sive inflammations and proliferating granulations containing the 
and hyaline degenerated cells. 

Rhinoscleroma occurs chiefly in eastern Austria and southw 
Russia; isolated cases have been observed also in Silesia, Italy, ] 
Belgium, Sweden, Switzerland, and Central America It is a c¢ 
disease progressing for years, beginning in the nose (Wolkowitsch ) 
rarely in the pharynx, larynx, or palate, and extending thence to 
boring parts—the external nose, lips, lachrymal duct, trachea, et 
the nose the disease is characterized by a thickening of the nas: 
which is sometimes diffuse, sometimes elevated or nodular. The 
nal skin takes on a red or brownish-red color, becomes stiff and fi: 
and covered with scales. In the throat and respiratory tract dense 
tilage- -like infiltrations are sometimes present, at other times a con 
ing cicatricial tissue is formed. The infiltrations may appear i 
form of nodes and nodules or as elevations and flattened are 
thickening, or they may be spread out more diffusely. By the trai 
mation of the infiltration into scar tissue marked deformities < 





1G. 4.— Section of rhineweleromatous tistue, with numerous degenerates and vacuolated cells ¢ 
tng bariit Gamle weit, barmatexstin' Preparation by Stepanow. 340. 
Fic, 4. Cells In condition of hyaline deseneration. and hyaline epberules, trom rhinosclery 
tissne of the yowal cord und of the tion by Stepanor b,c, d, Hyalinedegenerat 
containing sinall hacllit; ¢, upsulated bacllitz f, qi cells ‘with hyaline sphert 
frow hyalane wpherules. @, Lafler's solution ; €, With huematoxylin ; hu wi 
in. 7 4%, 














affected organs may be produced. Deep destruction of the tissu 
absent ; superfieial ulcerations may, however, occur. On section the 
trated tissue appears yellowish, spotted, but not infrequently sho 
gray or grayish- redcolor. ‘The tissue of the affected areas consists p 
of granulation tissue, partly of fibrous connective tissue. If the fo 
extends to the epithelial covering there appear in part proliferation 
part. degenerative processes in the epithelial cells, the latter being ı 
acterized by the formation of vacuoles and by an infiltration of the 
with round cells. According to Stepanow the vacuoles may coi 
bacilli. 

The granulation tissue itself shows in many places no especial ] 
liarities; rather does it present the same conditions present in « 
inflammatory infiltrations and proliferations of connective tissue. 
other places, on the contrary, there may be found a larger or sm 
number of large connective-tissue cells containing one vacuole or 8 
ing a total vacuolar degeneration or a reticulated structure, inthe m 











RHINOSCLEROMA. ACTINOMYCOSIS. 649 


of which bacilli may be demonstrated (Fig. 493), some of the latter pos- 
sessing capsules. It cannot be doubted that the multiplication of the 
bacilli in the cells is the cause of the cell-degeneration. 

Besides the cells showing vacuolar degeneration there also occur cells 
of various shapes which have undergone hyaline change (Fig. 494, a, b, 
c, d, e). These also contain bacilli with and without capsules, and also 
coccus-like forms. Through the loss of their nuclei these cells may 
become converted into non-nucleated homogeneous lumps (d). Finally, 
there also occur cells which enclose hyaline spherules (/, g), and free 
spherules are also found lying in the tissues (kh). In places not yet 
affected by cicatricial retrogression the hyaline formations may be pres- 
ent in large numbers. 


Literature. 
( Rhinoscleroma. ) 


Alvarez. Rech. sur l’anat. pathol. du rhinosclérome. Arch. de phys., vii., 1886. 

Bender: Das Rhinosklerom. Cbl. f. Bakt., i., 1887. 

Chiari: Stenose des Kehlkopfes u. des Larynx bei Rhinosklerom. Wien. med. Jahrb., 
1X82, 

Cornil: Lecons prof. pend. le I. sem. de l’an., 1883-84, Paris, 1885. 

Cornil ct Alvarez: Mem. p. serv. & hist. du rhinosclérome. Arch. de phys., vi., 
PAYS. 

Dittrich: Ueber das Rhinosklerom. Zeitschr. f. Heilk., viii., 1887; Zur Aetiologie 
des Rhinoskleroms. Cbi. f. Bakt., v., 1889; Zeitschr. f. Heilk., viii. 

Frisch: Zur Actiologie des Rhinoskleroms. Wien. med. Woch., 1882. 

Jaffinger: Das Sklerom d. Schleimhaut d. Nase, etc., Wien, 1892. 

v. Marschalk6: Histol. d. Rhinoskleroms. Arch. f. Derm., 53, 54 Bd., 1900. 

Mibelli: Beitr. z. Histologie des Rhinoskleroms. Monatsh. f. prakt. Derm., viii., 1889. 

Mikulicz: Ucber das Rhinosklerom. Langenbeck’s Arch., 20 Bd., 1876. 

Nikiforoff: Ueber das Rhinosklerom. Arch. f. exp. Path., xxiv., 1888. 

Paltauf: Actiologie des Skleroms Wien. med. Woch., 1891, 1892. 

Paltauf ı. v. Eiselsberg: Zur Actiologie des Rhinoskleroms. Fortschr. d. Med., 1886. 

Pawlowsky: Ucb. d. Aetiologie des Rhinoskleroms. Cbl. f. allg. Path., i., p. 601. 

Pellizari: Il Rinoscleroma, Firenze, 1883. 

Rona: Rhinosklerom. Arch. f. Derm., 49 Bd., 1899. 

Stepanow: Ueber die Impfungen des Rhinoskleroms. Cbl. f. Bakt., v., 1889; Zur 
Aetiologie des Skleroms. Monatsschr. f. Ohrenheilk., 1893. 

Wolkowitsch: Das Rhinosklerom. Langenbeck’s Arch., 38 Bd., 1889. 

Zagari: Ricerche ctiol. sul Rinoscleroma. Giorn. internaz. d. Sc. Med., 1889. 


$ 172. The Actinomyces or ray-fungus is a polymorphous fission- 
fungus which appears in different forms of growth in the human and 
animal organisın as wellas in cultures. It is the cause of actinomycosis, 
a disease occurring in man as well as in cattle, swine, and horses, and 
characterized by a progressive inflammation that produces in part granu- 
lation tissue and connective tissue, and in part pus. The botanical posi- 
tion of the fungus is still unsettled. By many it is classed with the 
thread-fungi, others group it with the polymorphous bacteria. Bostrom 
places it in the group cladothrir ; Kruse, in the group streptothriz. 

The masses of fungus formed in the tissues by the organism were long 
ago observed by Langenbeck and Lebert, but their significance was not 
rightly interpreted. The observations of Hahn, supplemented by those 
of Bollinger and Harz, first led to a correct interpretation of the ray- 
fungus occurring in domestic animals. Israel shortly after found a simi- 
lar fungus in man; and Ponfick soon after gave his opinion in favor of 
the identity of actinomyces of cattle with the fungus discovered by Israel 
in man. 








652 THE PATHOGENIC FISSION-FUNGI. 


been found in the pus of actinomycotic foci, and that the swallow 
portions of plants (spike of grain [Bertha]), or the contaminat 
wounds with vegetable material, have in certain cases preceded t 
velopment of actinomycosis. It is, therefore, very probable th 
fungus is present upon the higher plants or upon wood. 

If the ray-fungus succeeds in settling in a tissue it excites an i 
mation in its neighborhood. While the fungus which has pene 
into the tissue develops a mycelium and a fungus-granule (Figs. 4 
497, a, 498, a) there is formed in its neighborhood a nodular fo 
inflammation, which at first consists of small round cells (Figs, 4 
c; 498, b); but later, in addition to pus-corpuscles (Fig. 497, c), als 
tains epithelioid cells and giant-cells (b, d). 

The fungus-granules may increase within the nodule and lead 
enlargement; and it very often happens that cellular nodules the s 
a peaand larger contain a large number of fungus-foci, which are us 
situated in the periphery of the same. At the same time new fu 
foci, and consequently new cellular foci, may appear in the neighbor! 
The further spread of the infection takes place by means of small 
and threads, which are broke 
from the larger masses, and 
be seen in the tissues partly 
and partly enclosed in cells. 

Larger nodules often unc 
in time a purulent liquefactic 
their central portions, leadiı 
the formation of small absc 
which may become confluen 
form larger pus-cavities or sir 
In the neighborhood of the cel 
areas (Fig. 498) there dev 
early an active proliferation of t. 
which leads to the formation o, 
sels (k) and young granulation ti 
which later becomes transfoı 
into connective tissue (ec, g. h) 
the com tissue prolifer: 
attai X considerable pre 
tions, it leads to an induration ( 
498), often also to an enlargement of the tissue. The connective-t 
proliferation may finally extend into the small-celled areas, and rey 
the latter, the fungi probably being destroyed in this way. 

If the connective-tissue proliferation’ becomes predominant t 
arises in the course of weeks and months a nodular formation of t 
(Fig. 499, a) wh attle may attain the of a man’s fist. or 
reach a much & The tumor con: partly of dense cor 
tive tissue, partly of granulation tissue, and partly of intermec 
stages between the two. It always contains small cellular foei or 
cavities due to disintegration, in the purulent. contents of which 
fungus-masses are found in the form of the granules described ab 
When the fungus develops within the jaw-bone there oceurs at 
same time an active new-formation of bone at the periphery ( 
499, a) of the process. 

A predominance of tissue-necre and of suppuration over ti: 
production gives rise to more or less extensive sinuous cavities 


























ACTINOMYCOSIS. 653 


branching fistulous tracts communicating with one another. The walls 
of these consist of granulation-tissue and hyperplastic connective tissue, 
and here and there contain fungus-foci. The masses of fungi may in 
part become calcified. 

In cattle the disease affects chiefly the lower jaw, but may involve 
also the upper jaw (Fig. 499, a), the tongue, throat, larynx, esophagus, 
stomach, intestinal wall, skin, lungs, and subcutaneousand intermuscular . 
tissues. In these regions it leads to the formation of more or less exten- 
sive nodular tumors of the character described above, and was formerly 
given various names, such as osteosarcoma, bone-cancer, bone-tuberculo- 
sis, lumpy jaw, wooden tongue, tuberculosis of the tongue, lymphoma, 
fibroma, worm-nodules, ete. In man the infection, so far as is known, 
takes place through the mouth, fauces, esophagus, stomach, intestine, 
and lung, or through some external injury. In the first-named region an 
infection of actinomyces may take its start from carious teeth (cavities 
or fistule), or from any injury to the soft parts of the jaw or cheek. 
“ Thence it spreads over the neighborhood and may finally involve the face 
and the hairy portions of the head, as well as the throat, neck, back, and 
breast. | 

With the advent of the process there arise swellings which later 
soften and give fluctuation. When the latter is the case, pus is formed 
which is at times thin and watery, at other times more viscid, and con- 
tains the characteristic granules. If these abscesses break externally there 
may be formed fistulous tracts, which may either close again, or continue 
to secrete pus. 

Besides these purulent foci, which sometimes are small, at other times 
extensive, there is constantly formed more or less granulation tissue, 
which at times may be very abundant. As aresult of fatty degeneration 
and disintegration of its elements the granulation tissue often becomes 
partially whitish or yellowish or reddish-white in color, and permeates 
the diseased tissue in an irregular manner. In other places it comes to 
a development of connective tissue, particularly in those places where 
the process is not spreading. 

Through this development of connective tissue a local healing result- 
ing in cicatricial indurations may take place, but in other parts the process 
usually makes further progress and may under certain circumstances lead 
to very extensive destruction. If the disease encroaches upon the bones 
of the spinal column or of the thorax these may be gradually destroyed 
from the surface, and become rough, eroded, and carious. In rare cases 
the jaw-bone may be attacked from within through an alveolar process, 
and so undergo destruction. From the base of the skull the process may 
extend into the interior of the skull and lead to actinomycotic meningitis 
and encephalitis. 

In primary infection of the respiratory apparatus the process takes 
the form of a bronchopneumonia characterized by the formation of nod- 
ular foci (Fig. 498, 6) the central portions of which at an early stage 
assume a yellowish-white color. Through the disintegration of the in- 
flammatory foci cavities may be formed which contain fluid, pus-corpus- 
cles, fatty detritus, spherules of fatty granules, disintegrated red cells, 
and masses of actinomyces. The tissue lying between the mycotic foci 
suffers a more or less extensive, often very marked, inflammatory thicken- 
ing and induration (Fig. 498, c), and throngh a new-formation of con- 
nective tissue may be transformed into a callous, slate-gray or gray and 
white mass, devoid of air, and later undergoing cicatricial contraction. 











654 THE PATHOGENIC FISSION-FUNGI. 


In this manner a large portion of the lung may become converted 
mass of connective tissue. 

From the lung the process sooner or later extends to the vi 
pleura, and from this to the costal pleura or to the pericardium, ; 
rise in these places to inflammatory exudations and proliferations 
sue, which may lead to adhesions between the opposite layers « 
pleura or pericardium. From the costal pleura the cellular intilt 
as well as the pus formation and the fatty degeneration and disin 
tion of the granulation tissue may extend between the ribs to th: 
side, and d in the contiguous soft parts, in the connective 
and museles, and may finally break through in places Fro: 
lungs a rupture may sometimes take place into the mediastinu 
pericardial sac, and finally into the heart. Under certain conditi 
rupture may occur through the diaphragm into the abdominal cavi 
the process may extend from the posterior mediastinum into the 
peritoneal connective tissue, 

The secondary areas of destruction lying outside of the lung 
reach an extremely large size, while in the lung the primary p: 
advances but little and undergoes eicatrization. At one time the 
lent softening predominates, at another time the formation of granu 
tissue and the induration. 

Primary actinomycosis of the intestinal tract begins with the fı 
tion of plaque-shaped whitish patches of the fungus (Chiari) or of 
lar mucosal and submucosal foci (Zemann), which contain the sp 
fungus, and lead to ulceration through the occurrence of disin 
From the intestine the process spreads over the peritoneum and the 1 
peritoneal connective tissue, as well as to the organs adjacent to thr 
mary focus—for example, the liver; and may finally break throug 
abdominal wall. At the places where the fungi develops the pro 
ating foci of inflammation described above are produced. If 
masses gain access to the tissues in case of intestinal rupture, gangre 
abscesses will . 

Metastasis may be associated with the local progression of the dis 
but is rather rare. It usually results from a direct rupture intua b 

The metastas rising from a pr focus in the intestin 
found especially in the liver; those arising from a primary foeus i: 
lungs are found in the skin, nv les, bones, brain, intestine, and kidı 
The metastatic nodules behave like the primary foci, In rare cases i 
oceur also primary foei of is in the internal organs—fo; 
ample, in the brain The portal of entrance in these cases 
not be demonstrable. 

Johne, Pontick, Bostrom, Wolff, and Isra@l have attempted ino 
tion experiments upon animals, and according to their reports 
obtained positive results in part (Johne, Ponfick, Wolff, and Isr 
Wolff and Israél, by the inoculation of rabbits and guinea-pigs, obta 
in almost all ca characteristic disease with the formation of int 
matory foci containing the fungus-masses. They were also able to a 
cultivate upon agar-agar the fungus contained within these foci. 




























































Lery, as wellas Arvac, assumes that there are two forms of actinomyces, an al 
cultivated by Bostrom, and an atrobie cultivated by Wolf, Israel, Aschoff, hi 
the two forms I related empt by Zery to change one form In! 
other was not although the atrobic form could be mada in mm ı 
anatrobie condi He regards the wefinomyees as well a8 the 

known as sfreptotlirir as belonging toa group, the 


















ACTINOMYCOSIS. 655 


formation of branching, probably unicellular mycelia and which multiplies through an 
acrogenic snaring-off of conidia-chains or through fragments of threads resembling ba- 
cilli. Since the ray-fungi do not correspond to any one of the known hyphomycetes- 
groups, he places them in a separate group, the Actinomycetes. In this group he also 
places the tubercle-bacillus, the lepra-bacillus, the diphtheria-bacillus, and the bacillus 
of glanders. Lubarsch regards the streptothrices, with which he classes the ray-fungi 
(to Which the tubercle-bacillus also belongs), as a transition form between the bacilli and 
the moulds. 

Berestnew also distinguishes different forms of actinomyces (cultivated by him from 
straw, hay, etc.), and, in addition to actinomycosis, recognizes a condition of pseudo- 
actinomycosis, Which runs a similar course to that of the former, but is caused by fungi 
which do not belong to the ray-fungi. Aruse likewise regards the etiological factor of 
an actinomycosis as being of varied nature and not representing a definite entity. 
Scharmayer emphasizes the variability of actinomyces according to the conditions of 
vrowth. 

Grozzolino found in the pus of a skin affection resembling actinomycosis granules 
and bacilli, from which a spore-producing bacillus (Bacillus filamentosus) was cultivated, 
which produced no branching threads. 

Recently Eppinger (“ Ueber eine neue pathogene Cladothrix und eine durch sie her- 
vorgerufene Pseudotuberculosis,” Bett. z. path. Anat. v. Ziegler, ix., 1891) found, in the 
pus of an old brain-abscess causing death through meningitis, a polymorphous fission- 
fungus, which he designated as Cladothrix asteroides. Its characteristics were deter- 
mined by cultivation and by inoculation into animals. Since the changes occurring in 
the lungs and bronchial glands of the affected individuals resembled those of tuberculo- 
sis, and as a disease suggesting tuberculosis resulted from the inoculation of this fungus 
into guinéa-pigs and rabbits, the disease caused by the fungus may be designated pseu- 
dotuberculosa cladotrichica. 

Buchholtz (“ Ueber menschenpathogene Streptothrix,” Zetts. f. Htyg., xxiv., 1897) 
found in a pneumonic lung containing a large disintegration cavity with ragged walls, 
that the diseased lung-tissue was infiltrated with fine, branching, and many times broken 
threads, which stained with Gram’s method. He regarded the fungus, which he was 
not able to cultivate, as a pathogenic streptothrix. 

According to Dunker (Zeitschr. f. Mikroskopie und Fleischschau, iii., 1884) and Hert. 
iq (Arch. f. wissensch. u. prakt. Thierheilk., xii., 1886) there occurs in hogs a ray-fungus 
which is always situated in the muscles, particularly in the diaphragm, abdominal and 
intercostal muscles, and causes a degeneration of the muscle fibres in its neighborhood 
and proliferation of the intermuscular connective tissue. The fungus-masses form 
radially arranged clubs. They readily undergo calcification and then form white 
points in the flesh. 

According to investigations by Kanthack (“Madura Disease and Actinomyces,” 
Jour. of Path., 1892), Boyce (“Upon the Existence of More than One Fungus in Ma- 
dura Disease,” Trans. Phil. Soc., vol. clxxxv., 1894; Jlyg. Rundschau, 1894), and Vin- 
rent (“ Et. sur le parasite de pied de madura,” Ann. de U’ Inst. Pasteur, 1894), it is very 
probable that the disease occurring in India, known as madura-foot or mycetoma, is 
due to a polymorphous fission-fungus closely related to actinomyces, and called by 
Vincent the Streptothriz madure. The disease consists in a gradual swelling of one ex- 
tremity due to the formation of nodular deposits, which through softening become 
changed into abscesses and fistulous tracts, that upon pressure discharge pecu- 
liar brown or black, fish-roe, or truffle-like granules. Kanthack regards the fungus 
which is contained in ihe granules as identical with actinomyces; but the investiga- 
tions of Vincent and Boyce do not support this view. According to Boyce the strepto- 
thrix madurr occurs in two varieties, one white with fine dichotomously branching 
threads, the other black with branching pigmented threads. Unna and Delbanco 
(“ Anatomie des indischen Madurafusses,” Monh. f. prakt. Derm., 1900) also distinguish 
different forms of ray-fungi. The parasite of the madura disease has been known since 
1874 (Carter, * Mycetoma or the Fungous Disease of India,” London, 1874; Lewis and 
Cunningham, “The Fungous Disease of India,” Calcutta, 1875; Hirsch, Virchow’s und 
Hirsch’s Jahresber., 1875, 1876), and was formerly known as Ohionyphe Carters. 


Literature. 
( Actinomycosis.) 


Drei Fälle von Aktinomykose. Beitr. v. Ziegler, xxii., 1897. 
mat. Stellung d. Aktinomyces. Cbl. f. Bakt., xxiii., 1898. 
ver Paeudoaktinomykose. Zeitschr. f. Hyg.. xxix., 1899. 
merkenswerthe Falle von Aktinomykose. Wien. med. Woch., 1888. 








656 THE PATHOGENIC FISSION-FUNGE. 





Bollinger: Eine neue Pilzkrankheitbeim Rinde. Cl. f. d. med. Wiss, 187 
Zeitschr. f. Thiermed., iti., 1877; Münch. med. Woch., 1887. 

Boström: Unters. über die Aktinomykose des Menschen. Beitr. v. Ziegler, i 

Chiari: Darmaktinomykose. Prag. med. Woch., 1864. 

Firket: L’actinomycose. Revue de méd., 1884. 

Gozzolino; Ein neues Fadenbacterlum, Zeitschr, . Hyg., xxxiti., 1900. 

Grill: Aktinomykose d. Magens u. d. Darms, Beitr. v. Bruns, xiil., 1885. 

Hesse: Ueber Aktinomykose. Deut. Zeitschr. f. Chir., 34 Bd., 1892. 

Hoche: Ilistogendse du nodule actinomycosique. Arch. de méd. exp., 1899. 

Howard: Actinomycosigof Central Nervous System (Lit). Jour. of. Med. Re 

Hummel: Entstehung d. Aktinomykose durch Fremdkörper. Bietr. v. Bru 


1895. 

lich: Beitr. z. Klinik d. Aktinomykose, Wien, 1892. 

Johne: Deut. Zeitschr. f. Thiermed., vii., 1881; Cbl. f. d. med. Wias., 1882; 
mykose im Samenstrang kastrirter Pferde. Fortschr. d. Med., ifi., 1885. 

Israöl, J.: Mykose des Menschen. Virch. Arch., 74, 78 Bd., and Cbl. f. 
Wise, 1889; Klin. Beitr. z. Kenntniss d. Aktinomykose des Menschen, 


1885, 
Israäl, O.: Kultivirbarkeit d. Aktinomyces. Virch. Arch., 95 Bd.; Cbl. f. 
Wiss., 1886. 
Krause: Zur Kenntn. d. Aktinomyces. Cbl. f. Bakt., xxvi., 1899. 
Kruse: Systematik d. Streptotricheen in Flügge. Die Mikroorganismen, i., 1 
Lebert: Anat. path. Ic, Atlas t. I pl., IL, Fig. 16. 
Levy: Ueber die Aktinomycesgruppen. Cbl. f. Bakt. xxvi., 1899 (Lit.). 
Liebmann: L’Attinomyce dell’ uomo. Arch. per le Sc. Med., xiv., 1890. 
Martin: Actinomycosis of the Brain. Journ. of Path., iii., 1894. 
Moosbrugger: Ucb. die Aktinomykose des Menschen.’ Beitr. v. Bruns, il., To 
1886. 








van Niessen: Aktinomyces-Reinkultur. Virch. Arch., 150 Bd., 1897. 

Partech: Die Aktinomykose des Menschen. Sammi. klin. Vortr., No. 306-7, 1 

Pawlowsky « ct Makeutoff: Phagocytose dans l’actinomycose. ‘Ann. de I'in: 
teur. 1893. 

Perroncito: Inoculation d'actinomyces. Arch. ital. de biol., vii., 1886. 

Ponfick: Bresl. ürztl. Zeitschr., 1879, 9 Mai; Berl. klin. Woch., 1879, p. 347; D 
nomykose des Menschen, Berlin, 1882. 

Schlegel: Aktinomykose. Ergebn. d. allg. Path., v., Wiesbaden. 1900. 

Schürmayer: Ucber Aktinomyces. Cbl. f. Bakt., xxvii., 1900. 

Virchow: Trichinosis u. Aktinomykosis bei Schweinen. Virch. Arch., 95 Bd 

Wolff u. Israél, J.: Reinkultur des A. u. Ucbertrag. auf Thiere. Virch. Arc 
Bd., 1891. 

Wright: Madura Foot. Jour. of Exp. Med.. 1898; Actinomycosis. Ref. Hai 
Med. Sc.. 2d ed., 1900. 





$173. In addition to those already described there is a large nu 
of bacilli pathogenic for animals which may also cause infecti: 
man. The most important animal diseases caused by bacilli are syı 
matic anthrax, swine-erysipelas, swine-plague, cattle-plague, and chi: 
cholera. 


The bacillus of blackleg or symptomatic anthrax (Bacteria du charton m 
matique) is a rod with rounded ends about 3-5 « long and 0.5-0.6 u broad, and 
times possessing independent motion. According to the investigations of Bol 
Feser, Arloing, Cornerin, Thomas, and others it is constantly found in blackleg. 

Blackleg occurs particularly in young cattle and in lambs, and is usually 
within two duys. It is characterized anatomically by a tumor-like swelling of th 
due to the exudation of a bloody scrous fluid attended by the formation of 
subeutancous, intermuscular, and muscular connective tissue. The bacilli are for 
the region of the exudation and gas-formation, as well as in the spleen and liver. 
do not stain with Gram’s method. 

According to Arloing, Cornerin, and Thomas, the bacilli may be cultivated, i 
absence of oxygen, in chicken-bouillon, to which a small amount of glycerin an 
phate of iron is added. A’fasato and Kitt cultivated them in guinea-pig bouillon, 
and gelatin in the absence of oxygen. They grow best at from 86'-88° C., and 
spores in the middle or at the ends of the rods, whereby the latter become som 
swollen, ‘The addition of sugar and glycerin to the nutrient medium aids the gr 























ANIMAL DISEASES DUE TO BACTERIA. 657 


The inoculation of cattle and sheep with bacilli which are attenuated by heating pro- 
duces an immunity against virulent bacilli. Cattle, sheep, poate, rabbits, guinea-pigs, 
swine, dogs, cats, and chickens are susceptible to the bacilli of symptomatic anthrax; 
black rats are immune; horses and donkeys occupy an intermediate position. 
The inoculation of guinea-pigs with virulent material—for example, with the dried 
juice of the muscle of cattle dying of blackleg—leads very quickly to a rapidly spread- 
g swelling atthe point of inoculation, due to the infiltration of the tissues with a 
bloody cedema. The bacilli spread with remarkable rapidity in the tissues, particularly 
in the subcutaneous and intermuscular tissue, and penetrate also intothe muscles. They 
cause severe lesions of the vessels, leading to hemorrhages and serous exudations, and 
after a time to an abundant emigration of leucocytes. The animals usually die on the 
second or third day after the swelling has spread over a portion of the body. The blood 
usually remains free from bacilli. Spores are not formed in the living body. 


Literature. 


Arloing, Cornevin et Thomas: Le Charbon symptomatique de beuf, Paris, 1887. 

Hess: Der Rauschbrand. Thiermed. Vortr., 1888, No. 4. 

Kitasato: Der Rauschbrandbacillus. Zeitschr. f. Hyg., vi., 1889, viii., 1890. 

Kitt: Der Rauschbrand. Cbl. f. Bakt., i., 1887; Deut. Zeitschr. f. Thiermed., xiii., 
1887. 

Roger: Charbon symptomatique. Rev. de möd., 1891. 

Bogowitsch: Wirkung der Rauschbrandbacillen. Beitr. v. Ziegler, iv., 1889. 


The bacillus of swine-erysipelas (Löffler, Lydtin, Schottelius, and Schütz) is a 
bacillus from 0.6-1.8 # long. It may be cultivated in bouillon, meat-infusion-peptone- 
gelatin, blood-serum, and sour milk. 

In gelatin-plates it forms peculiar radiating and branched figures. In stab-cultures 
it grows out in white streaks from the stab-canal like the bristles of a test-tube brush. 
In cultures the bacilli may form pseudothreads. They sometimes enclose shining spher- 
ules which are regarded as spores. By means of pure cultures the disease may be re- 
produced in susceptible swine. House-mice and pigeons die within two to four days 
after inoculation, and their blood contains numerous bacilli. 

In rabbits, inoculation is followed by an erysipelas-like inflammation which termi- 
nates either in a fatal general infection or in healing. Guinea-pigs and chickens are 
immune. 

According to investigations by Pasteur and Thuillier, and confirmed by Schottelius 
and Schütz, the virulence of the bacilli for swine may be attenuated by progressive in- 
oculations in rabbits. Susceptible swine inoculated with this vaccine do not die after 
inoculation and become immune to fully virulent bacilli. 

Swine-erysipelas occurs particularly in young herds of highly-bred (English) hogs, 
while the common breeds are nearly or wholly immune. The disease is characterized 
by fever and the dppearance of red spots, later becoming brown, upon the neck, chest, 
and belly. Intestinal hemorrhages occasionally occur. More than half of the infected 
animals die, usually within a few hours or within four days. The autopsy shows 
swelling and localized hemorrhages in the mucosa of the intestine, swelling and ulcer- 
ation of the follicles, particularly in the ileocecal region, swelling of the mesenteric 
lymph-glands, and petechis® of the serous membranes. 

The bacilli are found in the blood as well as in the lymph-glands, muscles, spleen, 
and kidneys, where they also lie in the blood-vessels. The majority are free; some are 
enclosed in leucocytes. They are stained by Gram’s method. 


Literature. 


Hess: Der Stäbchenrothlauf u. die Schweineseuche. Thiermed. Vortr., i., 1888. 

Kitt: Der Stäbchenrothlauf der Schweine und dessen Schutzimpfung. Jahresb. d. 
Thierarzneisch., München, 1885-86, Leipzig, 1887; Streptothrixform d. Bacillus. 
Cbl. f. Bakt., xxii., 1897. 

Löffler: Schweinerothlauf. Arb. a. d. K. Ges.-Amte, i., 1885. 

Lorenz: Schutzimpfung gegen Schweinerothlauf. Cbl. f. Bakt., xv., 1894. 

Lydtin und Schottelius: Der Rothlauf der Schweine, Wiesbaden, 1885. 

Schütz: Rothlauf d. Schweine. Arb. a. d. K. Ges.-Amte, i., 1885. 


The bacillus of swine-plague is a small bacillus with rounded ends, 1-1.5 # long, 
staining chiefly at its ends. It resembles the bacillus of chicken-cholera, and may 
cultivated upon various media. It is regarded as the cause of the disease known in 











658 THE PATHOGENIC FISSION-FUNGI. 


Germany as “ Schweineseuche” or Schweinepest, in England as hog-cholera or sine 
America as sirine-plague and hug-cholera, and in Sweden and Denmark as swine. 
but it is not yet detinitely determined whether the swine-diseases of different lan 
the exception of swine-rysipelas) are identical (see Preisz and Karlinski). 

The anatomical changes in swine-plague vary with the localization of the ir 
In the lungs there are found multiple areas of necrotic and hemorrhagic pne 
and pleuritis, Intestinal infection leads to hemorrhagic and diphtheritic ente 
(in chronic cases) to caseous inflammations, which are accompanied by corres 
changes in the mesenteric glands, and occasionally also by peritonitis. The 
besides being found in the infected areas, are present in large numbers in the 
acute cases.” Hogs, guinea-pigs, rabbits, and mice are susceptible to inoct 





Literature. 


Bleisch und Fiedler: Schweineseuche. Zeitschr. f. Hyg., vi., 1889. 

Friedberger und Fröhner: Pathol. der Hausthiere, 18 

chen der americanischen Schweineseuche. Zeitschr. f. H 

Marek: Histologie der Schweineseuche. Zeitschr. f. Thiermed., i.. 1 

Preiz: Schweinepest und Schweineseptikämie. Zeitschr. £, Thiermed.. ii.. Jen 
eruglin; Bakt. d. amerikun. Schweineplague und der deutschen Sch weine 

f. Bakt., 1890. 

Balmon, Billings, Smith: Jahresb. v. Baumgarte 

Schütz: Schweineseuche. Art. a. d. k. Ges.-Amte, 

Selander: Swinpest. Ann. de I'Inst. Pasteur, iv. 

Silberschmidt: Swineplague, Hog-cholera, Pneumoentéritis des porcs. 4 

Tinst, Past., 1895. 
Smith: The Hog-Cholera Group of Bacteria. Cbl f. Bakt., xvi, 1894, p. 281. 





ix., 











The bacillus of chicken-cholera, or arian typhoid, a disease occurring ¢ 
among chickens, is a small bacillus from 1-1.2 long, often somewhat con 
in its middle, It was first studied by Perroneito, then by Toussaint, Pasteur, ı 
Nerehiafara, Celli, and Kitt. The disease is characterized clinically by great « 
tion and stupor, occasionally also by diarrhial intestinal discharges; anatomic 
swellings of the liver and spleen, hamorrhages and inflammations of the intesti. 
also frequently by pleuritis and pericarditis. 
The ba are found in the blood and therefore also in the capillaries of the 
ent tissues. They may be cultivated upon nutrient gelatin, blood-serum. and n 
ized bouillon, as well as upon potatoes, They form white colonies. Feeding or 
lation of the bacilli causes in chickens a typical chicken-cholera; pigeons, spa 
pheasants, rabbits, and mice are also susceptible to the bacilli, In sheep, hors 
guinea-pigs they produce abscesses at the point of inoculation. 



























Literature. 





Actiologie der Hühnercholera. Chi. f. Bakt. 

fdgelcholera. Cbl. f. Bakt..i., 1887; Deut. Zeit 

: Compt. rend., xe.. 1880. 

Wertheim: Cholera gallinarum. a. f. exp. Path., 26 Bd.. 1 
ürn: Die Krankheiten des Hausgetlügels. Weimar, 1882 


. 1888. 
hr. f. Thiermed.. sii 





According to the view of Voges (“ Krit, Studien u. caper Untersuch. über die 
da hämorelug 5 Septikimie und die durch sie bewirkten Krankheitsformen,” Zeita 
1898) the German sırine-plague, rabbit-septicemia,“ Wildse 
'en- and duek-cholera,, American hog-cholera, meine-ferer and “ 
chensenche,” are all caused by the same disease-agent—the bacterlum of heemorr 
septiceemla—and represent one and the same disease, to which he and Hueppe 
name of hemorrhagic wplicrmia,Preie (“Schweinepest und Schweinese) ese tk q 
1898) distin uishes between Schireinepest ant 
ses caused by different bacilli Septicemia ir 
associated with swine-plague as a secondary infection. Swine-plague is charact 
by cascous plaques and ulcerations in the intestine, enlarged and in part necrotic I 
glands of the abdominal and inguinal regions, and necrotic infiltrations of the sk: 
kidneys mia, on the other hand, according to Preisz, by a hemorrhagic 
moni. iemorrhagic fibrinous pleuritis and pericarditis, and hemorrhages from th 
neys. Karlinski (“Schweinepest und Schweineseuche,” Zeit. f. Hug... xxviii. 

































THE SPIRILLA. 659 


expresses himself in a similar manner and also distinguishes between Schrreinepest and 
Schweinese uche. 

The Bacillus diphtheriz columbarum is a small, slender bacillus, which was 
isolated by Loffier (“ Mittheil. a. d. k. Ges.-Amte,” ii.) from the exudate of a pigeon 
dying of diphtheria, and is regarded (Babes and Puscarin, “ Unters. tiber die Diphtherie 
der Tauben,” Zeitschr. f. Hyg., viii., 1890) as the probable cause of pigeon-diphtheria, 
a disease resembling human diphtheria. Löffler was able to reproduce the disease in 

igeons but not in chickens by means of inoculations of pure cultures of the bacilli. 
Mice died in about five days after inoculation, and the bacilli were found in the blood- 
vessels of all the organs. 

According to Löffler (l. ¢.) a buctilus is also present in the diphtheria of calves, but 
be was not able to cultivate it pure or to determine its pathogenic significance. 

The diphtheria of caloes and chickens is etiologically different from human diph- 
theria (ser, “ Ist die Diphtherie des Menschen auf Kälber übertragbar,” Fortschr. d. 
Hed., vi., p. 324; Zoffler, “ Mittheil. a. d. k. Ges.-Amte.,” 1884; Pütz, Fortschritte d. Med., 
v., p. 187). 

Besides the above, there are many other bacilli which have been described as the 
cause of disease in animals. Thus, forexample, according’ to Jlöflich (“Die Pye- 
lonephritis bacillosa des Rindes,” Monatsh. f. prakt. Thierheilk., ref. Central. f. 
Bakt., x.) and Enderlen (“ Primire infectiöse Pyelonephritis beim Rinde,” Deutsch. 
Zeitschr. f. Thiermed., xvii., 1891, ref. Cent. f. Bakt., x.), the frequently occurring 
pyelonephritis of cattle is caused by a bacillus. Likewise, according to Nocard (“ Note 
sur la maladie des boufs de la Guadeloupe connue sous le nom de Farcin,” Ann. de 
Uln. Past., ii.. 1888) the worm disease of the or, which was formerly of frequent occur- 
rence in France; and according to Oreste and Armeanné (* Studii e ricerche intorno al 
barbone dei bufali.” ref. Cent. f. Bakt., ii., 1887) and von Ratz (“Die Barbonekrank- 
heit,” Deutsch. Zeitschr. f. Thiermed., xxii., 1896), the plague occurring among the Ital- 
ian buffalo known as barbone det bufuli is due toa bacillus (by Voges re ed as the 
bacillus of hemorrhagic septicemia). According to Nocard and Roux (“ Le microbe de 
Ja peripneumonie,” Ann. de U’ Inst, Past., 1898) the lung-plague of cattle is caused b 
an extremely small, motile bacillus, whose form is with difficulty determined. Accord- 
ing to Bang (* Aetiologie des seuchenhaften Verwerfens,” Zeitschr. f. Thiermed., i., 1887) 
bacilli should be regarded as the cause of the epidemic abortion of cows. Stegel and 
Busenius (“ Krankheitserreger der Mund und Klauenseuche,” Deutsch. met. Woch., 1897) 
have described a bacillus as the cause of foot-and-mouth disease; but accurding to C. 
Fränkei (* Der Siegelsche Bacillus,” Aygien. Rundschau, vii., 1897) its pathological 
significance remains to be proved. Whether the microorganism described by Babes and 
Proca (* Aetiologie der Maul und Klauensueuche,” Centralb. f. Bakt., xxi., 1897) is the 
cause of foot-and-mouth disease is likewise still to be determined. Zöffler and Frosch 
(Cbl. f. Bakt., xxiii., 1898, p. 871) are of the opinion that the nature of the infecting 
agent in foot-and-mouth disease has not yet been determined. Lundgren (“ Die Renn- 
thierpest,” Zeitschr. f. Thiermed., ii., 1898) found a bacillus similar to the bacillus of 
symptomatic anthrax, and pathogenic for mice and guinea-pigs, in an epidemic disease 
affecting the reindeer herds of the Laplanders in northern Sweden. 


3 THE SPIRILLA AND THE JDISEASES CAUSED BY THEM. 


7 


(a) General Remarks upon the Spirilla. 


$174. The Spirilla, or Spirillaces, or Spirobacteria are divided into 
two genera, one of them called Spirillum, the other Spirochete. Many 
writers recognize still another genus, Vibrio. 

The genus Spirillum is characterized by the formation of short, stiff, 
shallow spirals, which in part possess flagella and show an active swarm- 
ing movement. The wavy rods are also called vibriones by many 
writers. ; 

Spirillum sive Vibrio rugula (Fig. 500, 5) forms rods, from 6-16 » long 
and 0.5-2.5 » broad, simply bent or having a shallow turn, and moves by 
means of flagella. It occurs in swamp-water, frees, and in the slime 
from the teeth. . 

Spirillum sive Vibrio serpens forms thin threads from 11-28 » long, 
having three to four wavy turns, and is found in stagnating fluids. 


660 THE PATHOGENIC FISSION-FUNGI. 


Spirilum tenue has very thin threads about 3-15 long, havi 
serew-like turns. 

Npirillum undula (Fig. 500, a) consists of a thread from 1-1.5: 
and 8-12 » long, having from one and a half to three turns, and fu 
with a flagellum at one end. It occurs in various decomposing fl 

executes rapid twisting and darting move 
z s JS vb Spirillum volulans possesses threads 
thick and 25-30 long, with two and a 
= UU 5 three and a half turns, and bearing a flagel 
each end. 
Tr —_=sT > The genus Spirochete (Fig. 504) ix cha 
a ized by long, flexible, closely-turned spiral 
Aes The Spirochete plicatilis forms long, vei 
brio regula thy and Spirit. closely wound threads, from 100-: 
trom acl ft ion ot ney of frequent occurrence in swamp-wa 
ebony gutters, and makes very rapid movements. 
een at ai Spirochete buccalis sive denticola is 1 
Jong, pointed at both ends, and is not infre 
ly observed in the secretions of the mouth and nose (ef. Fig. 183 
appears to S$ no pathogenic signiticance. 

The spirilla, so far as th re not pathogenic, have been but 
studied. They are present in large numbers in the contents of 
vaults, Aceording to Prazmowski Spirillum rugula causes decor 
tion of cellulose, and forms terminal spores. According to We 
vibrio present in nasal slime presents many forms of growth. Es 
succeeded in cultivating a spirillum, ealled by him Spirilwm rubrum 
the various ordinary media. In bouillon it forms spirals of from 
three to fifty turns, Short: spirilla execute lively movements, bu 
ones, on the contrary, slow movements or are motionless. The ec 
in firm nutrient media are at the beginning pale, but in time the pc 
not. exposed to the uke ona wine-red color, Inthe spirilla : 
cultures there appear three to four elear, dull-glistening spots tl 
id are probably to be regarded as spores, Cultures 
iri Ia are more resistant to drying than others, but the 
















































The long spirals’ may break up inte short segments whi 
about three-quarters of a turn, but these may 
undergo di 





h posses: 











Literature. 
(Life-history of the Spirilla.) 


r die Reinkultur eines > lum, Chl. f. Bakt. 1887. 
Kitasato’ Reinkultur eines Spirillum aus faulendem Blute. Chl f. Bakt. 
entlora d. Düngerjnuche. Zeitschr. f. Hy 
Spirillum Undula minus u. majus. CbL f. Ba N . 1895. 
Prazmowsky: Unters. üb. die Entwickelun e einiger Bakterien, Ta 

TERS, 

Salomon: Spirillum a. zethiermagens, 
Weibel: Untersuchungen über Vibrionen, 













ix., 





tb 


The Spirillum cholere asiatice, or the Vibrio cholere, 
called comnucbacillus (bacillerirgule cholérigéne), was discovered b 


The Pathogenic Spirilla, 














THE PATHOGENIC FISSION-FUNGI. 





live in well water for thirty days, in sewage for seven da a 
p linen for three to four di Nicati and Reitsch found them 
after eighty > 

In culture 









1 joined in pairs; at other times they form long sy 
there also o¢ ight rods, and occasionally the ma, 
pw the curve “only ıperfectiy not 
ss they show active mov 
inging drops, According to in 
ity is dependent upon a terminal tlagellı 
Atace ustion of the food-material there freqr 
wolution- s, in which the rods are sometimes sh 
mes swollen, thus ere y of fe Ax 
swelling, as well as the formation of sy which do not. tak the; st 
cur as the result of degeneration, and hav 
reted as phenomena of fructitieation. 
u demonstrated, The addition of hydrochlo 
a to enltur sof cholera-spirilla in peptone-conta 
+ peptone-meat- n alkaline, one-per-cent. solutic 
peptone containing one per cent. of salt) causes the culture to as 
wseered or Burgundy-red cole ion of a colo 
matter, cholera-red. According to Salkowsl n onitre 
reaction. 
When gaining entrance to the äntestinal tract of man the spir 
as they are not destroyed by the action of the gast 
‘owth otherwise prevented, develop both in the small a 
nes, and their multiplieation is followed by a marked tran: 
the intestinal mucosa, so that the intestine becomes filled with a fui: 
sembling meal-soup or rice er, in which es of desquamated 
thelium which has undergone mucoid degeneration float about. 
‘The spirilla ave always present in great numbers in the i 
tents, and a und in the Toni [ i 
may penetrate between and bene 











fluid 1 
vhieh may 
ations by I 











in degree of ¢ 
























not be 





















illa. 

juice or 
i 
dation 




































testinal 
whence 













well as soiled linen, are suitable for the examination, since 
observations made by Koch, the pi ay multiply activel 
time upon moist linen and moist earth, In old 
ot the spirilla is more dificult but ne Ss succeeds in all 
i dle most surely by me ultures. In order to 
paration of el m other inte 
| the dejecta with double 
the mixtur 
ruin wneevered for twelve hours rom 30 40 
he spirilla requiring oxygen will develop particularly upon the surt 
and may be easily trans vl thence to plate-eultures. Koch ree 
mends for this purpose as f peptone with common salt. 
he presence of cholera-spirille in the intestine ereiten an inflamma 
whieh in the beginning finds expression in redness, swelling, mitt 
transndation, mucoid degeneration of the epithelium, and desq 
Tate FR nation of sloughs, and uleeration. It is e 
aistantly by a more or less marked cellular infiltration ot 
itary follicles and Peye patches are swollen eveı 
plac ra few hours ar after on 


























































ASIATIC CHOLERA. 663 


three days. If the disease lasts a longer time, the intestinal contents 
become more consistent and the intestinal mucosa shows ulcerative 
changes. 

According to our present knowledge, the spirilla produce poisonous 
substances which cause local damage to the mucosa of the intestinal 
canal, and when absorbed give rise to symptoms of intoxication and 
cause paralysis of the vessels. Small foci of degeneration are often pres- 
ent in the liver and kidneys, within which the gland-cells show cloudy, 
fatty, or hyaline degeneration, or are necrotic. Moreover, the kidneys 
may frequently show cloudiness caused by a toxic degeneration of the 
epithelium; occasionally also a swelling of the cortex. Ecchymoses in 
the epicardium are of frequent occurrence, and in the later stages patches 
of necrosis may also occur in the mucous membrane of the vagina. The 
long-continued presence of spirilla in the intestine may give rise to ulcer- 
ation. Finally, the spirilla may be crowded out by the putrefactive bac- 
teria present in the intestine, and ultimately die out. Through the 
absorption of the products of decomposition a new intoxication may 
arise, Which is not dependent upon the original spirilla. 

According to Koch, Nicati, and Rietsch, cholera-spirilla may also be 
found in the vomitus. Nieati, Rietsch, Tizzoni, and Cattani found them 
also in the ductus choledochus and in the gall-bladder. According to 
the statements of these authors the spirilla usually do not enter the 
blood, but in cases of severe infection they may be spread throughout 
the body. 

Koch demonstrated the presence of spirilla in a tank in India which 
furnished the inhabitants of the region with their entire supply of water 
for drinking and other purposes, at atime when a part of the inhabi- 
tants were sick and dying of cholera. Since then, they have often been 
demonstrated in water-supplies during cholera epidemies. 

According to investigations by Nicati, Rietsch, van Ermengem, and 
Koch, symptoms resembling cholera may be produced in experimental 
animals through the introduction of cholera-spirilla into the intestinal 
canal. This experiment succeeds when cultures are introduced directly 
into the duodenum or small intestine (Nicati and Rietsch); as well as 
when the gastric juice of the animals (guinea-pigs) is neutralized with a 
five-per-cent. solution of soda, the bowels being quieted by an injection 
of Le.e. of tincture of opium to every 200 gm. of the body-weight, and 
one or more drops of a pure culture of the spirilla then introduced into 
the stomach (Koch). 

The animals thus inoculated die with marked symptoms of collapse. 
The small intestine is found to be filled with a watery, flocculent, color- 
less fluid containing spirilla in great numbers; the intestinal mucosa is 
reddened and swollen. 

Asiatic cholera 1s endemic in Lower Bengal and never entirely disap- 
pears there. Thence it spreads at times throughout India, and is carried 
by transportation over a larger or smaller part of the world. Since the 
spirilla are easily killed outside of the body the transportation must be 
effected mainly by individuals suffering from the disease. The infection 
probably occurs exclusively through the alimentary tract, as the re- 
sult of the introduction of infected beverages, food, or some other sub- 
stance into the mouth; but without doubt not every introduction of 
cholera-spirilla into the intestinal canal is followed by infection. 

Moreover, it not infrequently happens that the spirilla increase in the 

lestine, but excite only slight changes, so that the infected individual 


a 


60,4 THE PATHOGENIC FISSION-FÜNGI 


siffers nomarked svinptomis, and the diaguesis (al only bee Lad Th 
the demonstration of spirtila in the stools. 

if the cholera->pirilla get inte the water-Suppiy ald there inen 
cholera may develop in the given region with Very preat rapudity 
on the contrary. the infection takes place ty direct or Dodi reat ta 
from nal to dian. the spread is slow, in that the diseame is confine 
these whe come into contact with the sick. or With artleies vo Ztamuin 
by the latter, The incubation period is trom ole to two days. 

Ju the intestines of convalescents the spirilla. aecomiing te Inven 
tions of Kolle. may dive for a dong time and multiply witheut giving 
to anv svinptols betraying their presence, Rolle was able te der 
strate thea in a nuinber of cases after five te eichteen dave. aud im! 
Vidal Gases as Jong as Twenty to torty- eight dad. 

One attack of cholera makes the individual immune for a cer 
time. The immunity depends upon the presence of bactericidal i 
bodies, Thronuh these bedies the organism 1nay be protected f 
Cholera: but in those who have already contracted the disease the pm 
five inflnenee is of no avail ef. 882. 


The poison whieh is produced by the chulera-baciilus and which causes the -: 
tinh ciitdeal -1l): Ten sl a chart infe ‘cHiadu is pet known.  Grteté et believes TL: 
T= fa Pathe yeee ee ale matin, Nele that dt isi pepTeue . ‚chrierstoXupepten:. Pr”. "ji a 

NWebien that it isan eniaented the er]i-beniv According te Meta} rean: 7 cr atte 
po na rated by ¢ tae ge lye Fu surırd and Tw? ‘aah We ld refer the m: bid sv Inu ve 
theta tea hoot pedsonite: sines nitrites in small deses cause reichirg. vonitin 
eharzeef thin are b heces, fall ef temp nature, heart failure. cyanosis, and Cran} 
te entre rien and muscles of the neek—that is. Symptoms resembling those of cli 

mie peter because the cholersspiriila are alie to form pitrites out of nin 

Contacedd jn he freu] 

Hi vere) aot chals-retureadifhrs creatiy, according to the place of origin 
Tite cate Te virile hee tfe-e reuse s wit ha thee aes se, Guinea-pigs Which are ve ry sus 
bee “aa intraperitunen ib it, eeiutiohscof aq hide Ta nay Tne protected aralust this ‘infec 


I. Vai GUS Taapocyates re u it vert teat ee re fa PER nite aluures. hit De absolute Immunity 
hoonetwedb inthis tas The bie er ru. f lesınan individuals that have recut 
Pre atte cher sheave pert eproperties fir wuinea-pigs for several wi 
ar cc ee 

oe lltes. Mob, peaetien dec atures a & thie chelera-spérilia is duc to the fact 
My beet tha da ds peptone sottiens seventy farms inde) but alse nitrites 


= tre FE, raged sets tree mitrous acid which forms a red oc 
nie Wied tte su. en Ae the Saar self Metsehaikeff, and the > 
out Pde be WE ap sb teat per rad ye Ted coier ed f the cultures oCeurs only u 
"an. Deinen SL ss Bar zen, When Litrous acid alone is added. 


. . .: : 0. 
Nu f le» "4 , Ad . - Sere “dae, 


In A oc ion Tay Tiese Observers in the deject 
tae eT ry the eda he sttas itor thee tse hire res have steed for some tin 
of sled „spirila. onivsanewhat loner 

toyed I. pr as She Maar misting ashid trem the latter only in the fact 
tape oate fo togistibetis grat ulato ane huawe a sharp contour, Gelat 


. tet oath oa tee syentiy in stab-enitures after twenty 
inl . eobuedthoaiesy iv Miia Fis Sen ds formed. which s cn ren 
a | f Hart a 


ee a | ee et al Doom % tp hee ATES, tlie Ay form within forty. 
tale owe elise rc sho otpex naarnaed ol from the substanee of 
re Lo ee ii, ana =; hou Sf arew at all st Feooory) - few 


"1 al.‘ bide: Tepper tae cs tetha tn Hu BE BR 
Potter (hey cate ben sue wing flee otnpest ih, ane are rather resistant to 
nen Intrerbacel irre the in Stine eo apatthes piss dw the method” ab 
rennen Nee te sti diar tthe eo used bach orn snirlla, but less 
Poetry otebt fad whether the Sof FT fe aad Prior po 
to renasrtante Jeorebeslerie-hestras, sited dhe m which the 


ASIATIC CHOLERA. 665 


obtained their cultures were not fresh; and other authors have failed to find the spirilla 
in corresponding cases ( Kartulis, “Zur Aetiologie der Cholera nostras,” Zeitschr. f. 
‘Byg., vi., 1889). Knist (Münchener ärstliches Intelligenzblatt, 1885), 
on the other hand, found them in the crecal contents of a suicide. 

(2) Spirillum tyrogenum, found in cheese by Deneke in Flogge’s 
Institute (Deut. med. Wochenschr., 1885), is also very much like the 
cholera-spirillum, but is somewhat smaller, and the long spiral 
threads are more closely wound. Cultures on Eelatin-plates form at 
first sharply contoured discs that by low maguitication appear dark, 
and liquefy the gelatin more rapidly than the spirillum of Koch. 
In stab-cultures they behave like the Finkler-Prior spirillum, but do 
not grow upon potato. 

(8) Spirillum sputigenum is a spirillum of the shape of a curved 
rod, somewhat longer and thinner than the cholera-spirillum. It 
occurs in the saliva, and cannot be cultivated upon the ordinary 


(4) Vibrio of Metschnikof (Gamaleia, “Vibrio Metschnikovi et 
see rapports avec le microbe du cholera asiatique,” Annal. d. 1 Inst. 
Past., ; ii, 1889; Pfeiffer, “Ueber den Vibrio Metachnikovi 
und sein Verhältuiss zur Cholera asiatica,” Zeitschr. f. Hyg., 1888) 
is @ fission-fungus isolated by Gamalela in an epidemic occurrin; 
in chickens in Odessa, which was characterized by diarrhoea an 
enteritis. When cultivated it shows a very great resemblance to 
the cholera-spirillum of Koch. The spirilium is most easily ob- 
tained pure by inoculating pigeons with the blood of diseased 
chickens. ‘The pigeons die In-from twelve to twenty hours and 
show the spirilla in the blood and in the intestinal tract. 








Literature. 
(Spirillum of Asiatic Cholera.) 


Barth: Die Cholera, Breslau, 1898. 

Brieger: Choleraroth. Deut. med. Woch., 1887; Stoffwechsel 
producte d. Cholerabacillen. Berl. klin. Woch., 1887. 

Bujwid: Chem, Reaction f. d. Cholerabakt. Zeitschr. f. Hyg., il., 
1887; Cbl. f. Bakt., iif., 1888. 

Dieudonné: Ucbersicht über die choleraähnlichen Vibrionen. Cbl. 
f. Bakt., xvi., 1884. Fis. 500. — 

Dunbar: Differentialdiagnose zw. Choleravibr. u. and. Vibr. — eulture,’in gel 
Zeitschr. f. Hyg., xxi,, 1896. of the Spirillum o 

ich u. Tsuboi: Die Cholera, eine durch die Cholerabacillen Finkter and Prior. 

verursachte Nitritvergiftung. Münch. med. Woeb., 1898. 

van Ermengem: Rech. sur le microbe du choléra asiatique, Bruxelles, 1885; Neue 
Untersuchungen über Choleramikroben, Wien, 1886. 

Finkler u. Prior: Deut. med. Woch., 1884; Forschungen üb. Cholerabakterien, Bonn, 
1886. 

Flügge: Verbreitungsweise u. Verhütung d. Cholera. Zeitschr. 1. Hyg., xiv., 1898. 

Erasnkel: Choleraleichenbefunde. Deut, med, Woch., 1608. 

allg. 
















eraepidemie in Hamburg, 1892, Berlin, 1893. 

Kitasato: Widerstandsfähigkeit d. Cholerabakterien gegen Eintrocknen u. Hitze. 
Zeitschr. f. Hyg., v., vi.; Verhalten d. Cholerabakterien im menschl. Koth u. in 
Milch. Ib., v., 1889. 

: Actiologie d. Cholera. Deut. Vierteljabrsschr. f. off. Gesundheitspflege, xvi., 
1884; Conferenz z. Erörterung der Cholerafrage. Deut. med. Woch., Tr; 
Choleradiagnose. Zeitschr. f. Hyg., xiv., 1898; Die Cholera in Deutschland wäh- 

rend des Winters, 1892-98. Ib., xv., 1898. 














666 THE PATHOGENIC FISSION-FUNGI. 


Koch u. Gaffky: Bericht über die Thätigkeit der z. Erforschung d. Cho 
188), nach egypten u. Indien entsandten Commission. Arb. a. d. K. 


Kolle: Ueber die Dauer des Vorkommens von Choleravibrionen in den Dejec 
Cholerareconvalescenten, Zeitschr. Hyg., zvül. 

Lehmann: Die modernen Choleratheori iol. Ghatetbi.. v.. 1885. 

Lustig: Bakteriolog. Studien Aber Cholera asiatica. Zeitschr. f. Hyg. 

Mots off: Toxine ct antitoxine cholérique. Ann. de I’Inst. Paste 

Neuhaus: Ueber die Geisseln an den Bacillen der asiat. Cholera. 
1889. 

Nicati et Rietsch: R. 











yg., v., vi., vi. 1887 
dlemiologiscle Theil des Berichtes über die Thatigkeit der zur Erfors 
Cholera im Juhre 1883 nach Aegypten und Indien entsandten Commission 
u Teipzig, 1888; Ueber Cholera. Münch. med. Woch., 1892. (bl. f. } 
1892, 


Pfeiffer 
1895. 

Riedel: Die Cholera, Entstehung. Wesen u. Verhntung derselben, Berlin, 18 

Rumpf: Die Cholera asiaticn u. nostras, Feng, 1808 

Rumpf u. Gaffky: Die Cholera, Verh. d. XII. Congr. f. inn. Med., Wiesbw 

Salkows] U das Choleraroth. Virch. Arch., 110 Bd., 1887. 

Sulla resistenza del bacillo virgolo di Koch nelle acque I 








Choleragift. Zeitschr. f. Hyg., xi., 1892; Antikörper d. Cholera. 








Scholl: Unters, über giftige Eiweisskörper bei Cholera. Arch. f. Hyg 

Schottelius: Nachweis der Cholerabac. in den Dejeetionen. Deut. ined, Wo o 
1889. 

Schuchardt: Ueber das Choleraroth. Virch. Arch., 110 Bd., 1887. 

Sobernheim: Choleraimmunitat. Zeitschr. f. Hyg.. xx., 1895. 

Stieda: Neue Arbeiten über Cholera asiatica. Cbl. f. allg. Path., iv., 1893. 

Tizzoni et Cattani: Rech. sur le choléra asiatique. Beitr. v. Ziegler, 

Tachistowitach: Verind. d. Gehirns bei Cholera. Virch. Arch., 144 Bd., 18 

Voges: Die Choleraimmunität. Cbl. f. Bakt., xix., 1896 (Lit. 

Wassermann: Unters, üb. Immunität gegen Cholera asiatica, Zeitschr. 
xiv., 1 














$ 176. The Spirochete Obermeieri (Fig. 504) is found const: 
the blood of patients suffering from relapsing fever during the 
of the fever, and the multiplication of these organisms in the boc 
cause of the dis. 
The spiroel Inete i is 16-407 long, and possesses numerous spira 
Ina fresh drop of blood it shows very active motion. Carter an 
succeeded in producing the disease 
. by inoculation with the spirochiet 
9-00 \ nothing definite is known of its n 
EN development and habitat outside 
ann blood. The whereabouts of the spi: 

\ 
° “wy of the disease are not known. The 


or of its spores during the afebril« 
va 0} @ _taneons inoculation into apes of blo 











taining the spirochete is followed on 
several days by an attack of fever, « 
spirochiete is found in the blood only 
the febrile stage. According to the a: 
findings observed in man, the spleen. 

Jen and contains numerous yellow foci of degeneration, and oft 









foroff the histological ex 
tion of the spleen e cell-necrosis and cell-degen 
(Fig. 505, ¢), as well as deposits of fibrin in the veins of the pu 
proliferative processes in the pulp-cells. Further, numerous larg: 





SPIRILLUM OF RELAPSING FEVER. 667 


cells (f ) enclose red and white blood-cells or the remains of such. Fi- 
nally, numerous spirilla are found, especially in regions which are not 





. 
hocytes with spirila x cy m mpbocytes d. large 
Maier air am Ted blood-cells and their remains’ o free red blood-cells. x Bout ‘ou 


wholly necrosed but contain degenerated and necrotic cells, in part free 
(a), and in part enclosed in leucocytes (5), partly well-preserved, and 
partly beginning to show disintegration. 

The spirochetes stain especially well, in cover-glass preparations, with 
alkaline methylene-blue and fuchsin. 


Literature. 


(Typhus Recurrens. ) 


Cantacuzina: Spirilloses des oles. Ann. de I’Inst. Pasteur, 1899. . 
Gabritschewsky:: Zur Pathol. d. Spirochaeteninfection. Cbl. f. Bakt., xxvi., 1899. 
Heydenreich: Der Parasit des Rückfalltyphus, Berlin, 1877. 

Honl: Febris recurrens. Ergebn. d. allg. Path., iii., 1897. 

Lubimoff: Patholog.-anat. Veränderungen bei Typhus biliosua Virch. Arch., 98 Bd., 


1884. 
Metzchnikafl Ueb. den Phagocytenkampf bei Rückfalltyphus Virch. Arch., 1 
Nikiforoff. Zur path. Anat. u. Histol. d. Milz bei Recurrens, Beitr. v. Ziegler, xii. 


1892. 
Obermeier. Cbl. f. d. med. Wiss., 1878; Berl. klin. Woch., 1878, No. 88. 
Ponfick: Anat. Studien über den Typhus recurrens. Virch. Arch., 60 Bd., 1874. 
Puschkareff: Zur pathol. Anatomie der Febrisrecurrens. Virch. Arch., 118 Bd., 1888 
Sudakewitsch: Rech. sur la tiévre recurrente. Ann. de l’Inst. Pasteur, v., 1891. 





CHAPTER XI. 


The Yeasts and Moulds, and the Diseases Cau: 
Them. 


§ 177. The yeasts (Blastomycetes) and the moulds (Hyphon 
belong, as do the schizomycetes, to the non-chlorophyllaceous 
phytes. With the schizomycetes they have no phylogenetic relati 
on the other hand, they are closely related to one another. 

The moulds and yeasts, like the schizomycetes, derive their 1 
ment from organic substances containing carbon. The major 
their food in dead organic substances, and belong therefore to th 
phytes ; some are able to obtain nourishment from living tissues, 
to be classed, at least at times, with the parasites. In human bein 
forms occur, 

Outside the organism the moulds are generally known as t! 
ducers of the different mouldy films which so frequently develo 
organic substances. They belong to different groups of fungi. 

The yeast-fungi are the cause of alcoholic fermentation, and fi 
scum on the top of alcoholic beverages. 





Literature. 
(Moulds and Yeasts. ) 
De Bary, A.: Vergl. Morphologic d. Biologie d. Pilze, Mycetozoen u. Bakterl 


Ciien, aus dem Gesammtgebiete der Mykologie, Heft i.-x. 





der Systematik u. spec. Pflanzenmorphologie, Leipzig, 188 

len Kern der Hefezellen. Cbl. f, Bakt., xiii, 1898. 

Torgense Mikroorganismen der Gührungsindustrie, Berlin, 1892. 

Koch: Jubresber. über die Fortschritte der Lehre von den Gührungsorganismı 
1900, 

Ludwig: Ichrb, der niederen Kryptogamen, Stuttgart, 1892. 

Raum: Zur Morphologie u. Biologie der Sprosspilze. Zeitschr. f. Hyg., x , 1 

Sachs: Vorles. über Pilanzenphysiologie, Leipzig, 1882. 

Tavel: Vergleichende Morphologie der Pilze, Jena. 1892. 

Uhlworm u. Hansen: (bl. f. Bıkt., II. Abth., Bd. 1-6, Jena, 1895-1900. 

Zopf: Die Pilze. Handb, d. Botanik v. Schenk, iv. 












$ 178. Yeasts occur in man in the form of naked or encapsulatı 
or round cells of varying size. They are found chiefly as harmless 
phytes, most frequently in the upper part of the intestinal canal- 
stomach—where they are almost constantly present; and when ber 
in the process of alcoholic fermentation are taken they may oc 
large numbers, and may also multiply. In the bladder they ma 
wise multiply, in case the urine contains sugar; and may cause f 
tation of the urine with evolution of earbonie-acid gas. 

As parasites no importance has been attached to them unt 
recently, but the investigatious of Busse, Buschke, Sanfelice, Curt 

668 








PATHOGENIC MOULDS. 671 


active penetration into living tissue—that is, first into the epithelium 
(c, d), but often also into the connective tissue (a, f), and into the 
blood-vessels, and from these portals of invasion there may develop 
metastases in the internal organs. Thus, Zenker has observed hyphs 
and conidia in an abscess of the brain; and Paltauf has reported a case 
in which a mould-fungus was conveyed from an intestinal ulcer to 
the brain and lung. Schmorl has described thrush-metastases in the 
kidneys. 

Moreover, growths of moulds in the lungs are not always confined to 
dead material or to the cavity of the bronchus, but it happens, though 
rarely, that they penetrate into the living respiratory parenchyma, form- 
ing small white or yellowish, nodular masses, within which the lung tissue 
is necrotic, while in the neighborhood there is formed an inflammatory 
infiltration. In the injured cornea they may likewise penetrate into the 
tissue and cause necrosis and inflammation. 

Local colonizations of moulds which penetrate into living tissue 
cause a more or less marked irritation of the surrounding tissues, and 
give rise to tissue-degenerations (Fig. 509, c) and inflammation. Such 
changes may be observed in mycosis of the lung, as well as of the intes- 
tine (c, d, f) andear. When invading the lungs they form growths of 
hyphe which resemble the granules of actinomycosis, and are surrounded 
by collections of cells. Their action, however, is always limited, and 
they produce no substances which are injurious to the organism as a whole, 
or cause symptoms of poisoning. The frequently reported finding of 
moulds in abscesses of the subcutaneous tissues and internal organs are 
probably to be interpreted as due to the fact, that along with the bac- 
teria causing the suppuration, moulds also get into the tissues, as well 
as into the circulation. A general spreading of mould-fungi does not 
occur in these cases, in that the further development of the same is con- 
fined to the place of the metastasis. _ 

The form of moulds which are saprophytic, or to a limited extent 
parasitic, in man, belong to the Mucor, Aspergillus, and Eurotium gen- 
era. From the ear various species have been obtained: Aspergillus fumi- 
gatus (Fresen), Aspergillus flavus or flavescens (Brefeld, Wreden), As- 
pergillus niger or nigricans (Van Tieghem, Wreden, Wilhelm), Aspergillus 
nidulans (Eidam), Eurotium malignum (Lindt), Mucor corymbifer, and 
Trichothecium roseum ; and, in so far as known, these are the same species 
which occasionally occur in the respiratory tract. 

In the majority of cases it is necessary, in order to determine the 
variety of mould, to make cultures upon suitable nutrient media (decoc- 
tion of bread, bread-agar, potato, gelatin, etc.). On these the conidia 
which are sown grow out into germ-tubes, and form simple or branched, 
unicellular or multicellular threads, on which arise the peculiarly con- 
strueted fruit-bearers characteristic of the species, which eventually pro- 
duce conidia. Many also form spores through the copulation of cells of 
the mycelia, especially when the supply of oxygen is lowered (Brefeld, 
Siebenmann ). 

In the mucors there appear especial fruit-bearers (Fig. 510, c), which 
according to the species are either single or branched, and on the ends of 
which there are knob-like swellings from which the sporangia (d)—that 
is, Spherical vesicles filled with conidia-spores—grow. 

Mucor corymbifer, for example, forms branched fruit-bearers (Fig. 
509, c). The sporangia (d) on the ends possess a smooth membrane and 
enclose at the time of ripening yellowish conidia-spores. 








2 THE PATHOGENIC MOTLDS AND YEASTS. 


The aspergilli form conidia-bearers, which swell out spherically: 
and then produce numerous serigmais—that is, cone-like outgr 
radially arranged, t 

and spr 

out from the uppeı 
From 


posit 
the fungus of thrush (qj 
is still unsettled. | 
erly it was called Oi 
albicans, and classe 
the family Oidium, ' 
occurs in different 5 
in the form of filmy 
ings upon organic 
stances. When culti 
from conidia it pro 
hyphe which bec 
jointed and develop 
dia through a transverse division of the threads, but form no pec 
fruit-bearers. 

According to Rees, Grawitz, Kehrer, the thrush-fungus grow 
budding and by the production of mycelia and conidia, which in 
produce at their ends, by a process of constriction, new conidia, 
manner similar to that which takes place in the forms of mycod« 
belonging to the yeast-fungi. 
Consequently this fungus should 
be designated Mycoderma_ albi- 
eans. Linossier and Roux are, 
however, of the opinion that the 
thrush-fungus does not belong 
at all to the saccharomycetes, 
and they regard its classiticati 
at the present time as impo: 
ble, Cao, who has investigated 

arietien of oidium, re- 
ell-defined 
anding between 
astomyeetes and the hy- 
phomycetes, whieh they ap- 
preach through their production 


























Hyphee with contdia-bearers of Aspe: 
a. Fruit-head in optical cros-sect 
‘seen from above. x 275. 





ording to Plaut the 

thrush-fungus is identical with a mould, Monilia candida, which o¢ 
frequently in nature. Kehrer suspects that it is one of the higher mc 
which has become degenerated through parasitism. 

According to Nermayer all revécticeop ponds are resistant to the digestive j 
and may pass through the human intestinal tmet without being killed. Withor 
coir t introduction of some fermentable substance they are harmless. They 
an influence upon the intestinal canal only when fermentable substances are introd 
whereby at the high temperature of the body abnormal products of fermentatic 
produced having an irritating action upon the intestinal tract. 














PATHOGENIC BLASTOMYCETES. 673 


Busse found (1894) great numbers of yeast-cells developing in the diseased areas 
present in a woman, thirty-one years of age, who died from multiple inflammations of 
the bones, skin, Jungs, kidneys, and spleen, partly tumor-like and partly abscess-form- 
ing. According to his findings it may be regarded as certain that the yeast was the 
cause of the disease. The yeast could be easily cultivated upon suitable media. Mice 
were particularly susceptible to inoculation, dying in from four to eighty-three days 
after the injection. At death the yeast-cells were found to have markedly increased 
both at the point of inuculation, and also in the internal organs. A proliferation of 
tissue occurred only after a long duration of the infection. 

Busehke found yeasts in multiple ulcers of head and neck, arising from acne-like 
lesions. (rilchrist and Stokes found yeasts in a lupus-like affection of the skin. 

Sunfelice experimented with yeasts from fruit-juices, and found among these one 
pathogenic for guinea-pigs (Succharomyces neoformans) and one pathogenic for chickens 
and dogs (Siccharomyces lithogenes). Curtis found, in multiple proliferations of the 
skin resembling myxosarcoma, yeast-cells which were pathogenic for rats, mice, and 
dogs. 

5 Sınfelice, Corselli, Frisco, Roncali, Binaght, Leopold, and others believe that blasto- 
mycetes may be the cause of true tumors, sarcoma and carcinoma; but true tumors have 
never yet been produced experimentally by inoculations of yeast-cells or by injections 
of the same into the blood. Only suppurations and inflammatory tissue-proliferations 
have been produced by such experiments: and the finding of yeast-like structures in 
true tumors, even if part of these were true yeast-cells, does not permit of the conclu- 
sion that tumors are caused by yeasts (cf. 8 122). 

According to investigations by Auch, Löffler, Lichtheim, Hückel, and Lindt, the 
conidia of Aspergillus fumigatus, A. flareacens, A. nidulans, Eurotium malignum ; Mu- 
cor rhizopodiformis, M. corymbifer, M. pusillus, and M. rumosus, grow at the body -tempera- 
ture, and, when introduced into the blood-current of animals, grow into the tissues and 
form hyphe, although there is no new formation of conidia, and consequently no pro- 
gressive infection of the animal extending beyond the area within which the spores 
have been introduced. Conidia of Mucor rhizopodiformis and M. curymbifer grow, 
when introduced into the blood-stream of rabbits, chiefly in the kidneys and the lym- 
phatic apparatus of the intestines, where they cause a hemorrhagic inflammation. 
According to Cao, there are different species of oidia which, when injected into 
rabbits, cause inflammations, abscesses, or proliferations of granulation tissue; and 
many produce also a toxic action upon the organism. 

Aspergillus mycoses of the respiratory tract are not rare in animals, espe- 
cially in birds, and the proliferating mycelia cause tissue-necrosis and inflammation. 
According to Chantemesse, Aspergillus fumigalus causes in pigeons diseased conditions 
of the mouth, lungs, liver, and kidney, that of the first two organs resembling diph- 
theria, that of the latter two closely resembling tuberculosis. It may, therefore, be 
designated pxendotuberculosis aspergillina, According to Potain the infection may be 
transınitted to man and give rise to ulcerative diseases of the lung. 

Eurotinm and Aspergillus, according to Stebenmann, are two different families, 
having, however, a close resemblance to each other, in that the mycelia and conidia are 
similarly formed. The essential differences between the two lie in the fact that Euro- 
tium forms perithecia in the form of shining, light-yellow or sulphur-yellow, translu- 
cent bodics the size of a grain of sand, delicate and easily crushed; while the true 
Aspergillus forms hard, woody sclerotia usually embedded in a thick, white matted 
mass of mycelia. The development of these takes place in two periods. The second 
part of the development occurs only when the sclerotium finds a lodgment upon a 
moist substratum. 

Aspergillus flarus of Brefeld (Eurotium Asperillus flacus of de Bary) forms golden 
yellow, green, and brown growths; round, yellow, olive-green, or brown fruit-heads; 
round, rarely oval, sulphur-yellow to brown conidia with minute warts on the surface; 
diameter 5-7. Aspergillus fumigatus of Fresen (Aspergillus nigrescens of Robin) forms 
green, bluish, or gray growths; the fruit-heads are long, in shape resembling an in- 
verted cone; conidia, round, rarely oval, smooth, mostly clear and colorless; diameter 
2.5-8u. Aspergillus niger of Van Tieghem (Eurotium Aspergillua niger of de Bary) forms 
dark chocolate-brown growths; conidia are round, brownish-black, or grayish-brown 
when ripe; surface smooth or warty; diameter 3.6-5 u. 

Aspergillus can develop upon the injured cornea and give rise to purulent inflam- 
mation. Leber (Graefe’s Arch., xxv.) cultivated it upon the cornea and in the anterior 
chamber of the eye of the rabbit. Finally, Aspergillus also appears in the pelves of 
the kidneys. Bubes (Biol. Centralbi., ii.) found the conidia and hyphe of a mould in 
wicers of the skin which were covered by scabs, and gave to it the name of Oidium enb- 
tile cutis. 





64 THE PATHUG 





#ENIC MOULDS AND YEASTS. 


Literature. 


¢ Pethagraic Blastomycetes,) 

















Pitheliomen,  Zeitsch 
Samal Kline Vorte, X 
Ber 












baden, 1900 (Lit.). 
CbL f. Bakt.. xviii. 1845 

‘. . de 1’Inst,, 1896. 

from Accidents 








f Amer 





3. 
Foulerton: 1 ‘ath 
Frothingham: 








Tumor like Des 
ws. dour. ot Med. Ros, 1 
Gilchrist und Stokes: Pocudelupus Causd by a Blastomyees.Tenr of Fag 
. DSHS, 

Gilkinet 


Ya Blast 
















a u. pn 
: Blastomyeeten als  Infeet 


Nichols: The: 
Ormsby ind Miller 
Rabinowitsch | 

Ricketts Ovtiomscos 














F 

F. 

G 

H 

K 

K. 

: 
. Non . . 
1 : \ . \ 
L ~ . - r 





FAVUS., 045 


Obici: Pathogene Eigensch. d. Aspergillus fumigatus. Beitr. v. Ziegler, xxiii., 1898 
(Lit.). 

Oppe: Schinimelmykose d. harten Hirnhaut. Cbl. f. allg. Path., 1897. 

Pearson: Pneumonomycosis due to the Aspergillus Fumigatus. Proc. of the Path. 
Soc. of Philadelphia, 1900. 

Perroncito: Mycose aspergillaire. Arch. ital. de biol., vii., 1886. 

Podack: Aspergillusmykosen im Respirationsapparat. Virch. Arch., 139 Bd., 1895 
(Lit.). 

Potain: Un cas de tuberculose aspergillaire. LL’ Union méd., 1891. 

Pusch: Fadenpilze bei Thierkrankheiten. Ergebn. d. allg. Path., iv., 1899. 

Rénon: Rech. clin. et exp. sur la pseudotuberculose aspergillaire, Paris, 1898; Etude 
sur Paspergillose chez les animaux et chez Vhomme, Paris, 1897 (Lit.). 

Ribbert: Der Untergang pathogener Schimmelpilze im Körper, Bonn, 1887; Ueber 
wiederholte Infection mit pathogenen Schimmelpilzen. Deut. med. Woch., 1888. 

Roeckl: Ueber Pneumonomykosen. Deut. Zeitschr. f. Thiermed., x., 1884. 

Rothwell: Experimental Aspergillus. Jour. of Patlı., vii., 1900. 

Saxer: Pneumonomykosis aspergillina, Jena, 1900. 

Schenck: Subcutaneous Abscess Caused by a Fungus, J. Hopkins Hosp. Bull., 1898. 

Schmorl: Ein Fall von Soormetastase in der Niere. Cbl. f. Bakt., vii., 1890. 

Schütz: Das Eindringen von Pilzsporen in d. Athmungswege u. die dad. bedinırten 
Erkrankungen d. Lune, Pilz d. Hühngrindes. Mittheil. a. d. K. Ges.-Amte, Ber- 
lin, 184. 

Siebenmann: Die Fadenpilze Aspergillus flavus, niger u. fumigatus, Eurotium re- 
pens, u. Aspergillus glaucus, Wiesbaden, 1883; Die Schimmelmykosen d. Ohres, 
Wiesbaden, 1889. 

Soltmann: Soor. Eulenburg’s Realencyklop., xxii., 1899. 

Virchow: Beitr. z. Lehre v. d. pflanzlichen Parasiten. Virch. Arch.. 9 Bd., 1856. 

Zenker: Hirnabscess. Juhresber. d. Gres. f. Natur- u. lleilk. in Dresden, 1861-62. 

Zürn: Die Schmarotzer in u. auf dem Körper unserer Haussäugethiere. ii., Weimar, 
1887. 


( Thrush, ) 


Bohn: Soor. Grerhardt’s Handb. d. Kinderkrankh.. iv. 

Cao: Qidien u. Oidiomykose. Zeitschr. f. Hyg.. 44 Bd.. 1900 ( Lit.) 

Fischer 1. Brebeck: Zur Morph. u. Syst. d. Kahmpilze. Monilia candida u. d. 
Soorerreger, Jena, 1884. 

Grawitz: Purasit des Soors. Virch. Arch.. 105 Bd.. 1886. 

Heller: Zur Lehre v. Soor. Deut. Arch. f. klin. Med.. 55 Bd., 1805. 

Kehrer: Der Soorpilz. Heidelberg, 1883. 

Linossier et Roux: Champiguon du muguet. Arch. de med. exp.. 1890. 

Plaut: Syst. Stellung d. Soorpilzes, Leipzig. I885: Neue Unters. z. syst. Stellung d. 
Soorpilzes. Leipzig, 1887. 

Rees: Soorpilz. Sitzungsber. d. Phys. -med. Sec. zu Erlangen. 1877, 1878. 
Schmidt, M.B.: Die Localisation d. Soorpilzes in den Luftwegen u. sein Eindringen 
in das Bindegewebe der Oesophagusschleimhaut. Beit. v. Zeigler, iii., 1890. 
Steiner: Zur Pathogenese d. Soorpilzes. Chi. f. Bakt.. xxi,. 1897. 
Teissier: Champignon du muguet. Arch. de med. exp., ix... 1897. 


x 179. Thread-fungi are to be regarded as the exciting cause of 
disease in certain affections of the skin, as farus, herpes tonsurans, 
pityriasis versicolor. erythrasma. In all of these diseases the epithelial 
parts of the skin contain colonies of hyphie and conidia, and there re- 
mains no doubt that their presence causes in part tissue-degenerations, 
and in part proliferations and inflammations. 

The fungus of favus (Fig. 507) is usually called Achorion Schönleinii 
(discovered by Schonlein in 1839). 

Favus (tinea farosa, scald-head) affects particularly the hairy portions 
of the head, more rarely other regions, as, for example, the substance of 
the nails. It is characterized by the formation of dises (favus seutula), 
varying in size from that of a lentil to that of a five-cent piece, of a sul- 
phur-yellow color, and indented or pierced by a hair. In an abortive 
course it may merely form scales similar to those of herpes. 








676 THE PATHOG IC MOULDS AND YEASTS. 
According tu Kaposi, the favus seutulum originates as a smal 
lying under the epidermis and penetrated by 
Ww Wee of. a lentil and then form: 
, indented d ing through the upper ly 
> The seutulum consists of hyphe and conidia spor 
cup-shaped depression of the s beneath the ho! 
ve it. If the mass be removed during life, thc 
red moist surface. The favus forms a white, ert 
mass whieh is easily disintegrated in water. 

If the seutula are not removed, they join together to foru 
When the epidern is desquamated the fav u: 
Land dries up inte Howish-white, mor ik 
appear lust covered with dust, and 
out, sinee the mycelia and conidia of the fungus penet 











































el 









© into 








t and hair-bulb, as well a: » the sheath of the} ot. 

Throngh the growth of the fungus the hairs may not 
shed, but the papill At the same time 
produced i i re or Tess 
inflammation wh y Sc cter. 

The development of achorion in the nails (onychomycosis Tara 








rise to sulphur-yellow depo: 
of the nails with simultaneous looseni 
same, 

Trichophyton tonsurans, the fungus of herpes tonsurans (i 
itch.” ringworm” +, consists of long narrow threads, branching bu 
and with few eonid: It forms no scutulous masses, but penetrate 
into the hair-shaft, and makes the hairs brittle. Tt shows certain 
ences of growth, according to whether the herpes develops upo 
surfaces or upon areas devoid of hairs. 
Herpes tonsurans cupillitii forms bare dises ¥ 
a five-cent piece to that of a doll: These spots in wh 
broken off short look like pli which the hair has 
The sur s smooth or covered with se 
the border of the dis 


prin thickenings of the pare: 
x and cheesy disintegratior 






















ize from 
bh the hi 
been badly s 
nd somewhat redd: 
If the fungus-threads penetrate into th 





















follicles, pustules and seabsare formed. Such dises may appear i 
places, and may constantly inerease in size until healing: final, 


s vesicles ı Herpes to, 
‘les ( Herpes tonsuraı 
mosus}. At times red spots appear in numerous places; these ¢ 
spread, and as rapidly heal, The fungus is found between the 
most st bene neum (K: 
|, the nail becomes cloud: 
off, and is easily broken—a condition designated as onychomyeosia 
phytina 

Streosix par s through the fact that the development 
fungus i rd by a severe inflammation of the hairy p: 
the skin, leading to infiltration and suppuration—that is, to the 
tion of pustules, absces and papillary proliferations, Accord 
nd others eczema marginatum is also caused by the triel 
ton tonsnrans. The condition occurs in those regions where two st 
of skin come into contact with each other and are macerated by 
and is characterized by the formation of vesieles, pustules, and 
which are situated in the periphery of a pigmented surface. 







































PITYRIASIS VERSICOLOR. ERYTHRASMA. BIT 


Microsporon furfur, the fungus of pityriasis or mycosis versicolor 
or dermatomycosis furfuracea, occurs likewise in the form of hyphw 
and conidia, which are somewhat smaller than those of other skin-fungi. 
The pathological changes produced by this fungus are characterized by 
the formation of pale yellow or is 
brownish-red spots, varying in size from that of lentil to th t of the 
hand, sometimes smooth and shiningsat other times dull and ¢ i 
and of irregular shape. They may be spread uniformly over large 
of skin; and are found chiefly upon the truuk, neck, and flexor surfaces 
of the extremit but never upon the hands, feet, or face. 

Microsporon minutissium is the name given to a thread-fungus, 
which is found in the skin affection known as erythrasma (von Bären- 
sprung). The disease is charac- 
terized by the formation, on the 
r side of the thigh, of brown 
ches, which 



































s large as the palm of the 
hand. The fungus is found in 
i smaller than 






ad-fungi occurring in 
the diseased areas of the skin 
be cultivated upon proper 
a (ag: agar-glycerin, 
gelatin, potatoes, blood-serum, 
ete. ), and on such the conidia de- 
velop into single and branching 
threads, which become jointed 
(Fig. 512, a), and form chains of 
short cell (b). Club-like forma- 

















tions which frequently appear 

ends of Is i 312. Culture of Trichophyton tonsurans. 
upon the ends of the threads in ,,F10,52 Culture of Trichophyton om ere ee 
cultures, are regarded by Quincke cate walls; D, threads with thick-walled, short seg- 


mente, some of them being spherical. x. 270, 





and Elsenberg as imperfeet spo- 
rangia. The botanical position of 
these fungi is not yet determined; and nothing is known with certainty 
concerning their distribution outside of the human and animal body. 

According to Quincke, three forms of fungi occur in favus-masses, 
two of these being varieties of one species of fungus. Elsenberg found 
only two, which he regards as being varieties of the same species. Pick, 
Plaut, and Biro believe firmly in the etiological unity of favus. 

Sabouraud advances the view that the fungi causing trichophytosis 
represent very different species, all of whieh belong to the genus Botry- 
tis. Krösing distinguishes three groups of trichophyton-fungi according 
to the different appearances of the cultures on potato, and emphasizes, 
moreover, the differences in their organs of generation and fructification. 
Rosenbach, who has studied the moulds occurring in deep suppurating 
inflammations of the skin, differentiates several trichophyton-fungi as 
the cause of these affections. 

According to Spietschka the Microsporon furfur may be cultivated 
from the scales of the skin, and in cultures can be very well differentiated 
from the other pathogenic thread-fungi. Through the inoculation of the 
fungus a typical mycosis may be produced in man. 


























678 THE PATHOGENIC MOULDS AND YEASTS. 


From the great number of recent investigations by var 
is impossible to deduce anything definite concerning the nu 
of favus- and trichophyton-fungi. It is, however, evide 
investigations that the nature of the nutrient medium is of ¢ 
of the growth (Sabouraud, Waelseh), and 
findings be referred in a great measure to differen 
trient media on which the moulds were grown, 

Tnoculations with fu grown in cultures, into the s 
ws, rabbit which were made by Grawitz, B 
and others, gave partly negative, partly positive results. 
Plaut the inocu give positive results when sy 
has already taken place in the cultures. 

Von Hebra has deseribed (Wiener mel. Blätter, 1881: = Die Kra: 
Haut,” Braunschweig, 1881) as dermatumyemis diffuer flerorym a pect 
inatosis, which occurs on the elhow und bend of the knee, and is thou 
by fungi, which are like those of pityriaain cersicalur, 

Farna and herpes tonsurans occur ulso in domestic animals, 
rata (ef. Frideerger and Fröhner. “Lehr, d. spec. 

Waelech inoculn it 






















































Intravenous in, 
lungs of these animals form of pee “Mut abereuen 
which fungus threads have developed in a manner 
cosis. ii 











i causes the so. 

pine-spider Gastropuchia ] 
kills the destructive carth-cat 
Cmpuet attack especially th 





el eh "Bh avin ‘lestrays th 
megaapermum, a dlack-colored fungus, 
segetum, Fungi belonging to the fam 
cabbage-butterfly (mpm radicama, and the house-tly (E! 
growing all through the caterpillar and tinally kilfing it. 
cording to Harz (Juhresdber, d. Münchener T’hierarzueisehnle, Y882-83 
the musculature of crayfish, and is the cause of the craytish-pest. 































Literature. 


(The Fungi of the Dermatomyeosex. ı 





Jour, of Dermatol.. 
Arch. f Derm., 1808. 
Vierteljahrsschr. f, Derm. u. Syph.. x 
a forina pemfigoide et polinenrite tr 
Arch, per le vi.. 1892 



















alfetto da 
Bukowsky 


s dermien. 2 
v. During: Dermatomy . E arg’s Jahr. 1896 (Lit. 
ber den Fay uspilz bei Favine herpeticn 
Fabry. Ucher Favus, Arch. f N 
180, 
Fox and Blaxall: Plurality of Ringworm Fungi. Trans, of the Path. : 
1807. 


















vus u. Herpes tonsurans. ‘th. Arch., 108 Bd., 18: 










Iymorphismus pathogener Hyphomyceten. Arch, f. Derm.. x 
Ti npil Arch. f. Dert 1896. 
f. Derm., 1891 


‘orresphl. £. Schweizer Aerzte. 1807. 

neuen Favusarten. Cbl. f. Bakı 
„N and d. Dermatomy kose 
sfrage. Arch. f. 


Pick: Favus. 
f. Derm., 
INOR, 

Pick u. Kral: Unters. über den Favus. Arch. f. Dom 

Pleut. Beitrag zur Favusfrage. Cb. f. Bakt., xi, 





1891, Ergiinz: 





THE DERMATOMYCOSES. 6,9 


Quincke: Ueber Favuspilze. Arch. f. exper. Path., xxii, 1886; Monatsh. f. prakt. 
Derm., vi., 1887, viii., 1889; Arch. f. Derm., 31 Bd., 1895. 

Roberts: The Phy siology of the Trichophyton. Jour. of Path., iii., 1895. 

Rosenbach: Ueber die tieferen eiternden Schimmelerkrankungen d. Haut, Wiesbaden, 


1894. 

Sabouraud: Trichophytie. Ann. de Derm., 1892; Trichophyties A dermite rofonde. 
Ann. de l'Inst. Pasteur, vii., 1893; My cose innominée de l'homme. viii., 
1894. 


Spiegler: Ekzema marginatum. Arch. f. Derm., 38 Bd., 1897. 

Spietschka: Microsporon furfur. Arch. f. Derm., 87 Bd., 1896. 

Unna: Drei Favusarten. Fortschr. d. Med., x., 1892. 

Waelsch: Anatomie des Favus. Arch. f. Derm., 31 Bd.. 1895: Anatomie d. Tricho- 
phytosis. Ib., 35 Bd., 1896; Mannigfaltigkeit d. Wachsthums d. pathog. Schim- 
melpilze. Tb... 37 Bd., 1896; Anatomie d. Pityriasis versicolor. Ib., 38 Bd., 1897; 
Favus bei Thieren u. dessen Bezieh. z. Favus d. Menschen. Prag. med. Woch., 
1898, 








CHAPTER XI. 


The Animal Parasites and the Diseases Prodıx 
Them. 


1. Protozoa. 


§ 180. Of the Protozoa occurring as parasites in man, only 
number was known up to a few years ago; and even the know 
possessed but slight significance, since there could be ascribed. 
no marked influence upon the 
Through the investigations of the 
years, however, different forms ha 
recognized as the cause of morbi 
esses; and it is quite possible th: 
are still other protozoa capable of « 

pathological changes in the huma 
The forms already recognized are 
sentatives of all four classes of prot 

Of the Rhizopoda there occur ir 
testine three amoebae, known as the 
coli vulgaris, the Amoeba coli mitis (Roos, Quineke), and the Am: 
enterie (Kartulis, Osler, Councilman, Latleur, Kruse, Pasquale 
nterie is certainly distinguishable from the oth: 
Ameeba coli vulgaris and the Ameeba coli mitis resem] 
very closely, and may possibly be identical. 

The Amoba coli vulgaris is a harmless intestinal parasite w 
not infrequently present in the intestine (Roos, Kruse, Pasquale 
Ameba coli mitis was observed by Roos and Quincke in cases of 
enteritis in patients who had alw lived in North Germany. 

The Ameeba coli mitis consists, according to Roos, of a prote 
cell-body, from 25-35 » in diameter (in the spherical condition ). 
hibits slow movements, and very frequently encloses foreign bod 
example, bacteria and food-remains (Fig. 513, a). Besides the 
form, there occur, according to Roos, also encysted, spherical 
which are surrounded by a double-contoured membrane, and 
clear, round vesicles in their interior (Fig. 512, 5). When fed 
mals (cats) no pathogenic properties are disclosed. 

The Ameba dysenteriz (identical with the Amoeba coli deser 
Loesch) has a diameter, according to Roos, of from 15-25 2, but 
ing to Kruse and Pasquale, from 10-50. In the cell-body the: 
be recognized a homogeneous ectoplasm and a variable granula 
plasm, the arrangement of which varies according to the form 
animal (Fig. 5l4,a). By staining, anucleus may be made visible 
the cell. The cells are eapable of active movement, and assume 1 
the most varied shapes (d). They very often contain foreign 
particularly red blood-cells or rem: of such (6), or are studdı 

680 












































AMCEBA. INFUSORIA. 681 











clear vacuoles (ce). ‘According to Roos, they may also become en- 
eysted (e). 
According to investigations by Koch, Kartulis, Kruse, and Pasquale, 
they are invariably present in the dysentery prevailing in Egypt, and 
are usually also demonstrable 
in the dejecta. They have a b 
also been observed in cases of & ® @ 
dysentery in Russia (Loesch, 

atin), in America (Os- 
ler, Councilman, Lafleur, Lutz, 
Dock), in Germany (Roos), 
and in Austria (Kovacs). Ac- 
cording to investigations by a6 {pe 2 
Kartulis, Councilman, La- 
Pa and othe ieee, ul Bika arte, nt te sch mit 

'asquale, and others, it can- am 

uot be doubted that they are AA racy irs una sa 
of some significance in the 
origin of certain forms of dysentery. It is only questionable whether 
they alone, or only with the aid of changes produced by bacteria, are 
able to bring about pathological changes. In support of the latter 
theory is the fact that, when present in the tissues, they are always ac- 
companied by bacteria. 

Amebic dysentery is characterized by the occurrence of & hemor- 
rhagic catarrh, and by the formation of circumscribed ulcers with under- 
mined edges. The amebe (Councilman, Lafleur, Roos, Kruse, Pas- 
quale) increase not only in the intestinal mucosa, but also penetrate into 
the mucosa and submucosa, and there form large colonies, in the region 
of which the tissue undergoes necrosis without the formation of any large 
amount of exudate. By the rupture of the submucosal foci through the 

mucosa there are formed ulcers with undermined 
edges, which, gradually increasing in size, may attain 
large dimensions. 

If abscesses of the liver arise during the course of an 
amoebic dysentery, these may also contain the amebee 
in addition to bacteria; and it may be assumed that 
the former also take part in the destruction of the 
liver tissue. 

The amebee of dysentery are pathogenic for cats, and, 
when fed to them or when introduced into the rectum 
of the animal, cause a rapidly progressive, often fatal 
dysentery, which is similar in all respects to amebic 
dysentery in man. The amcebe also penetrate into 
the mucosa and submucosa of these animals. 

Of the Infusoria, both flagellated and ciliated forms 
occur in man. Of the latter form the best known is 
the Paramecium or Balantidium coli. (Fig. 515). 
This is a large infusorium thickly set with cilie, 
which has been demonstrated many times in the large 
intestine and in the dejecta in cases of diarrhea, and 

may stand in a causal relation to the intestinal catarrh. Of the flagel- 
late infusoria, there may be mentioned first the Cercomonas intesti- 
nalis (Fig. 516), a pear-shaped form having a spinous process at its 
pointed end, and a flagellum at its blunt end. It has also been found 








he THE ANIMAL PARASITES. 


in the intestine in catarrhal conditions, and in cholera and ty 
cases, According to Bütschli and Perroncito it is identical with ı 
stoma entericum of Grassi and Megastoma intestinale of Blancharı 
is in part passed off in the firces in an eneysted form (Perron 








Oy 


In 
aN 








FIG. 516, -Cereomonas intedtis FUG. 515. Trichemenan vagin- 
alia, (After Davaine.) alis. (After Köcılker.s 





particularly when no diarrhaa is 
ut. 





present. It occurs also in mice, 
dogs, sheep, and rabbits (Grassi), and attaches itself firmly 1 
face of the intestinal epithelium. 

Kannenberg found a cercomona: sputum ina case of lung 
grene.  Inassociation with it there wa: found Monas fens, a sph: 
infusorium with a flagellum. Strong reports a similar finding. 

Of the genus Trichomonas an oval infusorium furnished with 
flagella and acomb-like unduiati its entire length, onc 
cies, Trichomonas vaginalis, oc sin the vagina (Fig. 517), anc 
other, Trichomonas intestinalis, in the intestine ( 18). 

Marehand found trichomonads with four thread-shaped flagella 
no undulating membrane in the urine of a man. These were prol 
identical with Trichomonas 5 s four fla; 
Miura reports a observation Grimm saw tlagellated infu 
in abscesses of the liver and lung. Lindner found ciliated) infusor 
the crusts of an itching eczema of the sealp. 












































Lait, on the ground of a thorough investigation, is of the opinion that leuk 
is an infectious disease caused by protozoa: a sc s se of the su 
parusites, a hemameba leukeemize magna and u hemameba leukzemis par 
voray), the first of which occurs in myelogenous leukwini 
ety, 1 is supporter 5 
ns changed by the disease, and he sue 
rating the presence in 
like and large amha like bodies, as well ass 
segmented bodies in the morula 
e appearances most thorough! 
: and was able through injections of blood or of pulp made froi 
ms of organs, into the ingu of the rabbits (the injections being direeted t 
the brain), to produce a dis und to tind ii the blood. of te {noe 
nimal the stru plated forms, Fürst has explained tl 
nothing more than artefacts. and regards tl 
al, swollen, washed-out, and macerated mast-cell granules. Léeét holds 
view in spite of this attack, un y the fact that his hema 
show a specific staini which the ma 
granulations and similar ¢ that the hemame! 
found in cells wit hat mulation as v ul that they 
. Whip-, and flagellate-forms, and ‘form bodies even as lurge s 
in diameter, and finally, that they do not occur in normal blood, 
Recently Léert has reported observations on the spore-like resisting forms ı 
mamarba leuk magna, which he Iul seen in the blood-forming organs of a ¢ 
The earlier described flagellate-forms of the parasite seen in infecte 
hits he interprets us forms standing in relation to the sexual reproduction of the | 
murhie, since the amarbw and flagellated forms unite with each other. In man th 
in said to reproduce chiefly by sehizogony, in rabbits by spor sporopony et. 
Df eaceiia und mulariıl plasmodin. SS 181, 189). To the parasftes van 























ial staininge netl 
bload-corpuseles of sinall granul 
spindle-, and erescent shaped. stru . 
Flagella were also observed, Lévrit studie 
























































FLAGELLATES. TRYPANOSOMA. 683 


which, according to his latest publication. he finds in the nuclet of the white blowl- 
cells. he gives the name Hamamaba leukemia parca intranuclearis, He finds these nu- 
eleoloid bodies also in pseudoleukemia, most abundantly in the spleen, to a less extent 
in the lymph-gla 

Hensen found infusoria with one to three flagella in the stomach-contents of a case 
of gastric cuncer. Jucoby and Sehaudinn describe two ciliated infusoria obtained from 
the intestinal contents of a man suffering with diarrhea; to these Schaudinn gave the 
names Bulantidium monatum and Nyctotherus faba. 





ing to the lates have been many times observed in the blood 
of animals. In 1875 Rättig re} 








and frogs. In 1894 Bruce discovered that the tartse disease (fly disease, nagana) which 
occurs in Zululand and affects the cattle, horses, asses, and dogs of South Africa, is due 
to flagellates trausmitted through the sting of the tsetse-fly. 

All the forms of flagellates observed in the blood of different aninuls are generally 
designated us Trypanosoma sanguinis (Gruby.)aud different species or varieties of the 
same are distinguished. Fon Wunielewski classes with the trypanosoma of Gruby only 
the blood-parasites of frogs and fishes, and would retain for the trypanosoma of manı- 
mals the name Herpetomonas given by Kent. The form known as Trypanosoma san- 
gninix is widely distributed among the wild ruts (brown rutsand gray rats), the infected 
Tats showing no recognizable symptoms. According to nun Wiunteewskt the parasite i 
8-30 u long, 2-3 broad, sat its posterior end a beuk-like process Fig, 519, A), 
o interior a flagellum (d), and on its side an undulating membrane (c). By proper 
staining (Romanowski's stain gives the best results) there may be made visible within 
the cella nucleus («), and at the same time it may be recognized that the flagellum is 
continued us a border along the outer edge of the undulating membrane (e), and takes 
{te rise at the posterior end of the animal from a rod-shaped body (0) lying upon the 
protoplasm-body. Rubinowitech und Kempner regard this rod-shaped body, which 
stains similarly to the nucleas, as a constituent of the nucleus separated in space from 
the vesicular chromatin-framework, and designate it the nucleolus. Likewise, Plim- 





















FIG, 519.-Trypanımoma {herpetommax) sanguinis murium in different stages of development. 
(After A. von were.) Ari developed paraate with nucleus (a). rod-shaped body (b}, undulat- 
‘membrane (c), and flagellum (d) : with two nue + C, parasit 
oe Nucleus abd two red-ehaped Godlee D, division into two parasives; Z, parasite with four nuctel 
and four flagelia; F, viduals united into a colony. X 1,500. 





mer and Bradford distinguish a macronucleus and a micronucleus; but according to von 
Wasielenski structure does not lie in the cell-plasma, but in the periplastenı, from 
which the flagellum and undulating membrane also 

‘As Rabinowitsch and Kena =. tha development and multiplication of 
the parasite can best he nsritoneal inoculation of healthy 
white and spotted r= taking place, partly in the 


+‘. EEE pene 


cores ° ° Loco lee Yaaraıl". - wil Ara on 


« - - t. - . me mene 
Bo a EU CS 1 
en TUT ALT IL Ir #* I Biel er > mon In 
PP Er . LOST MIT ne) te TEEN ee 2 tees 
- -- . wea ee ee OO eC a Teed Te 
- - m ~— v «=f € . a. bd aa ...ı2 2 = re ors 
. etl. La . MI. de oo. TUE sL 
- - - ae em ate Missa N oer - Ok 
wo Lan . Ten met Delta WTILI de Tet et eee no a 
Tone - . . . ln "he. 
” ° oe: . . ass a ne kh eer ame 7 iy TS ee Ten 
I. Tee oo be, u Le ae Dat tun FT“ 
"pn 7 - un un 7 a att ers ry 1.2, „eltm  @ 7-  Sl k 
a bee wea a ul. Oe eT art Tel 0 oc 8 Teen ST Ss 
ar ot? nee - L - ie ae | bee TT Gls lad FE et | _ 
eee Mae eee ee Te Te te Utne se il Dt Lat 
ee Lee u we ere eet Te Te nn “les 
ot ines I . 1 al . . = al - alt 
2. in mer. Let teat IT ent LT on det le 
or) ae id ma a II. ett ee oe ZImeeel ie it tor neem te lt In 
Moe en aso lhe eee La Seamer " 
wee Zuge Dil Ya 
oo reer 
BAS te bi ces Feen ee 
a. Sawa Det at eet Ten LI MI Bast nm lig 
ZT an te Dette LIE N TIL TI NT 5 
DERZEIT nn et es Se, ne 
+O oe .: ts ole tte Tene 38 Te uae War post lst 
Tera te et bette Le ntl AT OP ee 8 
. os - 
BE; 70. “ee 2 i eS auto Tom 
ts ats 
Perel zg a - ‚ en Duo We * State 
3.0.08 ta Fatt er nr oe ae 
Harc.z2 . . a men mn we 
Jarnwıa. ne Sent an ise 
Karta 1.0.0 Det le eee TF at SET Fat te nes 
poe emer ce Tt ia. „,i-Irureı “evel:  Hvrz 
arse! 
Kuvarı ie. Tm ee Dean To He N “eo 
Krune . RPasyaase 00-7 00 te nm. Leterme aes Zimt: Hee 
-'1., 
v. Leyner. Schasdın lest. 2 „nnr.nm in Asvites™ ssi: ft Desalen 
5 „. -.. Run. Neun Perl IS 
Lonhh "I: ernatte Era ae snap vor. Ternd. TEeexdarı Virech. Arch. 6° 


Lowit Yoo feudal ae Pit zoeniutectt og Wiestaaden 1900 Speeif. Farts: 
IDatatieotea de aCtib boasts. Beft) ov Ziecier, Navi. 1900, Weitere Be. 
Sone herab Parasiten ocer Te caddie Zeitschr. f Heilk.. xvi. 1900 

Lstz Zur Kenntnis ner Aridhenestertys. Ch fr. Bakt.. x.. 1801 

Mrasiutin Feber ee Amöbenaus Parasiten des Diekdarıms. Cbl. f. Bakt . vi 

Mereschowsky Arch. mikr. Arat. sel. INES, 

Onlor Urber die bei Dv-cnterie vorhandene Amiöbe. Chl f. Bukt.. vil. 18a 

Pfeiffer Die Protozen als Krankheitserrerer. Jena. 1805. 

Posner Armohen im Ilarn Beil. Klin. Woch.. 1893. 

Quincke Protozen nenteritis. Berl. klin. Woch.. 1899. 

Quincke tu Roos Amöhenenteritis. Berl. klin. Woch.. 1893. 

Roon Zu Kenntn ed Amöbenenteritis, Arch. f. exp. Path.. xxxiii.. 1804. 

Kehneidomubl Die Protozoen als Krankheitserreger. Leipzig, 1898. 

Hehuberp Du ganze itischen Amöben des menschl. Darıns. Cbl. f. Bakt., xiii., 


INFUSORIA. 685 


Tajardo: Amöbenenteritis und Hepatitis. Chbl. f. Bakt., xix., 1896. 

Tenoglia: Entéro-colite paramceba coli. Arch. ital. de biol., xiv., 1890. 

Türk: Ueber die Himamdben Löwit’s. Verh. d. Congr. f inn. Med., Wiesbaden, 1900. 
Wesener: Unsere gegenw. Kenntn. über Dysenterie. Cbl. f. allg. Path., iii., 1892. 


( Infusoria.) 


Bruce: Report on the Tse.se Fly Disease, Ubomobo, 1895, 1896. 

Danilewsky: Zur Parasitologie des Blutes. Biol. Cbl., v., 1885-86; La parasitologie 
du sang, Charkoff, 1889. 

Dock: Trichomonas as a Parasite of Man. Amer. Journ. of Med. Sc., 1896 (Lit.). 

Doehle: Blutbefunde (Geisselinfusorien) bei Masern. Chbl. f. allg. Path., iii., 1892; 
Zur Aetiologie d. Masern, Pocken, Scharlach, Syphilis (Protoplasmakörper im 
Blute und in Pockenpusteln). Chl. f. Bakt., xii., 1892. 

Eberlein: Infusorien im Wiederk&uermagen (kommen normal vor). Cbl. f. Bakt., 
xx., 1896. 

Ehrenberg: Die Infusionsthierchen, Leipzig, 1838. 

Francis: An Experimental Investigation of Trypanosoma Lewisii. Bull. U. S. Hy- 
gienic Lab. No. 11, 1903. 

Grassi: Protistes endoparasites. Arch. ital. de biol.. ii., iii., 1882-883. 

Grassi, B., u. Schewiakoff: Megustoma entericum. Zeitschr. f. wiss. Zool., xlvi., 


1888. 

Grimm: Leberabscess u. Lungenabscess mit Infusorien. Langenbeck’s Arch., 48 Bd., 
1894. 

Hausmann: Die Parasiten der weiblichen Geschlechtsorgane, Berlin, 1870. 

Hensen: Infusorien im Magen bei Carcin. ventriculi. Deut. Arch. f. klin. Med., 59 
Bd.. 1898. 


Jakoby u. Schaudinn: Neue Infusorien im Darm. Cbl. f. Bakt., xxv., 1899. 

Janowski: Flugellaten i. d. Fıwces. Zeitschr. f. klin. Med., 31 Bd., 1896; Balantidium 
coli im Stuhl. Ib., 32 Bd., 1897 (Lit.). 

Koch: Reiseberichte über Rinderpest, Bubonenpest, Tsetse- oder Surrakrankheit, 
Texasfieber, tropische Malaria, Schwarzwasserfieber, Berlin, 1898. 

Kölliker u. Scanzoni: Ucb. Trichomonas, In Scanzoni’s Beitr. z. Geburtsk., Würzb., 
1855. 

Lambl: Cercomonas et Echinococcus in hepate hominis. Russ. med. Bericht, 1874. 

Lang: Protozoa, Jena, 1901. 

Laveran: Des try panosomes parasites du sang. Arch. de méd. exp., iv., 1892. 

Lindner: Erzeug. v. Hautkrankheiten durch e. Protozoenart. Monatsh f. prakt. 
Derm.. xvi., 1893. 

Malmsten: Ucber Balantidium coli. Virch. Arch., 12 Bd., 1857. 

Marchand: Ucber Trichomonas intest. Virch. Arch., 64 Bd.; Trichomonas im Harn 
eines Mannes. Cbl. f. Bakt., xv., 1894. 

May: Cercomonas coli hominis. Deut. Arch. f. klin. Med., 49 Bd., 1892. 

Miura: Trichomonas vaginalis im Urin eines Mannes. Chbl. f. Bakt., xvi., 1894. 

Moritz u. Hölzl: Megastoma entericum. Münch. med. Woch., 1892. 

Motter: Zur Kenntniss des Balantidium coli. Inaug.-Diss., Kiel, 1891. 

Musgrave and Williamson: Trypanosomiasis of Halser in the Philippine Islands, 
U.S. Govt. Lab. Rep., 1903. 

Novy and MacNeal: Cultivation of Trypanosoma. Vaughan Festschrift, 1908. 

Perroncito: Ueber die Einkapselung des Megastoma intest. Cbl. f. Bakt., ii., 1887. 

Plimmer u. Bradford: Morphologie d. Tsetseparasiten. Cbl. f. Bakt., xxvi., 1899. 

Rabinowitsch u. Kempner: Rattentrypanosomen. Zeitschr. f. Hyg., 30 Bd., 1899 
(Lit.). 

Rättig: Ueber Purasiten des Froschblutes. Inaug.-Diss., Berlin, 1875. 

Rieck: Sporozoen als Krankheitserreger bei Thieren. Deut. Zeitschr. f. Thiermed., 
xiv., 1889. . 

Roos: Ueber Infusoriendiarrhöe (Megastoma entericum, Trichomonas intestinalis, Cer- 
comonas hominis, Cercomonas coli u. A.). Deut. Arch. f. klin. Med., 50 Bd., 1898. 

Rouget: Trypanosome des mammiféres. Ann. de l’Inst. Pasteur, 1896. 

Ruge: Ueb. d. deutsche Proteosoma (bei Sperlingen). Cbl. f. Bakt., xxix., 1901. 

Schmidt: Trichomonas im Auswurf. Münch. med. Woch., 1896. 

Sievers: Balantidium coli und Megastoma entericum. Zeitschr. f. klin. Med., 30 Bd., 
1896; Arch. f. Verdauungskrankh., v., 1900. 

Stein: Der Organismus der Infusorien, Leipzig, 1867-78. 

Stieda: Ueber Balantidium. Virch. Arch., 35 Bd., 1866. 

Streng: Infusorien im Sputum bei Lungengangrän. Fortschr. d. Med., x., 1892. 

Wasielewski u. Senn: Flagellaten d ttenblutes. Zeitschr. f. Hyg., 33 Bd., 1900. 





656 THE ANIMAL PARASITES. 





Wittich: Spirillen im Blute von Hamste CH. f. d. med. Wiss, 1881. 
Zenker: ('ercomonas intestinalis. Deut, Zeitschr. f. prakt. Med., 1879. 





X 181. Of the Sporozoa occurring as parasites in man and 
mammals, the coccidia are to be mentioned first. In their you 
they exist as non-encapsulated inhabitants of epithelial cells, part 
in those of the intestinal canal and its adnexa, the liver especia 














filled with ewenlia and Mned wit 
dia nodules (Maller's fluid, hae 
covered with epithellun : + 





ans of excretion. Some of the 
with a capsule and become chang: 
yal permanent cysts or odeysts (Schaudinn), which leav 
resting-place and usually also their host, and under certain cor 
form sickle-shaped sporozoites through the repeated division ¢ 
cell body (sporegony), Through the taking-up of sporozoite-con 
s into a new host there is produced an infection of the la 
the sporozoit re set free and seek out epithelial cells fo 
elopment. 

Besiden this form of multipli 





round 

























ation there occurs within the i 
an also a repreduction schizogony—that is, there are dev 
m mature but non-eneysted individuals, by means of segmetr 
a large number of new siekle-shaped i 
uals, the so-called merozoites, which s« 
epithe! Is, and develop further 
sun 























Coccidium oviforme (I* 21) is 
site of the intestine and biliary pa 
occurring especially in rabbits. K 
and Pitre ind similar coceidia in 
a ritie exudate.  Podwyssozki el 

—Cowerdia from the biliary observed them in the human liv 
ot th rant vie of og In the liver of rabbits the inva: 
ment (MAller's: uid, b coccidia leads to the fo ion of 
nodules which may reach the size of: 
nut, and are desig’ x corvidia-i 





























tptarn ef as ‘These nodules ¢ vhite, 
granular and partis be tis un lowish-white mass. essent 


EPITHELIOMA CONTAGIOSUM. 687 


dilated bile-passages, the inner surface of which is more or less richly 
furnished with papillary growths (Fig. 520), and whose lumen contains 
great numbers of. coccidia. 

‘The coccidia occur in the bile-passages partly in the form of non-encap- 
sulated protoplasmic structures, and partly in the form of encapsulated 
bodies. Thesmallest coccidia, which are regarded as the younger forms, 
exhibit a coarsely granular protoplasmic structure (Fig. 521, a, 5), 
within which a nucleus (a) may occasionally be demonstrated. The 
larger forms exhibit on their outer surfaces regularly arranged granules 
(c, d), which stain intensely with hematoxylin. ‘The encapsulated forms 
oceur as oval, doubly contoured, clear bodies (¢, f, g, h) within which 
lies a variously shaped mass exhibiting also various forms of grauulation, 
but. never entirely filling up the space within the capsule. 

To the coceidia belong probably also those parasites which occur in 
the epidermis of man and form there peculiar growths known as epithe- 
lioma contagiosum (Fig. 522). In its fully developed condition the 
growth consists of a small nodule, about the size of a pea or larger, 
which is elevated above the surface of the skin, shows a small groove in 
its centre, and possesses a waxy lustre. 

On section there may be seen a lobulated epithelial growth (Fig. 522, 
d), with a central cavity opening externally (g), thus forming a growth 
resembling a gland; and it has been many times mistaken for a hyper- 
trophic sebaceous gland. It therefore represents an independent new- 
formation of epithelium due to a parasite. The parasites develop inside 
of the epithelial cells of the lobulated growth (¢), but are pressed by the 














Fic, 522.—Eplthelloma contagiosuin, Section through greatest diameter (MAlier's Auld, bermatoxyiin). 
a. Epidermis; b, connective tissue; c, sebaceous gi gland-llke epithelial proliferations ; ¢, para- 
Sica 4 horny” cell mingied with parasites: g. dct lied with boray eriibelum And parasite.” 518. 


growth of the adjacent epithelium toward the central cavity of the new- 
formation (f), and lie there in a meshwork of desquamated and horny 
epithelial cells. 

The earliest stages of development of the parasites occur in the epi- 
thelial cells as small protoplasmic bodies (Fig. 523, a, 6), which can be 
distinguished from the cell-protoplasm only with difficulty ; occasionally 
they contain in their interior small, distinct granules, and are therefore 
more evident. Later they increase in size, and finally fill up completely 
the epithelial cell (c, d, e), pressing the nucleus to one side. At the 
same time the granules within the cell (c) increase, and grow to larger 
bodies, so that the parasite finally becomes divided into a greater or less 
number of finely granular structures (d, e. f) lying in a finely granular 




















638 THE ANIMAL PARASITES. 


network. The nuck 
epithelial cell is destrc 
this time. 

The epithelial cell 
close parasites devel 
distinct membrane, 
comes more and mc 
defined, and surround 
site. The parasites 
expelled from the 
oval bodies which : 


Fit. 323.— Ee mninttie fying li epi ells closed ina capsule an 
‘gus stages of development. Iying Inside epithelial ce jomogeneous appeara 

Gaoher's fluid, hematoxylin). , Epithelial cells, en- fi r 
ing a protoplasmic body Inside of which ite siogle stain deeply with heer 


me kranulee: c_epithellal cell almost completely i i 
BIS vl paranlıcn: def paraattes conpletely olling The contagious epi 


the epliheilal cells and divided Into numerous separate may appear in great 1 
Bas beer deatroyedin Ps abouts, Ms one and the same i 
and several persons 
gether may be either simultaneously or successively attac 
spread of the disease is therefore referred to a contagion. 

Our knowledge of the significance of the so-called Miesc 
is still incomplete. They are tube-shaped structures whic 
infrequently found in the muscles of the hog (Fig. 524, a, 
sheep (especially in the oesophagus), and mice. They vary i 
lie within the muscle-fibres. In mature parasites the conte 
tubes are differentiated into single segments defined by a 
(Fig. 524), which enclose spherical (¢), kidney-shaped, or sic] 
bodies. The parasite is classed with the Sarcosporidia. Th: 
segments are designated sporocysts or sporoblasts, since within 
round or sickle-shaped spores (Rainey's bodies) arise. From 
















Fic, f24.—Mleacher's sacs, from swine-musie. a. b. Musele cut longitudinally and transy 
c. Longitudinal section. 


new Miescher’s sacs may develop under favorable conditions: 
Ingestion of meat containing sarcosporidia is not dangerous fo: 


‘As carly as 1870 Himer published observations of the development of ı 
their life-history has been accurately determined only in recent years, thn 


REPRODUCTION OF COCCIDIA. 689 


vestigations of R. Pfeiffer, Simond, Léger, Schaudinn, Schuberg, Siedlecki, Schneider, con 
Wasielewski, Labbe, and others. Lithe has recently collected in an excellent manner the 
results of the more recent investigations concerning the sporozoa (Centralbl. f. Bakt., 
Ba. xxvil., xxvill.). 

‘According to his presentation, the reproduction of coccidla occurs Partly through 
sporogony, partly through schizogony. The first method serves for the spreading of in 
fection and the preservation of the species, the second increases the extent of the infec- 
tion within the infected host. Sporogony is closely connected with a previously occurring 





Fig. 525.—Cycle of development of Coccidium Schuberyi. (After Schaudinn and Lühe). 1. 
zolie (or meroaeite) penetrating Into an epithelial ceil: #. mauonuclesr echizoat In an apltnelial call: 3, 
multinuclear schizont; 4 division of the echizont (schizogony) into numerous 


\ded by I ent 7, terletion f the 

roun loosened micı 8} ‘of ne macrogametes by 

3, young eye 9. odeysts with sporoblasts: 0. Ooeyain with sporooysin Goat Sontalatag. two. sport. 
zoltes : 11, sporozolte. 


copulation which in its course suggests the fertilization of the egg of the metazoa. 
An alternation of generations also takes place. 

The development and reproduction take place in the following manner: In schiz- 
ogony the sickle-shaped germ (Fig. 525, 1) arising as a sporocoite or mcrowotte develops 
within an epithelial cell into a schfzont (2) in which there soon takes place a multiplica- 
tion of the nucleus (3). There then results (on the second day after the over-feeding of 
sporocysts) a formation of merozoites (4) corresponding in number to the nuclei, and a 
residual body which is left behind after the segmentation. 

‘The merozoites again seek epithelial cells, and the same development begins anew. 
If the affected organ, as the result of these processes, becomes overcrowded with para- 
sites, there are then formed sexual individuals (Schaudinn). Some of the merozoites 
grow into large cells, the macrogumetes (6, 6) or female cells, which when mature throw 
off a portion of their chromatin-substance (6), and either remain naked or surround 
themselves with a capsule, which is provided with a micropyle. At the same time 
other merozoites develop into the male sexual cells or microgametocytes (5a, 6a), the 
nuclei of which divide into many daughter-nuclei. The latter approach the surface of 
the cell, and, surrounded by a certain amount of protoplasm, are constricted off, (6a) 
and then represent the microgametes (corresponding to the spermatozoa of the higher 
animals). The copulation of the microgametes with the macrogametes takes place in a 
manner similar to that of the fertilization of the metazoan egg, in that the microgamete 

netrates the encapsulated form of macrogamete through the micropyle, and the naked 
form through a certain point which pushes itself outward to form a prominence (7), the 
36 





690 THE ANIMAL PARASITES. 


conceptional protuberance. Sporogony follows the fertilization—that is, the 
is formed, in which, through the division of the nucleus and protoplasın | 
four sporoblasts (9), each of which late T produces two sickle-shaped sporoeoites 

Sarcosporidia have been observed in mammals (Rosenberg reports the 
sarcosporidia in-the heart-muscle of a European, Aartulisa similar finding 
dominal muscles of a Sudanese), birds, and reptiles. Their life-history is nc 
quately known; and at the present time (Zuühe) a classification of the sarcosp 
not be given. 

Numerous authors hold the view that other local pathological conditi 
tissues in man than those described above may be referred to sporozww. partic 
cinoma, Darier’s disease, Paget's disease, peculiar diseases of the uriuary pas 
It may, however, be remarked that this assumption in part is based upon erı 
part has not been absolutely proved by the investigations which have been n 
the present time. 

So far as careinoma is concerned, in spite of the great number of works o 
je 80 numerous indeed that they can scarcely be perused (cf. § 122), no pro 

n given that protozoa, coccidia in particular, are present within the epitl 
liferation and are to be regarded as the cause of the same. All the ap 
described as occurring in carcinoma cells, even the sickle-shaped formations w 
been thought to be convincing and those provided with a sort of capsule, may 
wise interpreted, and may be explained in part as changed nuclei, in part 
protoplasm of the cancer-cells, in part as cell excretions, and finally in part as 
Of cell-fusion or of the tal up of leucocytes by the cancer cella. 

The disease described by Darier us pevrospermose folliculaire eegetante, an 
by him to the presence of sporozoa, is very probably only an inflammatory a: 
the skin characterized ‘by a pathological cornitication (keratosis folliculaı 
Withe), in which little horny plugs and pegs are developed successively in t 
lium of certain parts of the body, while the cutis shows slight inflammatory 
According to Buzzi, Miethke, Rieck, Krésing, Petersen, and others, the “cor 
described by Darier as parasites, contain kerotohyalin and cleidin, substances 
present in cornified cells but not in gregarinse. 

Paget's disease is an affection spreading from the nipple, beginning with a 
like inflammation, and leading to superficial ulceration, and finally ending 
nomatous infiltration of the skin. It has been referred by Darter, Wieckham 
and others to the presence of a parasitic sporozoon in the epithelial cells; bı 
ever, either an eczema arising from other causes, and finally leading to canc 
is a primary cancer accompanied by inflammatory processes (Zhrhardt), in wi 
far changes take place in the epidermis, particularly swelling of the proto 
nuclei, with formation of vacuoles, and further proliferative changes, the pı 
pearanccs of which might be mistaken for parasites. 

Pisenti, Sileock, Ere, Bland Sutton, and Jackson Clarke have pointed out 
bility that the cysts occurring in the descending urinary passages in ureter 
are of parasitic origin. Lubarach and Aschoff have opposed this view; ton K 
upheld it. 

A 














ding to Kess and Guillebeau, coceidia may occasion in young cattle 
the int embling dysentery. 

Guarnieri (* Ric. sulla patogenesi ed etiol. dell’ infez. vaccinica e variolc 
per le Se. Med., xvi., 1892; “Uller. ric. sulla etiol. dell’ infez. vaccinica,” F 
L. Pfeifer (" Die Protozoen als Krankheitserreger,” Jena, 1895; “ Vaccine-co 
Zeitschr. f. Hyg. 23 Bd., 1896), E. Pfeiffer (“ Züchtung des Vaccine-erregers,” 
f. Bakt., xviii, 1895), and others (cf. Waxieleweki, “ Zelleinschlüsse bei Va 
ungen,” Centralbl. f. Bakt., xxi., 189%) consider the small, easily stained b 
rounded by a clear zone, which are found in the epithelium in the early 
variola and vaccinia, to be protozoa. Guarnieri has designated the suppos 
as Cyturyctes taccine. The parasitic nature of these bodies has not yet be 
strated. After Salmon (“ Parasites de la vaccine et de In variole,” Ann. dei 
teur, 1897) had spoken against such a view, Mickel (“Die Vaccinekörperel 
ton Ziegler, ii., Supplh., Jena, 1898) proved, through exact and carefully 
investigations, that in vaccinia at the point of inoculation into the cornea e 
tions of the epithelial cells undergo especial disease changes, and that from t 
plasm there arise those peculiar structures which have been mistaken for par 























COCCIDIA. EPITHELIOMA MOLLUSCUM. MIESCHER’S SACS. 691 


Literature. 
( Coccidia ; Parasite of Epithelioma Molluscum ; Miescher’s Sacs.) 


Barrat: The Nature of Psorospermosis, Journ. of Path., iv., 1896. 

Beck: Molluscum contagiosum. Arch. f. Derm., 87 Bd., 1896. 

Bertram: Zur Kenntn. d. Sarkosporidien. Zool. Jahrb., 1892, ref. Cbl. f. Bakt., xiv., 
1893. . 

‘ Bizzozero e Manfredi: Sul mollusco contagioso. Arch. per le Sc. Med., i., 1876. 

Clarke: Mollusc. contag. u. Coccid. ovif. bl. f. Bakt., xviii., 1895. 

Councilman: A Preliminary Communication on the Etiology of Variola. Journ. of 
Med. Res., 1903. 

Delepine and Cooper: A Few Facts Concerning Psorospermosis. British Med. Journ., 
ii., 1893. 

Eimer: Ueber die ei- oder kugelförmigen Psorospermien d. Wirbelthiere, Würzburg, 
1870. 

Gilchrist: Protozoa, etc. Johns Hopkins Hosp. Rep., i., 1896. 

Grassi: Sur quelques protistes endoparasites. Arch. ital. de biol., ii., iii., 1882, 1888. 

Grunow: Protozoenerkrankung (Coccidien?) des Darms. Arch. f. exp. Path., 45 Bd., 
1901. 

Guillebeau: Coccidium oviforme bei der rothen Ruhr des Rindes. Cbl.f. Bakt., xiv., 
1893. 

Hess: Die rothe Ruhr (Coccidienruhr) des Rindes. Schweiz. Arch. f. Thierheilk., 34 
Bd., 1892. 

Israel: Epithelioma folliculare. Festschr. f. Virchow, Berlin, 1891. 

v. Kahlden: Ueber Ureteritis cystica. Beitr. v. Ziegler, xvi., 1894. 

Kartulis: Pathogene Protozoen. Zeitschr. f. Hyg. xiii., 1893. 

Klebs: Psorospermien im Innern von thierischen Zellen. Virch. Arch., 16 Bd., 1859. 

Kromayer: Histogenese d. Molluscumkörper. Virch. Arch., 182 Bd., 1898. 

Johnson: A New Sporozoan Parasite of Anopheles. Journ. of Med. Res.. 1902. 

Labbé: Sporozoa, Das Thierreich, herausgeg. v. d. Deutsch. zoo). Ges., 5 Lief., Berlin, 
1899. 

Lang: Protozoa, Jena, 1901. 

Lühe: Ergebn. d. neueren Sporozoenforschung. Cbl. f. Bakt., xxviü., xxviii., 1900 
(Lit.). 

Künstler et Pitres: Psorospermie trouvée daus une humeur pleuritique. Journ. de 
Micrographie, 1884. 

Malassez: Sur le psorospermose du foie chez le lapin. Arch. de med. exp., iii., 1891; 
Sur les nouvelles psorospermoses chez l'homme. Ib., ii., 1890. 

Miescher: Verh. d. Naturforsch. Ges. zu Basel, 1843. 

Neisser: Ueber das Epithelioma contagiosum. Vierteljahrsschr. f. Derm. u. Syph., 
1888; Der gegenwärtige Stand der Psorgspermosenlehre. Arch. f. Derm. Ergän- 
zungsh., 1892. 

Nocard: Coccidial Tumor from the Small Intestine of the Sheep. Journ. of Path., i., 
1893. 

Pfeiffer, L.: Pathogene Gregarinen. Zeitschr. f. Hyg., iii., iv., v.; Schwärmsporen 
und Dauersporen bei den Coccidieninfectionen und bei Intermittens. Fortschr. d. 
Med., viii., 1890; Die Protozoen als Krankheitserreger, Jena, 1891; Die Zeller- 
krankungen durch Sporozoen, Jena, 1893; Miescher’sche Schläuche mit Mikro-, 
Myxo-, u. Sarkosporidieninbalt. Virch. Arch., 122 Bd.. 1890. 

Pfeiffer, R.: Coccidienkrankheit der Kaninchen, Berlin, 1892. ° 

Pisenti: Parasitäre Natur. d. Ureteritis cystica. Chbl. f. allg. Path., 1893. 

Pluymers: Des sacrosporidies. Arch. de méd. exp., 1896 (Lit.). - 

Podwyssozki: Bedeutung der Coccidien. Cbl. f. Bakt., vi., 1889; Studien über Coc- 
cidien. Cbl. f. allg. Path., i., 1890; Entwickelungsgesch. d. Coccidium oviforme, 
Cassel, 1885. a 

Bainey: Philos. Transact., T. 147, 1857. 

Block: Bporozoen als Krankheitserreger bei Thieren. Zeitschr. f. Thiermed., xiv., 
1889, 

Rixford and Gilchrist: Protozoan Infection. Johns Hopkins Hosp. Rep., i., 1896. 

Rosenberg: Psorospermien im Herzmuskel des Menschen. Zeitschr. f. Hyg., xi., 1892. 

Schaudinn: Der Generationswechsel der Coccidien u. Hämosporidien. Biol Cbl., vi., 
1899. 

Siedlecki: Cycle evolut. de Adelea ovata. Ann. de l’Inst. Pasteur, 1899. 

Simon: Evolution du coccidium. Ann. de l’Inst. Pasteur, 1897. 


692 THE ANIMAL PARASITES. 


8jöbring: Cocciden der Vogel. Cbl. f. Bakt., xxii., 1897, 

Stroebe: Die parasitären Sporozoen. Chl. f. allg. Patb., 1894 (Lit.). 

Thelohan: ‚Lea myxospori lies, ref. Cbl. f. Bakt., xix., 1896. 

Thomas: Bone Tumor Surrounding Encysted Coceidia. Report of the E 
Hosp., 1899. 

Török u, Tommasoli: Ucb. d. Wesen d. Epithelioma molluscum. Cl. f. E 
1890. 


Tyzzer: Coceidium Infection of the Rabbit’s Liver. Journ. of Med. Res., 1 
v. Wasielewski: Sporozoenkunde, Jena, 1896. 
White and Robey: Molluscum contagiosum. Journ. of Med. Res., 1902. 
‘Wolters: Conjugation u. Sporozoenbildung bei Gregarinen. Arch. f. mikr. 
Bd., 1891. 
For literature concerning cancer parasites, see § 122. 


(Darier's Disease ; Paget's Disease.) 


Boeck: Vier Falle von Darier’scher Krankheit. Arch. f. Derm.. xxifi., 1891 
Derier: De In psorospermos folliculaire végétante Ann. de Derm.. x., 188% 
Ehrhardt: Ueber Paget's Krankheit. Zeitschr. f. Chir. "en 1899. 

Jarisch: Darier’sche Krankheit. Arch. f. Derm., xxxi., 1895. 

Karg: Das Carcinom. Zeitschr. f. Chir., 34 Bd. 

Kroesing: Zur Kenntn. d. Darier'schen Dermatosis. Monateh. f. prakt. Dı 


1892. 
Lindt: Ueber Paget's Krankheit, Basel, 1895 (Lit.). 
Mourek: Beitr. z. Lehre v. d. Dermatosis Darier. Arch. f. Derm., xxvii., 1 
Pawlow: Psorospermose follicul. végétante Darier. Arch. f. Derm. Ergü 


1898. 
Petersen; Ueber die sng. Psorospermien d. Darier’schen Krankheit. Chl. 
898. 


"Die parssitären Sporozoen. Cbl. f. allg. Path., v., 1894 (Lit.). 

Die neueren Arbeiten über Psorospermien d. Haut. Monatsh. f. pral 
.. 1892; Paget’sche Krankheit. Ib., xvi., 1893. 

Wickham: Maladie de Paget du mamelon. Arch. de med. exp., ii., 1890. 











§ 182. Through the investigations of Laveran, Marchiafav 
Golgi, and others it: has been demonstrated beyond doubt that n 
caused by parasites belonging to the Protiste, which are usuall: 
together under the name Plasmodium malaris (introduced 
chiafava and Celli). They are also frequently designated haemos 
The parasites are found in the blood of malarial patients in « 
forms, usually enclosed in cells; and, according to the observe 
Golgi, Celli, Marchiafava, and others, a definite relation can be 
strated between the number and the stage of the developmen 
parasite and the attacks of fever. The parasites pass through 
stages of development in the interval between the attacks of fev 
stages, according to the authors mentioned, differing in febris fi 


febris tertiana, and febris quotidiana. At the same time the par 


the different forms of fever exhibit certain differences in their 
logical characteristics. Supported by these facts, there may the: 
distinguished in man different species of the malarial plasmodi 
its narrower sense the designation Plasmodium malaria is used o 
reference to the parasites of quartan and vernal tertian fevers. 1 
site of estivo-autumnal or pernicious malarial fever, because of i 
movements, is called Plasmodium vivax (Grassi and Feletti) ; that 
dian fever, which also occurs in the autumn, is designated Pu 
precox. 

The development and increase of the plasmodia take place w. 
red blood-corpuscles, in which, first of all, small, colorless : 
bodies (Fig. 526, a) appear. In quartan fever the further deve 
of the parasite proceeds by an enlargement of the small amceba 


MALARIA. 693 


(Fig. 526, a, 6, c, d, e), so that the red cell becomes more and more filled 
up by the parasite. At the same time pigment-granules, which are 





FiG. 528..-Plasmodium malaria of quartan fever. in different stages of development. (After Golgi.) 
a, Red blovd-cell with a small non-pigmented plasmodium; b, c, d, e, pigmented plasmodia of varying 
size, inside the red blood-cells; /, plasmodium in nning segmentation, with centrally placed pigment : 
g. segmented plasmodium ; h, plasmodium divided into separate spherules; ¢, k, two differently-shaped, 
free plasmodia (sexual individuals). 


formed from the substance of the red cell, appear within the bodies of 
the plasmodia. When the plasmodia have attained a certain size, the 
pigment-granules move toward the centre, while at the same time a 
radiating cleavage sets in, so that daisy-like figures (“rosettes”) (f, g) 
are formed, which consist of a pigmented centre and non-pigmented, ra- 
diating club-shaped petals. Later the clubs become detached from the 
central mass of pigment and take on a circular form (A). 

According to Golgi the development and division of the plasmodia of 
quartan fever require three days for their completion, and the attacks 
of fever coincide with the division of the plasmodia. The red cells occu- 
pied by the parasites are destroyed; the young plasmodia just formed by 
division penetrate again into blood-corpuscles, and the cycle of develop- 
ment begins anew. The pigment-granules formed by the plasmodia are 
taken out of the circulating blood partly free and partly enclosed in cells, 
and deposited in different organs, particularly in the spleen, liver, and 
bone-marrow. 

In febris tertiana (vernal tertian) the cycle of development is completed 
in two days (Golgi). The plasmodia developing within the red cells 
(Fig. 527, a-d) show much 
livelier motion and lead much 
more quickly to a decoloriza- 
tion of the red blood-corpus- 
cles than those of quartan 
fever, so that the red cells be- 
come decolorized on the first 
day after the fever, while the 
plasmodia are still small. The 
protoplasın of the plasmodia of 
tertian fever is also ınore del- 
icate and less sharply con- 
toured and the pigment-gran- 
ulesaresmaller. Initsdivision a, First stages of development ; b. c, enlarged plasmodia 
each plasmodium splits up in- with See oa 
to from fifteen to twenty new with flagellum (microgametocyte). 
cells (e), while the parasite of 
quartan fever forms only from six to twelve. Finally, the red blood- 
cells in quartan fever are mostly crenated, while in tertian fever they 





bin 


694 THE ANIMAL PARASITES. 


retain their shape. According to Celli and Marchiafava, sp 
not infrequently occurs prematurely, from five to ten spore 
within a red corpuscle. 

The parasite of estivo-autumnal or pernicious malaria differs : 
hemosporidia of the vernal fevers, particularly in the fact that it 
smaller (Fig. 528, a, b, c, d) and executes lively movements w 
red cells. It completes its life-cycle in forty-eight hours. Di 
stage of multiplication the parasite collects in the internal o 
that the division-figures (d) must be sought in the spleen, liv 
marrow, and brain (where they are present in great numbers). 
the infected red cells become crenated and prickly, and of a bra 
(Marchiafava, Celli); they die prematurely, and blood-cells, w 
tain no parasites, are also destroyed. The attacks of fever c 
case of autumnal tertian fever become so prolonged that they 
one another, and the condition thereby assumes the character 
continuous or continuous fever. 

The parasite of the true @stivo-autumnal quotidian fever is stil 
than that of the autumnal tertian, completes its development ir 
four hours, and produces but little pigment. According to Mar 
and Celli there also occurs a quotidian parasite very similar to tl 
but producing no pigment at all. 

According to Celli, Marchiafava, and Bignami, nuclear bodie: 
demonstrated, during certain stages of development, in the pr: 
of all the endoglobular forms of malarial hwmatozoa. Acco 
Ziemann, in sporulation there first occurs a division of the chrom 
small clumps, and then later the division of the cell-body, so th 
elump of chromatin is surrounded by a zone of protoplasm. 

Besides the forms of development already described which le 
intracellular increase of the plasmodia through schizogony, the 
particularly extraglobular, in part also endoglobular, round ai 
sickle- or crescent-shaped structures (Figs. 526, i, k; 528, e, f) 
as round bodies with flagella (Figs. 527, f; 528, g), which also 
a nucleus and pigment. The crescent forms occur particular! 
pernicious (stivo-a 
tertian) fever (Fig. 52 
Celli regards them as 
nostic feature of this 
fever; and Ziemann al 
that typical crescents 
formed in the other + 
of malaria, 

The last-named fo: 
veran had already di 
as structures belongin 
cycle of development 
16. 528. Plasmodium virar of autumnal tertian, sbow-  plasmodia, while Gol; 
DE EN EEE isang Alle Cell” Marchiafan 
Beine, ad pe m HARTE ham, Bastiauelli, 2 
J. 0. free plasinodia (wexun cells). and others regarded 1 

sterile vegetation 
First through the investigations of Manson, Bignami, Ross, an 
Callum, to which were later added those of Grassi, Bastianelli, B 
Celli, Laveran, Koch, Schaudinn, and others, it was shown 1 
crescents, the oval bodies, the spherical bodies, or spheres, as wel 





MALARIA. 695 


flagellate bodies known as polymitus, are intended for the reproduction of 
the parasites by copulation. The flagella-producing hyaline spheres aris- 
ing from the crescents are male serual individuals or microgametocytes, 
and the flagella developing from them, in whose formation the chro- 





iG. 30. Fig. 590. 
-Anophelese laviger. (After Meigen, loc. cit.) > 4. To the right a wing at higher mag- 





mosquito. {After Grassl.) 


matin of the cell takes an essential part (Sacharoff), have the signifi- 
eanee of seminal cells, spermatozoa, or microgametes ; while the non-flag- 
ellated spheres arising from the granular crescents have the significance 
of female sexual cells or macrogametes, The crescents leading to the for- 
mation of the sexual cells appear only after the infection has lasted for 
several days. In the chronic cachexia following malaria the forms lead- 
ing to schizogony are absent, and the crescents alone are present. 

The copulation of the malarial parasites of man takes place normally in 
the stomach of the mosquito, in different species of Anopheles (Fig. 529), 
which take up the malarial parasites during the sucking of blood from 
malarial patients. 

The copula arising from the union of the macrogamete and micro- 
gamete is designated oökinete (Schaudinn), a long, motile structure 
(described earlier as vermiculus by Danielewsky) which penetrates into 
the stomach-wall of the mosquito (Fig. 530), where through the forma- 
tion of a capsule it becomes the odcyst. The latter then enlarges, and 
forms numerous daughter-nuclei, and then sporoblasts, which break up 
into the sporozoites (Fig. 531) and the residual body. 

The sporozoites, which are formed in enormous numbers, pass into 
the body-cavity after the rupture of the ode: nd collect principally 
in the salivary glands, and through the bite of the infected mosquito are 
again transmitted to man, in whose blood they multiply within the red 
blood-cells through schizogony. 

‘The. pathogenic significance of the malarial plasmodia rests in the first. 
place upon the destruction of red blood-cells. In the pernicious form 
this may be so extensive that hemoglobinuria may take place. The 
melanotic pigment formed in the parasite is a product of the vital activ- 
ity of the parasites. In addition, as the result of the destruction of 
-hemoglobin, there occur deposits of hemosiderin in the bone-marrow, 
spleen, liver, and occasionally also in the kidneys. The massing of the 
parasites of pernicious malaria in the cerebral capillaries may cause eir- 
eulatory disturbances with the oceurrence of numerous hwmorrhages, 




















606 THE ANIMAL PARASITES. 








and consequent severe cerebral symptoms (perniciosa comatosa, s< 
apoplectica, meningitica). 

As the result of the retention of pigment-containing malarial p 
and the deposit of the products of blood-destruction, there a 
marked swelling of the spleen 
ated with hyperemia, followed 
by tissue-degenerations and in 
tissue-proliferations. 

After a long duration of the 
the spleen may become marke 
larged, pigmented, and greatly « 
in structure. Likewise, in tl 
there may be found in part de 
tions and pigmentations, and 
also indurative proliferations. 

Certain. varieties of the pla: 
correspond to the individual 1 
fever, as given above, but it 1 
noted that the fever-forms kn 
quotidian, subeontinnous, and ¢ 
Fig. 531 Odevat of human pernicious me ous (“comitata”), may also arise { 
Horzolae Wi the cence the blood of d 

generations of the plasmodia of 
or quartan fevers, 80 that daily a portion of the parasites comes tc 
lation. In this way there arise quotidian forms of fever, which 1 
regarded as a double tertian infection (quotidiana triquartanaria) 

It is not yet determined whether the malarial parasites produ 
ins; such production has been many times assumed, but never 
strated. The recurrences of mala fever weeks and months a 
original infection like nnot be explained. The assumption a 
that the crescents, which may be found in the cireulating blood 
the interval, aid in the production of the recurrence, is opposed by 
(Celli). According to Plehn basophile granules are found in 
cells as long as the infection lasts; when it ceases they disappear. 

The malaria occurring in northern countries corresponds in ; 
to the vernal forms of Italy, while the estivo-autumnal form is fc 
the tropies. 
















Heemosporidia—that is, sporozoa which live at the cost of the red blood-c 
thereby produce diseases which are to be classed with malaria—occur very frv 
in animals. Those of birds are best known (Danilewsky, MacCallum, 
Diontsi, Celli), and the life-cycles of the hwmosporidia of the pigeon, owl, and 
have been determined. _/adbé distinguishes two genera in birds, Halteridium ı 
teosoma ( Tlemoproteus of Kruse); as to the number of undifferentiated species, 
can be said at the present time. Celli obtained from the birds mentioned thi 
defined species. 

Of the Mammalia, cattle in particular suffer in different countries (Souther 








pear-shaped, and pair 
icance they determined 
taining the parasites. They 
place through pamsitic ticks living u 
cattle, the infection being tran nt by the sume tick which takes up the 
blood, but only through the generation descending from the same. This mo 
fection was confirmed by Koch in the hemoglobinuria of cattle occurring in 
East Africa and by (rasi in that occurring in cattle in Italy. The mode of « 
ment of the pireplaema in the body of the tick is still unknown; and it therefor 






697 
be decided whether the parasite should be classed with the known malaria parasites. 
Against a near relationship with the latter speaks the fact ( Zühe) that it increases within 
the red blood-cells by a repeated simple division. According to Kole, there occurs in 
South Africa, besides Texas-fever, another malarial disease of cattle (Febris malaria- 
formis), which is caused by a similar endoglobular parasite. 

According to Bonome and Cells hemosporidia also cause malaria in sheep and lambs, 
according to Prana and Galli- Valerto also in dogs, according to Koch and Kossel also in 
apes, and according to Dionisi in bats; but the life-history of all these parasites is 
unknown. 

Danilewsky and Cells have described hemosporidia in the frog, and the latter ob- 
server determined also the development of the parasite in the blood. 

Whether the malarial parasites of man can be transmitted to animals, or whether 
the malaria of animals can lead to an infection of man through the medium of mos- 
quitos, is not decided with certainty, but appears improbable. The plasmodia of the 
bat most closely resemble those of man, yet attempts at inoculation made by Dionisi 
gave no positive results. It may therefore be assumed that malaria would die out in 
a given region, either when all susceptible anopheles were killed, or all infected human 
individuals healed or protected from mosquito bites. 

The malarial plasmodia are stained best by the Romanowski stain, which differen- 
tiates the nucleus. 

The view that mosquitos were concerned in the distribution uf malaria is very 
old. and has obtained in Italy since Roman times. Koch found it held as a popular belief 
also among negroes. In recent times Manson (1896) and Bignami (1896) were the first 
to turn their attention to the problem and to give hypotheses concerning the röle played 
by mosquitos in the spread of malaria. Biynami carried out experiments along this 
line. but came to no positive result. Ross was the first (1897-88) to determine the cycle 
of development of the malarial plasmodium of birds (usually known as proteosoma). 
According to his investigations, the parasites taken up with the blood of the infected 
bird into the intestinal canal 
of mosquitos penetrate into 
the intestinal wall and there 
change into cysts in which in- 
numerable rod-shaped germs 
develop. Becoming free, 
these germs gain entrance in- 
to the salivary glands of the 
mosquitos, and thence into 
the organism of the bird dur- 
ing the act of blood-sucking. 
Ross found the parasites in 
the blood of the infected bird 
in from five to nine days after 
the infection. 

About the same time, 
Grassi found through pains- 
taking observations that the 
distribution of malaria in 
man corresponded to the dis- 
tribution of Anopheles clariger 
(Fabricius) (Fig. 529), and not 
to that of the common mos- 
quito (Culer pipiens). Basing 
his experiments upon this 
observation, Bignami suc- 
ceeded in producing malaria 
in healthy men by means of 


DEVELOPMENT OF PROTEOSOMA. 





Fig. 532.—Cycle of development of Proteosoma. 
dinn and Lühe.) 1, Sporozoite (or merozoite) within a red blood- 


(After Schau- 


the bite of anopheles. Later 
Grasst, in codperation with 
Bastianelliand Bignami, suc- 
cecded in determining the 
life-cycle of the malarial par- 
asite. It was then shown 
that several species of ano- 


corpuscle: 2, schizont ; 3, schizont with numerous nuclei; 4, schiz- 


ogony, formation of merozoites: 5, macrogamete (female cell) 
arising from a merozoite; 6, fully developed macrogamete after ex- 
trusion of the karyosome ; 5a, microgametocyte (male cell) arising 
from a merozoite; 6a, microgametocyte surrounded by loosened 
microgametes (spermatozoa) ; 7, fertilization of the macrogamete ; 
8, oökinete ; 9, oöcysts with sporoblasts ; 10, oöcysts with sporozoites ; 
11, free sporozoite. 


pheles native in Italy (Anopheles claviger [ Fabricius] or Anopheles maculipennis [ Meigen], 
Anopheles superpictus, pseudopictus, bifurcatus) spread the malaria occurring in man, 
while Culez pipiens is the host of the parasites of bird-malaria. 

The cycle of development of the malaria plasmodium isas follows: Within the 





698 THE ANIMAL PARASITES. 


blood (of man as well as of birds) the multiplication takes place first by schia 
young form of the plasmodia, represented by a small, unplgm ented body, nay 

the red cells (Fig. 582, 1) into a larger dy (2) in whose central 
anus collect. This cell-body known as «ci ‘Hiaont shows in preparation for 
an increase of nuclei (8), and then divides into a number (varying with th« 
spores or merozoites (4) with the abandonment of a pigmented residual body. 
zoites then seek a red blood-cell (7), and the cycle is again begun. 

In sporogony the merozoites develop into sexual individuals, macro; 
microgametocytes (2). When taken up into the stomach by bl 

uitos, the sexual individuals become ripe for fertilization, the macr 
throwing off the karyosome (6), the microgametocyte through ‘the formatio 
s (Ga). Copulation then follows (7). From the copula arises the mot 
in the wall of the mosquito’s intestine becomes the odcyst. in whi 
ion of the nucleus the sporoblasts (9) are formed, which in turn br 
a large number of sporozoites (10), which (77), becoming free, collect chiefly 
vary glands, and are thence transferred by the bite of the mosquito to an 
whose blood they increase through schizogony (1-4). 

The larvıe of anopheles live chiefly in slowly flowing water. The egg: 
eles claciger require about thirty days at 20°-85° C. for the development 
sects, and these in turn lay eggs when twenty days old, The pupe are 
drying, to cold, and to contamination of the water. The mosquitos fly 
evening and night, but do not rise very high above the level of the earth, 

0 very far away from the place of development. According to Grass, Bi 
Fustianelli, the iestivo-autumnal parasites will not develop in anopheles a at 
ture of 14°-15° C., and grow only slowly at 20°-29° C.; at 30° C. they 
entire development up to the formation of sporozoites in about seven va 

‘The literature concerning malarial parasites is extremely rich. The re: 
latest investigations are given in the publications of Mannaberg, Nuttall, Ce 
afava, Bignami, and Lihe (see below). The last-named treats particularly o 

ion of the position of the malarial parasites in the zoological system and th 
to the other sporozoa, in particular to the coccidia. 
























Literature. 
(Hemosporidia.) 
Babes «ı Gheorghiu: DI. formes du pmmsite de la malaria, Arch. de mé 


Barbacei Aetiologie d. Malaria, Chl. f. allg. Path., ifi., 1892 (Lit.); New 
Malaria, Ibie 





3 Johns Hopkins Hosp. Rep., 1895. 
Anatom. patolog. delle perniciose. Atti della R. Accad. Med. di 
1. 1890, ref. Chl. f. ale, path. ii; Chron. Malaris 

















Jopedique des sciences méd., F 


‘ohiimatozoen d. Schafe (Amöbo-Sporidien). Vin 






Studi sulle inf 
xv. and Arch. 
u 
und 
1890. 

Cattaneo « Mondi: .Alı iche dei corp, rossi del sangue. Arch. 
Mcı., xül., 1888. 

Celli: Le Rome, 1899; Die Malaria. Berlin, 1900 (Lit.). 

Celli ¢ Guarnieri: Sulla intima struttun del Plasmodium malarie. Cbl. f. 

der Malariainfection, Fortschr. d. Med., vii., 1889; Ar 

i.. 1889. 

Celli e Marchiafava: Die Veränderung der rothen Blutkörperchen bei 
kranken, Fortschr. d, Med,, i., 1883, ii.. 1885, ix. 1891: Arch. p. le 
ix., 1885, xi. 1N86, xii, 180 1890: Ueber die Pa 
körperchen. Internat. Beitr, estschr. f. Virchow. il., Berlin, 1891. 

Celli u. Sanfelice: Die Parasiten d. rothen Blutkörperchen. Fortschr. d. 

1891. 


Celli u. Santori: Die Rindermalaria ind. Campagna,  Cbl. f. Bakt., xxi., 1 
Councilman: Unters. über Laveran’s Organismus d. Malaria. Fortschr. d. 





ione malaricn, Torino, 1889. Arch, per le Se. A 

.. Intorno_a receuti lavori sui para 
Ueber die purasitäre Varietät “ Laveran’sche Ha 
chen Ficher, die davon abhängen. Fortschr. d. A 





mul: 


















n der rot 








MALARIA. 699 


1888; Further Observations on the Blood in Cases of Malarial Fever. Med. News, 
i.. 1889. 

Crookshank: Flagellated Protozoa in the Blood of Diseased and Apparently Healthy 
Animals. Journ. of the Roy. Microsc. Soc., Ser. ii., vol. iv., 1886, 

Danilewsky: Zur Parasitologie des Blutes. Biolog. Cbl., v., 1885-86, Arch. slaves 
de biol., 1886; Cbl. f. d. med. Wiss., 1886; Nouvelles rech. sur les parasites du 
sang des oiseaux, Charkow, 1889, ref. Biol. Cbl., x.; sur les parasites de l’infection 
malarique aigué et chronique chez les oiseaux et chez l!’homme. Ann. de I’Inst. 
Pasteur, iv., 1890; Ueber Polymitus malaris. Cbl. f. Bakt., ix., 1891; Contr. a 1’ét. 
de la microbiose malarique. Ann. de l’Inst. Pasteur, v., 1891. 

Dionisi: Les paras. endoglobulaires des chauves-souris. Arch. ital. de biol., xxx., 
1899. 

Dolega: Blutbefunde bei Malaria. Fortschr. d. Med., viii., 1890. 

Ewing: Pathological Anatomy of Malarial Fever. Journ. of Exp. Med., vol. vi., 
1902; Malarial Parasitology. Journ. of Exp. Med., vol. v. 

Fajardo: Hämatozoarie der Beri-Beri. Cbl. f. Bakt., xxiv., 1898; xxvii., 1900. 

Glogner: Malariaerreger im Malaischen Archipel. Virch. Arch., 158 Bd., 1899. 

Golgi: Sull’ infezione malarica. Arch. p. le Sc. Med., x., 1886, xiii., 1889; Gaz. degli 
Ospitali, 1886; Fortschr. d. Med., iv., 1886, vii., 1889; Arch. ital. de biol., ix.; Il 
fagocitismo nell’ infezione malarica. Rif. Med., iv., 1888; Ueber den angebl. Ba- 
cillus malariz v. Klebs, Tommasi-Crudeli, und Schiavuzzi. Beitr. v. Ziegler, iv., 
1889; Intermittirende Fieberformen der Malaria mit langen Intervallen. Ib., vii., 
1890; Sur le cycle évolutif des parasites malariques dans la fievre tierce. Arch. 
ital. de biol., xiv., 1890; Demonstration der Entwickelung der Malariaparasiten 
durch Photographieen. Zeitschr. f. Hyg., x., 1891; Ueber die im Sommer und im 
Herbst in Rom auftretenden Malariafieber. Cbl. f. Bakt., xv., 1894. 

Grassi: Intorno a alcuni protisti endoparassitici, Milano, 1882; Rapports entre Ja 
malaria et cert. insects particuliers. Arch. ital. de biol., xxx., xxxii., 1899. 

Grassi u. Feletti: Ueber die Parasiten der Malaria. Cbl. f. Bakt., vii., 1890; Arch. 
ital. de biol., xiii.; Malariaparasiten in den Vögeln. Cbl. f. Bakt., ix., 1891. 

Grassi et Dionisi: Le cicle évolutif des hemosporidies. Arch. ital. de biol., xxxi., 
1899. 

Koch: (Flage.laten im Blute von IIamstern.) Mittheil. a. d. Kais. G.-A., Berlin, 1881; 
Die Entwickelung der Mulariaparasiten. Zeitschr. f. Hyg., 32 Bd., 1899. 

Kolle: Parasit im Blute von Rindern in Süd-Africa. Zeitschr. f. Hyg., 27 Bd., 1898. 

Kossel: Malariaähnlicher Blutparasit beim Affen. Zeitschr. f. Hvg., 83 Bd., 1899. 

Kruse: Ueber Blutparasiten (im Froschblut). Virch. Arch., 120 Bd., 1890. 

v. Kubassow: Die Pilze des Paludismus, Berlin, 1898. 

Labbe. Parasites du sang des vertébrés. Arch. de Zool., 1894, ref. Cbl. f. Bakt., xvi., 
1894. Sporozoa, Das Thierreich, herausg. v. d. zool. Ges., 5 Lief., Berlin, 1899. 

Lang: Protozoa, Jena, 1901. 

Laveran: Nature parasituire des accidents de l’impaludisnie, Paris, 1881; Traité des 
fitvres palustres, 1884; Les hématozoaires du paludisme. Ann. de l’Inst. Pasteur, 
i., 1887; Arch. de méd. exp., i., 1889; ii., 1890; Du paludisme et de son héma- 
tozonire, Paris, 1891; Traite du paludisme, Paris, 1897. 

Laveran ct Blanchard: Les hématozoaires de l’homme et des animaux, Paris, 1895. 

Lieberkühn: Ueb. Bewegungserscheinungen d. Zellen (Amöbe im Froschblut), Mar- 
burg, 1870. 

Lühe: Ergebnisse d. neueren Sporozoenforschung. Cbl. f. Bakt., xxvii., xxviii., 1900 
(Lit.). 

MacCallum: Hematozoan Infections of Birds. Journ. of Exper. Med., iii., 1898. 
Mannaberg: Die Malariaerkrankungen, Wien, 1898 (Lit.); Die Malariakrankheiten, 
Wien, 1899 (Lit.); Malaria. Ergebn. d. allg. Path., v., Wiesbaden, 1900 (Lit.). 

Manson: The Mosquito and the Malaria. Brit. Med. Journ., ii., 1898. 

Marchiafava e Bignami: Sulle febbri malariche. Boll. della R. Accad. di Roma, 
xviii., 1892; Malaria. Twentieth Century Practice, New York, 1900. 

Marchoux: Ie paludisme du Sénégal. Ann. de !’Inst. Pasteur, 1897. 

di Mattei: Infez. malarica sperimentale. Arch. per le Sc. Med., xix., 1895. 

Mitrophanow: Beitr. z. Kenntniss der Hämatozoen. Biol. Cbl., iii., 1888. 

Neumann: Das melanämische Pigment. Virch. Arch., 116 Bd., 1889. 

Nuttall: Die Rolle d. Mosquitos bei Verbr. d. Mal. Cbl. f. Bakt., xxv., xxvi., 1890; 
xxvii., 1900 (Lit.). 

Opie: (n the Hxmocytozoa of Birds. Journ. of Exper. Med., iii., 1888. . 

Plehn; Beitr. z. Kenntniss d. tropischen Malaria in Kamerun, Berlin, 1896; Weiteres 
über Malaria, Jena, 1901. 

Ross: Mosquitos and Malaria. Brit. Med. Journ., i., 1899; Ann. de l’Inst. Pasteur, 
1899. 








700 THE ANIMAL PARASITES. 


Rouget: Trypanosome des mammiftres. Ann. de "Inst, Pasteur, 1896. 

Bakharof; Le parasite des Müvres paludéennes irrégulléres. Ann. de i'Tns 
v., 1891. 

Sambon: Life History of Anopheles. Brit. Med. Journ.. i., 1901. 

van der Scheer: Tropische Malaria. Virch. Arch., 189 Bd., 1895. 

Schaudinn: Der Generationswechsel d. Coceidien u. Hamosporidien. Zool 


1899. 
Scheube: Schwarzwasserfieber. Eulenb. Jabrb., viii.. 1898; Die Kranl 
warmen Länder, Jens, 1900 (Lit.); Texasfeber. Eulenb. Realeneyelc 
1900 (Lit.). 
Schneidemühl: Die Protozoen als Krankheitserreger, Leipzig, 1898. 
Schwalbe: Beitr. z. Malariafruge, 1. it, Berlin, 1900. 
Smith: Die Actiologie der Texasfieberseuche des Rindes. Cbl. f. Bakt., : 
N. Y. Med. Journ., 1899. 
Spener: Ueber den Krankheitserreger der Malaria, Biol. Centralbl.. xi., 181 
Stein: Structur des Paras. der Malaria tertiana. Virch. Arch., 159 Bd., 190 
Thayer and Hewetson: Malarial Fevers of Baltimore, Johns Hopkins Pres 
Wilde: Ergebnisse der Malariaforschung. Münch. med. Woch., 1901. 
Ziemann: Blutpurusiten bei heimischer u. tropischer Malaria. Cbl. f. B 
1896; Ueber Malaria und andere Blutparasiten, Jena, 1898. 


Il. Vermes (Worms). 
A. PLATYHELMINTHES (FLAT-WORMS). 
1. Trematoda, Sucking Worms. 


§ 183. The Trematodes or sucking-worms are flat-worms of t 
leaf shape. They possess a clinging apparatus in the form of 
sucking-cups of varying number, and are sometimes furnished wi: 
or clasp-like horny projections. The intestinal canal is without 
and is usually forked. The development takes place either by tl 
growth to maturity of the embryos (miracidium) hatching from t 
or by the method of alternate generation through the formation ı 
within the host. The wiracidium, or ciliated embryo, penetrate: 
snail or mussel, and there grows into a germ-sac (sporocyst), withi 
there later develops, either directly or after the formation of a 
mediate generation of germ-sacs (redi@), a swarming generation 
carie, which are provided with rudder-like tails. These lose th 
and penetrate into a new host (mollusks, arthropods, fish. am; 
apsulated, and attain sexual maturity as soon as the 
The germ-sacs which produce cercarie are des 
germ-sacs (“Immen”); if they first form redie and tl 
cari, they are called secondary germ-sacs (“ Grossammen”). 

Distoma hepaticuın, or liver-fluke, is a leaf-shaped suckin, 
about 28 mm. long and 12 mm. broad (Fig. 533). The cepha 
projects like a beak, and bears a small sucking-eup, in which the 
is placed. Close behind this, on the ventral surface, is a second sı 
cup, and between the two lies the sexual orifice. 

The uterus consists of a convoluted, globular sac behind the px 
sucking-cup. On each side of the hinder part of the body lie th 
sacs, and between the same are found the testicular canals, which 
many times. The forked intestinal tract (not visible in Fig. 
repeatedly branched. 

The eggs (Fig. 534) are oval, 0.13 mm. long and 0.08 mm. bro: 
water there develops an embryo, the miracidium (Fig. 535, A 















TREMATODA. 701 


cellular germ-balls (a); with the aid of its ciliated covering the embryo 
swims about, and seeks out a new host from the family of mollusks 
(Limneus minutus). On penetration into the snail the cutaneous layer is 
thrown off, and the miracidium, which possesses an intestine, an excre- 
tion-organ and a brain-ganglion, becomes changed into a sporocyst (B), 
in which the intestine and nervous system atrophy, while the cellular 

rm-balls develop further (B, a) and form a second generation of germ- 
sacs, the redie (B, b). The redix (C), which 
possess an intestine ((, a), produce then 
within the same host the cercarie (D) from 
cells which are loosened from their germ- 
matrix ((C, 6); these abandon the host and 
with the aid of a rudder-like tail swim about 
in the water. With the loss of their tails they 
become encysted upon almost any foreign 
body, and then reach their final host (usually 
through the food), in which they attain sex- 
val maturity. The sexually mature animal 
inhabits the biliary passages; more rarely it 
is found in the intestine or inferior vena 
cava. The liver-fluke is rare in man, but 
common in the ruminants. The results of its 
invasion, especially when it is present in 
great numbers, are obstructions and ulcerative 
strictures of the bile-passages, formation of 
biliary concretions, inflammation of the tis- 








Fig. 54. 


Fig. 533. - Distoma hepaticum with male und female sexual apparatus. (After Leuckart.) X 32. 
iG, 534. — Eggs of Distoma hepaticum. (After Leuckart.) X 200. 


sues in the neighborhood of the bile-ducts, and hyperplasia of the con- 
nective tissue of the liver with atrophy of the glandular tissue. 

Distoma lanceolatum is only 8-9 mm. long and 2-2.5 mm. broad, is 
lancet-shaped, and the cephalic portion is not especially marked off 
from the body (Fig. 536). 

The skin of the body is smooth. Two irregularly lobed testicles (4) 
lie close behind the ventral sucking-cup, in front of the ovary (0) and 
the uterus (u), the coils of which shine through the transparent body. 
The anterior coils are black with the ripe eggs, the others are rusty red. 
The yellowish-white yolk-sacs (d) lie in the middle of the lateral 
margin. 

The oval eggs are 0.04 mm. long, and while still in the uterus contain 
an embryo which escapes only after several weeks following the casting- 
off of the eggs. Its metamorphoses are unknown. 

Distoma lanceolatum likewise inhabits the bile-passages, but is very 
rare in man. It is of more frequent occurrence in sheep and cattle. 














102 THE ANIMAL PARASITES. 


When present only in small numbers, it causes no marked cha 
the presence of large numbers may excite inflammation and pri 
of the periportal connective tissne. 





sporoupe win erhal {oan rede (93 Gerede, ith Jake a) and ger Cb 
at with (aa mi 
with mouth (a), abduminal sucking-cup (b), intestine (c), and glands (d). 


Distoma spathulatum (Fig. 537) is a sucking-worm oc 
man in Japan and China. It is 10-14 mm. long and 2.5—4 m 
The eggs are 0.027-0.03 min. long and 0. 
mm. broad. The parasite inhabits usual 
passages and the gall-bladder, but may 
access to the pancreatic duct (Katsurada) 
out into the intestine. When occurring 
numbers (Katsurada counted 4,361 in o: 
causes an obstruction to the outflow of th 
often excites a more or less severe inflamı 
proliferation of connective tissue. 

The parasite is found also in cats 
(Katsurada). 

Distoma Westermanni (Kerbert), o 
pulmonate (Baelz) also occurs in Japan, ¢ 
Corea. The worm is 7.5-10 mm. long, 

road, egg-shaped, with slightly flatten 
surface, The oval eggs are 0.09 mm. 
0.056 mın. broad. The internal organiza 
538) resembles that of the other trema 
occurs in man as well as in cats and do; 
rada). It is found most frequently in + 
but occurs also in other organs: the pleu 
liver, intestinal wall, peritoneum, orbit 
eyelid, scrotum, ete. In each case it 
intesines sr posterior Small cavities surrounded by newly foi 
wucking-cup; "h, testicles nective tissue,and occurs occasionally in 
Cin wouter Sian; the lung it may be found also in the br 
& duct of Laurer and shell; walls of which show inflammatory chan, 
Se ating 0 ‘the hell rada). Its presence in the lung may Ri 


an xa!) ® heemoptoö and cause death. The numbe 








TREMATODA. 703 


flukes may run from twenty to thirty or even higher. Healing of 
the disease is possible after death of the parasite. 

Distoma felineum (Rivolta) or Distoma sibiricum (Winogradow) is 
a flat, almost transparent sucking-worm, of from 8-18 mm. in length and 
1.5-2.5 mm. broad, which is present in the bile-passages of the cat and 
dog, and in a few countries (Siberia) has been observed in man. Ac- 
cording to Winogradow it is the most common parasite in Tomsk. 
Askanazy recently observed a case in Königsberg. 

The inflammatory proliferations which the different forms of distoma 
cause in the liver of man, as well as in animals, may be followed by the 
development of carcinoma. 

In Distoma hematobium or Bilharzia hematobia (Fig. 539) the two 
sexes are separate. The mouth and ventral cups lie very close together 
on the tapering anterior extremity. In both sexes the sexual openings 
lie close behind the ventral sucking-cup. The male is 12-14 mm. long. - 





Fig. 537. Fig. 538, 


Fi. 637.—Distoma spathulatum. (After Katsurada.) a, Mouth sucking-cup; b, intestine; ¢, uterus; 
4, teaticles ; ¢, yolk-stalks; f, sperm-pouch ; g,orarlum. X 6. 

F1a. 538.— Dittoma Westermannt, fattened by pressure, in the ventral position. (After Katsurada.1 
@, ay, Mouth and abdominal sucking-cup respectively; b, intestinal loops: c, testicles; d, ovarlum: c. 
yolk-sialks ; f, shell-gland; g, uterus: h, excretory vessel. X 7.2. 


The body is flat, but in its posterior portion is rolled together to form a 
tube (Fig. 539) which serves for the reception of the female. 

* The female is 16-19 mm. long and nearly cylindrical. The eggs are 
an elongated oval (Fig. 540), 0.12 mm. long, and possess a terminal or 


. slateral spine. According to observations by Sonsino, no altneration of 


generations occurs in the development of Distoma haematobium. The 


04 THE ANIMAL PARASITES. 


part of intermediate host is taken by small crustacea, into 
ciliated embryo, swimming around in water, bores its way 
encapsulated in the tissues of its host. It is therefore probak 
infection may be transmitted through the drinking of wat 
with the larve. 

The wormsare found in the trunk and branches of the por 
the splenic vein, mesenteric veins, as well as in the vessels of 
and bladder; and may pass through the inferior mesenteric v: 
hemorrhoidal and vesical veins, the veins of the ureter an 
and by chance into the inferior vena cava, and thence intc 
Their eggs are distributed therefore especially throughout | 
and submucosa of the ureters, bladder, and rectum, and occas 
in the liver, lungs, kidneys, and prostate. While still within 
passages the cylindrical embryos (miracidia) covered with fin 


g 


Fis. 





Fia. 539.—Distoma hasmatobium. (After Leuckart.) Male and female, the latter Iyir 
gynscophorus of the former. X 10. 


Pia. 40.—Eggs of Distoma heematobtum. (After Leuckart.) a, Egg with termin 
with lateral spine. x 150. 


develop. Kartulis found them also in the skin of the leg an: 
is of the opinion that the infection may take place not only t! 
intestine, but also through the skin. 

The deposit of eggs causes severe inflammations which lea 
tissue-destruction and in part to proliferations of the tissue, 
pear in the mucous membranes as papillary and polypoid form 
the bladder it may lead to incrustations and formation of c 
and also to the development of fistulous tracts. In the liver 
leads to a connective-tissue induration. Following the im 
process, a development of carcinoma may take place in tt 
seminal vesicles, prostate, and in the skin (Kartulis). 

The parasite is found along the entire eastern coast of 1 
also in Zanzibar, Tunis, Lake Nyassa, in Beyrout, and in Si 
most common in Egypt, where about twenty-five per cent. of 
population suffer from the disease. 


Literature. 
(Distoma.) 


Albarran et Bernard: Tumeur épithél. duc a Ja Bilharzia. Arch. de mé 
Askanazy: Dist. felineum beim Menschen. Cbl. f. Bakt., xxviii., 1900. 
Aschoff: Ein Fall v. Distoma lanceolatum in der menschl. Leber. Vire 


Baelz: Einige neue Parasiten des Menchen. Berl. klin. Woch., 1888. 


2. 1m 


CESTODA. 705 


Biehringer: Arbeiten z. Entwickelungsgeschichte des Leberegels. Biol. Cbl., viii., 
1883. 

Biermer: Leberdistoma. Schweiz. Zeitschr. f. Heilk., ii., 1868. 

Bilharz: Distomum haematobium u. Veränd. d. Harnorgane. Wien. med. Woch., 
1865. 

Bostrém: Leberdistoma beim Menschen. Deut. Arch. f. klin. Med., xxxiii., 1888. 

Braun: Die Wohnsitze d. endoparasitischen Trematoden. Cbl. f. Bakt., xiii., 1898; 
Leberdistomen d. Hauskatze. Ib., xiv., 1893; Für d. Menschen neues Distomum. 
Ib., xv., 1894. 

Brock: On the Bilharzia FHamatobia. Journ. of Path., ii., 1893. 

Chaker” Etude sur l’hematurie d’Egypte causée par la Bilharzia haematobia, Paris, 
1890 

Fritsch: Zur Anatomie der Bilharzia haematobia Cobb. Arch. f. mikr. Anat., xxxi., 
1888. 

Griesinger: Arch. f. physiol. Heilk., xiii., 1854. 

Kartulis: Vork. d. Eier des D. haemat. in den Unterleibsorganen. Virch. Arch., 99 
Bd., 1885; Pathol. Anat. der Bilharzia. Ib., 152 Bd., 1898. 

Katsurada: Dist. spathulatum u. D. Westermanni. Beitr. v. Ziegler, xxviii., 1900 
(Lit.). 

Leuckart: Ucber den grossen amerikanischen Leberegel. Cbl. f. Bakt., xi., 1892. 

Looss: Zur Lebensgeschichte der Bilharzia haematobia. Cbl. f. Bakt., xvi., 1894; 
Trematodenfauna Aegyptens. Zool. Jahrb., xii., 1899; Cbl. f. Bakt., xxxiii., 1892. 

Lutz: Zur Lebensgeschichte des Distomna hepaticum. Cbl. f. Bakt., xi., 1892. 

Mvinecke: Dist. haematobium in d. Blasenwand. Jahrb. d. Hamb. Krankenanst., v., 
1897. 

Poirier: Contrib. & histoire des trématodes, Paris, 1885, and Note sur une nouvelle 
espéce de distome parasite de homme, le distomum Bathousi. Arch. de zool. exp., 
v., 1887. 

v. Ratz: Leberegel in der Milz der Schafes. Cbl. f. Bakt., xxvi., 1899. 

Riitimeyer: Ueber Bilharziakrankheit. Mittheil. a. d. Klin. d. Schweiz, Basel, 1894. 

Schaper: Die Leberegelkrankheit der Haussäugethiere. Deut. Zeitschr. f. Thiermed., 
xv., 1889. 

Schauinsland: Embryonalentwickelung der Trematoden. Jen. Zeitschr. f. Naturw., 
xvi., 1883. 

Scheube. Die Krankheiten der warmen Länder, Jena, 1900. 

Sonsino. Discovery of the Life History of Bilharzia Heematobia, The Lancet, 1893. 

Ward: Trematoda, Ref. Handbook of Med. Sc., 2d ed., 1908. 

Winogradow: Eine neue Distomaart. Cbl. f. allg. Path., iii., 1892. 

Yamagiva: Zur Aetiologie der Jackson’schen Epilepsie (Eier von Distoma pulmonale 
im Gehirn) Virch. Arch., 119 Bd.; Ueber Luugendistomenkrankheit in Japan. 
Ib., 127 Bd., 1892. 


2. Cestoda (Tapeworms). 


§ 184. The tapeworms are flat-worms devoid of mouth or intestine, which 
increase after the method of alternate generation through the germination 
of a pear-shaped primary head or scolex, and remain united to the latter 
for a long time as a (usually) long, band-shaped colony. The single 
segments of this colony, the sexually active individuals, or proglottides, 
increase in size the more widely they become separated from their place 
of origin by the formation of new members, but outside of this are de- 
void of any outward distinguishing peculiarity. The pear-shaped head 
or scolex, on the other hand, is provided with from two to four suckers, 
and usually also with curved claw-like hooks. With the aid of these 
elinging organs the tapeworms fasten themselves to the intestinal wall 
of their host, which appears to be invariably one of the vertebrate ani- 
mals. The scolices develop from a round embryo having four to six 
hooks, and are found as the so-called “measles” in the most diverse or- 
gans, chiefly the parenchymatous ones, from which they later pass by a 
passive migration into the intestine of their future host. 

The tapeworms occurring as parasites in man belong to different families 
—the Teniade and the Bothriocephalide. The first occur in man either 


as ‘‘measles” or as tapeworms, the latter only as tapeworms. 
27 














706 THE ANIMAL PARASITES. 


§ 185. Tsenia solium in its fully developed condition 
length of 2-3 metres. The head (Fig. 541) is of the size of 
head, is spherical in form, with rather prominent sucking 
crown of the head is not infrequently pigmented and bears a 
rostellum with about twenty-six plump, close hooklets havin; 
processes. Following the head there is a thread-like neck 
inch in length. Atacertain distance from the head segmenta 
the first segments being very short, but their length increase 
distance from the head (Fig. 542); they become quadratic 
longer than broad. The mature segments appear about 130 cm 





Fra. 542, 

Fig. 541. Head of Tenia woltum with protruding rostellum (carmine, bala). 
Fic. 542,—Hulf-developed and fully matured segments. Natural size. (After Leu 
Fic. 543.— Two proglottides with uterus. (After Leuckart.) X 2 


head, although the sexual organs are fully developed in earlie 
The ripe segments (Fig. 543) are, when stretched out, 9-1( 
and 6-7 mm. broad, and have rounded corners. The sexua 
situated laterally just behind the middle of the segment. 
which is filled with eggs, possesses seven to ten lateral bra: 
are separated from each other by a wide interval, and bre: 
varying number of boughs branching like a tree. 

The parenchyma of the body of mature as well as of imma 
tides, or tapeworm segments (Fig. 544), is divided into two ¢ 
the con! one being designated the middle layer, the perip 
the cortical layer. The middle layer contains the sexual app 
544, ¢, d, 6,5, 9, h, i, k, 1, m, n), as well as the water vascular 
an excretory apparatus which traverses the whole tapewor. 
head to the last segment in the form of two canals lying in 
border of the middle la, The canals are connected with e 
the posterior end of each segment («') and also send out nw 
subdividing branches into the body-parenchyma. 











CESTODA. 707 


The secual apparatus consists of male and female sexual organs, which 
lie close together. A number of small, clear vesicles serve as testicles 
(e), they lie chiefly in the anterior portion of the middle layer The vas 
deferens (e), which is con- 
nected with the testicles by 
the seminal ducts (d), emp- 
ties into a grooved papilla 
situated on the lateral border 
(Rh). The coiled end (f, 9) 
lies in a muscular bag and 
may be protruded through 
the sexual opening (cirrus). 
‘The female sexual opening 
lies close behind the male 
orifice in the same sexual 
cloaca, The vagina (i) leads 
thence to the posterior border 
of the segment. Before this 
is reached it widens into the 
seminal vesicle, and behind onder in front of nine; n, wens. 
this into the fructifying can- 
al and the so-called “globular body.” The germ-preparing organs, 
which must be sought in the immature segments, consist of a double ovary 
(k) and a single albumin-gland (2); these are sac-like or tubular organs 
lying in the posterior portion of the segment and communicating with the 
globular body. The latter is joined to the anteriorly located uterus (n), 
which at the time of sexual maturity forms a straight canal. When the 
eggs enter the uterus from the globular body, in which they pass their 
first stage of development, the above-mentioned lateral branches sprout 
out and become filled with eggs. During this process the remaining sex- 
ual organs disappear. 

The cortical layer of the proglottides is essentially muscular in nature, 
but in addition contains a larger or smaller number of so-called calcareous 
bodies, which are not entirely wanting in the middle layer as well. The 
musculature consists of smooth fibres, which form special groups in the 
suckers of the head. The surface of the tapeworm is covered with a 
clear cuticle, which forms the hooks 
on the heads. 

The eggs in the ovary are thin- 
skinned, pale and yellow, nearly 
globular cells, In the uterus they 
change into yellow balls having a 
thick, more or less opaque shell, 
covered with closely set spicules 

Tha. 545. Tha. 546. (Fig. 545, a). The latter is often 

Tho, 545.—Egus of Tenia soltum. b, With prim Surrounded by a second layer, an 
Se Reem Cine cay SE Dy a membranes and init there 
opel head in iu ARG Lach) ee are embedded granules (primitive 
vitelline membrane). The diam- 

eter of the eggs, not including the vitelline membrane, is about 0.03 mm. 

The thick-shelled spheres are not undeveloped eggs, but contain an 
embryo with six hooklets. An intra-uterine development of the em- 
bryo therefore takes place, the ripe segments are pregnant 











708 THE ANIMAL PARASITES, 


The further development of the embryos enclosed in the browni 
takes place ordinarily in a new host. Should they gain acce 
stomach of a hog, the egg-shell is dissolved, and the embryos, 
free, penetrate into the 
or intestinal wall. Th 
pass either by the bloc 
or by an active mig 
through the tissues in! 
that organ. Having ı 
resting-place, the eml 
dergo various metan 
and become changed : 
two or three months iı 
filled with serum (Fig. 
inner wall of which she 
into a bud from: which 
velops a new tapeworn 
scolex, as Well as a sac: 
the same, a receptaculum 

The cyst. containing 
worm head is know 
««measle”’ or cysticer 
ulose. Thescolices, w 
developed, possess a « 
hooklets, suckers, a w 
cular system and nume 
careous bodies in the 
parenchyma. If they gz 
to the human stomach, 
is dissolved, and there ¢ 
through the formation 
ments from the scolex 
a new chain of proglc 
new Tenia solium. 
solinm, in the epl- The Tenia solium in 
of a hog, small intestine of man, x 

quired by the eating of ı 
les” belonging to this parasite oeeur almc 
By means of its sucking-cups and it 
of hooks it clings y to the mucosa of the intestine; the nm 
portions float freely in the intestine. Usually but a single ps 
present in the intestine, although the presence of several at 
time is not rare. Occasionally as many as thirty or forty have 
served in one individual. They excite irritation of the intest: 
cosa, colie, and reflex disturbances of the central nervous syste 

The “ineasles” occur in the tissues of the hog, sometime 
sometimes in great numbers (Fig. 547), and individual organ 
heart, for example, may be closely studded with them. 
an, eysticerei occur in the most varied tissues—the musele 
in, ete. In the meninges and in the brain the measle 
pear in the form of mulberry or grape-like collection of eysts, } 
eysticerens racemosus (Zeuker). 7 are for the greater par 
though some of them may contain a scolex. 

The importance of the measle depends upon its location, but i 








FIG. 547..-Cvstieerch of the Ti 
cardium and myecard 








pork, since the “m 
in the hog and 









































710 THE ANIMAL PARASITES. 


The development follows a course similar to that of 
Malformations of this tapeworm are of very frequent occur 

The parasite is acquired by man through the eating of 
has not been definitely settled whether the “measles” of th 
in man, but some authors (Arndt, Heller) believe that st 
rence does take place. 

By means of its powerful suckers the parasite is able 
firmly to the intestinal wall. Stieda has observed a cas 
tenia 15 cm. long had penetrated through the wall of the d 
the pancreas, and had caused tissue-necrosis and hemo 
neighborhood. 


Teenia cucumerina or elliptica is 15-20 cm. long, and 
tellum and circle of hooklets. It is of very frequent occurrence in dog 
rare in man. Its cysticercoid inhabits the louse and flea of the dog 
flea of human beings (Grau). 

Teenia nana, a small tapeworm of from 8 to 15 mm. in length, 
four suckers and a circle of hooklets. It has been observed chlefiy 
Italy. B. Grassi was able to obtain several thousands of specimens f. 
who had suffered from severe nervous disturbances. According to h 
the tenia passes its entire development, from the embryo on, withi 
Viseonti (Rendiconti R. Istituto Lombardo, xviii., 1886) found, at 
young man from northern Italy, great numbers of Tenia nana in the 
ihe ileum. "In Germany it has been obmerved in only a few eases (Merte 

öder). 

Teenia diminuta (Rud.) or flaropuncta ( Weinland), minima (Grass 
20-60 mm. long, and has a head without hooklets. It is of common a 
and mice, and has also been observed in a few cases in man. Accordi 
Rorelli, the measles live in a small butterfly, as well us in beetles. 

Von Länstow has recently described as Teenla africana a large 
scolex devoid of hooklets, which he observed among the negroes of Ger 

Besides those which also occur in man, twniee are of frequent a 
domestic animals, both in the carnivora and in birds, as well as in th 

Tania marginata of the dog is a tapeworm, 1-5 m. long, provid 
circle of hooklets. Its cysticercus forms cysts of varying size in and 
membrancs of sheep, cattle, goats, and hogs. 

Tania serrata is a tenia found in the dog. It is 50-100 cm. long 
circle of hooklets.. The cysticerci are found in rabbits and hares. 

Tenia cenurua is a tapeworm of the dog, 40-100 cm. long, and 
hooklets. It passes its cystic stage most frequently in sheep, where it 
nervous system and forms cysts varying in size from that of a millet 
hen’s cgg, which contain great numbers of scolices. Its presence in th 
to the so-called “staggers” of sheep. 

Tenia plicata (10-25 cm. long). Tenia mamillana (1-8 cm. long), : 
Hata (3-5 cm. long) occur in horses. Tenia expanea (4-5 m. long) an 
lata (25-80 cm. long) are the common tapeworms of cattle. Further. 
of teni occur more rarely as parasites in sheep and cattle. 








Literature. 
(Tenia as Intestinal Parasites.) 


Blanchard: Cestodes monstrucux, Paris, 1894, ref. Cbl. f. Bakt., xvi 
Blochmann: Plasmatische Längsgefüsse bei Taenin sag. u. Taenia so 


xii., 1892. 
Beasn. Din amhrunnale Butwinkslune dar Grotadan Chl Rate 


CESTODA. 111 


Joseph: Dag centrale Nervensystem d. Bandwürmer. Tagebl. d. Naturforschervers, 
Berlin, 1886. 

Kahane: Anatomie von Taenia perfoliata. Zeitschr. f. wiss. Zool., xxxiv. 

Kitt: Lehrb. d. pathol.-anat. Diagnostik, ii., Stuttgart, 1895. . 

Leichtenstern: Taenia nana u. flavopunctata beim Menschen. Deut. med. Woch., 
1892. 

v. Linstow: Taenia nana u. murina. Jen. Zeitschr. f. Naturwiss., 1896. 

Lutz: Beobacht. üb. Taenia nana u. flavopunctata. Cbl. f. Bakt., xvi., 1894. 

Mingazzini: Sur le mode d’adhesion des cestoides a la paroi intestinale. Arch. ital. 
de biol., xxxii., 1899. 

Niemie: Ueb. d. Nervensystem d. Cestoden. Arb. a. d. Zool. Inst. d. Univ. Wien, 
xii., 1886. 

Nuttall: The Poisons Given Off by Parasitic Worms in Man and Animals. Amer. 
Nat., 1899. 

Peiper: Thier. Parasiten d. Menschen. Ergebn. d. allg. Path., iii., 1897 (Lit.). 

Röder: Tuaenia nana in Deutschland. Münch. med. Woch., 1899. ) 

Sommer: Ueber Bau u. Entwickelung der Geschlechtsorgane v. Taenia mediocanellata 
u. Taenia solium, Leipzig, 1874. 

Stieda: Durchbohrung d. Duodenums u. d. Pankreas durch. e. Täniae. Cbl. f. Bakt., 
xxviii. 1900. 

Stiles: The Type Species of the Cestode Genus Z/ymenolepis. Bull. U. 8. Hyg. Lab., 
No. 13, May, 1903. 

Stiles and Hassall: A Revision of the Adult Cestodes of Cattle, Sheep, and Allied Ani- 
mals, Washington, 1884; Tapeworms of Poultry, Washington, 1896. The Inspec- 
tion of Meats for Animal Parasites, U. S. Dept. Agr. Bull., 19, 1898. 

Ward: A New Human Tapeworm (Tenia confusa). West. Med. Rev., 1896; Zool. 
Anz., 1897; Cestoda. Ref. Hdb. of Med. Sc., 2d ed., vol. ii. 

Weinland: Human Cestodes, Cambridge, 1858. 

Zschokke: Studien über den anatom. u. histol. Bau der Cestode. Cbl. f. Bakt., i., 
1887; Rech. sur Ja structure des Cestofes, Bale, 1889. 


(Cysticercus in Man. ) 


Askanazy: Cysticerkenbildung an der Hirnbasis. Beitr. v. Ziegler, vii., 1890. 

Bitot ct Sabrazés: Etude sur les cysticerquesen grappe de l’enc&phale et de la mo8lle 
chez Vhomme. Gaz. med. de Paris, 1890. 

Dolina: Intraoculärer Cysticercus. Beitr. v. Ziegler, v., 1889. 

Hirschberg: Cysticercus im Auge. Eulenburg’s Realencyklop., 1885. 

v. Kahlden: Cysticercus d. IV. Ventrikels. Beitr. v. Ziegler, xxi., 1897. 

Kratter u. Böhmig: Freier Gehirncysticercus. Beitr. v. Ziegler, xxi., 1897. 

Lewin: Cystieercus cellulose der Haut. Eulenburg’s Realencyklop., 1885 (Lit.); 
Arch. f. Derm., 26 Bd., 1894 (Lit.). 

Mennicke: Cysticercus racemosus d. Gehirns. Beitr. v. Ziegler, xxi., 1897. 

Richter: Cysticercus racemosus in den inneren Meningen. g. med. Woch., 1891. 

Zenker: Ueber den Cysticercus racemosus des Gehirns, Bonn, 1882. 


§ 185. The Teenia echinococcus lives in the intestinal canal of the 
dog. It is 4-5 mm. long and possesses only four segments, the most 
posterior of these surpassing in length all the rest put together (Fig. 
551). 

The small hooklets have coarse root processes and are implanted upon 
a rather bulging rostellum. Their number runs from about thirty to 
fifty. 

The cyst-worm (hydatid) alone is found in man. It results from 
the introduction of tenia eggs into the intestinal canal. 

If the embryo wanders from the intestinal canal into any organ, it 
changes into a cyst, which is not capable of active motion. It consists of 
an outer lamellated, very elastic cuticle (Fig. 552, a) and a parenchyma- 
tous layer (6) lying internal to this, consisting of granular masses and 
cells, and containing muscle-fibres and a vascular system. When the 
cyst has reached about the size of a walnut (sometimes earlier), there are 
formed from the parenchymatous layer small brood-capsules (c) which 








712 THE ANIMAL PARASITES. 


produce a great number of scolices. The first stage of these tap 
heads consists of coarsely granular protoplasmic masses (d) lying 
wall of the brood-capsule; these develop further anc 
cavities (e) communicating with the cavity of the 
capsule, and later become differentiated into a tapeworı 
(f) furnished with a circle of hooklets. The head (h) 
now protrudes into the lumen of the brood-capsule ( 
about 0.3 mm. long, possesses a rostellum with small, 
hooklets, four suckers, a water-vascular system, and nu! 
chalky bodies in its parenchyma. Frequently the a 
part of the body is telescoped into the posterior part (g 

In many cases the echinococcus cyst remains : 
Its only change consists in an enlargement to the size 
orange or fist, through the formation of new brood-c: 
and heads. The surrounding tissue forms a connective 
capsule, in which the cuticular eyst lies. The cavity 
eyst is filled with a clear tluid, which does not coz 
through boiling or on the addition of acids, and contain 
or but little albumen, but on the other hand does c 
sodium chloride, calcium oxalate, triple phosphates, uri 
sugar (in the liver), and often also cholesterin. The 
o capsules are always situated on the inner surface, in cas 
are not mechanically dislodged; and are visible throu 
transparent parenchyma as small white points. Oceasi 
the cyst remains sterile. 

In many cases daughter-cysts (Fig. 553, ¢) are formed. The 
velopment proceeds in the depth of the cuticle independently of tl 
parenchymatous layer. Between two lamell® of the cuticle there 











.—Wall of an echino 
Membrane; h, pare 
in different wtages of di 





containing brood-capsules and scolices (alcohol. cart 
Inyen, ity verdeular cells; ey Dronataeapatiten el « 
x 100, 








a collection of granules, which surround themselves with a cuticl 
thereby become the centre of a new set of layers. As the num 
layers increases, the cavity grows larger and the contents become 





ECHINOCOCCUS. 713 


If the daughter-cysts grow they bulge out the wall of the mother-cyst 
like a hernial sac, until it finally gives way and liberates its contents. 
If they now pass outward by the side of the parent-cyst, they obtain from 





Fig. 558.—Echinococcus hydatidewus, a, Surface of liver: 
danguter-cysta within a parentcyet, which bias been opened by a 
n. 


: P gingurated connective 
in ineiston ds adhestons. Threwäfuis 


the parenchyma in which they lie an external capsule of connective tis- 
sue, and then produce brood capsules in the same manner as the primary 
cysts arising from the six-hooked embryos. 

An echinococcus with an exogenous proliferation is called echinococcus 
granulosus (scolecipariens Küchenmeister), or sometimes also echinococ- 
cus veterinorum from the fact that it is of frequent occurrence among 
the domestic animals. 

A second compound form of the echinococcus is the echinococcus 
hydatidosus. It is characterized by the presence of inner daughter-cysts 
(Fig. 553, c). According to statements made by Naunyn, and also con- 
firmed by Leuckart, the scolices and broud-capsules undergo a cystic 
metamorphosis, and so become changed into danghter-cysts which occa- 
sionally produce grand-daughter cysts. Through the formation of numer- 
ous daughter-cysts the chief cyst may attain a very large size. 

The infection of man follows the ingestion of the eggs of the tenia 
which occurs in dogs. The cysts are most often found in the liver, 
but the echinococcus occasionally occurs in the most diverse organs—for 
example, in the lungs, spleen, kidneys, intestine, in a bone or in the 
heart. With the exception of the disturbance of the tissues from press- 
ure and of the local inflammation which it causes (the latter leading to 
the formation of a connective-tissue capsule in many organs) the cyst often 














714 THE ANIMAL PARASITES. 


produces no harmful effects upon the affected individual. It ofteı 
on attaining a certain size (that of a walnut to that of an apple 
fluid is absorbed, the cyst contracts, and there remains within it a1 
cheesy detritus, which often calcifies to a mortar-like mass. The | 
lets are preserved for a very long time. 

In other cases the echinococeus becomes larger, particularly 
endogenous or exogenous daughter-cysts develop. It may become 
gerous through its size alone. Severe inflammations are occasic 
produced, particularly after trauma or after rupture of the cyst int 
of the body-cavities. Rupture into a blood-vessel may also occu) 
lead to the metastasis of cysts and an embolic blocking of vessels. In 
favorable cases rupture may take place externally or into the intest: 

The spontaneous spread of brood-capsules and scolices in the 





jon of an Kehinococeus multilocularis. a, Alveolar echinococcus tis 
¢. cavily produced by softening ; ıl, fresh nodules. Natural size. 






host, as well as the experimental transplantation of the same into anc 
host: (Alexinsky) may lead to the formation of new cysts. 

The form of the parasite known as echinococcus alveolar 
multilocularis presents itself as a hard tumor, situated usually iı 
liver, rarely in other organs (brain, spleen, adrenal), and possess 
alveolar structure (Fig. 554), in that a firm, dense connective-tissue 
encloses numerous cavities. Its contents are translucent and gelati: 
or consist of fluid and a gelatinous substance. The cavities are in 
spherical and in part irregular in shape. Usually, through the 
ening and disintegration of the parenchyma, ulcerative cavities (« 
formed. In other places the tissue is fibrocaseous, necrotic or calcific 
is impregnated with bile. At times the caseation of the proliferatir 
sue is the most prominent feature of the process; at other times the 
olar structure. When the development of the colonies has progi 
further, there appear in the tissue gray and yellowish nodules (d) in ' 
cavities containing colloid plugs (chitin-eysts and coils) are devel 





ECHINOCOCCUS. 715 


The exquisite alveolar structure has given rise to the theory that this 
form of echinococcus is an alveolar, colloid-containing tumor of the liver. 
Virchow first recognized the true nature of the condition, and demon- 
strated that the so-called colloid masses were echinococcus cysts. 

According to the investigations of Melnikow-Raswedenkow the alve- 
olar echinococcus is to be regarded as a different species, which increases 
in the tissue of the host in a peculiar manner, suggesting the mode of 
development of the Trematodes; and in many grees spreads by both 
hematogenous and lymphogenous metastases from the primary focus of 
development to other organs (lvmph-glands, lungs, brain). 

The embryo migrating from the intestine into the liver becomes 
changed into a multilocular chitinous coil, which possesses on both inner 
and outer sides granular masses of protoplasm, from which in part sco- 
lices, and in part ovoid embryos develop. These, through virtue of their 
motility, become distributed in the tissues and give rise to proliferations 
of granulation tissue with the formation of epithelioid cells and multina- 
clear giant-cells, terminating partly in tissue-indurations and partly in 
caseation. The latter process is particularly prominent in metastatic 
foci. Among the structures which arise from the granular protoplasm 
of the parasite there may be distinguished the following forms: (1) 
ovoid embryos with thin homogeneous membrane; (2) embryos with thick 
fibrous capsules; (3) scolices. 

The embryos which are capable of migration are to be found inside of 
the chitin-cysts as well as free between the tissue-cells. A part of the 
embryos wandering thence into the connective tissue of the organ develop 
within the vessels into complicated chitin-cysts or coils which again form 
an after-growth of embryos; another part die and are taken up by phago- 
cytes or are infiltrated and disintegrated. 

Scolices form from the granular protoplasm of the embryo (prosco- 
lices) inside of the chitin-structure as well as outside of the same. The 
proscolices entering the tissues may also be changed into chitin-cysts. 

The life-history of the alveolar echinococcus outside of the paren- 
chyma of the organ is unknown; the feeding to dogs has given no posi- 
tive results. It appears that the embryos and scolices of the same are not 
capable of development in the intestine of the dog. 

The ordinary echinococcus is widely distributed, though not very 
common. It is of most frequent occurrence in Iceland, where the inhabi- 
tants live in very close association with dogs. The alveolar echinococcus 
has been observed chiefly in Switzerland, South Germany, Austria, and 
in Russia. 


. Literature. 


( Echinococeus. ) 


Abee: eber multiloculären Echinococcus. Virch. Arch., 157 Bd., 1899. 

Alexinsky: Verimpfung von Echinococcus in d. Bauchhöhle. Langenbeck’s Arch., 
56 Bd., 1898. 

Bider: Echinoc. multilocul. des Gehirns. Virch. Arch., 141 Bd., 1895. 

Carriere: De la tumeur hydatique alvéolaire, Paris, 1888. 

Doebbelin: Knochenechinokokken d. Beckens. Deut. Zeitschr. f. Chir., 48 Bd., 1898. 

Erlanger: Der Geschlechtsapparat d. Taenia echinococcus. Zeitschr. f. wiss. Zool., 
50 Bd., 1890. 

Gerulanos: Multiple Muskelechinokokken. Deut. Zeitschr. f. Chir., 48 Bd., 1898 
(Lit). 

Guillebeau: Histologie des multiloculären Echinococcus. Virch. Arch., 119 Bd., 1890. 

Houzel: Cystes hydatiques du rein. Rev. de chir., 1898. 








716 THE ANIMAL PARASITES. 


Huber: Bibliographie d. klin. Helminthologie, i., München, 1891. 

Klemm: Fütterungsversuche m. Ech. multilocul. Bayr. ärztl. Correspbl., 1883. 

Madelung: Beitr. z. Lehre von den Echinokokken, Stuttgart, 1885. 

Mangold: Ueb. d. multiloc. Echinococcus. Berl. klin. ., 1882. 

Melnikow-Raswedenkow: Stud. über den Alveolarechinococcus. Beitr. v. Zie 
iv., Supplh.. Jena, 1901. 

Mosler: Ueber Milzechinococcus, Wiesbaden, 1884. 

Müller: Zur Kenntn. d. Taenia echinococcus. Münch. med. Woch., 1893. 

Naunyn: Entwickelung d. Echinococcus. Dorpat. med. Zeitschr., 1870. 

Neisser, A.: Die Echinokokkenkrankheit, Berlin, 1873. 

Oster feb. d. Ech. multil. bei Rindern u. Schweinen. Deut. Zeitschr. f. T 

med., xvii., 1890. 

Posselt: Die geographische Verbreitung des Blasenwurmleidens Stuttgart, 19004. 
Riemann: Keimzerstreuung d. Echinococcus. F 

v. Bruns, xxiv., 1899. 

Sommers: Statistics on Echinococcus Disease ir 
United States. N. Y. Med. Journ., 1896. 
Tschmarke: Beitr. z. Histologie des Echinocc 

multilocularis. Inaug.-Diss., Freiburg, 1891. 
Vierordt: Abhandlung über dm multiloculären ] 
nococcus, Freiburg i. B.. 
Virchow: Verh. d. phy: ec Ges., vi., Würzt 
855; Virch, Arch.-8 Bd., 1854. 
Wilms: Echinoc. multiloc. d. Wirbelsäule. Beit 
Bruns, xxi., 1898 (Lit.). 














































x 186. Bothriocephalus latus (Brem: 
or pithead is the most formidable tapew: 
of man, measuring from 5-8 metres in len; 
and consisting of three thousand to 1 
thousand short but broad segments (1 
555), which are broadest in the middle res 
and narrower again at the end. The ler 
of the largest segment is about 3.5 mm., 
breadth about 10-12 mm. 

The head (Fig. 556) has a long oval 
club shape, is about 2.5 mm. long and 1 1 
broad. It is somewhat flattened, and ] 
sesses on each lateral margin a slit-like 
pression, and is mounted upon a filiform ne 

The body is narrow and 
like a ribbon, with the except 
of the central parts of the: 
ments which project somew 
outward. At this spot the u 
us is found, in the shape oc 
single canal, which forms 
number of coils (Fig. 557, 
When the eggs colleet here 
great numbers the lateral e 
of the uterus arrange themsel 
in folds, so that a remark: 
rosette-li ppearance is y 
ephalux latus, (After Leuck- duced. The sexual openings 
Neu of Ruthrinerphate tatu of i the middle line of the ven 
Aten Heller.) Fnlantenl surface, near to the ante 

border of the segment, the 
male orifice (0) being close behind the male opening (f). 
The ovary (g) is a double organ which lies in the middle layer; 



































Fig. 585.— Ne 
art.) Natural sl 








BOTHRIOCKPHALUS LATUS. TT 


yolk-chambers (h), on the other hand, are located in the cortical layer. 
The shell-gland (k) lies behiud the collecting-tube (i) of the yolk-cham- 





Fi. 557.—Median portion of a proglottis of Bothriocephalus latus, seen from the dorsal surface. The 
‘cortical layer of the segment has been removed except a border on each side, and the middle layer thus ex- 
Posed. (After Sommer.) a, Lateral vessels ; h, testicular vesicles ; ¢, teaticular canalicull ; d, seminal ducts; 
&, posiertor. f. anterior holiow-muacie apparatus (cirrussac of vas deferens) ; g, ovary; I yolk-chambeı 

cortical area; 6, nich ‘lead ventrally to 


the yolk. 
chambers ; k, shell-glan orifice of 
uterus opening on the u 











bers. The testicles consist of clear vesicles (b) which lie in the lateral 
portions of the middle layer, and communicate by means of fine canals 
(ce) with the vas deferens (d), which terminates in the cirrus-sac (e, f ). 

The eggs (Fig. 558) are oval, and are about 0.07 mm. long and 0.045 
mm. broad. They are surrounded by a thin, brown shell, the anterior 
pole of which forms a sharply outlined 
cap-like cover. 

The Bothriocephalus latus occurs chiefly 
in Switzerland, in the northeastern parts 
of Europe, in Holland and in Japan, and 
lives, as does the Tenia, in the intestine 
of man. According to Bollinger it is 
rather frequent in 
Munich. The _ first 
stage of development. 
of the eggs takes place 
in water. After the 
lapse of months there 
develops an embryo 





(Oncosphera) armed een 
with six hooklets and ¥iG, 558.—-Eggn of Bothrincephalus lat one right 
covered with eilire having been emptied ot it Jolr-coutenta. “(tier Leachate) 


(Fig. 559). This de- ya!" 8%,cPrmyembrye of Bothrtooophalus latus with elated en- 











718 THE ANIMAL PARASITES. 


velops, in some intermediate host as yet unknown, into a measle (Pl 
cercoid), which, according to the investigations of Braun in the Russ 
Baltic provinces, seeks out as second intermediate host the pike or t 
pole, and develops in the muscle or internal organs of these animals i 
a sexless tapeworm. According to Grassi and Parona, the measle 
Bothriocephalus latus in Italy occurs in the pike and in the river-per 
In Japan it is found most frequently in the Onchorhynchus Perryi (1jiı 
Leuckart). Zschokke found it in the Lake of Geneva in the follow 
forms of fish: Lota vulgaris, Perca fluviatilis, Salmo umbla, Esox luc 
Trutta vulgaris, and Trutta lacustris. It is found most often in the tad] 
(Lota vulgaris) and in the perch (Perca fluviatilis). Should the measle g 
entrance, through the ingestion of the fish mentioned, into the intest: 
canal of man, it again attains sexual maturity. According to Braun: 
Parona the measles may also be brought to development in both dogs: 
cats. The presence of Bothriocephalus in the intestine gives rise ı 
gradually increasing anemia, which resembles pernicious ansmia. ' 
diminution of the red blood-cells and of the hemoglobin content of 
blood is probably due to the fact that after the death of the tapewı 
poisonous products arise having an injurious action upon the blood~ 
puscles, 


Bothriocephalus cordatus (Leuckart) is a tapeworm, of 80-115 cm. long, and 
a heart-shaped head, whose sucking-grooves are flattened. The breadth of the 
segments is about 7-8 mm. ; the length, about 8-4 mm. In Greenland and Iceland 
a frequent parasite of the dog, seal, and walrus, and is found occasionally in mun. 
measles likewise occur in fishes. 

Bothriocephulus Mansoni (Cobbold) or liguloides (Leuckart) is the measle (plerocere 
of a tapeworm which has been observed a few times (Manson, Ijima, Murata) in 
body-tiasues and in the descending urinary passages or in the urine. Its origin is 
known. 


Literature. 
(Bothriocephatus Latus.) 


Bollinger: }othrioceph. latus in München. Deut. Arch. f. klin. Med., xxxvi., 18 

Braun: Virch. Arch., 88 u. 92 Bd.; Zur Entwickelungsgeschichte des breiten Bs 
wurmes, Würzburg, 1885; Ueber den Zwischenwirth des breiten Bandwurt 
Würzburg. 1886; Die thier. Parasiten des Menschen, Würzburg, 1895. 

Grassi, B., ¢ Rovilli: Contrib. alla sindio dello sviluppo del Botriocefalo lato. Gi 
della R. Accad. di Med., 1887, ref. Cbl. f. Bakt., iii., 1888. 

Leuckart: L. c r Bothriocephulus-Frage. Cbl. f. Bakt. u. Parasitenk., i., ıı 

Parono: Rendiconti Ist. Lomb., vol. xix. 

Schaumann: Zur Kenntniss der Bothriocephalus-Anämie, Berlin, 1894. 

Schaumann u. Tallqvist: Blutkörperchen uuflösende Eigensch. d. breiten Ba 

Deut. med. Woch., 1898. 

ch. d. Bau htsreifen Glieder v. B. latus, Leipzig, 1872. 

as de Bothrioeéphalic en Belgique. Bull. de ’Ac. Roy. de Belgique, xv 




















t.). 
Zschokke: Bothrioeph. latus in Ganf. Cbl. f. Bakt., i, 1887; Zwischenwirth 
Bothr. latus. 1b. iv., 1888. 


B. NEMATHELMINTHES (ROUND WORMS). 


§ 187. All the round worms which occur as parasites belong to 
Nematoda. They possess a slender, cylindrical, elongated, at ti 
filiform body without segments or appendages. The cuticle is thick: 
elastic. The mouth opening is found at one extremity, and is provi 


ASCARIS LUMBRICOIDES. 719 


sometimes with soft and sometimes 
with horn-like lips. The elongated in- 
testine, together with the pharynx and 
chyle-stomach, extends through the en- 
tire body-cavity (Fig. 560) and opens 
upon the ventral surface a short dis- 
tance from the (usually) awl-shaped 
posterior extremity. The sexual or- 
gans and their openings are also found 
on the ventral surface. The female 
sexual orifice is located at about the 
middle of the body, less frequently 
near the anterior or posterior extremity 
(Fig. 560, A,a). Inthe male the sex- 
ual opening and the anus are located 
together (B, ce). The chitinous cover- 
ing of the’ lower gut forms in the male 
the means of clinging during the act 
of copulation. The males are usually 
smaller than the females. The de- 
velopment is direct, and the metamor- 
phoses are not striking. The nema- 
todes occurring in man are in part 
harmless parasites of the intestine, and 
in part very dangerous, sometimes even 
fatal, parasites of various organs. 

§ 188. Ascaris lumbricoides, the 
common round-worm (Fig. 560) is a 
light-brown or reddish, cylindrical 
worm with tapering ends. The female 
(A) is 25-40 cm. long, the male (B) is 
much smaller, and the posterior ex- 
tremity of the latter is bent in the 
form of a hook and provided with two 
spicules (c) or chitin processes. 

The mouth opening (5) is sur- 
rounded by three muscular lips bearing 
fine teeth. The female sexual opening 
(A, a) lies anterior to the middle of 
the body. The eggs which the mature 
female contains in enormous numbers 
possess in their fully developed con- 
dition a double shell (Fig. 561) and 
around this an albuminous envelope. 
They are about 50-70 in length. The 
worm inhabits the entire intestinal 
tract, but most frequently the small in- 
testine. It is the most common par- 
asite of man, and is found frequently 
in very great numbers. When mature 
fomales are present the feces Contain 
‘he eggs in great numbers. These are 

7 resistant to external influences, 

@, to drying and freezing. 





orifice ; ¢, the two spicules of the male: b, 
the (enlarged) oephalleend with thethreetipe. 

Fig. F61.—Egg of Ascarie lumbricutdes, * 
with shell "and albuminous covering. (After 
Leuckart.) x 200. 


720 THE ANIMAL PARASITES. 


The eggs require no intermediate host (Lutz, Leuckart, Grassi, I 
stein). Man is infected by the ingestion of eggs which have bt 
expelled from the bowel and have matured in the faces. According 
feeding-experiments which Epstein carried out on human beings w 
eggs which had been cultivated in damp feces for a long time, the row 
worm attains its maturity in from ten to twelve weeks after the ingest: 
of the eggs. At this time the male is 13-15 cm. long, and the fem 
from 20-30 cm. Their presence in the intestine does not cause any 
ticeable disturbance. Only when present in large numbers do they sor 
times, especially in children, cause intestinal catarrh, vomiting, nervı 
disturbances and convulsions. Occasionally the worm crawls into nort 
and pathological openings in the wall of the intestinal canal, and int 
way causes trouble. Thus, when it crawls into the ductus choledoch 
it may produce bile-stasis. If it penetrates through an ulcer into 
peritoneal cavity or into a hernial sac, it may excite inflammation 
the tissues concerned, According to Leuckart it may also penetrate : 
uninjured intestinal wall. It is very frequently passed with ‘the sto 
per anum, but at times per os in vomiting. From the pharynx it m 
wander into the larynx. 


In the domestic animals ascarides are of frequent occurrence. Ascaris lum 
coides is found in awine (Ascaris enilla) and in cattle (Ascaris rituli). “Ascaris 

a round worm whose female is 18-87 cm. long, isa common parasite of 

horse and donkey. Ascaris mystaz, whose female reaches a length of 12 cm., is for 

frequently in dogs and cats, and has also been observed in man. Various species, ¢ 

ignated as Heterakis, occur in birds. Heterakis maculosa, the round worm of pigec 

may cause the death of the pigeon when occurring in large numbers within its intesti 





Literature. 
(Ascaris Lumbricoides.) 


Epstein: Uchertmgung des Spulwurms. Jahrb. f. Riuderheilk.. 39 Bd. 1808. 
Grassi: Intorno all’ Ascaris lumbricoides. Gazz. degli Ospetali, ii., 1881, u. Cbl. 
Bat, ii, 1888; Trichoeephalus- und Ascurigentwickelung, Tbid., i, 1887. 
Huber: Bibliographie der klin. Helminthologie, München, 1898. 

Kitt: Lehrb. d. path.-anat. Diagnostik, ii., Stuttgart, 1895. 

Leuckart: Ucbergangsweise des Ascaris lumbricoides, Cbl. f. Bakt., ii., 1887. 
Lutz: Zur Frage der Invasion von Tuenia elliptica u. Ascaris lumbricoides. Cbl. 
Bakt., ii., 1887; Uebertragung des menschlichen Spulwurms. Ib., iii., 1888. 
Peiper: Thierische Parasiten. Ergebn. d. allg. Path., iii., 1897. 
Saltykow: Ascaridosis hepatis. Zeitschr. f. Heilk., xxi., 1900. 








§ 189. Oxyuris vermicularis, awl-tail, pinworm, or threadworm is 
small round worm (Fig. 562), the female being about 10 mm. long (a, 
and pointed at the caudal extremity like an awl, while the male is abo 
4 mm. long (e) with a blunt posterior end, the anus being provided wii 
a spieulum. 

The eggs (563, a), which the body of the female often contains i 
very great numbers, are 50 » long and 24 „ broad, have a flat and 
curved surface, and a shell which is covered by a thin albuminous laye 
Oxyuris vermicularis inhabits the large intestine and the lower portion: 
the small intestine. According to Zenker and Heller only the imprg 
nated mature females are found in the large intestine, the young indiviı 
uals and the males remain in the small intestine. They occur very fn 
quently in larger or smaller numbers. At night they often wander fra 
the rectum over the anal region, and may enter the vagina; they excil 


ANCHYLOSTOMA DUODENALE. 721 


itching of the affected parts. The scratch- 
ing thus produced sometimes leads to der- 
matitis, erections, masturbation, ete. 

For the development of the eggs (Fig. 
563 a-c), it is necessary after their expul- 
sion with the feces that they again be 
taken into the stomach of man or beast. 
It: is very probable that the original host 
may again infect himself with oxyuris, in 
that, for example, the eggs becoming at- 
tached to his finger during the act of 
scratching may later get into his mouth. 

The eggs are very resistant to drying, 
and in this condition may he widely scat- 


tered. 


$ 190. Anchylostoma duodenale 
( Dochmius duodenalis, or Strongylus duodena- 
lis, or Uncinaria duodenalis, also Uncinaria 
Americana [Stiles]), Hook-worm, is a small 
worm belonging to the family of Stron- 
gylides, which inhabits the upper part of the 
small intestine (Fig. 564). 
body of the female is 5-18 mm. long, that 
of the male 6-10 mm. The cephalic end 
(Fig. 565) is curved toward the dorsal sur- 
face, and possesses a bellied mouth-capsule 
(d). It is almost completely divided dor- 
sally, and the cleft is covered by two chitin- 
ous layers. On the ventral border there 
are four incurving teeth (6), on the dorsal 


ly placed (c), all being held together by 


chitinous bands. 


The cylindrical 





. Fig. 562. — Oryuris vermicularta. 
border two teeth which are perpendicular- a, Sexually mature female; h, female 


full of eggs; c, male. (After Heller.) 


The male is provided at its caudal extremity with a threefold bursa 
(Fig. 564, i), and two thin, fishbone-like spicules (p). In the female 
the posterior end is pointed, and bears an awl-shaped spine; the vulva 





Fic. 563. — of Oxyuris 

5 vermieularis and stages 
y of development. (After Zenker 
and Heller.) b, c, Segmenta- 

f tion of yolk; , tadpole-shaped 
y om omen ¢, worm-shaped embryo. 


38 


lies posterior to the body centre. The oval 
eggs (Fig. 566) are 44-67 a long, 23-40 u 
broad. They undergo the first stages of cleav- 
age in the human intestine (a-d), develop 
further in muddy water (e, f ), and may then, 
if brought into the human intestinal tract, de- 
velop again intosexuallymatureanimals. With 
its teeth the worm works its way into the 
mucous membrane as far asthe submucosa, and 
sucks itself full of blood. Its point of attack 
is distinguishable later by a small ecchymosis 
in the middle of which there is a white spot 
with a central perforation. Occasionally there 
are found in the intestinal mucosa small cav- 
ities filled with blood, within each of which 
there lies a coiled-up worm. The parasites, 
when present in large numbers, cause a con- 
tinuous and serious loss of blood, which may 


123 THE ANIMAL PARASITES. 


lead to the most severe forms of anemia (Egyptian chlorosis), but they 
are not infrequently found in individuals who present no symptoms of 





Fa. 585,—Cephalte end or Anchieaone duodenale. (After Schulthess.) a, Mouth-capeule B; tert 
of ventral border; ¢ teeth of dorsal border; d. mouth cavity: ¢, skin protuberance on ventral side of 
head; femuscular layer: g, dorsal grooves 

Fıa., 566.—Fggs of Anchyloxtoma unicnates (After Perroneito and Schulthess.) a-d, Different 
stages of segmentation; ¢, /, exes with embryos. X 200, 


disease. The parasite is very common in the tropics, and also in Japan. 
According to Griesinger and Bilharz about one-quarter of the native 


STRONGYLIDES. | 723 


Egyptians suffer from this disease. The parasite was very often ob- 
served in the workmen engaged in the Saint Gotthard tunnel. Accord- 
ing to Menche and Leichtenstern the brick-fields of the Rhine provinces 
are to a great extent infected with anchylostoma (brick-burner’s ane- 
mia). (For the distribution of Uncinaria Americana, see Stiles, Bull. U. 
8. Dept. of Agric., 1902.) 


Eustrongylus gigas, a palisade-worm of red color, whose female reaches a length 
of 1 metre, is a very rare parasite, which has been observed only a few times in the kid- 
ney-pelvis of man. It occurs very frequently in dogs. It possesses a mouth-opening 
with six papilla; the male has on its posterior extremity a bursa with a single spicu- 
lum. The eggs are oval, 0.06 mm. long, and provided with a rough ous 
capsule. 

P Strongylus longevaginatus, a thread-like, white worm, 26 mm. long, was once 


observed in the lung of a boy. 

In the domestic animals Btrongylides occur in much greater numbers than in man, 
and are in part inhabitants of the intestine, and in part of the lungs (Müller, “ Die 
Nematoden der Säugethierlungen,” Deut. Zeitschr. f. Thiermed., xv., 1886). 

Dochmius trigonocephalus and Dochmius stenocephalus occur in the intestine of dogs, 
and give rise to anemia. 

rongylus armatus is a common parasite of the horse, which enters the intestinal 
tract as an embryo, bores into the intestinal wall (Ol), thence into the liver, by way of 
the portal vein, and further into the lungs and the organs of the major circulation. 
Following this migration, it may develop in the most diverse organs and cause the 
formation of fibrous nodules, which become calcified after the death of the parasite 
enclosed in them. In the intestinal wall it may develop after direct migration or after 
embolic lodgment in the part, and leads to the formation of cavities, from which it 
again breaks through into the intestinal lumen. In the mesenteric arteries it attains 
sexual maturity, and causes thrombosis and the formation of aneurisms. The male of 
the mature worm is 20-80 mm. long; the female, 20-55 mm. 

Strongylus tetracanthus, which inhabits the large intestine of the horse, causes a 
hemorrhagic enteritis when present in large numbers. 

Strongylus paradorus is an extremely common parasite of the lungs of hogs. 
Strongylus capillaris, Str. commutaius, and Str. filaria are frequent parasites of the 
lungs of goats and sheep, and different species may be present in the same Jung at one 
time (Schlegel, “ Die durch Strong. capillaris verursachte Lungenwurmseuche der Ziege,” 
Arch. f. wiss. Thierheil., 25 Bd., 1899). The latter causes in sheep a bronchitis and 
nodular proliferating pulmonary inflammations; through the swallowing of many 
embryos inflammations of the intestine may also be produced. 

rongylus rufescens and Str. paradorus, Nematodium oris pulmonalis (Lydtin), or 
Pseudalius ovis pulmonalis (Koch) are also inhabitants of the lungs of sheep, the last- 
named causing a pseudotuberculosis. Str. commutatus and Str. pusillus occur in the 
lungs of the hare and rabbit; Str. syngamus and bronchtalus in the trachea of birds; and 
excite inflammations. Str. micrurus (Strose, “Bau von Strongylus micrurus,” Deut. 
Zeitschr. f. Thiermed., xviii., 1892) occurs in cows and calves, in arterial aneurisms as 
well as in the respiratory passuges. 

Strongylus pusillus causes in cats a pulmonary disease resembling tuberculosis 
(Jeanmaire, “ Ueber die hist. Veränd. der Lunge bei der verminösen Pneumonie der Katze 
und des Hasen,” Inaug.-Diss., Freiburg, 1900). Syngamus trachealis (Klee, “Der ge- 
paarte Luftröhrenwurm des Getlügels,” Deut. Thierdretl. Wochenschr., 1899) is a dan- 
gerous parasite of birds, particular y of pheasants, in the trachea of which it appears 
in great numbers, and attaches itself to the mucous membrane. It is easily recognized 
by its red color. Similar to the last-named is Syngamus bronchialis, which has been 
pbserved a few times in geese and ducks. 


Literature. 
( Anchylostoma. ) 
Bäumler: Anchylostomiasis. Correspbl. f. Schweizer Aerzte, 1881, 1885. 
Bozzolo e Pag : Giornale della Societä Italiana d’Igniene, ii., Milano, 1880. 


Bugnion . Anchylostome duodenal et anémie du St. Gotthard. ‘Rev. méd. de la Suisse 
rom., i., . 


Ernst: | Einige Fälle von Anchylostomiasis mit Sectionsbefund. Deut. med. Woch.. 


24 THE ANIMAL PARASITES. 


Griesinger: Arch. f. physiol. Heilk., 1854. 

Huber: Bibliographie d. klin. Helminthologie, München, 1893. 

Kitt: Lehrb. d. path.-anat. Diagnostik, ii., Stuttgart, 1895. 

Leichtenstern: Anchylostoma. Cbi. f. klin. Med., 1885, 1886; Deut. med. Woch., 
1885, 1886, 1887, 1888; Wien. klin. Rundschau, 1898. 

Looss: Lebensgeschichte d. Anchylostomum. Cbl. f. Bakt., xx., 1896, xxi., 1897; 
xxiv., 1898. 

Lutz: Samm!. klin. Vortr. v. Volkmann, No. 255, 256, 265. 

Menche: Anchylostomiasis. Zeitschr. f. Klin. Med., vi. 

Olt: Wanderungen des Strongylus armatus. Cbl. f. Bakt., xxix., 1901. 

Perroncito: Arch. p. le Sc. Med., v., Torino, 1881; Arch. ital. de biol., ii., tii., 1888. 

Prowe: Anchylostomiasis in Central America. Virch. Arch., 157 Bd., 1899. " 

Schulthess: :iträge z. Anat. des Anchylostoma. Zeitschr. f. wiss. Zool., xxxvii., 
1882. 

Sonderegger: Anchylostoma duodenale. Correspbl. f. Schweizer Aerzte, 1880. 

Stiles: Prevalence and Geographic Distribution of Hookworm Disease (Uncinariasis or 
Anchylostomiasis) in the United States. Bull. of Hyg. Lab., Pub. Health and 
Marine- Hospital Service of the United States, 1903. 

Ward: Nematoda. Ref. Hdb. of Med. Sc., 2d ed., vol. vi. 

Zinn u. Jacoby: Anchylostomum duodenale, Leipzig, 1898 (Lit.). 


§ 191. Anguillula intestinalis (Fig. 567) is a worm of 2.25 mm. 
length, which is found in the intestine, particularly in the tropics, and in 


-. - 

‘ hy 
.. - 
wt 


> 
er 
EN 


he een Bann 
Te 


a 
aloes 


vu; 


ij 
RE Y 
i 
ye u 
v Ri 





Fic. 55.—-Anguillula intestinalie. Fic. 568.—Female of Anguillula stercoralis, with 
(After Braun.) eggs and embryos. (After Perroncito.) X 885. 


Italy, and has been occasionally observed in Switzerland, Germany, Bel- 
gium, and Holland (probably transported from Italy), under similar con- 


ANGUILLULA. 725 


ditions as the Anchylostoma duodenale. According to the observations 
of Leuckart, Golgi, Grassi, Leichtenstern, Zinn and others, the Anguillula 
intestinalis is a hermaphrodite, the eggs of which develop even in the 
intestine to embryos of 0.2 mm. in length; and in the presence in the 
intestine of numerous parent-worms are found in the faces in great num- 
bers. In the stools they become changed within about twelve hours into 
filaria-like larvie, which, when gaining entrance into the human intestine, 
again grow into parasitic anguillule, which are again able to produce 
eggs capable of development. In addition there also occurs a develop- 
ment with an intermediate sexual generation, a heterogony. 

In the event of a sexual development the embryos grow outside of the 
body in about three days into sexually mature animals (female 1.2 mm. 
long, male 0.88 mm.) which are known as Anguillula or Rhabditis sterco- 
ralis (Fig. 567), and were formerly regarded as a separate species. The 
embryos of the separate sexual individuals develop into filaria-like larve, 
which, entering the intestine of man, again grow into parasitic anguil- 
lul. 

According to Leichtenstern and Zinn the filaria-like larve of the 
direct development are more resistant than those of the sexual. ‘The 
sexual mode of multiplication occurs particularly in the anguillula, com- 
ing from the tropics, while in the indigenous form (brick-laborers of 
Germany, Belgium, Holland) the direct. metamorphosis predominates. 
Leichtenstern has explained this by the assumption that the tropical 
anguillula after its transportation into a temperate zone has adapted 
itself to the less favorable climatic conditions of the latter in such a 
manner that the anguillula of the temperate zone favors more the much 
simpler mode of development which is the more independent of the 
climate—namely, the direct transformation of the embryo into the filaria- 
shaped larvs, which in turn grow directly into parasitic anguillule. 

According to the statements of various authors Anguillula stercoralis 
when present in large numbers causes diarrhea. According to Normand, 
Grassi, Golgi, Leichtenstern, and others, the worms are found chiefly in 
the upper parts of the small intestine. According to Leichtenstern and 
Askanazy the mature animals and the larve penetrate not only into the 
erypts of Lieberkiihn, but also into their epithelium and into the con- 
nective tissue of the mucosa, and iu individual cases may break through 
the muscularis mucose. The mother animals lay their eggs in the intes- 
tinal crypts. The embryos when hatched out wander out into the intes- 
tine. 


Literature. 
(Anguillula Stercoralis and Intestinalis. ) 


Askanasy : Invasion d. Ang. intestinalis in die Darınwand. Cbl. f. Bakt., xxvii., 1900. 

Golgi e Monti: Sulla storia naturale delle cost dette anguillule stercorali e intestinali. 
Arch. per le Sc. Med., x., 1886. 

Grassi e Perona: Arclı. per le Sc. Med., xiii., 1889. 

Grassi e Segré: Nuove osservazioni sull’ eterogenia del Rhabdonema (Anguillula) in- 
testinale. Rendic. della R. Accad. dei Lincei, 1887, ref. Cbl. f. Bakt., il., 1887. 

Huber: Bibilogr. d. klin. Helminthologie, Suppl., Jena, 1898. 

Leichtenstern: Ang. intestinalis. Deut. med. Woch., 1898; Cbl. f. Bakt., xxv., 1899. 

Normand: Du röle etiologique de l’anguillule. Arch. de méd., 1878. 

Orley: Die Rhabditiden und ihre medicinische Bedeutung, Berlin, 1886. 

Pappenheim u. Braun: Ang. intest. in Ostpreussen. Cbl. f. Bakt., xxvi., 1899. 

Perroncito: Arch. p. le Sc. Med., v., 1881; Arch. ital. de biol.. ii. u. iii.; Ann. R. Ac- 
cad. di Agricoltura di Torino, xiii. ; Journ. de l’anat. et de la phys., xviii. 


726 THE ANIMAL PARASITES. 


Teissier: Anguillule stercorale. Arch. de méd. exp., 1896. 

Thayer: On! the Occurrence of Strongyloides Intestinalis in the United States. Journ. 
of Ex ed., 1901. 

Zinn: Ueber Anguillula intestinalis. Cbl. f. Bakt., xxvi., 1899. 


§ 192. Tricocephalus dispar, the whipworm, is a common and rela- 
tively harmless parasite, though according to Askanazy it sucks blood 
from the intestinal mucosa. It inhabits the cecum and the neighboring 
“ portions of the intestine. It is found also in the domestic animals. The 
male and female are about 4—5 cm. 
in length (Fig. 569). The anterior 
body-half (a, b) is very thin, thread- 
like; the posterior, which bears the 
sexual organs (f, 9, l, 0, p) is much 
thicker, in the female (B) cylin- 
drical, and in the male ( A) rolled up 
and provided with a spiculum (g). 

The eggs (Fig. 570) are an el- 
ongated oval, 50 « long, and possess 
a thick brown shell, which shows 
at both poles a peg-shaped, glassy 
swelling. 

The first stage of the develop- 
ment of the embryos takes place in 
water and in moist earth. It ad- 
vances slowly, even in summer 
lasting four to five months, and in 
the colder months of the year much 
longer. The eggs are very resist- 
ant to cold and drying. (For the 
literature see Huber, ‘ Bibliogra- 
phie der klin. Helminthologie,” 
München, 1893, p. 213; Askanazy, 
“Der Peitschenwurm,” Deut. Arch. 
Ke Oe epee dispar: wrens f. klin. Med., 57 Bd., 1896; Heine, 


end of female; a, cephalic end; b, anterior portiono “ Anatomie d. Tricocephalus,” Cdl. 


of bodv with ceso hagus; c, stomach ; d, intestine ; „se 
e, cloaca ; f, seminal duct; g, penis; U, bell-shaped J. Bakt, xxviii, 1900). 





Fig. x. Fig. 570. 


sheath, with end of penis: m, intestine of the H : 
emale; n, anus; «©, uterus; p, vaginal opening. . S 193. Trichina spiralis occurs 
“9. in two forms—the trichina of the 
Fic, 5i0.— Bag of, Tricocephalus dinpar. (After intestine and the trichina of the 
Heller.) x 815. muscles. 


The intestinal trichina (Fig. 
571) is the sexually mature form, and is a small, white, hair-like worm 
scarcely visible to the naked eye. The female (4) is 3 mm. long, the 
male (B) is much smaller. The posterior part of the body is elongated 
in both sexes, and in the male (B) is provided on the dorsal half with 
two conical terminal pegs, which are directed toward the belly and 
are separated from each other by four knob-like papille. Instead 
of a spiculum the muscular cloaca is protruded outward | during copu- 
Jation. 

The intestinal canal begins with a muscular mouth, which becoming 
wider passes into the esophagus, which throughout its entire length is sur- 
rounded by the so-called cell-body—that is, by rows of large cells. The 
stomach, which follows the &sophagus, is a flask-shaped dilatation of the 
intestine, and is lined with finely granular cells. The stomach passes 


TRICHINA. 


797 


without any essential change of structure into the intestine, which in the 
male unites with the seminal duct at the posterior end to form the cloaca. 
The testicles consist of a pouch, which begins near the caudal end us 


a blind sac, proceeds as far forward as the cell- 
bodies, and bending there, passes over into the 
seminal duct. 

The sexual organs of the female (A) consist 
of a single ovary, a uterus and a vagina, which 
opens externally at the junction of the first and 
second quarters. The ovary likewise forms a 
pouch lying close to the posterior end of the 
body, in which the round eggs develop. The 
pouch passes anteriorly into the sac-shaped uterus. 

The eggs develop within the uterus into em- 
bryos which are set free at birth. 

The muscle-trichina (Fig. 572) is a worm 
0.7-1 mm. in length, which lives in the muscles 
of the body. It is usually rolled into a spiral 
and lies in a capsule, which occasionally contains 
lime-salts. Between the coils of the worm there 
is a finely granular mass. 

A single capsule may contain three to five 
trichine. 

If a piece of muscle containing living tri- 
chine is taken into the stomach of a host—for 
example, man—the capsule is dissolved and the 
triching are set free. In the intestinal canal they 
attain sexual maturity within two and a half days, 
when copulation takes place. On the seventh day 
after the ingestion of muscle trichin® the birth 
of embryos begins, which continues some time, 
even for weeks. A single female trichina may 
bear from one thousand to thirteen hundred 
young. According to Pagenstecher, Chatin, Cer- 
fontaine, and Askanazy, the female trichin pen- 
etrate into the intestinal villi and deposit the 
embryos in the chyle-vessels, whence their migra- 
tion begins. To what extent they are swept along 
passively by the lymph, or to what extent active 
migration is concerned in their spreading, is a 
difficult. matter to determine. When arriving in 
the muscles they penetrate the primitive fibres, 
bring the adjacent contents of the fibre to degen- 
eration, and grow in about fourteen days to fully 
developed muscle trichin®. In the neighborhood 
of the triching there occurs a proliferation of 
the muscle-nuclei and an inflammation of the 
connective tissue. At. first the musele-trichine 
are enclosed only by the sarcolemma, which ap- 
pears thickened and hyaline about them. Later 
there occurs in the neighborhood an inflammatory 
proliferation of granulation tissue which leads to 
the production of connective tissue on the outside 
of the sarcolemma and penetrates even within the 





richie. “A, Female; B. 
male, (Atlet Leuckart.) 


128 THE ANIMAL PARASITES. 


sarcolemma tube, the muscle-nuclei being destroyed. Fat cells may 
appear later in the connective tissue of the capsule, the development of 
the latter being especially marked at the poles. 

The intestinal trichinge have a limited life of from five to eight weeks. 
The muscle-trichinw, on the other hand, may live for a very long, possi- 
bly an unlimited time--that is, until the death of the affected individual ; 
or at any rate for years, although, according to Ehrhardt, a few may die 





Pig, 572.—Eneapeulated muscle trichine. (After Leuckart) x 60, 


before the encapsulation. After some time there frequently occurs a 
deposition of lime-salts in the capsule, especially at the poles, causing it 
to appear glistening-white by reflected light, and cloudy and dark by 
transmitted light. In rare cases the trichine after dying also become 
calcified. 

Trichinse have been observed, besides in man, also in the hog, cat, 
dog, rat, mouse, marmot, polecat. fox, marten, badger, hedgehog, and 
raccoon. Through the feed'ng of trichinous meat muscle-trichine may 
also be developed in rabbits, guinea-pigs, sheep, dogs, etc. Man becomes 
infected through the eating of uncooked pork. The invasion of the tri- 
ching produces various phenomena in man. The introduction of trichin- 
ous meat into the intestine is followed by the symptoms of an intestinal 
eatarrh. With the invasion of the muscles there are produced pain, 
swelling, cedema, paralysis, and not infrequently fever. The symptoms 
are most severe in the fourth and fifth weeks. Death not infrequently 
results. 

The trichine are found most abundantly in the diaphragm, tongue, 
intercostal muscles, the muscles of the neck and larynx, the lumbar mus- 
cles, and are scattered most sparsely in the distant muscles of the extremi- 
ties. They are usually most numerous about the insertions of the 
tendons, 


Literature. 
(Trichina Spiralis ; Trichinosis.) 
: Zur Lehre von der Trichinose. Cbl. f. Bakt.. xv., 1894: Virch. Arch., 
'ontr. A 1'ét, de In trichinose. Arch. de biol., xill., 1898; Cbl. f. Bakt., 





1897. 
Ohatin: La trichine et In trichinose, Paris. 1888. 


FILARIA. 129 


Ehrhardt: Muskelveränderungen bei Trichinose. Beitr. v. Ziegler, xx., 1896. 
Graham: Naturgesch. d. Trichina spir. Arch. f. mikr. Anat., 





Hertwig: Entwickelung d. Trichinenkapsel. Münch. med, 
Woch., 1896. 
Johne: Der Trichinenschaucr, Berlin, 1888. 
Langerhans: Ueber regressive Veriind. d. Trichinen u. ihrer 
pseln. Virch. Arch., 130 Bd., 1892. 
Lewin: Zur Diagnostik u. path. Anat. d. Trichinose. Deut. 
Arch. f. klin. Med., 49 Bd., 1892. 
Riess: Trichinenkrankheit. Eulenburg’s Realencyklop., 
xxiv., 1900. 
Soudakewitsch: Modific. des fibres muscul. par la trichinose. 
Ann. de !’Inst. Past., vi., 1892. 
Stiles: Trichinosis in Germany. Bull. 30, U. S. Bureau of 
Animal Indus., 1901. 
Virchow: Die Lehre von den Trichinen, Berlin, 1866. 
Volkmann: Trichinose. Beitr. v. Ziegler, xii., 1894. 
Williams: The Frequency of Trichinosis in the United 
States. Jour. of Med. Res., 1901. 
Zenker: Virch. Arch., 18 Bd.; Deut. Arch. f. klin. Med., 
Viii. ’ 


§ 194. Filaria or Dracunculus medinensis, the 
Guinea-worm (Fig. 573), is a thin, thread-like 
female worm from 60 to 100 cm. in length. The 
males (observed by Charles) which were attached 
to female filarie, were only 4 cm. long. The an- 
terior extremity is rounded off, while the posterior 
tapers intq a pointed tail which is curved toward 
the belly. The external cover- 
ing consists of a firm cuticle, 
which at the cephalic end is 
thickened in the form of a 
shield. The intestinal canal is 
narrow and has no anus. The 
uterus, filled with young, takes 
up nearly the whole of the body- 
cavity. Theembryos, which are 
set free by the bursting of the 
mother-worm, havea firm cuticle 
and an awl-shaped tail. As in- 
termediate host, the embryos 
seek out small crustacer, in 
which they are probably taken 
into the stomach of man with 
the drinking-water. In Africa 
and Asia the worm is of fre- 
quent occurrence. It develops 
in the skin to sexual maturity 
and causes abscesses of the af- 
fected region. It is usually 
found on the lower extremities, 
especially in the region of the 


~— heels. 
Fic. 673. Fig. 574. Filaria sanguinis hominis is 
„Eis. 578. — Filaria sive Dracunculus medinenste. the name given to the larve (Fig. 
After Leuckart.) Natural size. 574) of a worm, which occur in 
„ng a Embere of aria Bancroft were the blood and lymph of mai, 


730 THE ANIMAL PARASITES. 


and are about 0.35 mm. in length. The sexually mature worm is fili- 
form, the male about 15 em. long and the female 8cm. It is called 
Filaria Bancrofti after its discoverer. The worm inhabits the lymph- 
vessels, particularly those of the scrotum and lower extremities, and may 
be present in large numbers. It causes lymph-stasis and inflammations 
which lead to swellings of the lymph-glands and to elephantiasis-like thicken- 
ing of the tissue, associated with cedema and lymphangiectasis. Purulent 
inflammations, Iymph-abscesses, buboes, chylous hydrocele, and chylous 
ascites may appear in consequence of its presence. 

From the lymphaties of the limbs and scrotum the eggs and embryos 
(0.35 mm. long) (Fig. 574) pass into parts of the lymphatic system and 
into the blood, giving rise to hwmaturia, chyluria, and chylous diarrhea. 
According to Manson and Scheube the filarie are present in the blood 
taken from the skin only during the night; von Linstow explains this 
pheuomenon as due to the fact that during sleep the peripheral vessels 
become dilated, and so permit the entrance of the filaris, while the cap- 
illaries, being narrower during the day, do not permit such entrance. 
The hematuria is the result of the collection of embryos in the blood- 
vessels of the urinary tract. The chyluria and the chylous diarrhoea, on 
the other hand, are due to the obstruction by the parasites of the thoracic 
duct, thus causing a lymph-stasis which extends to the lymphatics of the 
bladder and intestine and there occasions the escape of lymph. Accord- 
ing to Scheube the rupture of the lymphatics is also attended by a rupt- 
ure of blood-vessels, so that blood becomes mixed with the lymph. The 
embryos may pass out from the urinary apparatus through the urine. 

The distribution of the embryos is, according to Manson, accomplished 
by means of mosquitos, which take up the parasite during the act of blood- 
sucking. In the mosquitos they pass through a second stage of develop- 
ment and are then (James) after two or three weeks ready for the infec- 
tion of a new host. Manson formerly heid the opinion that they entered 
the water, and in a free condition were taken up in the water into the 
intestinal tract. The investigations of James, Low, Grassi, and Noé, who 
followed their development and migration in the body of mosquitos, 
make it seem probable that they are transmitted to a new host through 
the bite of the mosquito. 

The Filaria sanguinis occurs, so far as is known, only in the tropics 

(Brazil, Egypt, Algiers, Madagascar, Zanzibar, Soudan, South China, 
Caleutta, Bahia, Guadeloupe). 


Mackenzte estimated the number of filaria-embryos present in the total bulk of the 
blood of a case of hwmatochyluria closely studied by him at from thirty-six to forty 
millions. The patient died from empyema; during the disease the filarie died. 

In the domestic animals numerous filaria-specics occur and inhabit different parts 
of the body. Filarta papillosa is a common parasite of the horse, donkey, and cattle; 
it lives in the serous cavities and reaches a length of from 5-18 cm. F¥tlaria hamalica, 
a worm 13-15 cm. long, inhabits the right heart and the pulmonary artery of the dog, 
and in this situation gives off its embryos to the blood-stream. It occurs particularly 
in America, China, and India. 


Literature. 
( Filaria. ) 


Barth: De la filaire du sang et ses rapports avec l’el&phantiasis des Arabes et quelques 
autres maladics des pays chauds. Ann. de derm. et syph., 1881. 

Clanchard: Filaria loa. Arch. de parasitol., ii., 1899. 

Charles: Ilistory of the Male of Filaria Medinensis. Scient. Mem. Med. Office Army 
of India, vii., Calcutta, 1892. 


ARTHROPODA. 731 


Hirket: Dela flaroee du sung, Accad. R. de méd. de Belg., Bruxelles, 1806. 

Goetze: Die Chylurie, Jena, 1887. 

Grassi: Filaria inermis, ein Parasit des Menschen, des Pferdes u. des Esels. Obl. f. 
Bakt., i., 1887; Entwickelungseyclus von 5 Parasiten des Hundes (Tenia cucu- 
merina, ‘Ascaris marginate, Spiroptera sungulnolenta, Filaria immitis Leidy und 
Hematozoon Lewis). Ibid. Ir., 1688; Homatozoon Lewis (Filaria des Hunde) 

».» Wil, ). 

Grassi'u. Nob: Ücbertrag. d. Blutfluria durch Stechmücken. Col f. Bakt, zuvill, 

Havelburg;; Ueber Filaria Sunguinis und Ohylurie. Virch. Arch., 89 Bd., 1882 

Huber: Bibliographie d. Klin, Helminthologie, Suppl., Jons, 1808. 

James: On the Metamorphosis of Filaria sanguinis In Mosquitoes, Brit. Med. Journ. 
ii., 1900. 

Laveran et Blanchard: Les vers du sang, Paris, 1895. 

Lewis: Geschlechtsreife Form der Filaria sanguinis, Cbl. f. d. med. Wiss, 1877. 

y. Linstow: Ueber Filaria Bancrofti Cobbold. Cbi. f. Bakt., xii., 1892. 

Lothrop and Pratt: Two Cases of Filariasis. Amer. Journ, of Med. Be., cxx., 1900 
(Lit ). 

Low: Filaria nocturna in culex. Brit, Med. Journ., i., 1900. 

Mackenzie, St.: Transactions of the Pathological Society of London, 1892. 

Manson: The Filaria Sanguinis, London, 1883; The Filaria Sanguinis Hominis Major 
and Minor, Two New Species of Hematozos. Lancet, 1891; ref., Cbl. 1. allg. 
Path., i., 1891. 

Murata: Zur Kenntniss der Chylurie. Mittheil. d. med. Fac. der Universitat, Tokio, 


1888. 

Rieck: Filaria immitis u. ihre Embryonen im Blute v. Hunden. Deut. Zeitschr. f. 
Thiermed., xiv., 1889. 

Scheube: Die Krankheiten der warmen Lander, Jena, 1900. 

Sonsino: The Life-history of Filaria Bancrofti. Brit. Med. Journ., i., 1900. 








Ill. Arthropoda. 
1. Arachnida. 


195. The parasites included among the Arachnida are chiefly epizoa, 
which either temporarily or permanently inhabit the skin. Only one 
species— Pentastoma—occurs in the larval 
form within the tissues. The most com- 
mon parasites of this group belong to the 
Mites (Acarina). The pentastoma be- 
longs to the family of tongue-worms 
(Pentastomide or Linguatulide). 

(1) Acarus scabiei or Sarcoptes 
hominis, the itch-mite, is a parasitic 
mite the size of a pinhead with a turtle- 
shaped body, provided on the ventral 
surface both anteriorly and posteriorly 
with two pairs of legs, each of which is 
furnished with bristles (Fig. 575). The 
anterior pairs of legs extend out into 
pedicled clinging-dises. The same ar- 
rangement is found in the posterior two 
pairs in the male, while in the female 
both of the posterior pairs end in long 
bristles. Several bristles are also found zo. 575,.—Femule iteh-mite, ventral ser- 
along the border of the posterior portion face. << 40, * 
of the body, while the back is studded 
with tooth-like knobs. ‘Che head is round and likewise set with bristles. 
The female is nearly double the size of the male. 





132 THE ANIMAL PARASITES. 


The mite lives in the epidermis (Fig. 576, a, d) in which it forms 
burrows, some of which are 10 cm. long. 

In the burrows the female (d) lays the eggs, which develop in situ 
into the young itch-mites (e), which penetrate still deeper into the epi- 
dermis, and after repeated sheddings of their skins grow into sexually 
mature animals. The skin responds to the irritation produced by the 





Tia. 576.—-Rcabies (alcohol, carmine). a, Horny layer of the is perforated by numerous bar 

with ER Aart as ia pmo I ze: a ‘section en lly deve a ie ~h-mit enges and 
cx cuts Im Pton | 7 ch mite: 

qmibryos of diiterent sizes’ 7, feces, en “ 


presence of the mites by an increased production of epithelial cells (a) 
and inflammation (¢c). The latter is still further increased through the 
seratching of the spots which itch in consequence of the invasion. 

2. Leptus autumnalis, the harvest-mite (Fig. 577) is the red-colored 
larva of a variety of Trombidide, which lives upon grasses and bushes 
and upon grain, and when occasion offers alights upon the skin of man, 
where it penetrates the epithelium and causes itching and inflammation. 

3. Demodex or Acarus folliculorum hominis (Fig. 578) occurs either 
singly or in numbers in the hair-follicles of the face, as well as in the 
ducts of the sebaceous and Meibomian glands. Hausche found the de- 
modex on the eyelashes in seventy-nine per cent., and Joers in sixty-four 
per cent. of the cases examined. Children under one year of age were 
free. The female is 0.4 mm. long, the male 0.3 mm. The eggs are de- 
posited upon the shaft of the hair or upon any other portion of tissue, and 
develop after two sheddings into sexually mature animals which are found 
in the entrances to the hair-follicles and sebaceous glands, with their heads 
directed inward. The assumption that the demodex causes inflammation 
(acne, blepharitis acarica) is not supported (Joers, Hausche), since in 
spite of its presence in the great majority of cases signs of inflammation 
are wanting. 

It is about 0.3 mm. long, and has on its anterior ventral surface four 
pairs of short thick feet. ‘The head possesses a snout and two feelers. 

4. Ixodes ricinus, the wood-jack or wood-tick (Fig. 579) is a fairly 


PENTASTOMA. 733 


large yellowish-brown member of the Arachnida belonging to the ticks. 
It has a black head provided with a sucking apparatus, and a very dis- 
tensible leathery body. It is of common occurrence upon grass and 
bushes, and sometimes alights upon man or beast. By means of its 
sucking apparatus it draws blood from the skin and swells up to a very 
remarkable extent. 

5. Pentastoma denticulatum is the larva of Pentastoma tenoides, 
a lancet-shaped animal belonging to the tongue-worms or Pentastomide. 
It inhabits the nasal, frontal, and maxillary cavities of various animals, 
especially of the dog, very rarely of man (Laudon) and occasions inflam- 
mations. The female of the mature animal is 50-80 mm. long, and an- 
teriorly from 8-10 mm. broad; the male is 16-22 mm. long, and anteriorly 
from 3-4 mm. broad. The body consists of eighty-seven to ninety seg- 
ments, the most anterior of which bear lateral segment-appendages, the 
pairs of limbs. The eggs, which are produced in very great numbers, 
areoval. The larvais4—5 mm. long, 1.5mm. broad, plump, flattened, and 
inhabits chiefly the liver, lung, or spleen, or more rarely the other organs 
of man and the herbivora. It occurs in the form of a small nodule encap- 
sulated in connective tissue. The body consists of about fifty ring-shaped 
segments which are provided at the borders with spines (Fig. 580), and 


ne. 579. 





ha. 677. Fra. 578. 





Fıs. S77.—Leptus autumnalis. (After KOchenmeister and Zürn.) 

Wha. 578.—Acarus folliculorum hominis. (After Perla.) x 300. 

Tio. 579. Irodes ricinus, sucked half full of blood. x 2. 

ia. 580.—Cephalic end of Pentastoma denticulatum. (After Perls.) X 40. 


the cephalic end is provided with four hook-shaped feet. The eggs are 
taken in from the external world through the intestinal tract. The para- 
sites set free in the intestine wander by means of a boring apparatus 
through the mesentery into the mesenteric lymph-glands, or penetrate 
directly into the blood-vessels, and are carried by the blood-stream 


734 THE ANIMAL PARASITES. 


to the liver or even to the lungs, where after shedding they develop 
into the encysted larve. The larve may in their wanderings gain access 
to the nasal cavity of their host, and develop into mature animals, al- 
though the further development usually takes place only after their re- 
ception into a new host. 


According to the published reports of Tanaka a small rad mite occurs in greet 
numbers in different parts of Japan during midsummer, and clinging firmly to the skin 
of man causes the so-called Kedani-disease, which is characterized by inflammation of 





Fa. 581. Fra. 582, 


Mi. 581.—Male of Dermatophagus communis seen from the ventral side. (After Pütz.) x 50. 
Wa, 582. — Male of Dermatocoptes communis, seen from the ventral side. (After Pütz.) X 50 


the skin and lymph-glands, with high fever, and often ends futally. It is probable that 
these ‘symptoms are due to secondary infections (proteus and streptococci) in the bites 
of the mite. 

In the domestic animals living mites occur very frequently as parasites of the 
akin, and represent different species of various families. 

Sarcoptes hominis, the burrow-mite or ttch-mite of man is found also in horses and 
Neapolitan sheep. In addition still other different species of sarcoptes may be distin 
guished as parasites of the domestic animals—for example, Sarcoptes equamiferusin dogs, 
hogs, sheep, and goats, and Sareoptes minor in cats and rabbits. 

Dermatophagus, the decouring-mite (Fig. 581), with a broad head, occurs in different 
animals, and different species may be accordingly distinguished. They live upon the 
cells of the epidermis and cause a desquamation of the skin. 

Dermatocoptes, the sucking-mite (Fig. 582), with long narrow hend, takes blood and 
lymph from the skin and causes inflammation. Dermatocoptes communis occurs in 
horses, cattle, and sheep. Dermatocoptes cuniculi is a parasite of the rabbit's ear. 

biotes equi of Gerlach is a mite which occurs chiefly upon the feet of the heavy 
English and Scotch horses, and causes a moist dermatitis, often incorrectly called ma- 
‚nders. 

Dermanyssus avium is a long, red, blood-sucking mite, about 1 mm long. and is 
often found upon birds, 

Of the tick family there occur on dogs, cattle, and sheep different species of Izodes, 
on pigeons Argas rejlerus, and others. Argas reflezus can, according to D’ Ajutolo, occur 

on man. 

Leptus autumnatis occurs also on dogs and chickens. 

Different species of Demodez occur in dogs and swine, and cause pustular erup- 





8. 
Pentastomata occur also in cattle, sheep, and goata, and in certain regions are very 
common in the first named. 


INSECTA. 7135 


2. Insecta. 


§ 196. The parasites belonging to the class of Insecta are for the greater 
part epizoa. In part they are but transient inhabitants of the skin, 
deriving from it their nourishment; in part they are permanent inhabi- 
tants and utilize the skin structures for the deposit of their eggs. Of the 
numerous species belonging to this class the following may be mentioned: 

(1) Pediculus capitis, the head-louse (Fig. 583), inhabits the hairy 
portions of the head, and derives its nourishment (i.e., blood) from the 
skin, by means of its feeding apparatus. Its eggs (nits) are barrel-shaped 
and white, and are attached to the hairs by means of a chitinous shell. 
The embryo hatches in about eight days. In consequence of the scratch- 
ing induced by the itching there often arise inflammations of the skin, in 
particular eczemas, which are often relatively severe. 

(2) Pediculus pubis, the felt or crab-louse (Fig. 584), inhabits the 
hairy parts of the trunk and extremities. Its habits of life are the same 
as those of Pediculus capitis. 

(3) Pediculus vestimentorum, the clothing or body-louse (Fig. 585), 
lives in the wearing apparel, and lays its eggs in the same. It gets 
upon man to obtain its nourishment. 

(4) Cimex lectularius, the bedbug, dwells in beds, floors, closets, etc. 
During the night it gets upon man to suck blood. It causes wheals in 

e skin. 

(5) Pulex irritans, the common fiea, also draws blood from the skin. 

At the point: where it has sucked there is found a little punctate hemor- 





Fig. 583. iG. 584. Mra. 586. 


Mia. 583.—Femule of Pediculus capttts, seen from the ventral surface. (KOchenmetster and Zürn.) x 18, 
ING. 584.—Mule of Pedliculus pubis, seen from the ventral surface. (Küchenmeister and Zürn.) X 13. 


Fic. {85.--Female of Prdiculu reatimentorum, seen from the ventral surface. (KOchenmelster and 
zam.! x 


rhage. Occasionally it causes wheals and swellings. It lays its eggs in 
the cracks of floors, in sawdust, ete. 

(6) Pulex penetrans, the sand flea, occurs in South Africa in the 
sand. The female lays her eggs in the skin, thereby causing an intense 
inflammation. 

(7) Mosquitos provided with stinging and sucking apparatus (Culici- 
de and Tipulide), horse-flies (Tabanide), and flies (Stomozyide) draw 
blood frequently from the skin of man. Various flies (stride or biting 


736 THE ANIMAL PARASITES. 


flies, Muscide or blow-flies) occasionally lay their eggs in the skin, in ulcers, 
or wounds, or in the accessible body-cavities, in consequence of which 
the maggots developing cause local destruction of tissue and inflammation 
(myiasis). Under certain conditions their larve may get into the intesti- 
nal tract with the food and there undergo further development (myiasis 
intestinalis). This is especially likely to occur when abnormal conditions 
which interfere with digestion are present in the stomach and intestine. 
The eggs of the Muscide (in Europe 
usually of Sarcophilia Wohlfarti, 
in America of Compsomyia or 
Lucilia macellaria and Musca an- 
thropophaga), when laid upon the 
mucous membranes or in wounds, 
hatch after a few hours, and cause 
destruction of the neighboring 
soft parts through their efforts to 
obtain nourishment. In the au- 
ditory canal, nose, and antrum of 
Highmore, the bones may be laid 
bare (myiasis mucosa). In the 
course of about a week the larve 
Fi. 5.-Gastrophilus equi. (After Brater.) a, leave the ulcers and pass into the 
Hes, larva. pupa stage in the earth. The 
Gstride (in Europe, Hypoderma 
bovis and Hypoderma Diana ; in America, Dermatobia nozialis or Cuterebra 
cyaniventris) lay their eggs upon wounds or in the intact skin. The 
larve, hatching very soon, penetrate into the cutis by means of their 
hooklets, and after several sheddings grow in from one to six months into 
larger larvee about 2 cm. long. They cause, particularly in their later 

stages, painful swellings of the neighboring tissue (myiasis wstrosa). 
Regarding the significance of different species of Anopheles as conveyers 

of malarial infection see § 182. 





Parasites belonging to the Museicda and (stride play a more important röle in the 
case of the domestic animals than in man; and the larvee of the species of Gistrus in 
particular occur as parasites in animals. For example, the larve of Gastrophilue epi 
(Fig. 586), Gast. pecorum and Gast. hemorrhoidalis inhabit the stomach and adjacent 
portions of the intestinal tract of the horse, where they complete their development up 
fo the pupa-stage, when they leave the animal, 

trus ovis lays its larve in the nasal cavities of sheep, whence they may wan- 
der, under certain conditions, into the frontal, nasal, and maxillary cavities, or even 
into the cranial cavity, and excite inflammation. 

The larva of Hypoderma or strus boris is 5-15 mm. long. It inhabits the skin and 
spinal canal of cattle, completing its development up to the pupa-stage, at which time 
it leaves the animal. "According to Schneidemühl the larvx do not always enter through 
the skin, but are more often taken in with the food, whereupon they penetrate through 
the wall of the cesophagus toward the skin and spinal canal. The latter follows from 
the fact that they are found in the wall of the oesophagus from October to January, 
and under the skin, on the other hand, from January to April. 





Literature. 


(Parasitic Arachnida and Insecta.) 
Er argus reflexus parasita dell’ uomo. Mem. della R. Accad. di Bolog- 
1899. 





Monographie der Oestriden, Wien, 1863. 
Csokor: Ueber Pentastomen u. Pentastoma denticulatum aus d. Leber des Pferdes. 
Zeitschr. f. Veterinärk., i., 1887; Cbl. f. Bakt., i., 1887. 


THE ANIMAL PARASITES. 7137 


Dubreuilh: Les diptéres cuticoles chez homme (Lit.). Arch. de méd. exp., 1894; 
Dermatozoaires, Paris, 1900. 

Hausche: Demodex folliculorum im Augenlide. Münch. med. Woch., 1900. 

Hoffmann: Fliegeniarven im menschl. Magen. Münch. med. Woch., 1888. 

Huber: Bibliographie d. klin. Entomologie, i.-iv., Jena, 1898-1900. 

Joers: „carus folliculorum u. 8. Bez. z. Lidrandenztündung. Deut. med. Woch., 
Joseph: Ucber d. Fliegen als Schädlinge u. Parasiten d. Menschen. Deut. Medicinal- 
Zeit., 1887; Ueber Myiasis externa dermatosa. Monatsh. f. prakt. Derm., 1887. 

Kitt: Lehrbuch d. path.-anat. Diagnostik, i., Stuttgart, 1900. 
Kulagin: Naturgeschichte des Pentastomum denticulatum. CbL f. Bakt., xxiv., 


Lallier: Etude sur la myase du tube digestif, Paris, 1897 (Lit. ). 

Lampa: Fliegenmaden im Darm des Menschen. Cbl. f. Bakt., iv.. 1888. 

Leuckart: Bau u. Entwickelungsgeschichte des Pentastoma, Leipzig, 1880. 

Lublinski: Fliegenlarven im menschl. Magen. Deut. med. Woch., 1885. 

Majocchi: Demodex follic. nelle ghiand. Meibom. Arch. p. le Sc. Med., 1899. 

Nuttall: Insects, Arachnids and Myriapods as Carriers of Disease. Johns Hop. Hosp. 

ep., . 

Osborne: Insects Affecting Domestic Animals. U. 8. Dept. of Agric. Bull., 1896. 

Peiper: Fliegenlarven als gelegentl. Parasiten d. Menschen, Berlin, 1900. 

Bählmann: Blepharitis acarica. Deut. med. Woch., 1892; Monatsbl. f. Augenheilk., 
1899. 

Salmon and Stiles: Sheep Scab, Washington, 1898. 

v. Samson-Himmelstierna: Ein Hautmaulwurf. Arch. f. Derm., 41 Bd., 1897. 

Bandahl: Ueb. d. Vorkommen v. Insecten im menschl. Organismus. Cbl. f. Bakt., 
v., 1889. 

Scheube: Die Krankheiten d. warmen Länder (Sandfloh, Fliegenlarven), Jena, 1900. 

Scischka: Anatomie der Scabies. Arch. f. Derm., 53 Bd., 1900. 

Schneidemühl: Entwickelungsgesch. d. Bremsenlarven. Cbl. f. Bakt., xxii., 1897. 

Schöyen: Ueber das Vorkommen von insecten am menschl. Körper. Biol. Cbl., iv., 
1885. 

Shipley: Revision of the Linguatulide. Arch. of Parasit., 1898. 

Sommer: Pentastomum denticulatum: Eulenburg’s Realenc klop.. xviii., 1898 (Lit. ). 

Tanaka: Actiologie u. Pathogenese d. Kedani-Krankheit. eb. . Bakt., xxvi., 1899. 

Ward: Arachnida. Ref. Handb. of Med. Sc., 2d ed., vol. i. 

Wilms: Myiasis dermatosa oestrosa. Deut. med. Woch., 1897. 


(Animal Parasites. ) 


Blanchard: Parasites animaux. Traité de path. poe. par Bouchard, ii., 1896. 

Braun: Die thierischen Parasiten des Menschen, Würzburg, 1895. 

Davaine: Traité des entozoaires, Paris, 1877. 

Huber: Bibliographie der klin. Helminthologie, München, 1891-98; Bibliographie der 
klin. Entomologic, i.-iv., Jena, 1898-1900. 

Küchenmeister u. Zürn: Die Parasiten des Menschens, Leipzig, 1882. 

Leuckart: Die menschl. Parasiten, Leipzig, 1863-76; 2te Aufl., 1879-1901. 

Moniez: Traité de parasitologie. Paris, 1896. 

Müller: Statistik der menschl. Parasiten, Erlangen, 1874. 

Neumann: Traité des maladies parasitaires des animaux domestiques, Paris, 1888. 

Parona: L'Eimintologia Italiana, Genova, 1894 (Lit. bis z. J., 1890). 

Perroncito: I parassiti dell’ uomo e degli animali utili, Milano, 1882. 

Stein: Die parasitären Krankheiten des Menschen, i., Lahr, 1882. 

Ward: Articles on Purasites, Arachnida, Nematoda, etc., in Ref. Handb. of Med. Sc., 
2d ed 


Zechokke, F.: Rech. s. l’organisation des vers parasites des poissons d’eau douce, 
Paris, 1885. 

Zürn: Die Krankheiten d. Hausgeflügels, Weimar, 1883; Die Schmarotzer auf und in 
dem Körper unserer Haussäugethiere, i., Weimar, 1883-89. 


39 


GENERAL INDEX. 


ABDOMINAL cavity, faulty closure of, 511 


Abortion, 496 
Abrachius, 516 
Abrin, poisoning by, 27 
Abscess, 385, 574 
burrowing, 368 
chronic, 863 
cold, 621 
congestion, 363 
Abscess-membrane, 858 
Acardiacus acephalus, 582 
amorphus, 582 — 
peeudoacormus, 532 
Acarina, 781 
Acarus folliculorum hominis, 782 
scabiei, 781 
Acervuloma, 480 
Acervulus cerebri, 223 
Achirus, 519 
Achorion Schönleinii, 675 
Achromatopsia, 55 
Achyla prolifera, 678 
Acids, corrosive, 22 
Acme of a fever, 94 
Acne, 574 
Aconitine, poisoning by, 29 
Acrania, 
origin of, 507 
Acromegaly, 212, 268 
Actinomyces or ray-fungus, 649 
Actinomycosis, 649 
Acuminate condyloma, 862 
Addiment, 118 
Addison’s disease, 89 
pigmentation of skin in, 232 
Adenocarcinoma, 463 
deveiopment of, 455 
Adenocystoma, 442, 485 
papillary, 446 
Adeno-cysts, 477 
Adenoma, 487 
alveolar, 440 
carcinomatosum, 458 
conversion of, into a carcinoma, 455 
destruens, 458 


umbilical, 518 


Adenomata and carcinomata, difficulty of 


distinguishing between, 441 
Adenomyoma, 405, 477 
Adenomyosarcoma, 485 


Adenosarcoma, 468 
Adipose tissue, atrophy of, 193 
development of, 290, 291 
pathology of, 198 
Adipositas, 52, 191 
AH gagropile, 226 
Equatorial plate, 278 
Aétrobes, 548 
Age, predisposition in old, 50 
Agenesia, 178 
partial, of the cranium, 504 
Agglutination of colon bacillus, 504 
of typhoid bacillus, 109, 592 
Agglutinins, 110 
Agnathia, 509 
Agrotis segetum, 678 
Air, entrance of, into the right heart, 71 
embolism, 71 : 
Albinism, 250 
Albuminoid bodies, protective, 105 
Alcohol, poisoning by, 28 
Alexins and immunitoxins, 118, 119 
protective, 105, 106, 118 
Alkaloids, toxic cadaveric, 88, 41, 549 
vegetable, 18 
Algor mortis, 167 
Alveolar sarcoma, 420 
Amelus, 516 
Amides, 542 
Amido-acids, 542 
Amins, 542 
Amitotic nuclear division, 276 
Amme, 700, 708 
Amnion, pathological conditions of, 480 
Amniotic adhesions a cause of 
tions of the embryo, 490 
Ameba coli felis, 681 
coli mitis, 680 
coli vulgaris, 680 
dysenterie, 680 
Amphibolous stage of fever, 94 
Amphimixis, 61 
Amputation neuroma, 802, 411 
Amyelia, total or partial, 499 
Amyloid concretions, 214 
degeneration, 208 
local infiltration of, 218 
Anabiosis, 11 
Anzsmia, 129 
chronic, 126 
collateral, 188 
due to tapeworm, 718 
general, 126 


mal! forma- 


740 


Anemia, localized, 129, 182 
Anaérobes, 543 
Anaplasia, 458 
Anasarca, 150 
Anatomy, general pathological, 8 
Anchylostoma duodenale, 721 
Americana, 721 
Androgynes, 527 
Anencephalia, 504 
origin of, 507 
Anencephalus, total, 505 
Aneurism, cirsoid, 397 
Angioma, 393 
arteriale plexiforme, 397 
arteriale racemosuin, 397 
cavernosum, 395 
fissural, 394 
hypertrophicum, 397 
lymphaticum, 399 
plexiforme arteriale, 397 
simplex, 898 
venosum (varicosum), 395 
Angiomyoma, 405 
Angiosarcoma, 424 
Anguillula intestinalis, 724 
stercoralis, 725 
Anhydr&mia, 126 
Aniline, poisoning by, 27 
Animal diseases caused by cocci, 579 
parasites, 45, 680 
Anopheles, 695 
Antagonism, bacterial, 545 
Anthrax-bacilli, 584 
attenuation of, 588 
Anthrax, protective inoculations against, 
588 


symptomatic, 656 
Antiautolysin, 119 
Antibodies, 109, 115 
Antitoxins, 106, 109, 114, 115, 118 
of diphtheria, 117 
Anus, condyloma latum of the, 633 
Aphthex, 672 
Aplasia, 165 
Aprosopia, 508 
Apus, 516, 519 
Apyrexia, 95 
Arachnida, 33, 46, 731 
Area cerebrovasculosa, 505 
medullovasculosa, 500 
Argas reflexus, 734 
Argyria, 249 
Arrhinencephalus, 506 
Arsenicismus, pigmentation in, 242 
Arseniuretted hydrogen, poisoning by, 26 
Arterioliths, 146 
Arteriosclerosis, 216 
Artery, obliteration of, 148 
terminal, 160 
Arthritis urica, 224 
Arthropoda, 731 
parasitic, 33, 46 
Ascaris lumbricoides, 720 
megalocephala, 720 
mystax, 720 
Ascites, 151 
chylous, 164 


GENERAL INDEX. 


Ascococci, 540, 559 
Asiatic cholera, 660 
Aspergillus flavescens or flavus, 671 
fumigatus, 671 
nidulans, 671 
niger, cr nigricans, 671 
Aspergillus-mycoses, 673 
Asphyxia, 6 
local, 170 
Astrocyte, 300 
Atavism, 58 
Atheroma, 252 
Atmospheric pressure, effect of an in- 
crease of, 13 
effects of sudden lowering of, 12 
Atresia ani, 515 
ani vesicalis, 516 
ani urethralis, 516 
ani uterina, 516 
ani vaginalis, 516 
oris, 509 
recti, 515 
urethre, 515 
Atrophy, 182 
active, 185 
brown, 188 
degenerative, 184 
disuse, 187 
excentric, 188 
neuropathic, 187 
passive, 185 
pigment, 183 
pressure, 186 
senile, 186 
simple, 184 
Atropine, poisoning by, 29 
Attenuation of bacterial virulence, 118 
Attraction-spheres, 275 
Auditory meatus, cholesteatomata in, 436 
mould-fungi in, 670 
Autochthonous pigment, 231 
teratomata, 473 
thrombi, 144 
Auto-intoxications, 75, 78, 80 
Autolysin, 119 
Autosite, 536 
Awl-tail, 720 
Axis-cylinder, sprouting of, 300 


BACILLACEA, 580 

Bacilli, 580 
pathogenic, 584 
saprophytic, 582 

Bacillus aceticus, 583 
acidi lactici, 582 
atrogenes capsulatus, 603 
amylobacter, 582 
anthracis, 584 
butter, 618, 629 
butyricus, 582 
caucasicus, 582 
coli communis, 593 
comma, 660 
cyanogenes, 582 
diphtherie, 597 
fluorescens liquefaciens, 588 
icteroides, 606 


GENERAL INDEX. 741 


Bacillus influenzse, 596 


lepre, 639 

mallei, 644 

mucosus capsulatus, 596 
adematis maligni, 602 
pertussis, 597 

pestis, 604 

phlegmones emphysematosex, 603 
pneumonie of Friedlander, 595 
prodigiosus, 582 

proteus vulgaris, 583 
pyocyaneus, 583 

smegma, 613 

subtilis, 581 

tetani, 601 

typhi abdominalis, 589 


Bacillus of anthrax, 584 


of blackleg, 656 

of bubonic plague, 604 

of chancroid, 607 

of chicken-cholera, 658 

of contagious pleuropneumonia, 659 
of diphtheria of calves, 659 

of diphtheria of chickens, 659 
of diphtheria of pigeons, 659 
of foot-and-mouth disease, 659 
of glanders and farcy, 644 

of hemorrhagic septicemia, 658 
of influenza, 596 

of leprosy, 639 

of malignant cedema, 60! 

of ozeena, 596 

of pseudodiphtheria, 600 

of pyelonephritis of cattle, 659 
of rhinoscleroma, 647 

of swine-erysipelas, 657 

of swine-plague, 657 

of symptomatic anthrax, 656 
of syphilis, 631 

of tetanus, 601 

of tuberculosis, 607 

of typhoid fever, 589 

of yellow fever, 606 

of whooping-cough, 597 


Bacteria, 540 


action of, 548 
acid-resisting, 613 
atrobic, 543 
anatrobic, 543 
association of, 552 
attenuation of, 552 
cultivation of, 553 
degeneration, forms of, 542 
ectogenic, 35 
endogenic, 35 
metastasis of, 551 
movements of, 541 
multiplication, 541 
oligomorphous, 540 
parasitic, 540 
pathogenic, 35, 551 
phosphorescence of, 549 
polymorphous, 541 
products of, 548 
saprophytic, 582 
spores of, 542, 545 
structure of, 541 


Bacteria that cause suppuration, 574 
transmission to feetus of, 551 
Bacteriacese, 580 
Bacterixmia, 39, 40 
Bacterio-try psins, 548 
Bacterium, 580 
coli commune, 593 
Bacterium of hemorrhagic septicemia, 658 
lactis atrogenes, 596 
pneumoni, 595 
typhi, 589 
vulgare, 583 
Balantidium coli, 681 
monatum, 683 
Barbone dei bufali, 659 
Barlow’s or Moeller’s disease, 158 
Basedow’s disease, 88 
Bedbug, or cimex lectularius, 735 
Bedsore, 177 
Beggiatoa, 541 
Benign tumors, 378 
Beri-beri, 19 
Bezoar stones, 226 
Bigerminal tissue-implantation, 480 
Bile-pigment, 244 
Bilharzia hematobia, 703 
Bilirubin, 244 
Biophores, 62 
Birds, malaria of, 696 
tuberculosis of, 628 
Biting-mite, 734 
Black death, 605 
Black gangrene, 176 
Blackleg, 656 
Bladder. urinary, papillary epithelioma of, 


Blastomycetes, 668 
Blebs, hemorrhagic, 157 
Blennorrhma, 385 
of the eye, 577 
Blister, 324, 327 
Blood, antibacterial properties of, 104 
coagulation of, 135 
extravasations of, 156, 235 
parasites of, 682, 692, 696 
protective powers of, 114 
Blood-cells, red, new formation of, 293 
white, new formation of, 292 
Blood-corpuscle cells, 236 
Blood-corpuscles, red and colorless, 294 
Blood-current, slowing of, 138, 139 
Blood-hyalin, 219 
Blood-mole, 497 
Blood-plates, 140 
escape of, from the blood-vessels, 318 
thrombus of, 139 
Blood- poisons, 24 
Blood-serum, bactericidal action, 105 
immunizing power, 113 
Blood-vessels, alterations of walls of, 815 
hyaline degeneration of the walls of, 
new formation of, 283 
Body-louse, 735 
Bone, in dermoid cysts, 483 
necrosis of, 360 
pathological new formation of, 362 


743 GENERAL INDEX. 


Bone, reproduetion of, 288 
Bone-marrrow, reproduction of, 290 
Bones, supernumerary, 525 
Bone-tissue, new formation of, 288 
Bothriocephalus cordatus, 718 
latus liguloides, 718 
latus Mansoni, 718 
Botryococcus ascoformans, 580 
Botryomyces, 580 
Botryomycosis, 580 
Botrytis Bassiani, 678 
Botulismus, 18 
Brachygnathis, 509 
Brain, concussion of, 16 
development of, 507 
telangiectatic tumor of, 384 
Brain-hernias, 505 
Brain-sand, 223 
Brain-substance in dermoid cysts, 482 
Branchial cysts, 509 
fistule, 509 
Breast, see also Mammary gland 
adenoma of, 489, 441 
Breasts, supernumerary, 525 
well-developed, in men, 525 
Bronchial calculi, 226 
Bronchitis, purulent, 334 
Bronchopneumonia, 834 
Brood-capsules, 711, 712 
Buboes in plague, 605 
Bubonic plague, 604 
Budding-fungi, 668 
Budding of cells, 277 
Burns 


Butter-bacilli, 613 


CACHEXIA, 166 
suprarenal, 90 
thyreoprival, 85 
tumor, 379 
Cadaveric alkaloids, 38 
petechie or lividity, 131, 167 
Cadaverin, 38 
Calcaneus, chondroma of, 387 
Calcification, 220 
Calculi, biliary, 227 
bronchial, 226 
dental, 226 
intestinal, 226, 280 
prostatic, 227 
salivary, 226 
urinary 228, 230 
Callus, 262, 352 
Calvarium, atrophy of the, 185 
Cancer, see also under Curcinoma, 449 
cells, 451 
cells, hydropic, 190, 467 
cylindrical-celled, 468 
endothelial, 370, 423 
etology of, 450, 452 
flat-celled, 462 
horny, 463 
medullary, 464 
milk, 451 
plugs, 460, 462 
umbilication, 451 


Cancroids, 458 
Cantharidin, 23 
Carbon-dioxide, influence of, upom devel- 
opment of bacteria, 543 
Carbon-monoxide gas poisoning, 3 
Carcinoma, 449 
acinosum, 464 
adenomatosum, 461, 463 
branchiogenic, 477 
calcification in, 467 
chorionic, 458 
colloides, 466 ° 
cylindrical-celled, 454, 463 
cylindromatosum, 467 
development of, 449, 458 
different forms of, 463 
durum, 464 
etiology of, 450, 452 
formation of metastases in, 471 
gelatinosum, 466 
giganto-cellulare, 467 
hyaline degeneration in, 467 
infiltration of, 451, 471 
medullare, 464 
metastasis of, 451, 471 
mucosum, 466 
my xomatosum, 467 
papilliferum, 469 
parasites a possible cause of, 450, 452 
petrifying, 468 
physaliferum, 467 
placental, 458 
retrograde changes in, 451 
scirrhosum, 
simplex, 464 
solidum, 461 
squamous-celled, 462 
structure of, 460 
tubular, 460 
Carcinomata, 449 
complete petrification of, 468. 
Cardiac muscle, new development of, 298 
Caro luxurians, 364 
Cartilage, hyaline, reproduction of, 288 
in dermuid cysts, 482 
pigmentation of, 284 
transformation of, into reticular tis- 
sue, 311 
Caseation, 173 
in tubercles, 618 
Castration, effects of, 90 
Catarrh, 824 
chronic, 363 
desquamative, 327 
mucous, 327 
purulent, 337 
serous, 826 
Cattle, actinomycosis of, 640 
tuberculosis of, 628 
Cattle-pest, 116, 579 
Cattle-plague, 116, 580 
Caustics or corrosive agents, 21 
Cavernous tumor, 385 
Cavity-formation in tuberculosis, 631 
Cebocephalia, 506 
Cell-division, 278 
Cell-protoplasm, division of, 376 


GENERAL INDEX. 


Cells, hyaline products of, 218 
Central corpuscles, 274 
group, 118 
nervous system, regeneration of, 200, 


Centrosomes, 274 

Cephalocele, 505 

Cephalothoracopagus, 535 

Cercari, 700 

Cercomonas intestinalis, 681 
Cerebrospinal canal, deficient closure of, 


meningitis, epidemic, 572 
Cerebrum, glioma of, 409 
malformations of, 504 
Cestoda, 705 
Chain-cocci, 540, 559, 561 
Chancre, hard, 682 
soft, 607 
Cheese-poisoning, 18 
Cheesy degeneration, 178 
Cheilo-gnatho-palatoschisis, 506 
Chemicals, as producers of suppuration, 
7 


Chemotaxis, 358, 545 
and chemotropismus, negative and 
positive, 103 
Chemotropismus, 358 
Chicken-cholera, 658 
Chilblains, 10 
Children, predisposition of, 50 
Chills, 95 
Chionyphe Carteri, 655 
Chloasma uterinum, 231 
Chloral hydrate. poisoning by, 29 
Chloroform, poisoning by, 28 
Chloroma, 429 
Chlorosis, Egyptian, 722 
Cholsmia, 80 
Cholera, Asiatic, 660 
protective inoculations against, 664 

Cholera-red, 662 
Choleratoxopeptone, 664 
Cholesteatomata, 436, 475 
Cholesterin, 198 
Cholesterin-calculus, 227 
Cholin, 41 
Chondroblasts, 287, 288 
Chondroitin-sulphuric acid, 200 
Chondroma, 886 
Chondromy xoma, 888 
Chondromy xosarcoma, 387 
Chondrosarcoma, 388 
Chordoma, 888 
Chorio-epithelioma, 458 
Chorionic villi, carcinomatous transforma- 

tion of, 458 
Chromatin, 278 
Chromatophores, 282 
Chromosomes, 274 
Chylangioma, 400 
Chylopericardium, 164 
Chyluria, 164 
Cicatricial tissue, 246 
Cicutoxin, poisoning by, 38 
Cimex lectularius, 735 
Cinnabar, in a tattooed skin, 248 


143 


Circulation, collateral, development of, 
182, 183 


of the blood and of the lymph, dis- 
turbances in, 123 
Cirrhosis of the liver, 365 
Cirrus, 707 
Cirrus-sac of Bothriocephalug latus, 717 
of tenia solium, 707 
Cirsoid aneurism, 397 
neuroma, 412 
Cladothrix, 541 
asteroides, 655 
Clavus, 262 
Cleft-foot, 519 
Cleft-hand, 519 
Cleft of the abdominal wall, 511 
Clefts, 498 
of the face, median, 508 
of the face, oblique, 508 
Climate, influence of, upon man, 34 
Clitoris, malformations of, 515, 528 
Cloaca, formation of, 515 
Clostridium, 540 
butyricum, 582 
Clothing-louse, 735 
Clots, post-mortem, 134 
lardaceous, 184 
Cloudy swelling, 188 
Clubbed-hand, 521 
Club-foot, congenital, 521 
Clustered cocci, 540 
Coagulation, 184, 317 
Coagulation-necrosis, 172 
Cocaine, poisoning by, 29 
Cocci or coccacere, 540, 559 
pathogenic, 560, 561 
Coccidia, 686 
Teproduction of, 686, 689 
Coccidium oviforme, 686 
Schubergi, 689 
Coccus mesenterioides, 560 
Cocey geal region, bigerminal teratoma of, 


Colchicine, poisoning by, 28 
Cold, effects of, 10 
abscesses, 621 
Colds, 11 
Collateral circulation, development of, 1388, 
34 
Collidin, 41 
Colliquation-necrosis, 174 
Colloid, 203 
cancer, 466 
different uses of the term, 205 
production of, by epithelial cells, 208 
Color-blindness, 55 
Colorless blood-corpuscles, emigration of, 
316 


increase of, relatively to the red, 816 
marginal disposition of, 316 
Coma diabeticum, 82 
Commotio cerebri, 16 
Compensatory hypertrophy, 8, 260 
of the heart-muscle, 236 
Complement, 118, 119 
Compsomyia, 736 
Conceptional infections, 64 


744 GENERAL INDEX. 


Conceptional infections of syphilis, 688 
of tuberculosis, 627 
Concretions, 220 
amyloid, 214 
calcareous, 223, 230 
free, in the body, 226 
uric acid, 230 
Concussions, effects of, 16 
Condyloma acuminatum, 363 
latum, 638 
Congenital predisposition, 47 
Congestion, 129 
Congestive-abscess, 363 
Conglutination, 139 
Conidia-bearers, 672 
Conidia-spores, 669 
Coniine, poisoning by, 29 
Connective tissue, hyaline degeneration 
of, 215 
transformation of, into bone, 312 
Connective-tissue structures, regeneration 
03, 
Constitutio epidemica, 33 
pestilens, 33 - 
Constitutional diseases, 52, 81 
Contagium, definition of, 32 
animatum, 34 
Continuous fever, 94 
Convalescence, 94 
Cor villosum, 328 
Cordyceps militaris, 678 
Corn, 262 
Cornification of epithelium, 206 
Cornu cutaneum, 257 
Cornutin, 23 
Corpora amylacea, 214 
Corpulence, 52 
Corrosive agents, 21 
Corynebacterium, 599 
Cows, tuberculous, milk from, 608 
Crab-louse, 735 
Craniopagus, 534 
frontalis, 535 
occipitalis, 535 
parietalis, 535 
Craniorachischisis, 504 
Cranioschisis, 504 
Cranium, faulty development of, 504 
partial agenesia of, 504 
Crayfish pest, 678 
Crenothrix, 541 
Cretinism, 86 
operative, 87 
Crisis, in fevers, 94 
Crossed embolism, 67 
Croupous exudate, 327 
membrane, formation of, on mucous 
surfaces, 328 
pneumonia, 332, 570 
Cruor, 134 
Cry ptogenic infections, 41, 568 
Cry ptorchismus, 520 
Culicid:e, 735 
Culture, methods of bacterial, 558 
Curarine, poisoning by, 30 
Cutancous horn, 257 
Cuterebra cyaniventris, 736 


Cyanosig,. 131 
Cyclencephalia or cyclocephalia, 506 
Cyclopia, 506 
Cylindrical-celled cancer, 454 
Cylindromata, 431 
Cystadenoma, 442 
multilocular, 442 
papillary, 446 
Cyst-formation, 251 
Cysticercus bovis, 709 
cellulose, 708 
racemosus, 708 
Cystin, 81 
Cystin-calculi, 230 
Cystocarcinomata, 469 
papilliferum, 469 
Cyst of echinococcus, 711 
Cystotibroma, 447 
Cystomata, 442 
multilocular, 442 
papillary, 442 
simplex, 442 
Cystomyxoma, 447 
Cystosarcoma, 447 
Cysts, branchial, 476, 509 
degeneration, 253 
dermoid, 475 
ectodermal, 475 
entodermal, 475, 476 
mesodermal, 475, 476. 
retention, 251 
simple teratoid, 475 
traumatic epithelial, 459 
Cyst-worm, 711 
Cytaster, 278 
Cytoplasm, 219 
Cytoryctes vaccine, 690 


DALTONISM, 55 
Darier’s disease, 690 
Dau ghter-cysts of echinococcus, 712 
Daughter-stars, 275 
Daughter-tumors, 375 
Deaf-mutism, 55, 56 
Death, 166 
apparent, 168 
Deciduoma, malignant, 458 
Decomposition, 549 
Decubital necrosis, 171 
Decubitus, 171, 177 
Deer-disease, 658 
Defect, 2, 269 
Defervescence, period of. in fevers, 94 
Degeneration, amyloid, 208 
colloid, 203 
fatty, 190, 194 
granular, 188 
glycogenic, 200 
hyaline, 215 
hydropic, 190 
lardaceous, 208 
mucoid, 201 
parenchymatous, 188 
waxy, 178 
Degenerations, 165, 184 
Deiter’s cells, 300 
Demodex, 732. 734 


GENERAL INDEX. 


Dermanyssus avium, 734 
Dermatobia noxialis, 736 
Dermatocoptes, 734 
communis, 734 
cuniculi, 734 
Dermatocysts, 475 
Dermatoinycosis diffusa flexorum, 678 
furfuracea, 677 
Dermatophagus, 734 
Dermoid cysts, 475, 481 
Dermoids, 475, 486 
Desmobacteria, 540 
Desmoid tumor, 380 
Destructive placental polyps, 458 
Determinants or determining pieces, 62 
Deuterotoxin, 599 
Development, disturbances of, 488 
Diabetes mellitus, 82 
Diabrosis, 157 
Diapedesis, 157, 316, 319 
Diarrhoea, due to coccidiy, 690 
Diastatic ferments, 548 
Diastematomyelia, 502 
Diathesis, hemorrhagic, 158 
uric acid, 224 
Dicephalus and diprosopus, 534 
Digitalin and digitalein, poisoning by, 30 
Diphtheria, 597, 598 
bacillus of, 597 
blood-serum treatment of, 117 
columbarum, 659 
of calves, 659 
of chickens, 659 
of pigeons, 659 
Diphtheritic inflammations, 839 
Diphtheritis, 339 
Diplococci, 559, 578, 579 
Diplococcus intracellularis meningitidis, 
572 
lanceolatus, 570 
pneumonie (Fraenkel, Weichselbaum), 
570 
Diprosopus, 534 
Dipygus, 535 
parasiticus, 538 
Disease, extrinsic causes of, 5 
intrinsic causes of, 47 
latency of, 2 
the symptoms of, 2 
Diseases, cause, origin, and course of, 1 
constitutional, 81 
general, 2, 75 
inheritable, 56 
local, 2 
Dispirem, 278 
Displacement of tissue asa cause of tumor- 
formation, 873, 474 
Dispora caucasica, 582 
Distemper of dogs, 580 
Distoma felineum, 703 
hematobium, 703 
hepaticum, 700 
lanceolatuin, 7Ot 
pulmonale, 702 
sibiricum, 703 
spathulatum, 702 
estermanni, 702 


Distomia, 509 
Disuse atrophy, 187 
Diverticulum, Meckel’s, 512 
Dochmius duodenalis, 721 
stenocephalus, 723 
trigonocephalus, 723 
Double monsters, 132, 531 
symmetrical, 533 
unequal, 536 
Dracunculus medinensis, 729 
Drill-bone, 392 
Dropsy, 150 
Druse, 650 
Ductus thoracicus, obstruction of, 164 
occlusion, 152 
rupture of, 164 
Ductus omphalomesaraicus, 512 
thyreoglossus, 476 
Duplications, 523 
Duplicitas anterior, 533 
parallela, 536 
posterior, 534 
Dura mater, endothelioma of, 422 
osteoma of, 391 
psammoma of, 480 
Dust-diseases, 15, 362 
Dust-particles, entrance of, into the body, 
67 


ınetastasis of, 67 
Dwarfs, 52, 179 

formation of, 179 
Dyschromatopsia, 55 
Dyscrasia, 166 

from bacteria, 42 
Dysentery due to ameebe, 681 
Dystopia renis, 520 


EBURNEOUS ORTEOMA, 389 
Ecchondrosis, 887 
physalifera sphenooccipitalis, 888 
Ecchynioses, 156 
Echinococcus granuiosus, 713 
hydatidosus, 713 
multilocularis, 714 
scolecipariens, 713 
veterinorum, 713 
Echinococcus-cyst, 712 
Eclampsia, 69 
Ectodermal cysts, 475 
Ectogenic bacteria, 35 
Ectopia cordis, 512 
interna, 520 
intestini, 512 
testis, 520 
vesice urinari®, 512 
Eczema, 574 
marginatum, 676 
Egyptian chlorosis, 722 
Elastic fibres, development of, 287 
Electric discharges, powerful effect of, 13 
Elephantiasis, 256 
Greecorum, 689 
hwmangiomatosa, 256 
lipomatosa, 256 
lymphangiectatica, 256 
ncuromatosa, 236 
Embolism, 66, 148 


748 


Embolism, crossed, 67 
paradoxical, 67 
retrograde, 67 
Embolus, riding, 70 
septic, 148 
straddling, 70 
Embryoid tumors, 484 
Embryoma, | 
Embryonal tissue, transplantation of, 307 
Embryonic tissue, 286 
development of, in a thrombosed ar- 
tery, 351 - 
Emigration of white cells, 316 
Emphysema of the skin, 72 
Emphysematous gangrene, 176, 608 
Empusa, varieties of, 678 
Empyema, 395 
Encephalocele, 505 
Encephalomeningocele nasofrontalis, 505 
Enchondroma, 
End-artery, 132, 160 
Endocarditis, 567 
Endochondritis sy philitica, 687 
Endothelioma, 420 
hemangiotic, 397 
lymphangiotic, 403 
Endothelial cancer, 423 
Endothelium, proliferation of, 284 
Engastrius, 538 
Enostoses, 889 
Enterocysts, 477 
Enterogenous intoxication, 79 
Enteroliths, 226 
Entodermal epithelial cysts, 476 
Entogenic bacteria, 35 
Entozoa, 45 
Enzymes, 100, 105, 548 
Eosinophile cells, 218, 219 
Ephelides, 401 
Epidemic, definition of, 32 
Epidermoids, 437 
Epigastrius, 538 
Epignathus, 538 
Epipygus, 588 
Epispadias, 514 
Epistaxis, 156 
Epithelial cysts, ectodermal, entodermal, 
and mesodermal, 475 
after transplantation, 308 
dermoid, 475, 481 
epidermoid, 475 
traumatic, 459 
Epithelial pearls, 207, 468 
Epithelioid cells, 297, 344, 609 
Epithelioma, 484 
contagiosum, 687 


papillary, 434 
Epithelium, atypical growth of, in capci- 
noma, 449 
hyperplasia of, 280 
metaplasia of, 312 
misplaced, development of a cancer 
from, 458 
pathological cornification of, 206 
protective powers of, 99 
regeneration and hy perplagia of, 280 
transplantation of, 306, 476 


GENERAL INDEX. 


Epizoa, 45 
Ergotism, 23 
Erysipelas, 562 
Erythema multiforme, 567 
Erythrasma, 677 
Erythroblasts, 293 
Erythrocytolysis, 185 
Erythrocytorrhexis, 185 
Erythrocytoschisis, 185 
Ether, poisoning by, 28 
Ethmocephalia, 506 
Ethmoid bone, osteoid sarcoma of, 420 
Eurotium, 671 
malignum, 671 
Kustrongylus gigas, 723 
Eventration, 512 
Exencephalus, 505 
Exhaustion due to excessive functional] 
activity of an organ, 7 
Exhaustion-theory of immunity, 113 
Exostosis, 389 
cartilaginous, 890 
connective-tissue, 390 
Exstrophia intestini, 612 
vesicee urinarie, 512 
Extravasate, 156 
Extravasations of blood, 156, 235 
Extremities, defective development ef, 
1 
duplication of, 528 
Exudate, cellular, 384 
croupous, $27 
fibrinous, 827 
fibrinopurulent, 836 
hemorrhagic, 832 
purulent, 
serofibrinous, 827 
serous, 326 
Exudates, absorption of, 341 
Eye, regeneration processes in, 808 


Face, malformations of, 508 
Facial hemiatrophy, 187 
Facies leontina in leprosy, 641 
Facultative anatrobes, 543 
Fallopian tube, dropsy of the, 118 
Farcy, 644 
Fastigium, 94 
Fat-embolism, 69 
Fat-granule cells, 196, 197 
Fats, the, 198 
Fat-tissue, atrophy of, 198 
new-formation, 290 
Fatty degeneration, 194 
deposit, 191 
Favus, 675 
Febris continua, 94 
intermittens, 94 
recurrens, 95 
remittens, 94 
subcontinua, 94 
Feet, abnormal positions of, 516, 521 
Felt-louse, 735 
Femur, absence of, 518 
Fermentation, 549, 550 
Ferments, diastatic and inverting, 548 
Ferret-disease, 658 


GENERAL INDEX. 


Fever, 92 
bactericidal action of, 110 
continuous, 94 
etiology, 96 
intermittent, 94 
malarial, the cause of, 692 
relapsing, 95, 666 
remittent, 94 
stages, 93 
ellow, cause of, 606 
Fibrillated connective tissue, development 


Fibrinopurulent exudates, 381, 386 
Fibrinous deposits, 327 
exudates, 827 
Fibro-adenoma, 440 
conversion of, into a carcinoma, 455 
intracanalicular, 441 
papilliferum, 441 
pericanalicular, 881 
Fibroblasts, 287 
Fibrolipoma, 384 
Fibroma, 380 
intracanaliculare, 441 
multiple, 381, 412 
cedematous, 381 
papiilare, 441 
pericanaliculare, 381 
Fibromatosis of the nerves, 413 
Fibromyoma, 406 
Fibronıyxoma, 382 
Fibrosarcoma, 418 
Filaria Bancrofti, 164, 730 
hematica, 730 
medinensis, 729 
papillosa, 730 
sanguinis hominis, 164, 728 
Filar mass, 278 
Fingers, dwarfing of, 519 
malformations of, 519 
Finkler- Prior spirilla, 664 
First intention, repair by, 346 
Fish-poisoning, 19 
Fission-fungi, 540 
methods of examining, 553 
pathogenic, 551 
Fissura abdominalis, 511 
abdominalis intestinalis, 512 
genitalis, 512 
sterni, 512 
vesice urinari#, 512 
Fistula colli congenita, 509 
Fistulous tracts, 336 
Flagella, 541 
Flagellates, 681, 683 
Fiat foot, 521 
Flea, or pulex frritans, 735 
Flemming’ 8 germ-centres, 388 
Flesh-thrombus, 497 
Fleshy moles, 401 
wart, 403 
Flies, biting (stride), 785 
common (Stomoxyide), 785 
stinging (Muscide), 786 
Fotal an. persistence of, 476 


147 


Fetal glands, remains, development of. a 
cancer from, 
Foetus papyraceus, 532 
syphilitic infection of, by cither the 
sperm or the ovum, 638 
Food, effects of lack of, 6 
Foot-and-mouth disease, 580 
Foot, cleft, 519 
Foreign body in inflammation, 858 
in cyst, 2538, 358 
in giant-cell, 358 
Formative cells, 287 
stimuli, 270, 271 
Fowls, typhoid of, 658 
Fractures, effects of, 288 
Fragmentation, 276 
Freckles, 232 
Freezing, effects of, 10 
gangrene due to, 176 
Frettchenseuche, 658 
Friedländer’s pneumobacillus, 595 
Frog foetus, 504 
Fructification, act of, 61 
Fuchsinophile bodies, 218 
Fungous granulations, 364 
Fungus medullaris, 368 
Furuncle, 574 


GADININ, 549 
Gall- ducts, adenocystoma of, 448 
Gall-stones. 226, 227 
Ganglion-cells, new-formation of, 290 
Gangrene, 175 

emphysematous, 176, 603 

due to ‚reezing. 176 

due to heat, 176 

infectious, 177 

marasmic, 177 

neuropathic, 177 

pressure, 177 

putrid, 176 

senile, 176 

symmetrical, 177 

toxic, 177 
Gangrenous inflammation, 340 
Gäs, irrespirable, 22 
Gas-phlegmon, 603 
Gastropachia pini, 678 
Gastrophilus equi, 736 

hemorrhoidalis, 736 

pecorum, 736 
Gastroschisis, 511 
Genitals, external, development of, 530 

malformations of, 514 
Germ-centres of Flemming, 298 
Germ-sac, intermediary, 700 

primary, 700 

secondary, 700 
Germ-variation, primary, 60, 489 
Germinal anlage, misplaced, a4 
Giant-cell sarcoma, 418 
Giant-cells, 276, 358 

embolism of, 69 

foreign body, 858 

in tubercles, 610 

multinuclear, 276, 858 
Giant growth, general, 52, 255, 522 


148 


Giant growth, partial, 255, 523 

Giants, 52, 255 

Giraldés, organ of, 529 

Gland-activity, cessation of, 82 

Glanders, 644 

Glia-cells, new-formation of, 800 

Glioma, 408 

Glycogen, 199 

Glycosuria, 82 

Gnats (Culicide and Tipulidr), 785 

Goblet-cells, 201, 447 

Gonococcus, 576 

Gonorrhea, cause of, 576 

Gout, 52 

Gouty deposits, 224 

Granula, 218 

Granular degeneration, 188 

Granulation tissue, 343 
formation of, 344 

Granulations, chronic, 363 
fungus, 364 

Granulation tumors, infectious, 868 

Granules, hyaline, 206, 218 
nuclear, 273 
the so-called, 218 

Granulomata, 364 

Grape-mole, 497 

Gravel, 228 

Greenish coloration in decomposing ca- 

davers, 168, 242 

Grossammen, 700 

Growth, causes of, 270 

Guinea-worm, 729 

Gummata, 634 

Gynecomastia, 525 


HAMAMCBA LEUKAMIZ, 682 
Heemangio-endothelioma, 425 
Hemangioma, 893 
cavernosum, 395 
hypertrophicum, 397 
simplex, 393 
Hemangiotic endothelioma, 897 
H&mangiosarcomata, 424 
Hematemesis, 156 
Hemathidrosis, 156 
Heematocele, 157 
Heematochy luria, 730 
Hematoidin, 236 
Heematoma, 156 
Heematometra, 157 
Hematozoa, 698 
Hematuria, 156 
Hemochromatosis, 235 
Hemofuscin, 231, 233 
Hemoglobin, 236 
H&moglobinsmia, 239 
Hemoglobinuria, 239 
Hamolysin, 118 
Heemopericardium, 157 
Hemophilia, 158 
acquired, 158 
congenital, 56, 158 
Hemoptoé or hemoptysis, 156 
Hemorrhage, 156, 236 
diabrosin, 157 
diapedesin, 157 


GENERAL INDEX. 


Hemorrhage, rhexin, 157 
Heemorrhagic septicemia, 658 
Hemosiderin, 237 
Hemosiderosis, 237 
Hemosporidia, 692 
Heemothorax, 157 
Hairs in dermoid cysts, 475, 481 
Hairy polypi, 479 
tongue, 207 
Halteridium, 696 
Hand, cleft, 519 
malformations of, 516 
Hands, abnornml positions of, 52t 
Hanging ir -drop cultures, 554 
relip, 508 
Harvest-mite, 732 
Hay-fever, 49 
Head, malformations of, 504 
Head-louse, 735 
Healing powers of the human body, 108 
serum, 113 
Heart, action of, 123 
disturbed action of, 124 
“ fibroid area in, 353 
~ increased action of, 126 
Heart-muscle, compensatory hypertrophy 
a of, 260 
h pertrophy of, 126 
pigment of, 233 
rigor mortis of, 168 
Heart poisons, 28 
Héart-polypi, 144 
Heat-exhaustion, 9 
Heat-stroke, 9 
Helleborin, poisoning by, 30 
Helvellic acid, poisoning by, 26 
Hemiatrophy, congenital, 187 
acial, 187 
infantile, 187 
Hemicrania, 504 
Hepatitis, chronic, 365 
Hereditary pieces or determinates, 63 
Hereditary transmission, atavistic, 58 
collateral, 58 
direct, 57 
pseudo-form of, 65 
Heredity, degenerative, 57 
identical, 57 
transformational, 57 
Hermaphrodism, false, 528 
true, 527 
Hernia basalis, 506 
cerebri, 505 
funiculi umbilicalis, 511 
lateralis, 506 
nasoethmoidalis, 506 
nasofrontalis, 506 
occipitalis, 505 
sphenoorbitalis, 506 * 
sphenomaxillaris, 506 
sphenopharyngea, 506 
syncipitalis, 506 
umbilical, 511 
Herpes tonsurans, 676 
Herpetomonas Lewisii, 683 
Heterakis, 720 
Heterotopous tissue-growths, 474 


GENERAL INDEX. 


Histoid tumors, 367 
Hog-cholera, 658 
Holorachischisis, 499 
Holoschisis, 278 
Homo delinquens, 53 
sapiens, 54 
Hook-worm, 721 
Horn, cutaneous, 257, 485 
Horny warts, 257, 434 
Horse-flies (Tabanidx), 735 
Humerus, osteochondroma of, 388 
Hunterian induration, 632 
Hyalin, connective-tissue, 219 
epithelial, 208, 206 
Hyaline cartilage, reproduction of, 288 
Hyaline degeneration, 215 
of connective tissue, 215, 219 
of connective tissuc of heart, 217 
of connective tissue of vessel-wall, 217 
Hyaline exudations, 219 
products of connective-tissue cells, 
218. 219 
thrombi, 219 
tissue-necrosis, 219 
Hydatid mole, 496, 497 
Hydatids, 711 
Hydrencephalocele, 505 
Hydrocele colli congenita, 510 
Hydrocephalus, 607 
Hydrocyanic-acid poisoning, 25 
Hydrogen-sulphide poisoning, 25 
Hydromeningocele, 501 
Hydromyelocele, 501 
Hydropic degeneration, 190 
Hydrops, 150 
adiposus, 154 
chylosus, 154 
Hydrorachis, 499 
Hydrothorax chylosus, 164 
Hygroma colli congenitum, 400 
Hyoscyamine, poisoning by, 29 
Hyperemia, active, 129 
local, 129 
passive, 180 
venous, general, 130 
Hyperkeratosis, 207 
Hypermastia, 525 
Hyperonychia, 257 
Hyperostosis, 863 
Hyperplasia, 255 
Hyperthelia, 525 
Hyperthyreosis, 88 
Hypertrichosis, 257 
Hypertrophy, 255 
compensatory, 261 
due to lessened use, 261 
due to over-work, §, 260 
due to non-resolution, 261 
due to removal of pressure, 262 
inflammatory, 262 
of a muscle or gland, 8 
of the tissues and organs, 255, 258, 260 
Hyphe, 43 
Hy phomycetes, 667 
Hypochondria, 17 
Hypoderma bovis, 736 
Hypoplasia, 178 


Hyposarca, 150 
Hypospadias, 514 
Hypostasis, 131 

post-mortem, 131, 167 
Hypostatic congestion, 131 
llysteria, 17 


IcnTHYOSIS, 256 
congenita, 256, 257 
hystrix, 257 
Ichthyotic warts, 257, 433, 434 
Ichthyotoxin, 19 
Icterus, 244 
neonatorum, 244 
Idiosyncrasy, 49 
Immune-body, 119 
Immune-sera, 119 
Immunity, 47, 99 
acquiring of, 111 
Ehrlich’s theory of, 114, 117 
Immunization, active and passive, 114 
Implantation, 305, 308, 480, 486 
bigerminal, 480 
monogerminal, 480 
Inclusio fatalis, 538 
Indolent ulcers, 363 
Induration, Hunterian, 682 
Infarct, anemic, 160 
embolic, 161 
ha:morrhagic, 161 
healing of, 162, 352 
Infection, 33, 39 
by means of animal parasites, 45 
cryptogenic, 41, 568, 575 
double, 41 
hematogenous, 41 
intra-uterine, 40, 552 
origin of disease through, 89 
protection against. 99, 101 
secondary, 41. 626 
spread of, by mosquitos, 46, 697, 780 
spread of, from mother to fetus, 40, 
64, 552 
Infectious diseases, 31 
healing of, 109 
local, 89 
inheritance of, 64 
Infectious foci, metastatic, 39 
Infiltration, 321 
growth of tumors by, 375 
purulent, 385 
serous, 326 
small-celled, 334 
Infiltrations of the tissues, 165, 321 
Infiltrative mode of growth of carci- 
nomata, 451 
Inflammation, 814 
catarrhal, 326, 835 
chronic, 860 
clinical significance of the term, 318 
different forms of, 326 
diphtheritic, 339 
‘fibrinous, 327 
interstitial, 323 
necrotic, 838 
parenchymatous, 824 
superficial, 324 


750 


Inflammation, suppurative, 885 
termination of, 341 

Influenza-bacillus, 596 

Infusoria, 681 

Inheritance of pathological peculiarities, 


Initial sclerosis, 632 
Injection of sterilized cultures, 118 
Innervation, disturbances of, 16, 17, 77 
Inoculation, 111 
Inoculation of attenuated specific disease- 
germs, 112 
Insanity, inherited, 58 
Insecta, 735 
Insects, 46, 785 
Insolation, 9 
Insusceptibility to poisons, 100 
Interfilar mass, 278 
Intermediary body, 119 
Intermittent fever, 94 
Internal secretion, 82 
Interstitial inflammation, 323 
Intestinal intoxications, 38 
mucous membrane, adenoma.like pro- 
jection of, 476 
Intestine, abnormal positions of, 511, 520 
tubular adenoma of, 
Intoxication, origin of diseases through, 
18, 78 
Invasion-disease, 45 
Inversio intestini, 512 
vesice urinarie, 513 
Iodothyrin, 87 
Iron, assimilation of, 242 
deposit, 240 
insufficiency of, 7 
reaction, 237 
Iron-free pigments, 236, 242 
Irradiation, 13 
_ Ischemia, localized, 132 
Ischiopagus, 534 
Isolysin, 119 
Isthmus, the, of aorta, 127 
Itch- mite, 731 
Ixodes ricinus, 782 


JANICEPS, 535 
Janus-head, 535 
Jarrings of the uterus as a cause of mal- 
formations of the embryo, 489 
Jaundice, 244 
Jaw, upper, actinomycosis of, 652 
giant-cell sarcoma of, 419 
lower, absence of, 509 


KAKERLAKEN, 250 
Kakké, 19 
Karyokinesis, 273 
Karyolysis, 169 
Karyomitosis, 273 
Karyorrhexis. 169 
Kedani disease, 734 
Kephir, 582 
Kephir-ferment, 582 
Keloid, 382 
Keratin, 206 
Keratohyalin, 206 


GENERAL INDEX. 


Keratosis follicularis, 690 

Kidney, amyloid degeneration of, 212 
arteriosclerotic atrophy of the, 186 
cloudy swelling of, 189 
compensatory hypertrophy of, 282, 


contracted, 364, 365 
cystoma of, 444 
deposits of fibrin in the, 883 
senile atrophy of, 186 
streptococcus infection of, 568 
tubular adenoma of, 440 
Kinetoses, 17 
Kribbelkrankheit, 28 
Krumelzellen, 854 
Krystallwulst, 308 


LABIA MAJORA and minora, defective de- 
velopment of, 515 
Labium leporinum, 508 
Lardaceous degeneration, 208 
spleen, 208 
Larynx, papillary epithelioma of, 435 
syphilitic ulceration of the, 636 
Latency of disease, 2 
Lead- poisoning, 23 
Lead, deposit of, 249 
Leiomyoma, 404 
Lens, regeneration of, 303 
Lentigines, 282, 401 
Leontiasis ossea, 258, 528 
leprosa, 641 
Lepra (or leprosy), 639 
anesthetica, 642, 648 
maculosa, 642 
mutilans, 642, 643 
nervorum, 642 
nodosa, 642 
tuberosa sive tuberculosa, 642 
ulcerosa, 642 
Leprosy, 689 
white, of the Jews, 251 
Leptothrix, 540 
Leptus autumnalis, 732, 734 
Leucoblasts, 294 
Leucocytes, 106, 110, 334. 335, 844, 356 
emigration of, 316, 325, 353 
new-formation of, 292 
varieties of, 294 
Leucoderma, 250 
Leuconostoc mesenterioides, 560 
Leucopathia acquisita, 250 
congenita, 250 
Leucotrichia, 250 
Leukemia, 682 
Leydenia gemmipara, 683 
Lice, 735 
Life-trophoblasts or biophores, 62 
Light. effects of, 18 
influence of. upon development of 
bacteria, 543 
Lightning figures, 14 
Lightning-stroke, 18 
Linguatulicde, 731 
Lip, carcinoma of, 454 
malformations of, 508 
Lipochrome, 231, 283 


GENERAL INDEX. 


Lipofibroma, 384 
Lipoma, 884 
Lipomatosis, 52, 191 
Lipomyxoma, 884 
Lique action-necrosis, 174 
Lithocelyphopsdion, 498 
Lithocely phos, 498 
Lithopedion, 498 
Liver, abscess of, 681 
amyloid degeneration of, 209, 311 
angioma cavernosum of, 396 
chronic inflammation of, 865 
cirrhosis of, 865 
coccidia, disease of, 686 
corset, 187 
cystoma of, 448, 444 
foamy, 608 
gumma of, 685 
multilocular adenocystoma of, 444 
Liver-fluke, 700 
Livores, 181, 167 
Lucilia macellaria, 736 
Lungs, actinomycosis of the, 651 
Aibrinous exudates in the, 882 
induration of, 362 
mould-fungi in the, 671 
red hepatization of the, 333 
syphilitic disease of the, 637 
tuberculosis of the, 616, 619, 620, 622, 


623 

Lupus of the skin, 617 
Lustgarten’s bacillus of syphilis, 681 
Luxations, congenital, 521 
Lymph, antibacterial properties of, 104 

formation of, 151 

hindrance of flow of, 152 
Lymphadenoid tissue, reproduction of, 

‚291 

Lymphangioma, 899 

cavernosum, 400 

cystoides, 399 

hypertrophicum, 400 

simplex, 399 
Lymphangiosarcoma, 420 
Lymphangoitis, 46 
Lymph-fistula, 164 
Lymph-glands, action of, as filters, 104 
Lymphorrhagia, 163 
Lymphosarcoma, 416 
Lysis, in fever, 94 
Lysogenous substance of Fränkel, 109 


MACROCHEILIA, 400 
Macrogamete, 689, 698 
Macroglossia, 400 
Macrostomia, 509 
Madura disease or Madura foot, 855 
Maidismus, 38 
Malanders, 734 
Malaria, 692 

forms of, 692 

in animals, 696 

piasmodia of, 682 

the cause of, 692 
Malformations, 488 

congenital, 488 

iasmus, §44 


T51 


Malignant odema, 602 
tumors, 379 

Mallein, 646 

Malleus, 644 

Mal perforant, 177 

Mammary gland, adenoma of, 489 
carcinoma of, 462, 464 
endothelioma of, 428 
intracanalicular fibroma of, 441 
mucous carcinoma of, 465, 468 
papillary cystocarcinoma of, 827 

4 


papillary cystoma of, 448 
tubular adenoma of, 489, 457 
Marasmic thrombi, 144 
Marasmus, 6, 166 
Margarin crystals, 199 
Mast-cells, 318 
Mastoid antrum, scholesteatomate in, 186 
Measles of tzenis, 708 
Meat-poisoning, 18, 88 
Meckel’s diverticulum, 512 
Mediastinal dermoids, 476 
Medullary cancer, 464 
Megastoma entericum, 682 
intestinale, 682 
Melsna neonatorum, 159 
Melanin, 283 
Melanomata, 400 
Melanosarcomata, 428 
Melanosis of internal or 234 
Melasma suprarenale, 8 
Membrane, pyogenetic, 353 
Meningitis, epidemic cerebrospinal, 572 
Meningocele, 500, 505 
Meningococcus, 572 
Meningo-encephalitis sy philitica, 634 
Meningo-encephalocele, 505 
Menorrhagia, 156 
Merismopeiia, 540, 541, 559 
Merorachischisis, 499 
Merozoites, 689, 698 
Mesodermal epithelial cysts, 476 
Metabolism, bacterial, 548 
Metaglobulin, 141 
Metakinesis, 274, 278 
Metamorphosis, viscous, 189 
Metapluasia, epithelial, 812, 578 
of the tissues, 310 
Metastasis, 66 
direct, 67 
formation of, in carcinomata, 451 
hematogenous, 66 
in tuberculosis, 623 
lymphogenous, 66 
of pigment, 72 
paradoxical, 67 
retrograde, 67 
Metastatic daughter-tumors, 70, 875 
infectious foci, 71 
inflammations, 66 
Methemoglobin, 239 
the formation of, 26 
Methemoglobinuria, 239 
Methyl guanidin. 38 
Metrorrhagia, 156 
Miasm, definition of, 82 


752 


Miasmatic-contagious disease, definition 
oT, 
Miasms and contagions, boundary-line be- 
tween, 85 
Micrencephalon, 53 
Micrencephalus, 180, 505 
Microbacteria, 540 
Microbrachius, 516 
Microgamete, 689, 698 
Microcephalus, 180, 505 
Micrococci, 540, 559 
Micrococcus ascoformans, 580 
aurantiacus, 560 
botryogenes, 580 
cyaneus, 560 
gonorrheer, 576 
hematodes, 560 
in meningitis, 572 
in mycofibroma, 580 , 
in mycosis of parrots, 580 
in Pseudotuberculosis of guinea-pigs, 
0 


luteus, 560 
of foot-and-mouth disease, 580 
of hemoglobinuria of cattle, 580 
of lung-disease of horses, 579 
pathogenic, 560, 561 
pyogenes, 578 
pyogenes of rinderpest, 579 
tetragenus, 560 
tetragenus of udder-disease, 580 
ures, 560 
violaceus, 560 
viscosus, 560 
xantogenicus, 607 
Microgametocyte, 689, 698 
Microgyria, 180 
Micromelus, 516 
Micromyelia, 58 
Micropus, 516 
Microsomes, 278 
Microsomia, 496 
Microsporon furfur, 677 
minutissimum, 677 
Microstomia, 509 
Miescher, sacs of, 688 
Miliary tubercles, 611, 616, 624 
tuberculosis, hematogenous, 638 
Milk from tuberculous cows, 
Mineral poisons, 18 
Miracidium, 700 
Missed labor, 498 
Mites, 731, 734 
Mitome, 278 
Mitosis, 273 
Mole, 400 
hairy, 400 
hydatid, 497 
pigmented, 400 
Möller's or Barlow’s disease, 158 
Molluscum bodies, 687 
Monas lens, 682 
Monilia candida, 672 
Monobrachius, 516 
Monogerminal tissue-implantation, 480 
Monomorphous bacteria, 54 
Monopus, 516 


GENERAL INDEX. 


Monsters, 488 
double, 494, 531 
triple, 531 
Morbus Addisonii, 89, 231 
maculosus Werlhofii, 158 
Morgagni, hydatid of, 529 
Morphine, poisoning by, 29 
Morphea nigra et alba, 642 
Mosquitos, agency of, in spreading certain 
diseases, 46, 697. 730 
Mother-star, 274, 277 
Mouldering, 550 
Mould-fungi, 668, 669 
Mouth, development of, 510 
malformations of, 509 
Mucins, the, 202 
Mucor corymbifer, 671 
pusillus, 673 
ramosus, 673 
rhizopodiformis, 673 
Mucorini, disease-producing, 48 
Mucous degencration, 201 
membranes, carcinoma of, 454 
membranes, papillary epitheliomata 
or, 
tissue, reproduction of, 291 
Muguet, 670 
Müller’s duct, 529 


“ Multiple fibromata of the skin, 54, 412 


Mummification, 176 

Muscardine in silkworms, 678 

Muscarin, poisoning by, 30 

Muscide, 783 

Muscle, atrophy of, 185 
heart, hypertrophy of, 266 
heart, new-formation of, 298 
in dermoid cysts, 482 
non-striated, hypertrophy of, 298 
non-striated new-formation of, 298 
striated, hypertrophy of, 260 
striated, new-formation of, 296 
waxy degeneration of, 173 

Muscle-trichina, 727 

Muscles, cadaveric stiffening of, 168 
supernumerary, 525: 

Muscular system, pathological changes in 

the, 53 

Mussel poisoning, 19 

Mycelium, 669 

Mycetoma, 655 

Mycobacterium tuberculosis, 613 

Mycoderma albicans, 672 

Mycodesmoid, 580 

Mycofibroma, 580 

Mycoprotein, 541 

Mycosis of alimentary tract, 67 
of respiratory tract, 670, 678 
of skin, 675 
versicolor, 677 

Mycosozin, 105 

Myelocele, 501 

Myelocystoccle, 501 

Myelocystomeningocele, 502 

Myelocysts, 477 

Myelomeningocele, 500 

Myiasis, 736 

Myofibroma, 406 


GENERAL INDEX. 


Myolipoma inside the vertebral canal, 
474 
Myoma, 404 
levocellulare, 404 
striocellulare, 406 
Myosarcoma, 407 
Myositis ossificans, 58, 892 
Myxoangiosarcoma, 431 
Myxadema, 86 
Myxofibroma, 888 
Myxolipoma, 888 
Myxoma, 882 
Myxosarcoma, 882 


NAVUS FLAMMEUS, 394 
lymphaticus, 400 
pigmentosus, 400 
pilosus, 400 
prominens, 395, 400 
spilus, 
vasculosus, 895 
verrucosus, 895, 400 
vinosus, 894 
Nanosomia, 496 
Nasal muscous membrane, lymphosar- 
coma of, 416 
Navel stone, 227 
Neck, malformations of, 508 
Necrobiosis, 171, 173 
Necrosis, 169 
anemic, 170 
cheesy, 178 
cosgulation, 172 
colliquation, 178 
decubital, 177 
direct, 171 
indirect, 171 
marasmic, 171 
mummifying, 176 
neuropathic, 170, 177 
senile, 176 
thermal, 176 
Nemathelminthes, 718 
Nematoda, 718 
toxic, 177 
Nematodium ovis pulmonalis, 728 
Nerve- and heart-poisons, 28 
Nerve elements, new formation of, 299 
Nerve-fibres, peripheral, new formation 
Ol, 
peripheral, pathological changes in, 
54 


Nerves, fibromata of, 412 
fibromatosis of, 412 
leprosy of, 642 
regeneration of, 801 
Nervous system, central, pathological 
changes in the, 58 
Neurasthenia, 17 
Neuridin, 88, 549 
Neusin, 38, 549 
Neuroepithelioma, 409 
Neurofibroma, 411 
Neuroglia, hypertrophic growth of, 300 
regenerative growth of, 300 
Neuroglioma ganglionare, 409 
gliomatosum microcysticum, 410 


153 


Neuroma, 411 
amputation, 802, 411 
amyelinicum, 413 
cirsoid, 412 
ganglion cellulare verum, 413 
myelinicum, 412 
plexiforme, 412 
verum, 412 
Neuropathic atrophy, 187 
gangrene, 177 
necrosis, 170 
Neuroses, traumatic, 17 
Neurotization, 302 
Nicotine, poisoning by, 29 
Nitrate-of-silver poisoning, 28 
Nitrobacteria, 549 
Nitrogenous nourishment, importance of, 6 
Nitrous oxide, poisoning by, 28 
Nodes, gouty, 225 
Normal serum, 117 
Nuclear contents, 273 
framework, 278, 278 
granules, 278, 278 
Nuclear division, asymmetrical, 275 
atypical, 275 
direct, 278, 276 
indirect, 278 
plueripolar, 275 
segments, 274 
spindle, 274 
Nuclein, 273 
Nucleinic acid, 106 
Nucleus, composition of the, 278 
Nutrition, retrograde disturbances of, 165 


ÖBEsıTy, 52, 191 
Obligate anatrobes, 543 
Obturating thrombus, 144 
Ochronosis of cartilage, 284 
Odontoma, 889 
(Edema and dropsy, 150 
cachectic, 158 
collateral, 158 
due to obstruction of thoracic duct, 
152 
ex vacuo, 158 
hydremic, 158 
inflammatory, 158 
malignant, 
purulent, 336 
stagnation, 152 
(Bsophagus, growth of apnthe upon the, 


(Estrid®, 736 
(Estrus bovis, 736 
ovis, 736 
Oldium albicans, 672 
subtile cutis, 678 
Olein, 198 
Oligomorphous bacteria, 540 
Omentum, tuberculosis of, 626 
Omphalocele, 511 
Omphalomesenteric cyst, 513 
duct, 512 
Oncospheera, 717 
Onychogry phosis, 257 
Onychomycosis favosa, 676 


754 GENERAL INDEX. 


Parasites, metastasis of, 71 
Parasitic diseases, 88 
infection, 88 
Parasitism, origin of disease through, 31, 
33 


Onychomycosis trichophytina, 676 
Oöcyst, 686, 689, 698 
Odkinete, 697, 698 
Opium and morphine, poisoning by, 29 
Organs, weight of, 259 

volume of, 259 
Osteoarthropathie hypertrophiante, 263 
Osteoblasts, 290 
Osteochondroina, 388, 391 
Osteofibroma, 891 
Osteoid sarcoma, 480 

of ethmoid, 429 

trabecule, 480 
Osteoma, 889 

dental, 389 

disconnected, 389 


Parenchymatous cells, embolism uf, 69 
Parenchymatous degeneration, 188 
inflammation, 824 
Parietal thrombus, 144 
Parotid gland, angiosarcoma of, 426 
chondrofibroma of, 426 
chondromy xosarcoma of, 887 
my xoangiosarcoma of, 431 
Parosteal osteomata, 389 
Parrots, mycosis of, 580 
Pathology and pathological anatomy , the, 1 


durum seu eburneum, 889 clinical, 8 
heteroplastic, 389 general, definition of, 1 
medullare, 389 problems of, 1 
parosteal, 389 Pear! disease, 628 
spongiosum, 389 tumors, 486 


Pearls, epithelial, 207, 436, 463 
Pediculus capitis, 735 
pubis, 785 
vestimentorum, 785 
Pellagra, 19, 88 
Penis, duplication of, 535 
stunting of, 514 
Pentastoma, 781 
denticulatum, 788 
tsnioides, 738 
Peptotoxin. 549 
Peribronchitis, 884 
Peripheral nerves, pathological changes 
in, 54 
Perithecia, 678 
Perithelioma, 426 
Peritoneum, cystic lymphangioma of, 400 
Peritrichous flagella, 602 


Osteomyelitis, 574 
Osteophyte, 389 
Osteoporosis, 183, 184 
Osteosarcoma, 419 
Ovary, adenocystoma of, 445 
ermoid cysts of, 481 
multilocular adenocystoma of, 443 
papillary cystadenoma of, 445, 447 
papillary cystocarcinoma of, 470 
cystoma of, 446 
teratomuta of, 483 
Over-exertion, 7 
Over-heating, 9 
Overwork, hypertrophy from, 260 
Oxidation, intra-organic, 91 
Oxygen, effects of a diminution in the 
supply of, 5 
influence of, upon development of 


bacteria, 548 
Oxyuris vermicularis, 720 


PacnyakrriA, 263 
Packet-shaped cocci, 540, 560 
Paget’s disease, 690 
Palate, malformations of, 508 
Palhnitin, 198 
Pancreas, cyst of the, 252 
diabetes after extirpation of, 88 
Papillary adenomata, 440 
conversion of, into a carcinoma, 456 
cystomata, 446 
epitheliomata, 434, 436 
Papilloma, 380 
Paracholia 245 
nervous, 245 
Paradoxical embolism, 67 
Parakeratosis, 207 
Paralysins, 110 
Paramecium coli, 681 
Paramitome, 278 
Paramucin, 203 
Paraplasın, 278 
Parasite (in the case of twins), 536 
Parasites, 31 
animal, 679 
formation of cysts by, 253 


Perlsucht, 628 
Pernicious malaria, 694 
Perniones, 10 
Perobrachius, 516 
Perochirus, 519 
Perodactylism, 519 
Peromelus, 516 
Peropus, 516, 519 
Perturbatio critica, 94 
Pes calcaneus, 521 

equinovarus, 521 

valgus, 521 
Pest, 604 

bacillus, 604 
Pestilence, definition of, 32 
Petechi®, 156 
Petrifaction, 220 

in carcinomata, 468 
Petrifving sarcoma, 480 
Phagocytes, 99, 103, 856 
Phagocytosis, 99, 103. 856 
Phallin, poisoning by. 26 
Phimosis, hypertrophic, 515 
Phleboliths, 146, 227 
Phlegmon, 336 

wooden, 568 
Phloridzin diabetes, 84 
Phocomelus, 516 


‘ GENERAL INDEX. 


Phosphorescent phenomena, 549 
Physalides, 467 
Physiology, pathological, 1 
Pia mater, cholesteatomata of the, 437 
Pigeon-diphtheria, 659 
Pigment, autochthonous, 281 
extrinsic, 248 
hematogenous, 285 
metastasis of, 78 
pathological absence of, 250 
pathological formation of, 231 
Pigment-atrophy, 183 
Pigment-carrying cells, 286, 287 
Pigment-granule spheres, 857 
Pigmented mole, 400 
warts, 400 
Piroplasma bigeminum, 696 
Pithead tapeworm, 716 
Pityriasis, 675 
versicolor, 677 
Placental cells, embolism of, 69 
infections, intra-uterine, 552 
polyp, malignant, 458 
vill carcinomatous transformation, 


Piacentoma, 458 
Plague, bubonic, 604 
Plasma-cells, 354 
Plasmodium malaris, 692 
preecox, 692 
vivax, 692 
Plasmolysis, 185 
Plasmorrhexis, 135 
Plasmoschisis, 185, 169 
Plasmosomes, 278 
Plate-cultures, 558 
Platyhelminthes, 700 
Plerocercoid, 718 
Plethora, 126 
Pleura, endothelioma of, 422 
Pleuritis, fibrinous, 831 
Plenropneumonia, contagious, of cattle, 


Plexiform neuroma, 418 
Plugs, epithelial, in cancer of the skin, 460 
Pluripolar division, 275 
Pneumococcus, 570 
Pneumonia, croupous, 332, 570, 595 
infectious, of cattle, 659 
of horses, 579 
Pointed condylomata, 362 
Poisoning. definition of, 18 
Poisons, classification of, 21 
different varieties of, 21 
Poison-theory, of immunity, 112 
Polar area, 278 
corpuscles, 274, 278 
furrow, 
Poliosis, 250 
Polydacty lism, 528 
Polymastia, 525 
Polymelos, 537 
Polymitus, 695 
Polymorphism of cancer-cells, 451 
Polymorphous bacteria, 541 
Polypi, hairy, 479 
valvular, 145 


155 


Polythelia, 525 
Polyuria, 56, 82 
Post-mortem hypostasis, 181, 167 
Potassium chlorate poisoning, 26 
Predisposition, acquired, 48 
congenital, 52 
local, 48 
temporary, 48 
Prepuce, absence of, 515 
hypertrophy of, 515 
shortness of, 515 
Pressure atrophy, 186 
Pressure, continuous, effects of, 15, 186 
Froglottides, 708 
Proliferation, phenomena of, 343 
Proscolex, 715 
Prusoposchisis, 508 
Prosopothoracopagus, 586 
Prostatic concretions, 205 
calculi, 227 
Protective mechanisms, natural, 99 
Proteosoma, 696 
Proteus vulgaris, 588 
Prothrombin, 136 
Protophyte, 540 
Protoplasm, 275 
Prototoxin, 599 
Protozoa, parasitic, 680 
Psammomata, 430 
Pseudalius ovis pulmonalis, 728 
Pseudo-actinomycosis, 655 
Pseudodiphtheria bacilli, 600 
Pseudohermaphrodismus, 52% 
Pseudomelanosis, 238 
Pseudomucin, 202 
Pseudotuberculosis, 580, 628 
aspergillina, 629, 678 
cladotrichica, 629, 655 
due to animal parasites, 629 
due to bacteria, 629 
due to foreign bodies, 628 
due to hyphomycetes, 629 
vermian, 629 
Psorospermose folliculaire végétante, 690 
Psychoneurosis, 17 
Ptomatns, 88, 41, 548 
toxic, 88, 549 
Pulex irritans, 735 
penetrans, or sand flea, 735 
Pulmonary circulation, increase of resist- 
ance in, 127 
Pulse, acceleration of, 125 
venous, 125 
Puriform softening, 146 
Purpura, 158 
hemorrhagica, 158 
rheumatica, 158 
simplex, 158 
Pus, 335 
inspissated, calcification of, 353 
Pus-cocci, 574 
Pus-corpuscles, 335 
Pustule, 385 
Putrefaction, 88, 41, 549 
alkaloids, 88, 41 
zymoids, 41 
Putrescin, 38, 549 


156 GENERAL INDEX. 


Putrid gangrene, 176 
Pysmia, 40, 566, 575 
Pyelonephritis of cattle, 659 
Pygopagus, 588 

Pyknosis, 169 
Pyosepthemia, 566 
Pyosepticsmia, 40, 566, 575 


QUININE, poisoning by, 29 
RaBIEs, protective inoculations against, 
116 


Rabbit septicemia, 658 
Race, predisposition of, 51 
Rachicele, 500 
Rachipagus, 536 
Rachischisis, partial, 499 
total, 499 
Rag-sorters’ disease, 587 
Rainey’s bodies, 688 
Ray-figures, 275 
Ray-fungus, 649 
Rays, 275 
Recurrent fever, 95 
Receptaculum scolicis, 708 
Rectum, cancer of, 461 
Redis, or secondary germ-sacs, 700 
Reduplications, 528, 533 
Regeneration, 265 
causes, 266 
of degenerated tissue, 342 
partial, 267 
Regenerative capacity of tissues, 269 
Relapsing fever, 95. 666 
Remittent fever, 94 
Repair by first and by second intention, 
6 


Respiratory apparatus, aspergillus my- 
coses of, 673 
Resting-cells, 273 
Restitutio ad integrum, 267 
Retention cyst, 251 
Retina, glioma of, 409 
Retrograde changes, 451 
Rhabditis stercoralis, 725 
Rhabdomyoma, 406 
Rhexis, 157 
Rhinoscleroma, 647 
Rhizopoda, 680 
Ribs, supernumerary, 58, 525 
Rice-water intestinal discharges in cholera, 
662 
Ricin, 27 
immunity to, 117 
poisoning by, 27 
Rider’s bone, 392 
Rigor mortis, 168 
Rinderpest, immunization, 116 
Ringworm, 676 
Roscola syphilitica, 683 
Round-cell sarcoma, 416, 417 
Roundworms, 718 
Rudimentary twin, 480, 532, 536 
Russel's bodies, 206, 218 


SACCHAROMYCES ELLIPSOIDEUS, 669 
lithogenes, 673 


Saccharomyces neoformans, 678 
Saccharomycetes, 678, 679 
disease-producing, 669, 678 
Sacs of Miescher, 688 
Sago-spleen, 208 
Salts, caustic, 22 
Sand flea, or pulex penetrans, 735 
San tumors, 430 ing by. 29 
tonin, poisoning by, 
Saprophytes, 548 
Saprophytic bacilli, 582 
cocci, 560 
Sarcina lutea, 560 
ventriculi, 560 
Surcinee, 560 
Sarcoma, 414 
adeno-, 468 
angio-, 426 
alveolar, 420 
cysto-, 447 
etiology of, 415 
fibro-, 415, 416, 418 
iant-cell, 418 
rman gio-, 424, 426 
large round-celled, 417 
lym phadenoides, 416 
lymphangio-, 420 
lympho-, 416 
medullary, 415 
melano-, 428 
myo-, 419 
myxo-, 419 
organoid, 420 
osteo-, 419 
osteoid. 130 50 
petrifying, 
phyllodes, 447 
plexiforme, 426 
polymorphous-celled, 417, 418 
simple, 416 
small, round-celled, 416 
spindle-celled, 417 
telangiectatic, 415 
tubular, 420 
Sarcocarcinoma, 468 
Sarcophilia Wohlfarti, 786 
Sarcoplasm, 297 
Sarcoptes hominis, 781 
minor, 734 
squamiferus, 784 
Sarcosporidia, 688, 690 
Sausage-poisoning. 18, 88 
Scabies, 782 
Scald-head, 675 
Scall, 675 
Scar-tissue, 267 
Schistoprosopia, 508 
Schizogony, 682, 686, 689, 698 
Schizomycetes, 540 
Schizont, 689, 697, 698 
Scirrhus, 464 
Sclera, regeneration of, 808 
Scleroma respiratorium, 647 
Sclerosis, 216 
initial, 632 
of nerve-tissue, 300 
Scolex, 705 


GENERAL INDEX. 


Scrofula, 627 
Scrotum, malformations of, 515 
Scurvy, 158 
Scutula of favus, 675 
Sea-sickness, 17 
Sebaceous glands in dermoid cysts, 482 
Secale cornutum, 28 
Second intention, repair by, 846 
Secondary infection, 41, 626 
Secretion, internal, 82 
Segmentation, direct, 273 
indirect, 273 
Segmented skein, 274, 277 
Semilunar ganglia, pathological changes 
in, 90 
Sepsin, 41 
Sepsis, 40 
Septicemia, 40, 566, 575 
hemorrhagic, 658 
Septicopysmia, 40, 566, 575 
Sequestration of necrosed tissue, 171, 341, 
360 


Serpiginous ulcers, 363 

Serum, healing, 113 
protective, 118 

Sex, predisposition of, 51 

Sexual glands, teratoid tumors of, 481, 486 
removal of, 9 

Sexual organs, internal, development of, 

52 

Shock, erethistic and torpid, 16 

Sickness, causes of, 5 

Side-chains, 118 

Siderosis, hematogenous, 240 

Silver, deposit of, 28, 249 

Sirenomelia, 517 

Situs inversus, 520 

Bkein-like structure of the nucleus, 274, 
7 

Skeleton, pathological changes in the, 53 

Skin, absence of pigment of, 250 
cancer of, 453 
emphysema of, 72 
healing of wounds of, 346 
leprous nudule of the, 640 
lupus of the, 617 
melanotic alveolar sarcoma of, 429 
multiple fibromata of the, 54 
papillary epithelioma of, ‘488 
pathological alterations of, 55 
pigmentation of, 89, 231 

Skin- transplantation, 306 

Skull-cap, angioma cavernosum of, 397 

Slumber-cells, 325 . 

Smallpox, pustule, 334 
parasites of, 690 

Smear cultures, 558 

Smegma bacillus, 618 

Snake poison, 22 
immunization, 117 

Soft chancre, 607 

Special sense, organs of, new-formation of 

the tissues of, 303 

Specificity of the tissues, 266 

Spermin. 91 

Sphacelinic acid. 23 

Sphacelus, 176 


| 
or 
Sy 


Sphatrobacteria, 540 
Spheres, fatty granule, 196, 357 
pigmented granule, 857 
Spider cells, 300 
Spina bifida, 498 
anterior, 500 
cystica, 499 
lumbosacralis, 500 
occulta, 500 
posterior, 500 
Spinal column, pressure atrophy of the, 
1 


cord, development of, 507 
Spindle-celled sarcoma, 417 
Spindle-figure, 277 
Spindle, nuclear, 274, 278 
Spirilin, or spirillacese, or spirobacteria, 

65 


Spirillum cholere Asiatic, 660 
of Finkler and Prior, 664, 665 
rugula, 659 
serpens, 659 
sputigenum, 665 
tenue, 660 
tyrogenum, 665 
undula, 660 
volutans, 660 

Spirobacteria, 659 

Spirochete, 540, 659 
buccalis, 660 
denticola, 660 
Obermeieri, 666 
plicatilis, 660 
varieties of, 660 

Spleen, amy loid degeneration of, 208 
changes in, in relapsing fever, 666 
tissue, reproduction of, 290 

Sporangia, 671 

Spore-formation, 542 

Spores, 36, 542, 669, 698 

Sporoblasts, 688, 698 

Sporocyst, 688, 689 

Sporogenous ranules, 545 

Sporogony, 686, 689, 698 

Sporozoa, 686 

Sporozoites, 686 

Stab-cultures, 533 

Stadium amphiboles, 94 
decrementi, 94 
incrementi, 94 

Staggers, cause of the, 710 

Staphylococci, 540, 578 

Staphylococcus pyogenes albus, 576 
pyogenes aureus, 573 
pyogenes citreus, 576 

Stars, 274, 275, 277 

Starvation, 6 

Stasis of the blood, 149 

Stearin, 198 

Sterigmata, 672 

Sterilized cultures, injection of, 113 

Sternopagus, 586 

Stigmatization, 159 

Stomach, carcinoma of, 456 

Stomoxyid, 735 

Stones (concretions), 226 

Stone-cutter’s lung, 362 


758 


Straddling emboli, 70 
Strangles of horses, 579 
Streptococci, 540, 561 
Streptococcus articulorum, 569 
brevis, 569 
erysipelatis, 569 
lanceolatus, 570 
longus, 569 
meningitidis, 572 
puerperalis, 569 
pyogenes, 561 
scarlatinosus, 569 
Streptothrix madure, 655 
Strongylides, 723 
Strongylus armatus, 723 
bronchialis, 728 
capillaris, 728 
commutatus, 725 
duodenalis, 721 
filaria, 723 
longevaginatus, 723 
micrurus, 723 
paradoxus, 723 
pusillus, 723 
rufescens, 723 
syngamus, 723 
tetracanthus, 723 
trachealis, 728 
Strychnine, poisoning by. 29 
Substance, fibrinogenic, 141 
Substance, lysogenic, 109 
Substance, zymoplastic. 141 
Sucking-mite, 784 
Sucking-worms, 700 
Suffocation, 5 
Suffusion, 156 
Suggillations, 156 . 
Sulphur-methamoglobin, 26 
Sunstroke, 9 
Supernumerary organs, 58, 528 
Suppuration, cause of, 336 
Suprarenal cachexia, 90 
capsules, altered function of, 89 
Suprarenin, 90 
Surra. 684 
Susceptibility to infections at different 
ages, 50 
Sweat-glands in dermoid cysts, 482 
Swine-erysipelas, 657 
immunization, 115 
Swine-plague, 857 
Sycosis parasitaria, 676 
Symbiotes equi of Gerlach, 734 
Symmetrical gangrene, 177 
Symmyelia, 517 
Symptomatic anthrax, 656 
protective inoculations against, 115 
Sympus, 517 
Syncephalus, 585 
Syncope, 16 
Syneytium, 458 
Syndactylism, 519 
Syngamus branchialis, 723 
trachealis, 723 
Synophthalmus, 506 
Synotia. 509 
Syphilides, 633 


GENERAL INDEX. 


Syphilis, bacillus of, 681 
hereditary, 686 
transmission to foetus, 64, 688 
Syringomyelia, 58 
Syringomyelocele, 501 


TABANIDE, 735 

Tablet-formed cocci, 540, 541, 559 

Tactile irritability, 108 

Teenia Africana, 710 
ceenurus, 710 
cucumerina, 710 
echinococcus, 711 
denticulata, 710 
diminuta, 710 
elliptica, 710 
expansa, 710 
flavapuncta, 710 
mamillan&, 710 
marginata, 710 
mediocanellata, 709 
nana, 710 
perfoliata, 710 
plicata, 710 
saginata, 709 
serrata, 710 
solium, 706 

Tail, formation of a, in the human being, 
§25 


Talipomanus, 521 
Tapeworms, see also under Janta, 705 
Tarichium megaspermum, 678 
Tartar of the teeth, 226 
Tattooing of the skin, 248 
Teeth in dermoid cysts, 481 
supernumerary, 525 
Telangiectasia, 39 
lymphatica, 399 
Temperature, influence of, upon develop- 
ment of bacteria, 543 
Temperatures, high, of the body, 9 
low, of the body, 10 
Tendinous spot. 349 
Teratoid cysts, 473 
tumors, 473 
Teratoma, autochthonous, 480 
bigerminal, 480 
coccy geal, 479, 480, 588 
heterochronous and heterotopous. 474 
monogerminal, 480 
sacral, 475 ° 
of sexual glands, 481, 486 
solid, 483 
Terminal artery, 182 
Testicle, adenocystoma of, 444 
adcnorhabdomyoma of. 485 
angiosarcoma of, 425 
congenital adenocystoma of, 484 
dermoid cysts of, 486 
ectopia of, 520 
retention of, in the abdominal cavity, 
920) 
teratomata of, 485 
Tetanotoxin, 602 
Tetanus, 601 
antitoxin. 117, 608 
Tetanus-bacillus, 601 


GENERAL INDEX. 


Tetany, thyreoprival, 85 
Texas fever, 696 
Thallophytes, 668 
Thoracic cavity, faulty closure of, 512 
Thoracogastroschisis, 511 
Thoracopagus, 536 
parasiticus, 538 
Threadworms, 720 
Thrombin, 186 
Thrombo-arteritis purulenta, 147 
Thrombo-phlebitis purulenta, 147 
Thrombosis, 184 
sequele of, 146 
Thrombus, 144 
autochthonous, 144 
induced, 144 
laminated, 137 
mixed, 137 
red, 136 
white, 137 
Thrombus-mole, 497 
Thyreoprival cachexia, 85 
tetany, 85 
Thyroid, angiosarcoma of, 425 
extirpation of, 85 
Thyroiodine, 85 
Tibia, tuberculous disease of, 621 
Tipulidee, 735 
Ticks, 782 
Tinea favosa, 675 
Tissue-implantation, bigerminal, 480 
monogerminal, 480 
Tissue-lesion, 815 
Tissues, restitution of the, 265 
Toes, stunting of, 519 
Tongue, actinomycosis of the, 650 
Tongue-worms, 731 
Tophi, gouty, 225 
Torula-chains, 559 
Toxalbumins, 18, 38, 42, 549 
Toxenzymes, 18 
Toxic substances, 18, 37 
Toxinemia, 39 
Toxins, 549 
Toxoids, 100 
Toxons, 599 
Toxoses, 100 
Trarfsmissible pathological conditions aud 
tendencies, 56 
Transplantation, 305 
Transportation, retrograde, 67 
Traumatic epithelial cysts, 459 
neuroses, 17 
Trematoda, 700 
Trichina spiralis, 726 
Trichocephalus dispar, 726 
Trichomonas intestinalis, 682 
vaginalis, 682 
Trichophyton tonsurans, 676 
Tritotoxin, 599 
Trophoneurotic diseases of the tissues, 78 
Trypanosoma Brucii, 684 
sanguinis, 688 
Tsetse disease, 683 
Tubercle, 609 
solitary, 618 
Tubercles, miliary. 616 


Tuberculin, 116, 614 
Tuberculobactericidin, 614 
Tuberculomyces, 618 
Tuberculomycoprotein, 614 
Tuberculosis, 607 
avian, 628 
bacillus, 607 
bovine, 628 
hematogenous miliary, 625 
infection with, 608 
Tube-cocci, 540 
Tumors, 366 
adenocarcinoma, 461 
adenocystoma, 442 
adenoma, 487 
adenosarcoma, 468 
angiosarcoma, 424 
benign and malignant, 878 
cachexia accompanying, 379 
carcinoma, 449 
cavernous, 897 
chloromata, 429 
chondromata, 886 
chordoma, 888 
classification of, 869 
connective-tissue, 367 
cylindroma, 481 
cystic, 442 
cystocarcinoma, 469 
definition of, 366 
dermoid cysts, 472 
desmoid, 890 
different varieties, 380 
enchondroma, 886 
endothelioma, 420 
epithelial, 483 
etiology, 871 
fibroma, 880 
fibromyoma, 406 
fibrosarcoma, 415 
glioma, 408 
growth of, by infiltration, 375 
hemangiomata, 393 
histoid, 867 
keloid, 382 
leiomyoma, 404 
lipoma, 384 
lymphangiomata, 899 
malignant, 879 
melanosarcomata, 428 
metastases, 875 
myofibroma, 406 
myoma, 404 — 
my xochondroma, 388 
myxoma, 882 
my xofibroma, 882 
myxolipoma, 882 
myxosarcoma, 882 
neurofibroma, 411 
neuroglioma ganglionare, 408 
neuroma, 411 
organoid, 420 
osteoid sarcoma, 430 
osteoma, 389 
papilloma, 880 
psammoma, 480 
recurrence of, 378 


760 


Tumors, retrogressive changes in, 877 
rhabdomyoma, 406 
sarcocarcinoma, 468 
sarcoma, 414 
structure of, 867 
teratoid, 478 

T win-formations, rudimen , 480 

Tympanic cavity, cholesteatomata in, 486 

Typhoid fever, bacillus of, 589 
protective inoculations against, 116 
of fowls, 658 

Typhotoxin, 88 

Typbhus reourrens, 866 


ÜDDER-INFLAMMATIONS, 580 
Ulceration, tuberculous, 622 
Ulcer, 386 
chrunic, 863 
indolent, 863 
serpiginous, 368 
Ulcus atonicum, 368 
callosum, 368 
elevatum hypertrophicum, 868 
indolens, 863 
molle, 607 
Umbilical hernia, 511 
Urachus-cysts, 477 
Ureemia, 
Urates, deposit of, in gout, 224 
Ureteritis cystica, 690 
Urethra, abnormal narrowness of, 515 
absence of, 515 
atresia of, 515 
Urethritis, gonorrheeal, 577 
Uric-acid deposits, 224, 228, 280 
infarct, 228 
Urina calculi, 228 
Urobilin, 286 
Urobilinuria, 236 
Uterus, adenocarcinoma of, 461 
beginning carcinoma of cervix, 455 
myoma of, 404 
Uvula, bifurcation of, 508 


VACCINE, 690 
Vacuoles, 151, 169, 190, 822 
Valves, lesions of, 125 
Valvular thrombus, 144 
Variola, 690 
Vascular nevi, 304 
eyatem, pathological changes in the, 


walls, pathological alterations of, 815 
Vasculitis, proliferating, 850 
Vasomotor nerves, irritation or paralysis 
of, 159 
Vein-stones, 227 
Venous pulsation, 125 


GENERAL INDEX. 


Venous pulse, 125 
Veratrine, poisoning by, 20 
Vermes, 7 
Verruca carnea, 401 

senilis, 484 

vasculosa, 395 
Vertebre, supernumerary, 525 
Vertebral canal, deficient closure of, 498 
Vesicles, 824, 827 
Vibrio cholere, 660 

of Metschnikoff, 665 


serpens, 659 

Vibrion b butyrique, 582 
septique of Pasteur, 602 

Viscera, abnormal positions of, 5% 
duplications of, 525 

a pparatus, pathological conditions 

Oo 

Vitelline duct, cyst of, 518 

Vitiligo, 250 

Volatile poisons, 22 


WANDERING CELLS, 319 
Warts, fleshy, 400 

ichthyotic, 484 

senile, 484 

venereal, 262, 862 
Water, effects of lack of, 6 
Weights of different organs, 259 
Whip-infusoria, 681 
Whip-worm, 726 
White gangrene, 176 
Whooping-cough, bacillus of, 597 
Widal-Gruber reaction, 109, 592 
Wolffian body, 529 
Wolf’s jaws, 508 
Wood-jack or wood-tick, 732 
Worm-disease of the ox, 659 
Worms, 45, 700 

parasitic, 45, 700 
Worm-disease, 646 
Wound -diphtheritis, 340 
Wound-granulations, 345 
Wound-infection, 48 
Wounds, effects of, 15 


XANTHIN CALCTLI, 230 
Xiphopagus, 586 


YEAST-FUNGI, 668 
Yellow fever, 606 


ZONA DERMATICA, 500 
epithelo-serosa, 500 

Zodgica, 542 

Zymase, 550 

Zymoid, putrefactive, 41 


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STANFORD UNIVERSITY MEDICAL CENTER 
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