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Full text of "The pathology and differential diagnosis of infectious diseases of animals"

LIBRARY 

OF THE 

University of California. 



BIOLOGY 

Class UBH/R^ 



THE PATHOLOGY 



DIFFERENTIAL DIAGNOSIS 



INFECTIOUS DISEASES OF ANIMALS 



By VERANUS ALVA MOORE, B.S., M.D. 

Professor of Comparative Pathology, Bacteriology and Meat Inspection, 

New York State Veterinary College, Cornell University, 

Ithaca, Nev^' York. 



With An Introduction by 

DANIEL ELMER SALMON, D.V.M. 

Former Chief of the Bureau of Animal Industry, United States 

Department of Agriculture. 



THIRD EDITION REVISED AND ENLARGED 



WITH I2ZJLLUSTRATIONS 

'•■'^ OF THE \ 

ERSIT Y ) 

OF J 



ITHACA, N. Y. 

TAYLOR & CARPENTER 

I 908 



6 



K ' 









^\0^'- 



COl'YRIGHT I90S 

By Veranus Alva Moore 



PRESS OF 
JOURNAL JOB DEPARTMENT 



TO DANIEL ELMER SALMON 

LARGELY THROUGH WHOSE LABORS THERE WAS ES- 
TABLISHED IN THE UNITED STATES DEPARTMENT OF 
AGRICULTURE THE BUREAU OF ANIMAL INDUSTRY 
WHICH HAS MADE POSSIBLE EXTENSIVE INVESTIGA- 
TIONS INTO THE NATURE OF EPIZOOTIC DISEASES 
IN AMERICA AND WHO FOR TWENTY-ONE YEARS 
DIRECTED THESE INVESTIGATIONS 

THIS VOLUME IS DEDICATED. 



PREFACE 

The activity in the study of the infectious diseases of ani- 
mals has brought out many new facts pertaining to them since 
the pubhcation of the second edition of this volume. This 
rapid increase of new knowledge and the elimination of pre- 
viously employed methods and interpretations render thepr e- 
paration of a text-book suitable for student use more and 
more diflScult. 

In the present revision, the general plan of the arrange- 
ment of subject matter and the classification of the diseases 
followed in the previous editions have not been changed. The 
grouping of the infectious diseases in accordance with the clas- 
sification of their etiological factors is for student purposes at 
least proving to be satisfactor}-. The rapid accumulation of 
literature on the subject matter of this elementary work pre- 
cludes the pubhcation of a bibliography. The appending of a 
few references after the discussion of each disease to some of 
the more important articles has, however, proven to be of 
much assistance to students just beginning the study of in- 
fectious diseases. 

I desire to express my appreciation of the kind reception 
accorded to the second edition and the helpful reviews and 
criticisms that it has received. It is hoped that this edition 
will be of still greater aid both to the student and practitioner 
than the former ones. My thanks are especially due to Drs. 
S. H. Burnett and \V. J. Taylor of this department for helpful 

V. A. M. 



PREFACE TO THE FIRST EDITION 



The literature on infection and the etiology and morbid 
anatomy of infectious diseases of animals is exceedingly rich 
in the results of new discoveries and important investigations. 
However, students just beginning this study and following a 
prescribed curriculum have not the time nor are they prepared 
to read with profit the detailed records of original research. 
Such publications seem to be better adapted for those doing 
advanced or graduate work. Furthermore many of these 
publications are out of print and are only available for con- 
sultation. F'or these reasons it is believed that a volume con- 
taining the rudiments of the subject will be of use to the stu- 
dent and an aid to the teacher. It is also believed that such 
a work will be of assistance to practitioners. 

In preparing this volume the aim has been to bring to- 
gether in a concise form the fundamental facts in the path- 
ology of the more common infectious diseases of animals, 
especially those existing in the United States, with which 
sanitarians and the practitioners of comparative medicine must 
contend. To this end the current literature, the reports of 
the investigations made at various Institutions and Experi- 
ment Stations, as well as the standard works on comparative 
pathology have been freely drawn upon, to all of which full 
acknowledgment is hereby made. 

In order to bring into consideration the clinical value of a 
knowledge of morbid anatomy a few of the symptoms or ante- 
mortem manifestations have been included. It is hoped that 
this correlation of symptoms and lesions will stimulate a deeper 
interest in the study of comparative pathology and thus render 
it of more permanent and practical value for those entering 
into the practice of veterinary medicine. 

In selecting the subject matter care has been taken to 
avoid, as far as possible, the introduction of results concerning 



which there are controversies. It has seemed best to deal 
with those facts about which at the present time there is little 
or no doubt. After the discussion of each disease a few refer- 
ences to the literature are appended. These are intended sim- 
ply to bring the attention of the student to a few publications 
respecting the cause and morbid anatom}^ considered in the 
light of modern etiology, of the disease in question and to a 
few articles containing the results of original research. 

In order not to complicate or unnecessarily expand this 
text, a knowledge of general pathology and the principles of 
bacteriology has been taken for granted. 

The difficulties involved in the preparation of such a text 
are both numerous and obvious. The indication of errors or 
omissions with any other criticisms that will tend to better the 
volume and increase its efficiency for the student will be 
thankfully received. 

V. A. M. 



TABLE OF CONTENTS. 



PAGE 



List of Illustrations x 

List of Reference Books i. xiii 

Introdtction xiv 

CHAPTER I. 

GENERAL CONSIDERATION OF ETIOLOGY, INFECTION AND 
SPECIFIC INFECTIOUS DISEASES. 

Etiology I 

Infection 2 

Channels of Infection 5 

Wound infection . 6 

A specific infectious disease 11 

The differential characters of a specific infectious or epizootic 

disease 11 

Dissemination of infectious diseases 14 

Cause of variations in the course of an infectious disease 15 

Classification or grouping of infectious diseases 16 

Migula's classification of bacteria iS 

CHAPTER II. 

DISEASES ATTRIBUTED TO WOUND INFECTION. 

Botryomj'cosis 21 

Omphalophlebitis 25 

White scours in calves 26 

Infectious suppurative cellulitis 29 

Fistulous withers and poll-evil 31 

Infectious mastitis 32 

Miscellaneous infections 36 

CHAPTER III. 

DISEASES CAUSED BV BACTERIA — GENUS STREPTOCOCCUS. 

General discussion of streptococci 38 

Strangles 44 

Equine contagious pleuro-pneumonia 49 

Apoplectiform septicemia in chickens 57 

Streptococcus mastitis 60 

CHAPTER IV. 

DISEASES CAUSED BV BACTERIA-GENUS MICROCOCCUS. 

Takosis 6;^ 



Vlll CONTENTS 

CHAPTER V. 

DISEASES CAUSED BY BACTERIA— GENUS BACTERIUM. 

Pasteurelloses 69 

Swine plague 71 

Hemorrhagic septicemia in cattle 94 

Fowl cholera 105 

Goose septicemia in 

Fowl typhoid 114 

Swine erysipelas - 123 

Anthrax 129 

Glanders 151 

Tuberculosis 175 

Avian tuberculosis 203 

Johne's disease 230 

Ovine caseous lymph-adenitis 234 

Asthenia in fowls and pigeons 243 

Diphtheria in calves and swine 244 

CHAPTER VI. 

DISEASES CAUSED BY BACTERIA— GENUS BACILLUS. 

Hog cholera 246 

Tetanus 265 

Black leg 276 

Foot-rot in sheep 289 

Miscellaneous infections with bacilli 291 

CHAPTER VII. 

DISEASES CAUSED BY BACTERIA— FAMILY SPIRILLACE.^. 

Diseases of fowls caused by spirilla 294 

Disease of pigs caused by spirochaetes 297 

CHAPTER VIII. 

DISEASES CAUSED BY FUNGI. 

Actinomycosis 299 

Actinobacillosis 317 

Iveeches 321 

Pneumonomycosis 333 

Epizootic lymphangitis 342 

Farcy in cattle 346 

Mycotic stomatitis 347 

Blastomycetes, infection in horses 348 

CHAPTER IX. 

DISEASES CAUSED BY PROTOZOA— GENUS PIROPLASMA. 

Texas fever 349 



CONTENTS IX 

Ictero-heniaturia in sheep 3>(>^ 

Equine malaria 3^9 

Canine malaria 372 

CHAPTER X. 

DISEASKS CAUSED BV PROTOZOA — GENUS AMEBA. 

Infectious entero-hepatitis in turkeys 377 

CHAPTER XI. 
DISEASES CAUSED BV PROTO/OA— GENUS TRYPANOSOMA. 

Classification of Trypanosoma 39' 

Surra 4oo 

Dourine 4io 

Mai de caderas — 423 

Nagana 426 

CHAPTER XII. 

INFECTIOUS DISEASES POR WHICH THE SPECIFIC CAUSE IS 

NOT YET DETERMINED. 

Rinderpest 43° 

Contagious pleuro-pneumonia in cattle 44' 

Foot and mouth disease 454 

Rabies .__. 459 

Diphtheria in fowls 4'^5 

Influenza 499 

Dog distemper. 5o6 

Cerebro-spinal meningitis 5 '4 

Cornstalk disease in cattle 5i7 

Infectious abortion 523 

Variola in animals 529 

Epithelioma contagiosa 539 

Infective sarcomata in dogs 542 

Fowl pest 543 

CHAPTER XIII. 

IMMUNITY AND PROTECTIVE INOCULATION. 

Natural immunity 545 

Artificial immunity 547 

Hemolysins 55- 

Protective inoculation 555 

Prevention 560 

CHAPTER XIV. 

DISINFECTION. 

Disinfection 5^3 

Disinfection of stables 5^7 



X ILLUSTRATIONS 

ILLUSTRATIONS. 

PLATES. 

Tuberculosis of lung, pig ^ 

Map showing Texas fever line ^^ 



FIGURES IN TEXT. 



1. Purulent infiltration 7 

2. Micrococcus pyogenes aureus 8 

3. Streptococcus pyogenes 9 

4. Abscess in partially immunized rabbit '7 

5. Streptococcus of mastitis 3^ 

6. Section of cow's udder 34 

7. Morphology of streptococcus 39 

8. Micrococcus caprinus ^4 

9. Bacterium of swine plague 72 

0. Lung showing emphysema in interlobular spaces 78 

1. Right lung of pig showing areas affected with swine plague _ 79 
Portion of lung showing hemorrhagic interlobular infiltration 82 
Hemorrhagic kidney, pig ^3 

14. Hemorrhagic heart, cow 

15. Bacieriuin sanguinariuni 

16. Temperature chart of fowls affected with fowl typhoid .__ 

17. Diseased blood in fowl typhoid "8 

18. Congested liver in fowl typhoid i '9 

19. Phagocytic action of leucocytes on the red blood corpuscles. 120 

20. Bacterium of swine erysipelas 124 



13 



ICO 



116 



130 
132 



21. Anthrax bacteria from an impression preparation 

22. Cover-glass preparation from anthrax blood 

23. Bacterium anthracis, in blood '3^ 

24. Nasal septum and turbinated bone, glanders 15^ 

25. Nasal septum, advanced glanders ^57 

26. Nasal septum, showing scars, glanders 15S 

27. Glandered lung '59 

28. Section of glandered nodule i^i 

29. Farcy, cutaneous glanders '"2 

30. Mallein reaction '"7 

30. /lacieriuin tuberculosis '8° 

31. Lymph glands on side of cow's head iSj 

32. Dorsal aspect of bovine lungs '^5 

33. Bovine tracheal and bronchial lymph glands 186 

Posterior mediastinal glands ^^7 



34 



35. Section of very young tuberch 



ILLUSTRATIONS XI 

36. Tuberculous heart, cow 190 

37. Tuberculous focus in cow's lung 192 

38. Section of tuberculous lung, cow 193 

39 Tubercular pleiira 194 

40. Tubercles on mesentery 195 

41. Tubercles on omentum .._. 196 

42. Tuberculous ulcers, intestine, cow 197 

43. Section of a tuberculous ulcer 198 

44. Tuberculous spleen, pig 201 

45. Avian tubercle bacteria 204 

46. Culture of avian tubercle 205 

47. Tuberculous liver, fowl 208 

48. Section of a tubercle, fowl ._ 209 

49. Tuberculous mesentery, fowl 210 

50. Tuberculous skin, fowl 21 1 

51. Temperature curve, tuberculin 221 

52. Chart showing the effect of cold water on temperature 221 

53. Tuberculin curve of pig 222 

54. Non-tubercular temperature reaction 223 

55. Chart showing tuberculin reaction 224 

56. Bacterium of Preisz 236 

57. Caseous nodules on leg of rabbit 238 

58. Lung of sheep with nodules 239 

59. Bacillus of hog cholera 249 

60. Ulcerated intestine in hog cholera 254 

6t. Spleen of pig, normal and with hog cholera 255 

62. Bacillus of tetanus 266 

63. Bacillus of black leg 278 

64. Bacillus of malignant edema 287 

65. Bacillus necrophorus 290 

66. Necrotic area, liver, rabbit. 290 

67. Spirochaett- anserina 294 

68. Spirochaetes from pig 296 

69. Ray fungus 301 

70. Section of young actinomycotic growth 302 

71. Giant cells in actinomycotic growth 302 

72. Actinomycosis, head of steer 304 

73. Young actinomycotic growth 306 

74. Actinomycotic jaw, cow 307 

75. Section of actinomycotic jaw 308 

76. Actinomycosis of upper jaw 309 

77. Actinomycosis in tongue 310 

78. Actinomycosis in cow's lung 312 

79. Actinobacillosis 318 

8c. Leeches, lesions in lip of horse 325 



Xli ILLUSTRATIONS 

8i. Various forms of fungus 326 

82. Leeches, lesions in lip of horse 327 

83. Isolated nodule from lesion 32iS 

84. Club-like ends of hyphae fungus, "leeches" 329 

85. Section through nodule, "leeches" 330 

86. Aspergillus fumigatus 334 

87. Section of lung showing aspergillus 336 

88. Necrosis, kidney of rabbit 340 

89 Piroplas)iia bigeiniuniii 353 

90. Coccus form of Piroplasma higeniinmn 353 

91. Texas fever parasite in blood of kidney 354 

92. Coccus form of Texas fever parasite in kidney 354 

93. Invasion of corpuscles with /'/Vo/>/fl:5w«<z bigeininuin 355 

94. Adult male tick, Boophilus annulatus 355 

95. Bull suffering from Texas fever 356 

96. Adult female tick, y>'t)0/!'/n7«5 annulatus ^ 357 

97. Eggs and young tick, i>\;())!>/?z7«.T annulatus 35S 

98. Awcha nieleagridis 379 

99. Ceca of turkey with lesions of entero-hepatitis 383 

100. Cecum showing ulcers, in entero-hepatitis 384 

lor. L/iver of turkey affected with entero-hepatitis 385 

102. Early lesions in entero-hepatitis 386 

103. Trypanosoma Ihuci — 392 

104. Trypanoplasina Jlorrelli 392 

105. Trvpauosoma Le7uisi 393 

106. Map showing distribution of trypanosomiasis 396 

107. Trypanosoma Evansi 4ob 

108. Trypanosma cquiperduni 4'2 

109. Trypanosoma eqniperdu7n, dividing 4'3 

1 10. Negri bodies 4^2 

111. Section of normal plexiform ganglion, dog 480 

112. Section of plexiform ganglion from a case of rabies 480 

113. Diphtheria in fowls, eye 4^7 

114. Diphtheria in fowls, sinus 4^^ 

1 15. Early stages of diphtheritic necrosis 4''^9 

116. Advanced stage of diphtheritic exudate 49° 

117. Diphtheritic exudate, throat of pigeon 492 

118. Diphtheritic exudate, larynx, fowl 493 

119. Diphtheritic exudate, larynx and trachea, fowl 493 

120. Sections of heads of normal and diphtheritic fowls 496 

I2[. Epithelioma contagiosa, fowl 540 

122. Ehrlich's figures, complement 554 

123. IChrlich's figures, various receptors 554 

124. Ivhrlich's figures, free receptors 554 

125. Ehrlich's figures, anti-complement 554 



A LIST OF REFERENCE BOOKS. 



BouLEV ET REVNAi..— Nouveau Dictionaire pratitiue de Medecine de 

Chirurgie et d'Hygiene Veterinaires. 
Cadeac— Encyclopedic Veterinaire. 
DiECKERHOFF.— Lehrbuch der specielleu Pathologic und Therapie fiir 

Thicrarztc. 
EllenbKRGER. vSchuTz cnd Baum.— Jahresbericht liber die Leistungen 

auf dcm Gebiete der Veterinar-Medicin. 
Fleming —A manual of veterinary sanitary science and police. 
Friedberger und Frohner.— Lehrbuch der spezicllcn Pathologic u. 

Therapie der Haustiere. 
Galtier.— Traite des maladies contagieuses et de la police sanitaire des 

animaux domestiques. 
Hutyra uxd MarEK.— Spezielle Pathologic und Therapie der 

Haustiere. 
KiTT.— Lehrbuch der pathologischen Anatomic der Hausthiere. 
KOLLE UND Wassermann.— Handbuch der pathogenen Mikroorgan- 

ismen. 
Law.— Veterinary Medicine. (Especially Vol. IV.) 
LUBARSCH und'ostertag.— Ergebnisse der allgemeinen Pathologic 

und Pathologischen Anatomic des Menschen und der Tiere. 
NOCARD ET Leclainche.— Les maladies microbiennes des animaux. 
OSTERTAG.— Handbook of meat inspection. Authorized translation by 

U. V. Wilcox. 
Reynal— Traite de la Police Sanitaire des Animaux Domestiques. 
Schneidemuhl.— Lehrbuch der vergleichenden Pathologic und Ther- 
apie des Menschen und der Hausthiere. 
Waluey.— The four bovine scourges. 



For bibliography on all medical subjects, see Index-catalogue of 
the Library of the Surgeon-General's office. 

Annual reports, Special Reports and Bulletins on Animal Diseases 
issued by the Bureau of Animal Industry, U. S. Department of Agricul- 
ture, Washington, D. C. 

Proceedings of the American Veterinary Medical Association. 

The Bulletins on Animal Diseases issued by the various State Agri- 
cultural Experiment Stations. 



INTRODUCTION. 

An elementary treatise on the patholog}^ of the infectious 
diseases of animals— a treatise that states briefly, clearly and 
comprehensively all that is known, and excludes all that is 
not known — has long been needed not only by the students 
who are beginning this interesting subject, but by members 
of the veterinary profession who, as practitioners, investigators 
or teachers, wish to learn in the shortest time the present con- 
dition of our knowledge. A work which supplies this need 
will be welcomed and appreciated. 

There are few subjects more important to Americans than 
a thorough comprehension of the infectious diseases of ani- 
mals. An enormous amount of money is invested in the 
domesticated animals in the United States, and the security of 
this investment depends very largely upon our ability to pro- 
tect these animals from infectious diseases. There are many 
diseases of this class which spread among animals as smallpox, 
bubonic plague or cholera spreads among mankind; and it re- 
quires a thorough knowledge of all the characteristics of such 
diseases to guard against them, to recognize them when they 
appear or to control them. 

For a period already too long, exact knowledge of these 
diseases has been confined to a comparatively small number of 
men; but with the great property interests at stake it is ex- 
tremely desirable that this information should be distributed, 
that not only responsible officials but every practitioner should 
share it. With not far from three thousand million dollars 
worth of farm animals in this country, and with a single dis- 
ease that sometimes destroys a hundred million dollars worth 



INTRODUCTION XV 

of property in a year, it is not difficult to see the value of that 
precise knowledge which is required to deal promptly and 
efficiently vv'ith these plagues. 

It is a narrow and incorrect view to hold that the farmer 
who owns these animals is the only one who suffers from the 
ravages of the diseases which destroy them. Animal pro- 
ducts constitute a large part of the national food supply. If 
this food supply is diminished, made dearer and more difficult 
to obtain, want, misery, disease and death among mankind 
increase. At first the effects of a scarcity of the food supply 
ma3^ be almost inappreciable and felt only by the verv poor; 
but as the conditions of famine are approached, suffering is 
multiplied and intensified until whole communities are pros- 
trated or destroyed. An abundant supply of wholesome and 
nutritious food is therefore an essential condition of the wel- 
fare and prosperity of the people. 

The great commercial operations of nations also depend 
to a great extent upon the good condition of animals. When 
all of the horses are disabled by an epizootic, as they have 
been on rare occasions by influenza, the delivery of purchased 
goods has nearly ceased, the shipments of flour, iron, machin- 
ery and other products have been temporarily arrested and 
business has been almost at a standstill. Again, it should be 
remembered that we export annually from the United States 
forty million dollars worth of live animals, one hundred mil- 
lion dollars worth of meats, fifty-five million dollars worth of 
lard, tallow and other animal fats, and nine million dollars 
worth of dairy products. Let this traffic be stopped by the 
shortage of supplies or by prohibitive orders of other nations 
on account of the unrestrained prevalence of infectious dis- 
eases, and the earnings of steamships, and railroads, and 
banks, and commission houses, are at once diminished; men 



XVI INTRODUCTION 

employed in these enterprises are discharged, and in innumer- 
erable ways the welfare of people who have no part in the 
ownership of any of these animals or their products is affected. 

Finally the most serious of all is the case in which the 
animal plague, in addition to being destructive to animal life, 
is communicable to and fatal to man, as is true of anthrax, 
rabies and tuberculosis. Such diseases destroy property, dis- 
turb business, lessen the food supply, and directly threaten 
human life. What more is needed to impress upon the reader 
the supreme importance of studying and understanding the in- 
fectious diseases of animals ? 

The pathology of these diseases is in itself a large subject. 
Investigations concerning it have extended over more than a 
century of time and the literature of the subject is enormous. 
To concentrate this knowledge, to select the truth and discard 
the errors, and to develop a concise and systematic treatise is 
a task of great magnitude and one which has required much 
labor and thought. The writer has not seen the manuscript, 
but, from his long and intimate acquaintance with the author, 
he feels sure that the work has been patiently, carefully, intelli- 
gently and thoroughly done, and that it will be favorably 
received. 

D E. Salmon. 




CHAPTER I. 

GENERAL CONSIDERATION OF ETIOLOGY, INFECTION 
AND SPECIFIC INFECTIOUS DISEASES. 



§ I. Etiology. The development of the science of bac- 
teriology, together with a knowledge of the parasitic protozoa, 
has already demonstrated that a large number of the infectious 
diseases are the direct result of the invasion of the animal body 
by certain species of microorganisms. A specific etiology 
which teaches that for each of the various epizootics we have a 
single, definite cause has become recognized and been accepted 
by all pathologists. Although there are a number of distinct 
diseases for which such a specific agent has not been found, 
the evidence in the very nature of the maladies is conclusive 
that for each of these such an etiological factor exists. 

In studying the pathology of infectious diseases the idea 
of a definite and adequate cause should be kept in mind. It is 
no longer justifiable to attribute them to an unfavorable en- 
vironment, poor hygiene, or improper sanitation, conditions 
which may aid the specific cause but which cannot supplant 
it. It is often a troublesome task to differentiate between the 
morbid affections, often fatal in their results, brought about by 
improper care and food, and the maladies dependent upon a 
specific cause. The reason why many of the former theories 
accepted unsanitary conditions, certain kinds of food or other 
similar agencies as the etiology of distinct, infectious diseases, 
is found in the fact that the infectious microorganisms- were 
and still are often transmitted to the individual through such 
channels. It is important, therefore, that the limitations of 
both the exciting cause and the environment should be fully 
taken into account. Although for certain diseases such as 
rinderpest we do not know just what the specific cause is, 



2 ETIOLOGY 

the fact that its location in the body of the diseased animal 
is known, that with the morbid tissues the disease can be 
produced in healthy animals and that without this definite 
infection, no matter what the conditions are, the malady can- 
not be made to develop, argues against extraneous conditions 
as exciting causes. 

The mystery which formerly surrounded the origin, the 
course and the disappearance of animal plagues has in a large 
degree been cleared away ; and in its place we are confronted 
with the problems involved in the life history and the possi- 
bilities of invading microorganisms. In fact during the last 
few years the biological sciences have been brought into im- 
mediate use by the pathologists. Etiology has become per- 
manently linked to microbiology so that in seeking for the 
specific cause of an infectious disease we look for some species 
of organic life which may belong either to the animal or to the 
vegetable kingdom. The fact that certain microscopic animals 
and plants have become, if they were not in the beginning, 
parasitic on larger and higher forms of life has long been 
recognized ; but the idea came later, that the various infections 
giving rise to a wide series of phenomena, known as symp- 
toms and morbid anatomy, were actually and simply the results 
of the invasion of the individual with living microscopic plants 
(bacteria) or animals (protozoa). It is likewise true that for 
many of the disorders consisting of changes recognized in the 
terms of general pathology, the cause may be found in the 
conditions of life under which the individual has been forced 
to exist. Etiology, therefore, in a broad sense, includes both 
the infecting microorganisms that produce the specific infectious 
diseases and poor hygienic, unsanitary conditions and physical 
forces which may produce non-specific morbid changes often 
sufficient to cause death. 

§ 2. Infection. The term infection has come to be gen- 
erally understood to mean the entrance into the animal body, 
from without, of living microorganisms capable of multiplying 
within the living tissues and of producing in consequence of 
this multiplication a local or a general diseased condition and 



INFECTION 3 

possibly the death of the individual. The invading microor- 
ganisms may belong to any one of the three great groups of 
microscopic life, namely, bacteria, higher fungi, and protozoa. 
It is custotuary and convenient, if not altogether logical, to 
limit the term microorganisms to these forms, excluding alto- 
gether the entozoa and other animal parasites, most of which 
are not microscopic in size. 

A diseased condition produced by substances not capable 
of reproducing themselves, as, for example, organic or inor- 
ganic chemical compounds, is an intoxicative process. In an 
infection, the immediate cause of the symptoms and morbid 
changes in the tissues is an intoxication due to the action of 
the metabolic products (toxins) of the invading microorgan- 
isms. The theories of their mechanical interference with 
the normal functions of the body or that they absorb the 
nutriment, thus depriving the tissues of necessary food, wait 
for demonstration. The results of infection vary in their 
manifestations. 
/ If the invading organisms remain at the point of entrance 

and produce local tissue changes, the condition is spoken of as 
a u'Oiind infection. 

If the invading bacteria become widely distributed in the 
circulation and tissues, the condition is known as septicemia or 
bacteremia. 
/ If the infecting bacteria remain at the point of entrance 

^ and multiply there, elaborating a toxin which is absorbed and 
which causes symptoms and possibly death, the condition is a 
toxemia. 

If there is a febrile condition, resulting from the absorp- 
tion of the products of putrefaction caused by saprophytic 
bacteria, the condition is called sapremia. 

If the invading organism is one possessed of definite 
pathogenic properties, such as the bacterium of anthrax, giv- 
ing rise to a definite series of symptoms and lesions, the affec- 
tion is designated a specific, infectious disease. 

Through the agency of metastasis, invading microorgan- 
isms may be carried from the point of introduction to other 



4 INFECTION 

parts of the body, where they may become localized, multiply, 
and give rise to any one of many forms of lesions. It may 
happen that the point of entrance is so obscure that the result- 
ing morbid changes are not easily traced to an external 
infection. There are many illustrations of this in comparative 
pathology, such for example as suppurative cellulitis. For 
convenience in discussion, infections may be divided into two 
clinical groups, namely : wound infections and specific infec- 
tious diseases, although in certain instances they cannot be 
separated. 

In arriving at a clear understanding of the nature of infec- 
tions, it is well not to be too closely circumscribed by classifi- 
cations. It is better to look upon them as a series of processes 
going on in the animal world due to the activities of infecting 
or parasitic microorganisms. In other words, the lesions fol- 
lowing an infection are simply the results of parasitism. 

In the study of the various forms of infection in the lower 
animals, lesions have been found to contain, apparently as their 
causative factors, bacteria which suggest at least that certain 
of the supposed saphrophytic organisms may, under certain 
conditions, become parasitic and cause infections resulting in 
more or less local or general disturbance. Many lesions seem 
to be produced by bacteria which are harbored normally upon 
the skin. When these organisms are introduced by accident 
into the living tissues they multiply and acquire, if they did 
not already possess it, the power to produce tissue changes. 
We cannot, therefore, dismiss the subject of infection without 
a passing consideration of the possible etiological significance, 
under certain conditions, of many species of bacteria ordinarily 
considered harmless with which the animal body is constantly 
surrounded. In the search for the cause of many lesions sup- 
posed from their nature to be infectious, or in applying meth- 
ods for their prevention, it is well to take into consideration all 
microorganisms v/hich might possibly be the causative factors 
and not limit the search to the detection of the already recog- 
nized pathogenic species. Recent investigations point to the 
conclusion that domesticated animals frequently suffer as the 



CHANNELS OF INFECTION 5 

result of the invasion of bacteria at present not listed among 
the pathogenic microorganisms, and what is true in this regard 
for bacteria, may be hypothetically applied to the higher fungi 
and to the protozoa. 

§ 3. Channels of infection. There are a number of 
ways by which microorganisms may be introduced into the 
living tissues of the animal body. The more common of these 
are as follows, namely : 

1. Through the digestive tract. Bacteria gain entrance 
into the tissues from the digestive tract where they have been 
brought with the food or water. It is not clear in all cases 
how the invading organisms get into the tissues from the 
intestine. It has been demonstrated that tubercle bacteria will 
pass through the mucosa with fat globules in the process of 
digestion and absorption. 

2. Through the respiratory tract. Bacteria are taken into 
the lungs with the inhaled atmosphere. Pulmonary tuber- 
cular affection is often brought about in this way. 

3. Through abrasions of the skifi or intestinal mucosa. 
The wide distribution of bacteria in nature renders it highly , 
probable that in all wounds of the integument microorganisms 
will reach the fresh tissues. They may come from the cutting 
or tearing implement, the particles of dirt which may fall into 
or upon the cut surface, or from the ducts of the glands of the 
skin itself. It may happen that the fresh tissues thus exposed 
are infected with one or several species of bacteria. It may 
be that one or more of these species may be destroyed by the 
living juices of the body or by the leucocytes, or again it is 
possible that, from their saprophytic nature, they may not be 
able to multiple in this new environment ; in either case the 
infection is of no significance and clinically would not be 
recognized. It may happen that only one species of the infect- 
ing bacteria multiplies and produces the morbid changes. 
This would be a single infection. If, however, two or more 
species cooperate in the production of the lesions, it is called 
a mixed infection. This term is often used to designate the 



6 WOUND INFECTION 

condition where one species may be responsible for the tissue 
changes, although other bacteria are present but only in an 
accidental or passive way. 

4. Through the generative organs. Infection of the 
reproductive organs takes place in certain instances where they 
are the seat of the disease. This is especially true in case of 
maladie du coit. 

5. Through the agejicy of insects. Some insects carry the 
virus of certain diseases from the infected and introduce it into 
the susceptible individuals. Thus the mosquito carries the 
Plasmodium of human malaria, the cattle tick the piroplasma 
of Texas cattle fever, and flies are often the introducers of 
pathogenic bacteria, such as those of anthrax. In certain 
instances, as with malaria, a part of the life cycle of the micro- 
organism takes place in the body of the carrying insect. 

6. Transmission of the virus from the parent to the fetus. 
Occasionally the young of diseased parents are born infected 
with the disease with which one or both of its parents were 
suffering. In these cases the specific bacteria were transmitted 
either from the sire at the time of coition, or later to the fetus 
in the uterus from the dam. It is important not to confuse 
these rare cases with those in which the offspring are born 
uninfected but subsequently contract the disease. Many of 
the so-called hereditary diseases are the result of post-natal 
infection. 

§ 4. \A^ound Infection. Wound infections are the direct 
results of the entrance of certain microorganisms into trau- 
matisms and operative incisions. They fall very naturally 
into two classes: 

1. Those infections producing local, acute or more 
chronic inflammatory processes usually leading to suppuration 
and finally healing by granulation. This is the form most 
frequently encountered clinically. The tissue changes are 
those of acute or chronic inflammation. 

2. Infections which may in the beginning appear like 



WOUND INFECTION 







the first or cause so little disturbance as to be unnoticed at the 
time, but sooner or later result in a local or remotely situated 
lesion or lesions. Frequently these are recognized as distinct 
diseases although in some cases, such as scirrhous cord, the 
origin is easily traced to 
an operation where infec- 
tion was possible. This 
group of wound infec- 
tion lesions, such as 
scirrhous cord, botryo- 
mycosis, infectious cel- 
lulitis of cattle and sheep 
and still other disorders 
may not appear to be 
dependent upon wound 
infection ; but the results 
of recent investigations 
suggest this as their pri- 
mary cause. These affec- 
tions will be treated sep- 
a r a t e 1 y in subsequent 
paragraphs but their re- 
lation to wound infec- 
tion renders them worthy 
of note in this connec- 
tion. 

In wound infection, 
the invading organism 
is not always of the same 
species. It is because of 
the fact that wound in- 
fection lesions of a similar character anatomically may be 
caused by a number of different bacteria that they cannot be 
classed among the specific infectious diseases. It is observed 
further, that in many of these lesions two or more species have 
been responsible for the results. There is no symptom, or 
manifestation of tissue changes, bv which one can determine 



Fig. I. Wound infection. Purulent in- 
tiltralion from the ivall of an abscess in 
a horse shoiving the infiltration of the 
intermuscular tissue 7vith pus corpuscles. 
Draii'ing made icith i inch ocular and 
-S objective. 



8 



WOUND INFECTION 



the specificity of the exciting cause. If this is done, it 
requires a bacteriological examination. 

Another class of diseases that are sometimes called 
wound infections should be mentioned, namelj-, those specific 
diseases, such as tetanus and symptomatic anthrax, where the 
virus is supposed always to be introduced through a wound 
either in the skin or mucous membranes. 

Bacteria causing wound infection. A large number of 
species of bacteria and a few fungi are included among the 




Fig 2. Micrococcus pyogoies aureus. Drai^iug from a cover- 
glass preparation of a bouillon culture. Highly magnified. 



organisms which are known to produce wound infections in 
animals. Usually, however, the forms encountered are micro- 
cocci, especially those belonging to the staphylococcus group, 
streptococci, Bacillus pyogenes (Bacillus pyogenes bovis 
(Grips) Bacillus pyogenes suis (Kiinnemann) ), a few other 
bacilli, especially those belonging to the colon group and a 
few species of the genus pseudomonas. Fungi and protozoa 



WOUND INFECTION 9 

are rarely found in acute wound infection lesions excepting 
in specific diseases which they cause and where their entrance 
is through injuries or by means of the bites of insects. Many 
of the specific pathogenic bacteria may be introduced through 
wounds. As a rule, it seems to be true that in the domesti- 
cated animals, as in man, the pyogenic bacteria are the most 
common and important wound infecting microorganisms. In 
open wounds these are, of course, associated with a very large 
number of ordinary saprophytic bacteria. Frequently in 
closed lesions nonpathogenic organisms are present in addition 




Vie 3. Streptococcus pyogenes. Draiving made front a cover-glass 
preparation from a bouillon culture. Highly magnified. 



to the seemingly causative factors. It is worthy of note that 
it appears to be impossible to predict from the general charac- 
ter of the lesions, the kind of bacteria which are producing 
them, except it be in case of infections like tuberculosis or 
actinomycosis. These bacteria are usually recognized without 
trouble in cover- glass preparations made from the lesions. 



lO WOUND INFECTION 

Their species can also be easily determined by cultivating- 
them on artificial media/ 

Morbid anatomy of infection. The tissue changes resulting 
from an infection of the body with various microorganisms 
belong with those considered in general pathology under the 
headings of inflammations, degenerations, other retrograde 
disturbances and regenerative processes. The pathology of 
infection, therefore, is not a discussion of new deviations or 
disturbances of cells and fibers, but rather a grouping or com- 
bining of disturbances already recognized as the selective 
results of the activities of the particular invading organisms. 
Thus in ordinary wound infections the morbid changes are 
those of an acute inflammation leading to suppuration, necrosis 
or gangrene ; sometimes they are chronic in nature, resulting 
in formative changes, and again in the various forms of exuda- 
tion. In other instances infection results in hemorrhages of 
varying degrees. Occasionally the lesions may become local- 
ized, as in pneumonia, lymphangitis, intestinal ulcers, nephri- 
tis, hepatitis, splenitis and the like. The morbid anatomy of 
infection introduces few if any changes not known to general 
pathology. Because of this, the emphasis of the pathology of 
infection rests on the etiology and the possible variety and dis- 
tribution in the body of the tissue changes. It has been 
shown that certain infections are slow in bringing about tissue 
changes and consequently many lesions resulting from wound 
infection may, when they appear, be considered as distinct 
maladies. 

Preveyition of infectioji. In surgical operations, wound 
infection may be prevented where uninfected lesions are 
involved by disinfecting the field of operation. This is a much 
more difficult task than it appears. The habit of- bacteria of 
growing down into the hair follicles, sweat glands and beneath 
the dead epithelial cells on the surface, renders it necessary 
to use a disinfectant of much penetrating power in order to 



'For the specific cultural characters of each of the wound infection 
icteria the student is referred to manuals of bacteriology. 



A SPECIFIC INFECTIOUS DISEASE II 

sterilize the skin. In case of traumatic infection the wound 
itself must be disinfected. 

ij 5. A specific infectious disease. A specific infec- 
tious disease is the result of the multiplication within the animal^ 
body of a single species of microorganism. The lesions may 
be local or general, but the cause producing them is always 
the same. Thus, Bacterium ayithracis will produce a disease 
which is called anthrax, no other cause can produce it, and no 
matter how much the lesions may vary in different individuals 
if they are produced by this species of bacteria the disease is 
anthrax. It is clear, therefore, that there is no hard and fast 
line between a simple (single) wound infection and a recog- 
nized infectious or epizootic disease, except in the nature of the 
invading organism. The course of the disease may vary in 
different individuals and usually it does, especially if in differ- 
ent species of animals. If a man receives accidentlly a cut 
from a knife with which he is making a post-mortem on an 
animal dead from anthrax, the lesion is liable to be restricted 
to the point of inoculation, and while it is anthrax (malignant 
pustule) it would often be recognized as a simple wound infec- 
tion. If this accidental inoculation should occur in a guinea 
pig, the disease would not be recognized as a local lesion : but 
the animal would develop septicemia. 

As a class the specific diseases are differentiated from the 
lesions known clinically as wound infections in a number of 
ways. The bacteria of the epizootic diseases do not ordinarily 
produce wound infections following accidental injuries or sur- 
gical operations, although there are exceptions. Again, there 
is usually a difference in the mode of infection. The virus of 
the epizootic diseases is ordinarily introduced through the 
digestive or respiratory tract or by means of insects, while in 
wound infection the virus is introduced, as the term implies, 
through the injured integument or mucosa. 

i^ 6. The differential characters of a specific infec- 



'Plants suffer from specific infectious diseases caused by bacteria 
and fungi, quite as much as animals. 



12 A SPECIFIC INFECTIOUS DISEASE 

tious or epizootic disease. It is very important not to mis- 
take for an infectious disease some form of bodj' disturbance 
due to a local cause or condition. Animals often suffer from 
improper food and the conditions of life under which they are 
compelled to live. It frequently happens that as all ot the 
animals in a given herd are subjected to like conditions, a 
number of them, perhaps all, will manifest very similar symp- 
toms and more or less of them die. Such an occurrence often 
gives rise to the supposition that the cause of death is some 
form of infection. Deaths from such causes or under such 
conditions should be carefully distinguished from an epizootic. 
In differentiating a non-infectious disorder from a specific dis- 
ease, it is important, and usually sufficient, to take into 
account the appended characteristics of an infectious disease. 

1. Cause. An infectious disease is caused by a specific 
agent. This necessitates as the first requisite an exposure to 
and an infection with the specific organism. 

2. Period of incubation. The infection must be followed 
by a certain period of incubation before the development of 
symptoms. This is the time necessary for the invading micro- 
organism to become established in the body and to bring about 
the first symptoms of the disea.se. The incubation period var- 
ies in different diseases, and to a certain degree in the same 
disease, according to the mode of infection and the resistance 
of the individual. Usually the incubation period of a given 
disease is practically the same for all individuals of the same 
species when subjected to the same mode of infection. Ex- 
ceptions, however, are not rare. 

3. Lesions. The morbid anatomy of an infectious dis- 
ease is usually nearly the same in animals suffering in the 
same outbreak, especially when they were infected at or about 
the same time. It is more common for only a few individuals in 
a herd to be infected in the beginning and from these first cases 
for other animals to contract the disease. In many epizootics, 
the disease appears in an acute form in the first animals 
attacked while those infected later in the course of the outbreak 
suffer from a chronic form of the affection. In other outbreaks 



DIFFERKNTIATION 1 3 

the first cases are chronic in nature and the later ones acute. 

4. Dnrafio7i. In animals, as in man, most of the infec- 
tious diseases are self limiting, but, as a rule, the percentage 
of fatal cases is much larger among animals than in the human 
species. The period of convalescence is not so well marked in 
the lower .«;pecies as in man. It frequently happens that the 
course of the disease is so changed that an acute case which 
appears to recover, or at least to pass into the stage of con- 
valescence, becomes chronic or subchronic in nature and 
eventually terminates in death. The lateness in the develop- 
ment of the modified lesions often causes the nature of the ter- 
minal disease to go unrecognized. 

5. Trafismission by hioculation. Finally, it is necessary 
in making a positive diagnosis to find the specific organism, 
or to prove the transmissibility of the malady from the sick or 
dead to healthy animals. The extent of the spread of the 
virus of the disease through the available channels for its dis- 
semination will also aid in determining the infectious or non- 
infectious nature of the malady in an outbreak among 
animals. 

In diagnosing an epizootic disease investigations have 
shown that too much reliance can not be placed on the period 
of incubation, or the morbid anatomy. There are many pos- 
sibilities, therefore, that an erroneous diagnosis may be made 
when the clinical and post-mortem evidences of the disease are 
alone considered. It has also been determined that certain 
non- infectious disorders often assimilate, in their more general 
manifestations, the characters of infectious maladies. This 
fact necessitates much care in the differentiation of outbreaks 
of animal diseases. 

The dietary and other non-infectious disorders do not 
exhibit definite, uniform differential characters excepting per- 
haps in case of those caused by a few mineral poisons or by 
eating certain plants. As examples of the.se, lead poisoning 
and the Pictou or Winton disease of horses and cattle caused 
by eating a ragwort {Stmea'o jacoboea) may be mentioned. 
The non-infectious disorders are differentated from the infec- 



14 DISSEMINATION 

tious ones largely by eliminating the characters of the latter 
and finding, if possible, the causative agent. 

The necessity for an early and positive diagnosis in all 
outbreaks of epizootic disease, is to assure the enforcement of 
all possible measures to prevent its spread. The essential 
problem for the practitioner or sanitarian in the presence of 
these diseases, is to restrict the number of cases to the indi- 
viduals already infected. In order to do this, it is of much 
importance that modified or chronic cases of any infectious 
disease should not escape detection if there is danger of their 
spreading the virus or exposing susceptible animals. 

§ 7. Dissemination of infectious diseases. Al- 
though the discussion of the means by which each of the vari- 
ous diseases are disseminated will be found under the considera- 
tions of the individual affections, it is important to consider 
the general ways and means by which these different vital 
causative factors are spread from an infected individual to a 
non-infected one in the same herd and from one herd to 
another. As we understand them at the present time, each 
virus is dependent for its perpetuation upon its escape from 
one host (sick or dead) to another. As these organisms are 
without power of their own for such migration, they are depend- 
ent upon other forces and carriers to take them. In finding 
the cause of their spread, we must consider first how they 
escape from the infected individual and secondly how they are 
carried rom one individual to another. 

1. Escape of virus from infected individuals. The infect- 
ing organisms escape from the living body either with (a) the 
excreta, (b) the external discharge of ulcers and abscesses or 
both, and (c) the blood by sucking and possibly biting insects. 
After the death of the host they can escape only by the dis- 
integration of the dead body or by its being consumed by 
other animals or birds. The bacteria of several diseases 
can pass through the digestive tract of such animals un- 
injured. 

2. Dissemination of infectiyig orga7iisms. Pathogenic 



DISSEMINATION OF INFECTION I5 

bacteria are spread after they escape from the body in many 
ways, the following being the most common : 

(a.) By direct contact. 

(b.) They are carried on the hands, shoes or clothing 
of attendants, and on farm implements, such as shovels and 
hoes. 

(c.) They are carried in streams receiving the excreta 
or disintegrating bodies of the infected. 

(d.) They are scattered with the excreta of birds that 
feed upon the dead carcasses. Other animals, such as dogs 
and foxes, are also charged with the scattering of the virus by 
the same method. 

(e. ) The virus is often carried from one herd to another 
by introducing chronic cases or those already infected in which 
the symptoms have not yet appeared. 

(f.) Animals are often infected by shipping them in cars 
or crates that have previously contained diseased animals and 
that have not been thoroughly disinfected. 

(g. ) The pathogenic protozoa are transferred from 
infected to non-infected individuals by means of insects. They 
are carried from place to place in infected animals. 

§ 8. Cause for the variations in the course of an 
infectious disease. It is a recognized fact that there is much 
variation in the course of infectious diseases in different epizo- 
otics and often marked individual variations occur in the same 
outbreak. In explaining this interesting phenomenon, it is 
important to take into account the question of individual 
resistance or immunity,— partial or more complete. It was 
found in case of certain diseases that when an individual was 
partially immunized and then infected, that the lesions were 
very much modified. The teachings of a specific etiology 
point to this phenomenon as a result of certain biological or 
vital differences existing either in the parasite or in the host, 
possibly in both. The results of the investigations already 
made along this line suggest as a probable explanation, that 



l6 CAUSE FOR VARIATION 

the course of the disease varies on the one side with the resist- 
ance of the host and on the other with the degree of virulence 
of the infecting microorganism. This has been expressed in 
the formula 

-^ 

in which D = the disease, V - - the virulence of the infecting 
organism, and R ^- the resistance of the host or the individual 
attacked. As V or R change the disease is modified. For 
example, rabbits that are partially immunized against swine 
plague bacteria, when inoculated with a virulent culture of 
that organism, will live for several days and perhaps for weeks, 
and then die of peritonitis, pleuritis or extensive pus forma- 
tions, instead of perishing within twenty- four hours with sep- 
ticemia as they would if they had not been protected against 
this organism. In chronic cases of swine plague, as found in 
certain outbreaks, the bacteria are often attenuated so that 
when inoculated into susceptible rabbits the result is the same 
as when the rabbits protected by partial immunization were 
inoculated with virulent cultures. The above simple formula 
which was worked out and demonstrated for certain swine 
diseases seems to apply to infectious diseases generally. 

§ g. Classification or grouping of the infectious dis- 
eases. It will be found in the study of the morbid anatomy 
of the various specific maladies that the lesions in a given dis- 
ease vary in different species and in individuals of the same 
species to a marked degree. This fact precludes the possibility 
of classifying or arranging them after their morbid anatomy, if 
the idea of a specific etiology is to be adhered to. If the infec- 
tious diseases are to be considered as parasitisms, as they 
appear to be, the only logical method of classifying them, 
according to the writer's opinion, is the one suggested by their 
etiology, namely, that they shall be placed in groups corre- 
sponding to their causes. Thus a single lesion found in the 
glands of the head, in the lungs, in the liver, in the mesenteric 



CAUSE FOR VAKIATION 



17 




Fig. 4. Large abscess in partially immunized rabbit caused by sivine- 
plague bacteria. This rabbit lived 37 1 days after its inoculation with 
virulent swine plague bacteria. At death its -weight zvas 19S0 grams\ 
the tumor itself iveighing goo grams. 'J he abscess Jormed dorsad 0/ the 
peritoneum. [a) Cecum, [b] intestines, (c) abscess. The control rab- 
bit of same iveight and age died of septicemia in 16 hours. 



l8 CLASSIFICATION OF DISEASES 

glands, in the skin, in the joints, or in the generative organs, 
would be called tubercular if the bacteria of tuberculosis could 
be demonstrated to be its cause. The same conclusion would 
be maintained regardless of the character of the lesion, 
whether cellular, purulent, caseous or calcareous. These facts 
are enough to suggest that the most direct method of arrang- 
ing these diseases for purposes of study is in groups composed 
of like generic etiological factors. 

Most of the known specific causes of the infectious dis- 
eases of animals are bacteria. It is necessary, therefore, in 
carrying out this plan to choose from among the numerous 
classifications one to be followed in grouping the diseases ac- 
cording to the genera of bacteria producing them. Of the 
various systems, the one by Migula seems to be the simplest 
and most natural and consequently it is selected. The only 
radical difference between it and the others, so far as pathol- 
ogy is concerned, rests in the fact that the old genus Bnderiu?n 
is revived, but with a new meaning. All rod-shaped, non- 
motile bacteria are placed in this genus. This causes a change 
of the generic name from Bacillus to Bacterium of a number of 
pathogenic bacteria, such as those of tuberculosis, anthrax, 
swine plague and others of less importance. 

Because of the few species of fungi and protozoa that 
are pathogenic for animals, systematic classifications of these 
organisms are not introduced. For such classifications the 
student is referred to the various works^ou mycology for the 
fungi and the excellent work by Calkins, — " The Protozoa" 
for the protozoa. In this elementary pathology, all that seems 
to be necessary concerning the biology and classification of the 
pathogenic protozoa will be given in connection with genera 
and species under the " etiology ' ' of the diseases they produce. 

The chapter on diseases caused by fungi naturally fol- 
lows those on the bacterial diseases. 

§ ID. Migula's classification of bacteria. The genera 
of the five families are incladed. 



migula's classification of bacteria 19 

MIGULA'S CLASSIDCATION 

LOWER BACTERIA 



COCCACCAC 



Streptococcus 

Mtcrococcus 

Sarcma 

Planococcus 

Planosarcma 

Bacterium 

Bacillus 

Pseudomonas 

Spirosoma 
Mlcrospira 
Spirillum 
Spirochaeta 



,»»u 



• •••• 00 0000 



•• 5^ @.*. A-jJiflgj 



urn 



BACTERIACEAE 



#(^ 7f ^ 



SPIRILLACEAE 




MIGULA S CLASSIFICATION OF BACTERIA 



FAMILIES. 

I. Cells globose in a free state, 
not elongating in any direc- 
tion before division into 1,2, 
or 3 planes i. 

II. Cells cylindrical, longer or 
shorter, and only dividing in 
I plane, and elongating to 
twice the normal length be- 
fore the division. 

(i) Cells straight, rod-shaped, 
without sheath, non-motile, 
or motile by means of fla- 
gella 2. 

(2) Cells crooked without sheath 3. 

(3) Cells enclosed in a sheath 4. 

(4) Cells destitute of a sheath, 

united into threads, motile 
by means of an undulating 
membrane 5. 



Coccaceae. 



Bacteriacese. 
Spirillaceae. 
Chlamydobacteriaceae. 



Beggiatoaceae. 



I . Coccacete. 



Cells without organs of motion. 

a. Division in i plane i. 

b. Division in 2 planes 2. 

c. Division in 3 planes 3. 

Cells with organs of motion. 

a. Division in 2 planes 4. 

b. Division in 3 planes 5. 

2. Badcriaccie. 

Cells without organs of motion, i. 
Cells with organs of motion 

(flagella). 



Streptococcus. 

Micrococcus. 

Sarcina. 

Planococcus. 
Planosarcina. 



Bacterium. 



migula's classification of bacteria 

a. Flagella distributed over 

the whole body 2. Bacillus. 

d. Flagella polar 3. Pseudomonas. 

3. Spirillacece . 

Cells rigid, not snakelike or flex- 
uous. 

a. Cells without organs of 

motion i. Spirosoma. 

b. Cells with organs of mo- 
tion (flagella). 

1. Cells with one, very 
rarely 2-3 polar fla- 
gella 2. Microspira. 

2. Cells of polar flagella, 

in tufts of from 5-20- - 3. Spirillum. 

Cells flexuous 4- Spirocha^ta. 



4- 



ChhxDiydobactcriaceae. 



Cell contents without granules 
of sulphur. 
A. Cell threads unbranched. 

1 . Cell division always only 

in I plane i. Streptothrix. 

2. Cell division in 3 planes 
previous to the forma- 
tion of conidia. 

a. Cells surrounded by a 
very delicate, scarce- 
ly visible sheath 

(marine) 2. Pliragnudiothrix. 

b. Sheath clearly visible 

(in fresh water) 3. Cretwi/trix. 



22 miguIvA's classification of bacteria 

B. Cell threads branched 

(pseudo- branches) 4. Cladothrix. 

Cell contents containing sul- 
phur granules 5. Thiothrix. 

5. Beggiatoaceae. 

Only one genus known {Beggiatoa Trev.), which is 
scarcely separable from Oscillaria. Character as given under 
the family. 

REFERENCES. 

1. Berger. Vergleichende Untersuchungen iiber den Bacillus 
pyogenes bovis und den Bacillus pyogenes suis. Zeitsch f. Iiifektiou- 
skrankh. parasitare k'raiikh. und Hygiene der Haustiere, Bd. Ill 
(1907), S. loi. 

2. Grips. Ueber eine mit multipler Abszessbildung verlaufende 
Pleuritis und Peritonitis der Schweine und deren Erreger. Zeitschr. f. 
Fleisch- u. Milchhygiene, iSgS. 

3. Grips. Ueber einen pyogenen Mikroorganismus des 
Schweines. Inaugural-Dissertation. Giessen, 1902. 

4. KiJNNEMANN. Ein Beitrag zur Kenntnis der Eitererreger des 
Rindes. Arch. f. zviss. u. prakt. Tierheilk., 1903. 

5. MiGULA. System der Bacterien. 1897. 

6. vSmith and Moore. On the variability of the infectious dis. 
eases as illustrated by hog cholera and swine plague. Bulletin No. 6. 
U. S. Bureau of Animal Industry, 1894. p. 81. 

7. Welch. General bacteriology of surgical infections. Dennis^ 
System of Surgery. Vol. i , p. 249. 



CHAPTER II. 



DISEASES ATTRIBUTED TO WOUND INFECTION. 



§ II. Lesions which may be caused by several 
organisms that are recognized as distinct maladies. It 
has already been stated that the lesions following wound 
infections may be brought about by a variety of bacteria and 
also that certain of these disease processes are sometimes 
recognized as distinct maladies. There are a number of affec- 
tions which belong to this class. From some of these, such as 
botryomycosis, a supposedly specific organism has been isolated 
and described. A number of workers, however, have found 
that other bacteria may produce apparently the same morbid 
conditions. The more important of the affections which seem 
to be directly traceable to wound infection will be briefly de- 
scribed in the light of recent investigations. It should be 
stated, however, that the amount of work that has been done 
on these subjects is not sufficient to preclude the possibility of 
a specific etiological factor, but rather to suggest the lines 
along which valuable and more conclusive findings may be 
expected in the future. 



§ 12. Botryomycosis, This name has been given to a 
variety of lesions found more commonly in the horse but oc- 
curring also in cattle, swine and other animals. The thickened 
spermatic cord (scirrhous cord) which sometimes follows cas- 
tration is the most common form of this disease. Practitioners 
often designate as botryomycosis certain closed abcesses occur- 
ring in the subcutaneous or intermuscular tissue. Abscesses 
and nodules found in the internal organs have been included 
under this caption. Several investigators have isolated from 



24 BOTRYOMVCOSIS 

these lesions a species of microorganism which appeared to 
stand in a causative relation to them. It was first described as 
Zobgloea pulmonis equi, in 1870, b}^ Bollinger who found it in 
the nodules in the lungs of a horse. More recently he re- 
named it Botryococcus ascoformans. Rivolta designated it Dis- 
comyces equi. Rabe proposed the name Mkrococais botryogenes 
and Johne has called it M. ascoformans. The results of other 
investigations throw some doubt upon the specific nature of 
these lesions. Kitt, Hell, dejong, Gay and others have found 
in them micrococci which do not differ from M. pyogenes aureus. 
The writer has failed to find M. ascoformans but has isolated 
in its stead pyogenic micrococci and streptococci. In one very 
interesting case of thickened cord, the writer found masses of a 
fungus resembling that of actinomycosis within the pockets of 
spongy tis.sue sprinkled throughout the thickened fibrous cord. 
Bacteria was not found in this case. 

In the closed abcesses in the connective tissue, pyogenic 
bacteria have been found, excepting in certain cases of long 
standing where the cultures give negative results. Investi- 
gations which have been made into the bacterial flora of the 
skin of the horse show that pyogenic bacteria are frequently 
present in the deeper layers of the epidermis, in ducts of glands 
and about the hair shafts. With the possibility of infection 
from the integument plus all the other chances of having 
members of this and other groups of bacteria introduced into 
the body there seems to be abundant opportunity for infection 
wnth a variety of species. The evidence at hand points to the 
conclusion that botryomycosis is the result of wound infection, 
and that several species of microorganisms are capable of pro- 
ducing it, especially the form known as scirrhous cord. 

The source of infection in the cord is to be found in the 
unsterilized or non- disinfected skin, improperly sterilized in- 
struments, dressings, and hands of operator. For precautions 
to be observed in disinfecting the skin see chapter on disinfec- 
tion. The fact is worthy of note in this connection, that sep- 
ticemia, peritonitis, and other more distantly localized lesions 
occasionallv follow such infections. 



OMPHALOPHLKBITIS 



^13. Omphalophlebitis. This affection which is com- 
monly called navel- ill, consists of suppurative lesions in young 
animals caused by pyogenic bacteria. In the horse they are 
most often localized in the joints of the limbs. In certain other 
species the lesions are quite as likely to be situated elsewhere 
in the body. In some cases the morbid changes are restricted 
to subcutaneous and intermuscular suppurative cellulitis. 

The infection takes place in the umbilicus. As the cord 
is severed in the field or stable many species of bacteria may 
gain access to the end of the exposed and freshly severed cord. 
In the colt a streptococcous seems to be the most common 
species of bacteria capable of producing the joint abscesses. 
In the lamb, a variety of the colon bacillus has been associated, 
apparently as the etiological factor, with the subcutaneous 
cellulitis. The lesions resulting from navel infection illustrate 
in a most excellent manner the extent to which certain pyo- 
genic bacteria gaining access to the body may extend by 
metastasis to places remote from their entrance and produce 
diseased foci. 

In the case of navel-ill. the umbilical vein contains a large 
number of bacteria. The writer has found that in colts very 
few if any of the bacteria (streptococci) producing the joint 
lesions could be found in the parenchymatous organs. Occas- 
sionallv one or two of many tubes of media inoculated from 
the liver would develop into cultures of the infecting organism. 
In this disease, where many species of bacteria come into com- 
petition, one is impressed with the fact that seemingly very 
few of the ordinary bacteria are capable of gaining an entrance 
into the circulation or, at least, are possessed of vital powers 
sufficient to resist the destructive forces of the living animal 
body A brief description of a case with the bacterial findings 
win illustrate this point. The case referred to was from Dr. 
Williams' clinic. 

A colt, about three years old. It was in good condition ^^^^^^^^^'f 
to be perfectly well excepting for the diseased joints. It was killed tor 



26 WHITE SCOURS IN CALVES 

examination. The umbilical vein, from the umbilicus to the liver, was 
distended with blood, pus cells and bacteria. All the internal organs 
appeared to be normal. In both knee joints, and in one hock joint there 
was extensive suppuration. A bacteriological examination showed the 
umbilical vein to contain many species of bacteria, among which may be 
mentioned B. coli coniinunis^ Micrococcus pyogenes aureus and a strep- 
tococcus. One of several tubes of media inoculated from the liver de- 
veloped the streptococcus, the others remained clear. All media inocu- 
lated from the heart blood, spleen, kidney and glands remained sterile. 
All of the media inoculated with the pus from the diseased joints gave 
pure cultures of the streptococcus. 

The treatment in these cases is limited to the prevention. 
The proper disinfection and dressing of the umbiHcus at the 
time it is severed prevent this trouble. It is the only pre- 
ventative measure known to us. 



§ 14. W^hite scours or diarrhea in calves. This is 
a disease affecting calves from a few hours to as many days 
old, with a mortality ranging from 50 to 90 per cent. The in- 
vestigations which have been made in this country, especially 
those at the New York State Veterinary College, have sug- 
gested that it is due to certain forms of the colon bacillus. In 
these investigations characteristic lesions were not found. 

Nocard reported the results of his investigation of appar- 
ently a similar disease of calves in Ireland. He found that 
they usually die during the first week. In the more chronic 
cases, lung lesions were found. His inquiries tend to show 
that this is primarily due to a wound infection. He states in 
his report concerning the nature of this disease that it usually 
lasts from 3 to 6 days and is characterized by an intense intes- 
tinal discharge. The discharges are always of the nature of a 
diarrhea, white and frothy. The calves lose flesh rapidly, 
their flanks are hollow, abdomen retracted, back arched, eyes 
sunken, and hair dull ; they make violent expulsive efforts, 
the nose is hot and dry with slight discharge of mucus, and 
the temperature is elevated. 

In other cases, but not so commonly, the symptoms are 



WHITE SCOURS IN CALVKS 



27 



less severe and recovery seems to take place ; but most of the 
calves die several weeks later with pulmonary lesions. 

Nocard states that it is not rare to see, in these cases, 
the discharges mixed with blood in various quantities. In 
more chronic forms it is not rare to observe acute, multiple and 
very painful arthritis. 

The lesions found at the autopsy vary according to the 
course of the disease. Usually the umbilicus is large and the 
umbilical blood vessels have indurated walls, and contain 
blood clots which may be soft and purulent. Bloody extrav- 
asations are observed, sometimes ver\' extensive, along the 
umbilical vessels and the urachus, extending sometimes to 
the posterior third of the bladder. 

In rapidly progressing cases, lesions of true hemorrhagic 
septicemia are found. All the organs are congested ; their 
surface is covered with petechiae, ecchymoses or sub-serous 
blood infiltrations ; the capillary network of the peritoneum, 
the omentum, the pleura and the pericardium is very much 
injected. 

Nocard describes the lungs and articular lesions as follows : 

"The lungs are rarely entirely healthy ; most often they 
present here and there little diffuse centers of catarrhal pneu- 
monia, nodular broncho-pneumonia or only of atelectasis. The 
lesions are much more constant, extensive and dense when the 
animals have resisted longer ; they represent then the transi- 
tion between the simple atelectasis of the beginning and the 
suppurative lesion of lung disease. 

"Articular lesions, when they exist, are very interesting. 
The periarticular tissues are infiltrated with yellowish and 
somewhat gelatinous liquid ; the synovial serous membrane is 
covered with a rich vascular injection, which seems to extend 
to the borders of the cartilages of the articular surfaces ; the 
culs-de-sac of the synovials are distended by a great quantity 
of thick and limpid synovia, strongly yellow or reddish in 
color, and in which more or less dense and abundant clots ot 
fibrinous exudate are floating. When the lesion is older, 
instead of synovia, there are thick, dense, and firm fibrinous 



28 WHITE SCOURS IN CALVES 

exudates, which fill the culs-de-sac of the serous membrane 
and are infiltrated between the articular surfaces. In these 
cases the lesion resembles exactly those of peripneumonic 
arthritis of sucking calves." 

He found a microorganism (Pasteurella) in the organs 
and blood of the calves, with which he was able to produce 
the disease. After convincing himself that he had found the 
cause, he sought for the source of infection, which he found 
in the umbiliais. He advances three suppositions concerning 
the time and mode of entrance : i. intra-uterine, 2. vaginal, 
3. after delivery when the calf drops on the ground or floor 
and when the ruptured cord conies in contact with the fecal 
matter or dust of the stable. The latter he believes to be the 
actual method. His conclusion concerning infection after 
delivery may be summarized in the following observation 
which he makes : 

" We have witnessed in a well kept farm a case of labor 
in a cow. She was in an ordinary barn. Nothing had been 
prepared to receive the new-born. The calf was dropped on a 
bedding soiled with feces ; he only fell back a little, and there 
during 15 or 20 minutes, we watched him making his efforts 
to get up, falling back here and there to the right and to the 
left or on his belly, dragging the stump of his cord on the 
ground, in the urine, or even in the fecal matter. It was only 
after the mother had well licked her little one, well covered 
with salt, that the cord was ligated. I am not sure that the 
umbilicus was cleaned. 

" White scours is ordinarily the result of iDnbilical infection 
which takes place at the time of delivery, by the way of the 
wound made by the rupture of the cord." 

He states that this trouble can be prevented if the person 
in charge of the animals at the time of their delivery takes 
certain precautious to prevent infection. 

This disease described by Nocard does not seem to differ 
in many respects from the diarrhea in young calves in this 
country. Lesage and Delmar have described the disease in 
France. Ward and Fisher tested Nocard's method with quite 



SUPPURATIVE CELLULITIS 29 

satisfactory results In our cases the lung complications did 
not occur Our bacteriological examination of a number of 
young calves that died of this trouble showed that their blood 
and organs were teeming with a variety of B. coU communis. 
I have not found Bad. sept, hemorrhagicce (Pasteurella) in 
any of our cases. This suggests the possibility of serious 
umbilical infection with members of other groups of bacteria. 
The important finding of Nocard should stimulate further in- 
vestigation into this important trouble in this country. As 
the remedy which he recommends, and which has given good 
results is simplv one to prevent infection of the ruptured cord, 
the conclusion of the wound infection origin of this disease is 
strengthened. 



^ 15. Infectious suppurative cellulitis. Cattle and 
sheep suffer from more or less extensive inflammatory condi- 
tions of the subcutaneous tissues, especially of the lower 
extremities. Frequently the morbid process extends beneath 
the hoof, causing it to slough or to undergo resulting disinte- 
gration changes. When this condition exists, the affection is 
usually called "foot rot." If the inflammatory process attacks 
the skin also, the condition is often designated erysipelas. If 
it becomes circumscribed, resulting in a local suppuration an 
abscess or an ulcer is the result. The investigations which 
have been made concerning the cause of these lesions point to 
the conclusion that they result from an infection, probably 
through some slight abrasion of the skin. Thus far. the 
results show .streptococci* to be the etiological factors m the 
majority of these cases. It frequently happens that a number 
of animals subjected to the same conditions are attacked at the 
same time, giving rise to a condition resembling an epizootic. 

*Lu^et^s reported the results of bacteriologic examinations of 
fifty-two abscesses in cattle. From nine of these steptococci were 
obtained in pure culture, and in ten cases ^^ey were - -t-^^ ^ 
other bacteria.-^;/;/^/^.- de V Instilut Pasteur. Vol. I II(iS^3),P- .-^f- 



30 SUPPURATIVE CELLULITIS 

In cattle, — cases studied by the writer, — the lesions were, 
within certain limits, uniform in all of the affected animals. 
Usually but one foot or leg was attacked, although there were 
numerous exceptions. The first symptom noticed was a swell- 
ing, which usually appeared in the lower part of the leg, most 
often in the pastern. In some animals the swelling was re- 
stricted to a small area, but often it extended up the leg to 
and even above the knee or hock joint. There was evidence 
of pain. As the inflammator}' process continued, the subcutane- 
ous tissue became indurated, the skin thick and dry, and later 
it would crack, usually but not always, below the dew claws, 
and a thick creamy pus would be discharged. After discharg- 
ing, the swelling subsided and the normal condition was 
rapidly restored. The time necessary for the suppurative 
process and recovery to take place varied in different animals, 
but as a rule from ten to fifteen days were required. The 
exceptions were largely in those cases where the inflammatory 
process extended down to the coronary cushion. In these 
there was more or less sloughing of the hoof. These cases 
were the most serious. 

In the so-called foot-rot of sheep, we have, in the cases 
which have come to our notice, conditions similar to those 
found in the cattle which were suffering from suppurative cellu- 
litis. It may be of interest to cite a specific case with the 
result of the bacteriological examinations. 

May, 1899, two sheep that were suffering from so-called 
foot-rot were brought to Dr. Law's clinic. They came from a 
large flock in which forty or more animals were reported to be 
similarly affected. 

No. I. An adult female in very poor condition. All four feet and 
legs were affected and the nails on one foot were quite loose. There 
was a purulent discharge from openings either between the claws or in 
the skin just above the hoof. The microscopic examination of the pus 
from this opening showed a number of bacteria, but streptococci were 
especially numerous. They were not isolated in pure culture. The 
left knee was badly swollen and from the lower side of the swelling 
there was a discharge of thin purulent substance which contained strep- 



FisTULOiT.s \vithp:r.s 3! 

tococci in large numbers. A few other bacteria, mostl)" micrococci, 
were associated with them. 

No. 2. An adult female, black, emaciated, but in much better flesh 
than No. i. The two fore feet and the left hind one were affected. The 
hind foot and the right fore one were discharging. The left fore foot 
was badly swollen above the hoof but the swelling did not extend high 
up the leg. Fluctuation was marked. The skin was shaved, washed, 
disinfected and the abscess opened. A thick creamy pus was expressed. 
From this a number of tubes of media were inoculated and in each a 
streptococcus developed in pure culture. The pus from the discharging 
feet contained a streptococcus with other bacteria. The feet were 
treated locally with disinfectants by Dr. Law. In recovering there was 
considerable thickening of the interdigital tissue. In this case the 
suppuration had not extended under the nails. 



§ 16. Fistulous withers and poll-evil. Recent inves- 
tigations indicate that these very common and troublesome 
local diseased conditions are either directly or indirectly the 
result of bacterial invasion. This conclusion is tentatively 
drawn from the fact that the bacteriological examinations made 
from the pus and from recent lesions in these affections invari- 
ably reveal the presence of streptococci or micrococci, or both. 
Gaj' found a streptococcus in each of seven cases of common 
fistulous withers and in two cases of poll-evil. It was invari- 
ably a.ssociated with a micrococcus. He found in five cases of 
deep seated shoulder abscesses M. pyogenes aureus only. It is 
instructive to note, that bacteria closely resembling this organ- 
ism have frequently been found in the deeper layers of the skin. 
The mechanical injuries commonly attributed as the primary 
cause consist usually of little more than skin irritation from ill 
fitting harnesses, saddles or from blows. While these are 
mechanically not extensive, they are sufficient to liberate into 
the juices of the subjacent tissues the bacteria deeply seated in 
the integument. The inflammatory process leading to sup- 
puration, the formation of fistul^e, the new formation of fibrous 
tissue in the affected parts, and even the bone necrosis occa- 
sionally seen are all possible and rational results of the activi- 
ties of the pyogenic bacteria found in the lesions. There is 



32 



INFECTIOUS MASTITIS 



nothing in their character to suggest causative agencies other 
than microorganisms. The tissue changes involved in the 
deposition of fibrous tissue and the abscess formation are 
known as the results of infection and the inflammatory pro- 
cesses following them. These affections are mentioned in this 
connection simply because the accumulating evidence tends to 
strengthen the working hypothesis that they are the result of 
bacterial invasion. 



Cattle suffer frequently from 
an acute inflammation of the udder as the result apparently of 
an invasion by a number of bacteria. The results of the inves- 
tigation of this affection thus far reported suggest that the 
form which is transmitted from animal to animal is caused by 
a streptococcus. It is, however, 
difficult to distinguish between 
this affection and those caused 
by certain other bacteria. It 
t "••••' -j» ^ \ t seems likely that many cases are 

\ /^ i • * ,•••••••* primarily brought about by me- 

• '''''^. *To ••••••**>* • chanical injuries which render 

possible the entrance into the 
fresh tissues of the bacteria of the 
skin or of the milk ducts. Other 
cases may be due to infection 
through the teat of bacteria capa- 
FiG. 5. Streptococcics from a ^^j^ ^f producing, by means of 
case of infectious mastitis. , . ... j ^ ^-l • 

their metabolic products, the in- 
flammatory condition without a distinct injury to the mucous 
membrane. The former view that there was a sphincter mus- 
cle near the base of the teat which closed the duct sufficiently 
to prevent the entrance of bacteria to the secreting portions of 
the gland was not well founded upon anatomical facts (Fig. 6). 
The acute and more chronic inflammatory affections of the 
udder fall very naturally into two groups, namely : (i) those 
in which the parenchyma is most affected and (2) those in 




INFECTIOITS MASTITIS 



33 



which the stroma or fibrous tissue is involved. The form of 
mastitis more frequently encountered as an infectious (trans- 
missible) disease is characterized by very marked changes in 
the milk, accompanied by the usual symptoms of parenchymat- 
ous inflammation of the gland itself. The discharge from the 
udder usually contains flaky masses held in suspension in the 
clear or perhaps cloudy serum. The color varies, and occa- 
sionally the fluid is blood-stained. The microscopic examina- 
tion shows the presence of agglutinated fat globules, pus cells 
and often red blood corpuscles. 

A number of bacteria* considered of more or less etiologi- 
cal value have been found associated with lesions of doubtful 
specific origin. The results of Kitt, Nocard, Mollereau, Guille- 
beau, Zschokke, Bang and still others, in which a Bacterium, 
a Bacillus, a Micrococcus , a Staphylococcus, and a Streptococcus 
have been found and reported as standing in a causal relation 
to the trouble, indicate that a variety of microorganisms are 
active in producing those affections which are frequently 
grouped without distinction as infectious mastitis. The review 
of much of the literature on this subject shows that a number 
of cases reported as infectious were isolated or sporadic ones, 
/. e. , they were in dairies where the disease did not spread to 
other animals. While these may be truly infectious in their 
nature they should be differentiated from the rapidly spread- 
ing phlegmons which are easily recognized as infectious 
(^contagious). 

If we take into account the variety of anatomical changes 
which have been described in the various udder affections, we 
can reasonably admit that different agencies may have been 
instrumental in their production. The various species of bac- 
teria which have been isolated from the udder lesions may very 



*Among the bacteria which have been found in udder trouble and 
described as a possible or perhaps the more probable cause the follow- 
ing species may be mentioned : Bacterium phlegmasiic uberis. Strep- 
tococcus agalactitT contagioscc, Stapliylococcus tnastitidis, Galactococcus 
versicolor, G. fulvus, G. albus. 



34 



INFECTIOUS MASTITIS 




^ ^ 











^"->^ 






Fig. 6. Section of a quarter of a cow's udder through one teat; 
{a) cistern, (b) larger milk ducts, {0 secreting portion of mammary 
gland. 2, drawing of secreting portion of gland, enlarged. 



INFECTIOITS MASTITIS 35 

likely have been of etiological importance in their respective 
cases. 

Already the facts have been pointed out, that the udder is 
normally more or less extensively invaded with bacteria and 
that certain species of bacteria seem to persist in the milk 
ducts of the glands when once they become lodged there. If 
these results apply to cows generally as rigidly as they did to 
those examined, an explanation for the presence of a variety 
of bacteria in the affected udders is not difficult to find. 
Whether these particular organisms, under certain conditions, 
would become primarily responsible for udder disease is not 
known. The evidence suggests that a number of the bacteria, 
heretofore described as the cause of mammitis, were in the 
affected glands by virtue of their presence in the normal udder. 
Concerning these points additional investigations are much 
needed. 

The writer has examined the milk secretions from the 
affected cows in two quite serious outbreaks of mastitis. In 
the first, the milk was drawn in sterile bottles after the udders 
and the hands of the milker had been thoroughly washed in a 
I to I ooo solution of corrosive sublimate. In all, there were 
eight samples of milk taken from as many different cows. In 
six of the eight specimens streptococci appeared in pure cul- 
ture. In the other two cases micrococci were associated with 
the streptococcus. In the second outbreak, the milk from four 
diseased udders was drawn with aseptic precautions directly 
into tubes containing slant agar and promptly sent to the 
laboratory, where it was carefully examined. From two cases 
pure cultures of streptococci were obtained, while those from 
the others were impure. The streptococci obtained from the 
twelve cases appeared to be identical and the clinical aspect of 
the disease in the different animals w^as the same. 

In a dairy that was under close observation by Ward, one 
cow was found to be troubled in one quarter of the udder with 
an inflammatory process which produced thickened masses in 
the blood-stained milk. From this milk a streptococcus was 
isolated in pure culture. It could not be diff-erentiated from 



36 



MISCELLANEOUS INFECTIONS 



the one isolated from the cows in the outbreaks mentioned. 
Another cow in this herd was found to have her udder per- 
manently infected with a streptococcus. Another animal in 
the same dairy suffered repeatedly from acute streptococcus 
mastitis. 

There are a large number of morbid conditions more or 
less frequently encountered in domesticated animals, which 
seem to be due to infection of some kind but which are not 
demonstrated to be of such an origin. These will continue to 
be attributed by some to infection and by others to various 
general causes until the truth concerning their etiology is 
revealed. 



j^ i8. Miscellaneous infections. Attention should be 
called to the many morbid conditions, resulting from infection, 
that are encountered in different species of animals and 
are liable to be attributed to other agencies. Usually such 
lesions are referred to general pathological conditions, but a 
more careful inquiry will reveal the presence of infection. 
Among these, may be mentioned pericarditis in cattle, so fre- 
quently associated with punctures by foreign bodies. The 
extensive exudative inflammations in these cases are frequently 
associated with micrococci. The same has been true of certain 
cases of localized endocarditis resulting in the formation of fun- 
goid, purulent, or necrotic masses about the valves of the heart. 
When one considers the possibilities of infection from acci- 
dental causes, as well as from surgical interference, together 
with the agency of metastasis, it is not difficult to understand 
how such a variety of morbid conditions can come about. 
Infection, therefore, forms an important part of pathology, out- 
side of those specific organisms that cause epizootics of greater 
or less severity. 

REFERENCES. 

I. Bollinger. Mycosis der Lunge beim Pferd. Archiv fiir 
pathoL AnaL, Bd. XUX (1870), S. 583. 



REFERENCES 37 

2. DeJong. Untersuchunt(en iiber Rotryoniyces. These de Gies- 
sen, 1899. 

3. Dubois. An enzooty of acute streptococcic mammitis. /our. 
ofComp. Pathology and Therapeutics, Vol. 17 (1904), p. 159. 

4. Frohxkr. Ein Fall von generalisirter Botryomykose. Mouat- 
sheftefiir Thierheilk., Bd. VIII (1897), vS. 171. 

5. (tAV. a bacteriological study of fistulous withers, botryomy- 
cosis and infected wounds in the horse. Ainer. i^et. Reviei<.\ Vol. 
XXIV (i9oi),p. 877. 

6. JOHNE. Zur Actinomykose des Sameustranges. Deutsche Zeit- 
schr.Jiir Thierm., Bd. XII (1885 1, S. 73. 

7. LucET. Ann. de P Institut Pasteur. Vol. VI (1893) p. 324. 

8. M'Fadvicax. Metastatic lesions in Discomycosis. The Jour. 
Compr. Path, and Thera., Vol. XIII (1900), p. 337. 

9. MiGULA. System der Bacterien. 1897. 

ID. Moore. Suppurative cellulitis in the limbs of cattle due to 
streptococcus infection. Ainer. Vet. Reviezv, June, 1898. 

11. NocARD. A New Pasteurellose : White scours and lung dis- 
ease of calves in Ireland. Anier. Vet. Reviezv., Vol. XXV (1901), 
p. 326. 

12. Smith and Dawson. Injuries to cattle from swallowing 
pointed objects. Ann. Report U. S. Bureau of Auitnal Industry, 
1893-4, p. 78. 

13. W.-VRD. The invasion of the udder by bacteria. Bulletin No. 
ijS, Cornell Univ. Agric. Exp. Station, 1900. 



CHAPTER III. 



DISEASES CAUSED BY BACTERIA 
GENUS STREPTOCOCCUS. 



§ 19. General discussion of streptococci. The con- 
fusion which exists coucerning species in this group of bacteria 
and the variety of antistreptococcic serums on the market, ren- 
der a summary of the present knowledge concerning this group 
of bacteria somewhat desirable. The genus Streptococcus is 
based according to Migula on its method of reproduction or 
division. Streptococci are spherical bacteria that divide in one 
plane. The segments do not separate but are held together in 
short or longer chains, although the divisions seem to be com- 
plete. Just how the segments are held together is not fully 
determined. According to older and more commonly encoun- 
tered classifications, a streptococcus is simply a number of 
micrococci (spherical bacteria) united in the form of a chain. 
In some of the supposedly different species the segments are 
oblong and vary in size. Frequently, however, the segments 
vary in size and form in the same chain. 

The more usually observed cultural characters and bio- 
chemic properties of different streptococci are quite similar, 
although it is difficult to obtain two cultures that will exactly 
agree in all of their manifestations when grown on a large 
number of media. Their disease-producing powers, however, 
vary within wide limits. While variations in the physio- 
logical properties and pathogenesis are true for different cul- 
tures (species? ), it has been found that there is a possibility of 
much variation in the subcultures of the same species. As 
with certain other bacteria, their virulence is the first to suffer 
change. In differentiating species, therefore, the fact must 
not be overlooked, that the existing characters and properties 



STREPTOCOCCI 39 

possessed by the streptoccocus in hand may have been more 
or less influenced by its conditions of life. When, for example, 
two streptococci appear to be identical under the majority of 
tests, a slight deviation in a single property cannot be considered 
of great differential value especially if this particular manifes- 
tation is among those most subject to change. A fundamental 
difficulty in differentiating species among streptococci seems to 
be a lack of information concerning the possible variations 
brought about by different environments. The further diffi- 
culty of identifying any of the very large number of forms 
which have been assigned specific names is due to the brevity 

•••• 







Fig. 7. Si.v /briHS of streptococci, i. Long chains consisting oj 
small segments arranged ivith equal spaces beliveen them. 2. Long and 
shorter chains in ivhich the segments are arranged in pairs. The size 
of the individual segmeitts is considerably larger than those in the long 
chains, j. Short and longer chains where the segments are oval ivith 
the long diameter perpendicular to the long axis of the chain. 4. Long 
iTiterlacing chains. 5. Short and longer chains with one or more seg- 
ments very much larger than the others. 6. Chains shoiving divisions 
in two planes. This form of division has been observed in a feiv cases. 
The dividing in tivo planes is an exception xvhich is not satisfactorily 
explained. X about 1000. 



40 STREPTOCOCCI 

of their description and the failure of the author to nientiou 
any character or property, or combination of the same, which 
would distinguish it from others. However, such deficiencies 
cannot well be avoided in the time of rapid accumulation ot 
observations and the evolution of methods. 

§ 20. Classification of streptococci. A few investi- 
gators have tried to eliminate the confusion concerning species 
by classifying streptococci according to distinct morphologic 
characters and pathogenic properties. Of these classifications 
the following may be mentioned : 

I. The classification of von Lingelsheim. This author di- 
vides all streptococci into two groups, or species, namely : — 

{a) Streptococcus brcvis — which is non-pathogenic. 

{b) Streptococcus longus — which is pathogenic. 

This is a combination of pathogenesis and morphology 
which the author thought applicable to the entire genus. He 
worked very largely, however, with the streptococci from the 
human mouth and throat. 

n. The classification of Kurth. Kurth worked largely 
with the streptococci from cases of scarlatina. His system is 
practically the same as that of von Lingelsheim, with the ex- 
ception that he does not include pathogenesis as necessarily 
belonging to either group. The divisions are as follows : 

{a) Streptococcus rigidi — Streptococci growing in short 
chains, imparting a uniform turbidity to bouillon. 

ib) Streptococcus flexuosi — Streptococci which grow in 
long interlacing chains forming flocculi in bouillon, leaving 
the liquid clear. 

HI. The classification of Pasquale. Pasquale worked with 
thirty-three streptococci, including nearly all of the then 
known species. His work was quite exhaustive, but he had 
to deal with cultures of various generations. He divides them 
into four groups, as follows : 

(a) Short saphrophytic streptococci. 



DISTRIBUTION OF STREPTOCOCCI 4I 

(d) Long non-virulent streptococci. 

(c) Long pathogenic streptococci. 

i^d) Short highly infectious streptococci. 

Group (d) pertains largely to bacteria which are no longer 
recognized as streptococci, for example, the diplococcus {Hficro- 
tocciis lanceolaftis) of pneumonia. It is now known that strep- 
tococci which grow in short chains are often virulent. This is 
especially true of the pyogenic forms. 

The study of streptococci from various sources, more 
especially from tissues of diseased animals, suggests the desira- 
bility of delaying a further classification until more definite 
data are obtained concerning the natural history, not only of 
these, but also of the species normally present on the mucous 
membranes of animals and in nature generally. The specific 
name is, pathologically or even biologically speaking, of little 
moment unless we can attach a certain definite meaning to it 
concerning the morphologic characters, cultural manifestations 
and the degree of disease-producing power possessed by the 
organism designated. In a group of twenty-eight streptococci 
previously studied, the writer found the pathogenic forms, 
i. e. those able to produce disease in rabbits, guinea pigs, or 
mice, about equally divided between the long and short chains. 
Of the twenty-eight, nine possessed a certain amount of viru- 
lence for one or more of these animals. 

§ 21. Distribution of streptococci in nature. The 
fact has been pointed out in many publications that strepto- 
cocci are quite widely distributed in nature. The results of 
the bacteriologic examinations of normal mucous membranes 
show that they are frequently included in the bacterial flora of 
the mouth, throat, nares, intestines, vagina, and in a few cases 
they have been found in the bronchioles of the horse and rab- 
bit They are also present in greater or less numbers on the 
skin, especially in the deeper layers, presumably in the ducts 
of the sweat and sebaceous glands and along the hair shafts 
and follicles. They exist in soil and in water, and occasionally 
these forms are quite as delicate in their morphology and 



42 STREPTOCOCCI 

equally as sensitive to the influence of environment as those 
isolated from diseased animal tissues. In view of this wide 
distribution, the presence of a streptococcus in any abnormal 
condition cannot be considered necessarily a specific infection 
from a previous case of the same kind. In many affections 
where the specific organism has been demonstrated, such for 
example as diphtheria, tuberculosis and hog cholera, strepto- 
cocci frequently appear m the lesions. In these cases, they 
are considered as accidental or secondary invaders, although 
in some of these maladies, such as tuberculosis, they are be- 
lieved to be of more or less secondary importance. When, how- 
ever, the specific cause of the disease is not positively known, 
and streptococci which possess certain pathogenic powers for 
experimental animals are constantly present and seem to 
stand in a causal relation to the disease, the pathologist is 
confronted with a puzzling problem in trying to determine the 
source and the etiological importance of the organism in hand. 
In cases of infection leading at once to septicemia, peritonitis 
or suppuration, the explanation is more simple than in the 
epizootic diseases, such as Bncsiseuche, where the constant 
presence of streptococci in the lesions can be quite as easily 
explained on the ground of their invasion of the parts affected 
from a normal habitat as on the hypothesis of a specific in- 
fection. It is in these instances that we are seeking for the 
crucial test. 

We have found in a few test experiments that when cer- 
tain of the delicate streptococci which exist (are found; in ex- 
ternal nature (soil or water) are introduced within the tissues 
of certain animals they become, by reason of their activities, a 
source of irritation which causes local tissue disturbances. In 
a few cases they have produced septicemia with fatal results. 

In cases of infection resulting in septicemia, or in those 
where the disease is more localized, as in strangles or mastitis, 
and possibly in others where the affection spreads more or less 
rapidly, we cannot well escape from the feeling that the strep- 
tococci, present in such large numbers, must either stand in a 
causal relation to the disease or be accounted for bv their 



DISTKIHUTION OF STKRI'TOCOCCI 43 

rapid proliferation in native soil made favorable for their ex- 
cessive increase by the conditions produced by the true etio- 
logical factors. Their natural distribution is so wide and 
their virulence so capricious that a secondary invasion, which 
seems always to be possible, renders the fixing of etiological 
responsibility upon a streptococcus isolated from any diseased 
tissue a somewhat difficult task. The problems in this con- 
nection which concern us most and which need more extended 
investigation pertain (i) to the determination of the parasitic 
possibilities of streptococci existing in nature, /. e., those ordi- 
narily considered as saprophytes and (2) to the distinction, if 
it exists, between streptococci that are able to produce local 
inflammatory processes leading to suppuration and those which 
produce highly infective and rapidly spreading diseases, such 
as erysipelas and strangles. 

In view of the confusion respecting species in this genus, 
the identity of streptococci isolated from the lesions in the 
various diseases which have been attributed to streptococci is, 
at the present time, a matter of some uncertainty. There is 
also considerable skepticism concerning the primary etiological 
significance of the streptococci in a number of diseases in 
which they have, heretofore, been assigned as the cause. 
Recent investigations, especially those of Lignieres, tend to 
the conclusion that they are often secondary invaders in cer- 
tain of these diseases. Petruschky has pointed out analogous 
cases in human infections in showing that streptococci play an 
important role as secondary invaders in human diphtheria, 
scarlatina and tuberculosis. 

Pathogeyiesis. In the absence of verified results to prove 
the non-specific relation of streptococci to the diseases which 
have with reasonable certainty been attributed to the activities 
of this genus of bacteria, these affections are tentatively 
included among the specific streptococcic maladies. It is very 
important, especially when the use of antistreptococcic serums 
are in question, to take into account the apparently large 
number of forms, or species, commonly included in the general 
statement of a streptococcus disease or infection. In 1S97, 



44 STRANGLES 

Van de \^elde, in a very exhaustive series of experiments, 
showed that an antitoxin produced from one streptococcus will 
not immunize against another, save to a very slight degree. 
Better results are reported by the use of polyvalent serums. 
There are a number of acute local disorders, such as 
vaginitis in cows, that have been attributed to this genus. 

REFEREXCES. 

1. Klein. Seventeenth Annual Report of the Local Government 
Board. Supplement containing report of Medical Officer. London. 
1887, p. 256. 

2. KuRTH. Arbeiten a.d. Kaiserlichen Gesundhcitsamte, Bd. VII 
(i89i),S. 389. 

3. Moore. Bulletin No. j. U. S. Bureau of Animal Industry, 
1893. P- 9- 

4. Pasquale. Beitriige zur path. Anal. u. zur allgemeinen 
Palhologie, Bd. XII (1893), S. 433. 

5. Petruschky. Zeitschrijtf. Hygiene, Bd. XVII, S. 59. 

6. VON LiNGELSHEiM. Zeitschrift f. Hygiene, Bd. X (1891), 
S. 331- 

7. Welch. The Amer. Jour, of Med. Sciences, VoL CII (1891), 
P- 439- 



vSTRANGLES. 



Synonyms. Adenitis equorum ; Coryza contagiosa 
equorum ; Distemper: Goiirme ; Druse. 

§ 22. Characterization. Strangles is an infectious dis- 
ease of horses, asses and their hybrids occurring sporadically 
and in epizootics. It is characterized principally by a fever, 
followed by an acute catarrh of the mucosa of the upper air 
passages especially of the nares, and a suppurative inflamma- 
tion of the lymph glands of the submaxillary and pharyngeal 
regions. The lesions, however, are not restricted to these 
parts. It is a disease of young animals. 

v^ 23, History. Strangles was among the first equine 
diseases to be recognized. In 1664, Solleysel gives an account 
of it and points to the fact that it had been known for a long 



HISTORY OF STRANGLES 45 

time. Its infectious (contagious) nature was determined 
experimentally in 1790 by Lafosse and since that time by a 
number of other investigators. In 1873, Rivolta found in the 
pus of the abscesses a micrococcus which appeared in chains of 
from three to five segments. Baruchello, in 1887, described 
as its cause an organism, which he designated as Bacillus 
adenitis eqiii. Strangles has been thought by some to be 
identical with scrofula and measles. Sacco and Nasbot con- 
sidered it as horse pox. Viborg and Toggia and more recently 
Nasbot advocated the inoculation of horses with the lymph of 
horse pox as a prophylactic measure against strangles. Dela- 
motte demonstrated that this procedure was of little or no pre- 
ventive value. The supposed specific cause ^Streptococcus equi) 
of strangles was described first by Schiitz and later by Sand 
and Jensen in the same year (1888). This discovery has been 
confirmed by Poels, Lupka and others. More recently Lig- 
nieres has discovered a " coccobacillus " which he believes to 
be the primary cause. He considers the streptococcus of 
Schiitz as a secondary invader of no specific value. His con- 
clusions do not appear to have been confirmed. 

§ 24. Geographical distribution. Strangles is a wide 
spread disease among horses. It appears to stand in equine 
pathology very much as measles do in human medicine, — a 
disease of early life and consequently more prevalent where 
there are more young. It seems to exist in all countries 
where the horse kind are raised and to be more prevalent in 
breeding districts than elsewhere. 

§ 25. Etiology. Strangles is caused by Streptococcus 
equi, first described by Schiitz in 1888. With pure cultures of 
this organism Schiitz was able to produce the disease in 
healthy horses. It is fatal to mice, a maximum virulent virus 
destroying life in three days. In the writer's experience 
streptococci only have been found in the abscesses. 

The period of ivcubation varies, from four to eight days is 
the most usual time. 

J; 26. Symptoms. The first indication of this disease 



46 STRANGLES 

is a rise of temperature. There is loss of appetite, depression, 
and often great weakness. The general symptoms may con- 
tinue for a few days before the localization of the lesions is 
apparent. The first local manifestation consists usually in a 
catarrh of the nasal mucosa or swelling of the sub-maxillary 
and pharyngeal lymphatic glands. The nasal discharge is at 
first serous and somewhat viscid, but in from 3 to 5 days it be- 
comes purulent and of a yellowish green color. The catarrhal 
condition may exist in one or both nostrils. It may extend 
into the pharynx, larynx, trachea and even to the bronchi. In 
most cases, swelling of the sub- maxillary glands appears con- 
currently with the purulent nasal catarrh. The spreading of 
the inflammation to the connective tissue which surrounds the 
glands, and the stasis of the lymph in the efferent lymph 
vessels, often cause the development, from the sub-maxillary 
lymph glands, of very extensive swellings that may occupy 
the entire inter-maxillary space, and may spread even to the 
outer side of the maxilla. Abscesses form in most cases. 

In exceptional cases, strangles may present catarrhal 
symptoms without suppuration of the lymph glands. Jensen 
states that it may first assume the form of pharyngitis, purulent 
pneumonia, and pleuritis without any well marked morbid 
affection of the lymph glands. The urine generally remains 
alkaline ; it frequently contains a considerable quantity of 
albumen. 

At times, strangles is accompanied by a cutaneous exan- 
thema which takes the form of an eruption of w^heals, nodules, 
vesicles and even pustules ; these may appear, chiefly on the 
sides of the neck, shoulders and sides of the chest. These 
exanthemata are characterized by their sudden appearance, 
and often by their equally rapid disappearance. An eruption 
of vesicles may break out on the nasal mucous membrane. 
The contents of the vesicles is at first limpid, but later it 
becomes purulent. Rabe states that the streptococcus of 
strangles can produce ulcers on the nasal mucous membrane. 

§ 27. Morbid anatomy. The lesions in strangles are 



MORBID ANATOMY 



47 



interesting from the fact that in the beginning the disease is 
general but later in its course it becomes a series, exceedingly 
variable in different individuals, of localized morbid foci. 
The lymphatic glands seem to suffer most, although any organ 
may be involved. As indicated by the symptoms, the lesions 
in most cases are characterized by an acute inflammatory pro- 
cess followed by suppuration. 

The glandular swellings about the head usually terminate 
in suppuration, the pus discharging either externally or into 
the oral cavity. In other cases the pus undergoes caseation. 
Frequently the inflamed glands become confluent, resulting in 
a single large abscess. Small abscesses may occur under the 
pharyngeal mucosa. 

The inflammation may extend to the superficial lymph 
vessels of the skin, especially of the head, resulting in the for- 
mation of a large number of small abscesses. This may be 
followed by a diffuse phlegmonous swelling of the parts. 
Metastatic abscesses are liable to occur in a great variety of 
organs. The metastasis seems to take place through both 
lymph and blood vessels although the lymphatic glands are 
most often affected. Suppurating foci have been described in 
nearly every lymphatic gland in the body. The discharge of 
pus from the bronchial, mesenteric or other glands, within or 
adjacent to the pleura or peritoneal cavities, may give rise to 
a fatal pleuritis or peritonitis. There is no organ of the body 
free from possible suppurative lesions as a result of metastasis. 

Strangles may become chronic, especially when the nasal 
catarrh extends into the sinuses of the head, in the guttural 
pouches, or pharyngeal cavity. In these cases the animal be- 
comes emaciated. The lesions in these cases resemble some- 
what those of chronic glanders. Many complications are 
liable to arise. Mixed infections and secondary lesions often 
occur. The prognosis, however, is favorable. 

Death from strangles is caused usually by either septi- 
cemia, pyemia, pleuritis, peritonitis or suppurating (metas- 
tatic) pneumonia. 

The duration of the disease varies according to its .severity 



48 STRANGLEvS 

and the localization of the lesions. In mild cases conva- 
lescence begins in a few days, but in other cases restoration 
may require weeks and even months. 

The mortality, according to available statistics, does not 
exceed three per cent. 

i< 28. Differential diagnosis. Strangles is to be differ- 
entiated from : 

1 Purulent nasal eatarrh. In this affection, there is 
rarely suppurating sub-maxillary glands, although occasional- 
ly these glands may be swollen. 

2 Glanders. In glanders, the tissue changes are more 
persistent and the skin lesions, if they exist, do not heal as 
rapidly as in strangles. In chronic cases, the diagnosis is 
quite difficult. Here animal inoculation must be resorted to. 
Mice inoculated subcutaneously with the nasal, discharge suc- 
cumb to the streptococcus of strangles but they are resistant 
to the bacterium of glanders. Guinea pigs inoculated in a like 
manner will, in case of glanders, develop that disease from 
the lesions of which pure cultures oi Baeterium mallei may be 
obtained. 

3 Parotiditis. In this affection the swelling is localized 
and suppuration does not often occur. 

4 Abscesses due to pyogenic bacteria. The cases are rare 
where there would be any question as to diagnosis. The bac- 
teriological examination including the inoculation of animals 
would give positive aid unless the pyogenic organism hap- 
pened to be a virulent streptococcus in which case a differen- 
tiation might be difficult. 

§ 29. Prevention. Isolation of the infected and removal 
of healthy animals from the place where the diseased animals 
came down. If in stables the stalls should be thoroughly 
disinfected before being used for well animals. 

REFERENCES. 
I. LiGNiERES The etiology of equine influenza as infectious 
pneumonia. Jour. Compr. Patli. and Thera., Vol. XI {iSgS), p. 312. 
Translated from Recueil de Med. Vet., Vol. IV (1897). 



EQUINE PLEURO-PNEUMONIA 



49 



2. Poles. Die Mikrokokken der Druse des Pferdes. Forischr. 
der Med., Bd. VI (1888), S. 4. 

3. Reeks. Intracranial strangles, abscess in a mare. Jour. 
Compr. Path, and T/iera., Vol. XII (1899), p. 178. 

4. Sand and Jensen. Die Aetiologie des Druse. Deutsche Zeit. 
fur Thiermed., Bd. XIII (1888), S. 437. 

5. ScHUTz. Der Streptococcus der Druse des Pferdes. Arch, fur 
Thierheilkunde, Bd. XIV (1888), S. 172. 



EQUINE CONTAGIOUS PLEURO PNEUMONIA. 

Synonyms. Pleuro-pneumouia contagiosa equorum ; stable 
pneumonia; pjieninoenteritis; Bnistsenc/ie. 

ij 30. Characterization. This disease known as conta- 
gious pneumonia or contagious pleuro-pneumonia in the horse 
is characterized by a high temperature, rapid pulse, but occa- 
sionally without definite lung disturbances. Like strangles, 
both the symptoms and the lesions vary to such a degree that 
it is difficult to single out diagnostic features. 

§ 31. History. In earlier times, influenza and conta- 
gious pleuro-pneumonia of the horse were not distinguished as 
separate diseases. Falke differentiated the disease formerly 
known as influenza into contagious pleuro-pneumonia and 
influenza. Since his time they have been recognized as dis- 
tinct diseases. 

>j 32. Geographical distribution. Contagious pneu- 
monia, like strangles, is widely distributed. It appears in epi- 
zootic form, although in certain places it is reported to be 
almost enzootic. It prevails most extensively where large 
numbers of horses are congregated. It has frequently been 
reported as the cause of much trouble among the horses in the 
European armies. In the eastern part of the United States, it 
appears from time to time in more or less serious epizootics. 
It is quite common among horses shipped from the West. In 
these cases, it is designated as "western" or "stable"' fever. 



50 EQUINE PLEURO--PNEUMONIA 

>5 33. Etiology. There is some question concerning the 
specific cause of this disease. A large number of suspected 
microorganisms have been isolated and described, but the 
streptococcus of Schiitz seems to be the only one with which 
the disease has been produced experimentally. 

In 1887, Schiitz published the results of his investigations 
into the cause of BrustseMche. He described an organism 
which appeared as a diplococcus in tissues, but in bouillon 
cultures it grew in flocculi. From the description, it appears 
that this organism was a streptococcus, notwithstanding the 
fact that in the tissues it appeared more often as a diplococcus. 
In cultures, he speaks of it as chains growing in masses. He 
mentions a capsule, but in the cases described it does not seem 
to be invariably present and it is not mentioned in prepara- 
tions made from cultures. Chantemesse and Delamotte, Gal- 
tier and Violet, and Cadeac found streptococci in the lesions 
of animals suffering from this disease. Although differences 
seem to exist in the streptococci isolated and studied by these 
investigators, there is a striking similarity between them. It 
is not at all unlikely that difference in methods may explain 
the variations mentioned. 

According to Schiitz, cultures inoculated into horses pro- 
duce the disease when injected directly into the lungs by 
means of a hypodermic syringe. The resulting contagious 
pleuro-pneumonia exhibits the same symptoms and runs a like 
course to those observed in cases of the disease contracted in 
the natural or common manner. The essential changes shown 
on post-mortem examination were multiple gangrenous patches 
in the lungs with parenchymatous degeneration of the most 
important organs. The inoculated streptococci were found in 
the tissues of the artificially produced disease. According to 
Schiitz, the bacteria of contagious pleuro-pneumonia are found 
most numerously in the lungs or the exudate on the pleurae. 
They are also met with in the nasal discharge and in expired 
air (Rust). Nothing positive is known concerning the life 
history of the streptococci outside the animal body. They are 
supposed not to be able to live longer than six weeks within 



i-:tiology 51 

the animal body ; but in certain cases, especially in encysted 
deposits in the lungs, the virus may remain active for a much 
longer time. 

Baumgarten and Hell oppose the view that Schiit/.'s strep- 
tococcus is specific, while Rust and Fiedler support it. Hell 
maintains that with our present means of investigation, the 
bacteria of contagious pleuro-pneumonia cannot be differen- 
tiated from the pyogenic streptococci or from the strepto- 
coccus of erysipelas In fact, Hell believes that the strepto- 
coccus of Schiitz has a pathogenic effect in horses affected 
with pleuro-pneumonia ; but as there is no positive proof of 
its being specific, he maintains that we are justified in sup- 
posing that this ubiquitous microorganism simply has an injuri- 
ous influence on the course of the disease, contributing to the 
production of the secondary lesions. Hell further states that 
protective inoculation with Schiitz's bacteria, which at first 
promised good results, has not proven to be satisfactory. 
Fiedler, on the other hand, has obtained the same bacteriolog- 
ical results and has arrived at the same conclusion as Schiitz. 
He also states that he has experimentally produced pleuro- 
pneumonia in a horse by inoculation of cultivations of these 
bacteria. 

Lignieres believes that his cocco-bacillus stands in an 
etiological relation to this disease and that here, as in strangles, 
the streptococcus is a secondary invader. This view has not 
been confirmed. 

The writer made a bacteriological examination of the 
organs from five cases of fatal contagious pneumonia of the 
horse. In each case, the lungs were more or less hepatized, 
but the other organs were nearly normal in appearance. 
Without exception, a streptococcus appeared, usually in pure 
culture, from the lungs. The inoculated media from the other 
organs (liver, spleen, and kidney) remained clear. The strep- 
tococci isolated from the different cases were identical in 
their morphology, cultural manifestations and pathogenesis. 
A microscopic study of the lungs from the different horses 
showed streptococci singly, in pairs and occasionally in short 



52 EOUINK PLEURO-PNEUMONIA 

chains. Distinct capsules were not observed. In bouillon 
cultures, however. the\' appeared in long chains, leaving the 
liquid clear, as described by Schiitz. 

This streptococcus did not grow in gelatin, or on serum, 
or on potato. It would not develop in acid media. On agar 
the colonies were small and characteristic of streptococci, i. e., 
with a thickened, convex, grayish center surrounded by a 
thin, spreading bluish border, nearly equal in width to the 
diameter of the central portion. It fermented dextrose, lac- 
tose and saccharose, with the formation of acids but no gas. 
Milk remained unchanged in appearance. 

In mice and rabbits, it produced a rapidly fatal septicemia, 
but guinea-pigs were unaffected. A horse inoculated in the 
pleural cavity with a small quantity of the culture was killed 
lo days later. At the point of inoculation and extending over 
an area equal to one-half of the lung, there were strong adhe- 
sions between the lung and parietes. The subjacent lung 
tissue w^as hepatized. Pure cultures of the streptococcus were 
obtained from the exudate and from the hepatized lung. 

Although a few discrepancies exist between the descrip- 
tion of Schiitz's organism and this streptococcus, in the more 
essential features they seem to be identical. The cases were 
examined before the publication of Lignieres' results, and the 
methods employed did not meet the requirements of those used 
in isolating his cocco-bacillus. Although a very careful histo- 
logical study of the pneumonic tissue was made, Ligniere's 
organism was not detected. It is known that a bacterium, 
resembling that described by Lignieres, exists normally in the 
upper air passages of a certain number of horses. 

The period or inriibation is g\y&\\ as varying from one to 
fourteen days, but usualh- from lour to ten days elapse from 

the time of exposure to the development of the first symptoms. 

^ 34. Symptoms. The symptoms vary to a marked de- 
gree. When pneumonia develops early in its course, the dis- 
ease may appear suddenly ; and in addition to the elevation of 
temperature there is a cough with difficult breathing. Often 



SYMPTOMS 53 



the svraptoms differ from those of fibrinous pneumonia by the 
absence of distinct evidences of local lesions which are found 
in that disease. The first regular symptom is a rapidly 
increasing temperature frequently accompanied by a chill. The 
pulse rate is increased. There is general depression, usually 
lossof appetite and muscular weakness; the conjunctivae and 
other visible raucous membranes become congested. There 
may be from the beginning marked indications of localized 
lesions in the lungs, or the general symptoms may continue 
without evidence of pronounced lung disturbance. The dura- 
tion of the disease depends almost entirely upon its course. 
In the more tvpical cases, the fever lasts from 5 to 8 days. 
The period of convalescence is much longer, lasting from two 
to three weeks. Many symptoms may be exhibited, corres- 
ponding to the variations in the morbid processes. If the 
heart, digestive tract, liver, kidneys or brain become the local- 
ized seat of the disease, symptoms referable to impaired func- 
tions of these organs are in evidence. The septicemic form 
has been described as being followed by localized suppurative 
lesions. 

§ 35. Morbid anatomy. The morbid changes in the 
tissues and organs vary according to the course of the disease, 
which is exceedingly irregular. It may exhibit a regular 
form of lobar inflamation of the lungs or the disease may run 
an atvpical, complicated, acute, chronic, and not infrequently 
an abortive course. Further, authorities agree that many com- 
plications mav arise modifying or changing completely the 
morbid anatomv of the disease from the conditions found m 
the more tvpical cases. In the few cases examined post-mor- 
tem by the writer, the gross lesions were restricted to the lungs. 
They were either in a state of congestion, or exhibited 
changes of fibrinous pneumonia in the cephahc (anterior) 
portions of one or both organs. Pneumonia is the most com- 
mon localized lesion. Several quite distinct forms of lung 
disturbances are described. 

In the lobular form of pleuro-pneumonia. which it is 



54 EQUINE PLEURO- PNEUMONIA 

Stated furnishes the largest number of subjects for post-mortem 
examination, there are many hemorrhagic foci, possibly gan- 
grenous pneumonia with secondary pleuritis. Parenchymatous 
degeneration of other vital organs is reported. Areas of the 
lung tissue of greater or less size are thickened and hepatized- 
These are located more especially near the base of the lungs 
and in the lower (ventral) portions. Bright foci which are 
distinctly defined from the neighboring tissues are scattered 
through the hepatized areas and appear on the surface of sec- 
tions of the hepatized parts. Uusually several of these foci 
are present. They vary in size from a millimeter to 20 or 
more centimeters in diameter. In recent lesions, these areas 
are very small, of a grayish-red color and surrounded by a 
grayish zone consisting of leucocytes. In more advanced 
lesions they become yellowish, necrotic and finally cavities 
are formed varying from the size of a pea to that of a hen's 
egg. These cavities are surrounded by a smooth capsule. 
There are other foci which contain greasy, fetid, watery pus 
(gangrene of the lungs), by reason of the necrotic part of the 
lung undergoing liquefaction in consequence, it is stated, of 
the admittance of air. The lungs often contain suppurating 
foci composed of a whitish pus mixed with necrotic lung 
tissue. It sometimes happens that the foci just described are 
absent in the lungs, although during life distinct symptoms 
of such a localized affection may have been present. In these 
cases, it is assumed that absorption of the necrotic tissue has 
taken place. The remaining tissue of the lungs is more or 
less hyperemic or edematous. 

The pleurae show signs of a difi'use, exudative inflamma- 
tion, the starting point of which in the large majority of cases 
is from necrotic deposits which are situated in the periphery 
of the lungs. Pleuritis may occur, however, apparently as a 
primary lesion without the necrotic foci being present. The 
contents of a necrotic deposit in the lungs rarely break 
through into the pleural cavity. In some cases, the visceral 
and costal layers of the pleurae are congested, diffusely or in 
spots, and are sprinkled with hemorrhages. Frequently the 



MORBID ANATOMY 55 

pleurae are covered with soft red granulations over which are 
layers of a yellowish exudate which are partly membranous 
and partly coagulated in a reticular manner, and which can 
usually be easily removed. The pleural cavities generally 
contain a considerable quantity of fluid. Dieckerhoff states 
that from 30-40 liters of a serous fluid are occasionally present. 
The exudate is usually turbid and of an orange, grayish-red, 
brownish-red, or dirty-grayish color. It is generally mixed 
with numerous yellowish colored flakes which form a sediment 
when the liquid is allowed to stand in a glass. The pleuritic 
exudate sometimes consists of pure pus and less frequently of 
blood. The pleuritic exudate when present in large amount 
compresses the lungs and pushes them away from the thoracic 
walls. In cases of recovery, the pleuritic exudate may become 
organized, binding the lungs to the costal walls and diaphragm. 
Various forms of fibrous, villous growths develop on the 
pleurae. 

The records show that the other organs of the body are 
usually in a state of parenchymatous inflammation and fatty 
degeneration. The muscular tissue of the heart is, as a rule, 
brownish-gray in color, soft, and suffers from cloudy swelling. 
In severe cases, it shows well-marked fatty degeneration, is of 
a clay color, and is occasionally sprinkled with a large number 
of small, yellowish-white foci. The liver is enlarged, of a 
clay color or sometimes icteric, and presents signs of fatty 
degeneration. The spleen is flaccid, its pulp increased and 
often sprinkled with hemorrhages. The kidneys may be swollen, 
friable and sometimes show numerous hemorrhagic foci. 
The lymph glands, especially the bronchial and mediastinal 
glands, are enlarged, softened, and exhibit on section a grayish- 
red color. The muscles of the body are soit, and of a yellow- 
ish-brown color. Small hemorrhages under the serous mem- 
branes are frequently reported. Slight endocarditis may occur. 
The blood suffers less change than any of the solid organs. 
It contains an excess of polynuclear leucocytes. 

The mucous membranes of the stomach and intestines are 
frequently hyperemic, swollen, sprinkled with hemorrhages, 



56 EQUINE PLEURO-PXEUMOXIA 

and sometimes even ulcerated. The bronchial mucous mem- 
brane is swollen and inflamed. 

In other cases, the lesions are those of lobar pneumonia, 
in which the stages of hyperemia, red hepatization, gray hepa- 
tization and resolution fin favorable cases) follow each other 
in regular order. In a fatal case post-mortemed by the writer 
the right lung was entirely involved, the left one being but 
slightly hyperemic. In non-fatal cases, the crisis is reached 
on the 5th or 6th day, after which resolution begins. 

As already stated the lesions in this disease are so ex- 
ceedingly variable that, in addition to the more typical pneu- 
monia, almost any modification can be found. The detailed 
description of many of these variations as described by Dieck- 
erhoff are worthy of careful study. 

T/ir duratio7i of the disease is from two to three weeks. If 
there are complications the course may be much longer. 

The mortality is often very high. The literature shows it 
to vary from one to thirty per cent. It frequently leaves ani- 
mals practically worthless because of pleural adhesions and 
other complications. 

§ 36. Differential Diagnosis. This disease is to be 
differentiated from several disorders. 

1. Influenza. In the general form, where the localiza- 
tion of the lesions in the lungs does not occur, it is often con- 
fused with influenza. 

2. Bronchial pneumonia. The pneumonia which often 
follows colds must be differentiated from the epizootic form. 

3. Aspiration pneumonia. The pneumonia following the 
introduction of foreign substances into the lungs, as often 
happens in giving medicines, must be distinguished. The 
history, course of the disease, and the spread to other animals 
will do much to settle the diagnosis. In case of post-mortem, 
streptococci are often found in all the pneumonias. We have 
no positive lesion or organism by which to determine the 
diagnosis. 

§ 37. Prevention. The short period of incubation and 



SEPTICKMIA IN CHICK.KN.S 57 

the high temperature as the early symptom render it an 
easy task to detect the appearance of the disease. The well ani- 
mals should if possible be removed at once to other stables. 
The stalls occupied by the infected animals should be disinfected 
before being used for other animals. Isolation and disinfec- 
tion are the important factors in checking the spread of this, 
as of other infectious diseases. 

To prevent the introduction of this malady, all horses 
brought from a distance should be kept isolated for at least a 
week before allowing them to come in contact with the home 
animals. 

RHKKRKNCKS. 

1. Cadkac. Contributions a r etiologie de la pueunionie conta- 
gieuse dn cheval. Compt. rend de la Soc. de Biol., 1889, p. 316. 

2. Fleminc. Infectious pneumonia of the horse. The Veteri- 
nary Jour., Vol. XXXIII, p. I. 

3. SCHUTz. Die Ursache der Brustseuche der Pferde. Vircho7v's 
An-hiv, Bd. CVII, S. 356. 

4. SCHt^rT/.. Die genuine Lungenentziindung der Pferde. Archiv 
fur wissen. u. prak. Thierlieil/ciiride, Bd. VIII. 

5. SiEDAMGROTZKY. Ueber infectiose Pneumonien bei Pferden. 
Deutsche med. Wochenschrift, 1882, vS. 668. 

6. W1LI.IAMS. Contagious pleuro-pneumonia of the horse. Aiiier. 
Vet. Reviezv, Vol. XVI (1892^, p. 301. 



APOPLECTIFORM SEPTICEMIA IN CHICKENS. 

ji 38. Characterization, A rapidly fatal septicemia in 
chickens caused by a streptococcus. 

§ 39. History. This disease was recently discovered 
and described by Norgaard and Mohler. Although the symp- 
toms and lesions given correspond .somewhat closely to those 
mentioned by Mazza and Rabieux, there is a marked differ- 
ence in the etiological factor. The newly discovered disease 
is based upon the findings and investigations following a single 
epizootic among fowls. Thus far it has been identified in one 
other locality. 



58 SEPTICEMIA IN CHICKENS 

^ 40. Geographical distribution. The only locality 
from which it has been described is Loudoun Co., Va. It 
was observed and a few cases studied by Moore and Mack in 
an epizootic among fowls in the northern part of New York in 
1905. 

§ 41. Etiology. This disease is stated to be due to a 
streptococcus which grows in short or longer chains with seg- 
ments varying from 0.6 to o.8/< in diameter. In some cases 
elongated forms are observed. It is an aerobe, and a faculta- 
tive anaerobe. When cultivated on artificial media it does not 
liquefy gelatin, it does not change the appearance of milk, but 
causes slight acidity and thickening of the lower stratum with- 
out coagulation of the casein. The reaction of alkaline bouillon 
is changed to an acid one. It does not give a visible growth 
on potato. It stains by Gram's and Gram-Weigert's methods. 
In bouillon it grows in somewhat flaky masses while the 
medium remains clear. It was fatal to fowls, mice, rabbits 
and swine ; guinea pigs, dogs and sheep were not destroyed 
by inoculation. This organism has not been specifically named. 

^ 42. Symptoms. It is not at all uncommon to find the 
fowls dead and lying under the roosts. Occasionally capons 
were observed to be sick for from 12 to 24 hours prior to 
death. In these cases the feathers become ruffled and the fowl 
showed evidence of extreme depression. The onset of the 
disease is very sudden and its course a very rapid one, usually 
terminating in death. 

§ 43. Morbid anatomy. The authors describe the 
morbid anatomy as follows : "The spleen is more or less en- 
larged, showing hyperplasia of the Malpighian corpuscles. The 
pulp contains numerous areas of extravasated blood. When a 
stained section is examined by means of a hand lens a number 
of circular semi-transparent foci, the size of a pin hole, may 
be noted. These are found on microscopic examination to be 
centers of necrobiosis, consisting of parenchyma which has 
undergone coagulation necrosis, and surrounded by a more or 



DIFFERENTIAL DIAGNOSIS 59 

less well defined capsule of embryonic and further developed 
connective tissue cells and filaments. 

" On microscopic examination, the kidneys show slightly 
swollen epithelial cells of a beginning parenchymatous degen- 
eration to well pronounced disintegration of the renal 
epithelium of acute nephritis. The degree of degeneration 
depends, as a rule, upon the course of the disease. If a bird 
succumbs suddenly or in the course of a few hours the morbid 
changes are either not apparent at all or but slightly pro- 
nounced, while, on the other hand, the duration of three or four 
days to a week results in an acute exudative nephritis. The 
swollen or degenerate epithelium of the tubules surrounds irreg- 
ular masses of coagulated exudate and white blood corpuscles, 
among which are numerous short chains of streptococci. In 
very acute cases with sudden death the liver shows extreme 
hyperemia. The cells have a slightly granular appearance in 
addition to the fatty infiltration usually seen in the liver of 
well kept fowls. When death does not occur until after 
twenty- four hours the liver cells also show parenchymatous 
or fatty degeneration ; their outlines become indistinct, the 
body very granular, and the nucleus takes the stain but 
faintly. Interlobular and intralobular collections of round 
cells and leucocytes appear, and in more chronic cases centers 
of coagulation necrosis may be seen. The lungs become 
hepatized. The walls of the bronchioles are thickened and the 
streptococci may be seen in the minute capillaries. The air 
cells are filled with plasma, red blood corpuscles and epithel- 
ium, among which the microorganism is easily detected." 

^ 44. Differential diagnosis. This affection must be 
differentiated from fowl typhoid and chicken cholera. The 
positive diagnosis of each must rest with the etiological 
factor. A number of diseases of fowls have been described 
from various places in Europe and Africa, but none of them 
seem to be caused by a streptococcus. 

§ 45. Prevention. The separation of the well from the 
diseased fowls and placing them in uninfected houses or yards 



6o STREPTOCOCCUS MASTITIS 

is of the first importance. Norgaard and Mohler found that 
immunity may be produced in susceptible animals by the 
filtrate of bouillon cultures, by sterilized bouillon cultures of 
the specific streptococcus, and with the serum of artificially 
immunized animals. 

REFERENCES. 

Norgaard and Mohler. Apoplectiform septicemia in chickens. 
Bulletin No. 36, U. S. Bureau 0/ Animal Industry, 1902. 



vSTREPTOCOCCUS MASTITLS. 

^46. Characterization. The term "streptococcus mas- 
titis" has been given to an infectious disease of the udder of 
cows caused by a streptococcus. It is characterized by hard 
foci in the gland. 

§ 47. History. As early as 1848, Brennwold observed 
in Switzerland an enzootic mastitis that was difficult to cure. 
The affection was called ''gelber Gait:' Since that time this 
affection has been found in nearly all if not all countries. 
Among the more recent writers on this subject may be men- 
tioned Hess and Borgeand in Switzerland, Nocard and Mol- 
lereau in France, and Zschokke in Vienna. In America it 
does not appear to have been studied independently of the 
infectious form of mastitis described in § 17. The epizootic 
mastitis occasionally reported in this country may be identical 
with this supposed distinctively specific disease. Zschokke 
found the streptococcus in 297 of the 444 cases of altered milk 
examined. 

§ 48. Geographical Distribution. This affection has 
been reported from nearly every country where cows are kept. 

§ 49. Etiology. The organism that causes this disease 
was described by Kitt, as Streptococcus agalactia, and Guille- 
beau as Streptococcus contagioscc. It enters the udder through 
the ducts of the teats. 

The writer has been unable to differentiate this strepto- 



MORBID ANATOMY 6l 

COCCUS from the one he has found in cases of mastitis, and also 
in the milk of cows with healthy udders. Ward and Reed 
produced mastitis in a healthy udder with the streptococcus 
that they had isolated from a normal udder. 

The period of incubation is very short, one to three days in 
the produced cases. 

i^ 50. Symptoms. The first symptom is the diminution 
in the quantity of milk, usually in but one quarter of the 
udder. This is quickly followed by indurated foci in the 
affected glands. The part becomes inflamed. The discharge 
or secretion is thin, more or less colored, and contains pus 
cells and clumps of streptococci. The lesions develop slowly, 
and one quarter after another of the udder becomes involved. 
Later the milk secretion is liable to stop entirely. 

§ 51. Morbid Anatomy. The tissue changes are 
described as those of catarrhal inflammation of a mucous sur- 
face, followed by the development of new formed tissue and 
atrophy of the parenchymatous tissue. The gland is hard and 
in time becomes enlarged, due to the new formed tissue. The 
microscopic examination shows a thickened intertubular 
tissue, and the epithelial cells more or less disintegrated and 
sloughed from the tubular walls. The lymphatic glands and 
other organs of the body are not involved. The lesions are 
localized in the udder. 

The period of duration is variable, but always long. 

77z<?/;v^7/(7j^^ is grave for the gland itself, but is rarely 
fatal to the animal. 

§ 52. Differential Diagnosis. The diagnosis is made 
by finding the .streptococcus in pure culture. It is to be dif- 
ferentiated from the sporadic cases of mastitis caused primarily 
by some injury, and the infectious mastitis caused by other 
bacteria, largely micrococci. This can readily be done from a 
bacteriological examination of the udder secretions. 

§ 53. Prevention. This disease is spread from the 
infected to the non-infected largely by the hands of the 



62 STREPTOCOCCUS MASTITIS 

milkers. Recognizing this fact, the spread can be stopped 
by disinfecting (washing in a disinfectant) the hands of the 
milker after each animal. The diseased animals should be 
isolated from the others. It is one of the easiest infections 
to control. 

REFERENCES. 

1. Brennwald. Chronische Euteretitziindung, Archivf. Thier- 
heilk. Bd. X (1848), S. 40. 

2. Dubois. An Enzooty of Acute Streptococcic Mammitis. Jour. 
Contp. Path, and Thera. Vol. XVII {1894), p. 159. 

3. NoCARD ET MoLi-ERE.\u. Sur une mammite contagieuse des 
vaches laitieres. Bulletin de la Societe centr. de Med. vet., 1884, p. 188. 
Ibid. Ann. de PJnstiiut Pasteur, Vol. I (1887), p. 109. 

4. Reed and Ward. The significance of the presence of strepto- 
cocci in market milk. American Medicine, Vol. VII (1903), p. 256. 

5. ZSCHOKKE. Weitere Untersuchungen iiber den gelben Gait. 
Schweizer-Archiv fi(r Thierheilk., Bd. XXXIX (1897), S. 145. 



CHAPTER IV. 



DISEASES CAUSED BY BACTERIA 
GENUS MICROCOCCUS. 



§ 54. General discussion of the genus Micrococcus. 

^h.Q: genus Micrococcus includes the spherical bacteria that divide 
in two planes. The micrococci, therefore, may be single spher- 
ical organisms or they may be united in pairs (diplococcus), 
in fours (tetracoccus), or in small clumps or masses (staphy- 
lococcus). This genus contains many important species but 
they are largely among those forms producing wound infection, 
such as Micrococcus pyogenes aureus. These infections are not 
characteristic in their manifestations and consequently the 
disturbances they produce have not been classed among the 
specific infectious diseases. At present, we seem to have 
recognized but one specific malady of animals attributed to 
them. In the human species they cause a number of diseases. 



TAKOSIS. 



§ 55. Characterization, Takosis, meaning to waste, is 
a destructive, infectious disease of angora goats. It is char- 
acterized by great emaciation and weakness, with symptoms 
of diarrhea and pneumonia. 

§ 56. History. The name Takosis was given to this 
disease of goats by Mohler and Washburn in 1903. They in- 
vestigated the disease, described its symptoms and morbid 
anatomy. They found a micrococcus which they believed to 
be its cause and which they named M. caprimis. 

In 1875, a disease was reported among angora goats in 
Virginia which may have been this infection. Pegler describes 
it somewhat fully in his work entitled, ' ' The book of the goat ' ' 



THh 

R31TY i 



64 TAKOSIS 

as " a disease peculiar to goats." The identity of this disease 
and the various affections of goats, largel}' pneumonia, 
described bj^ Duquesnoy, Hutchens, Pusch, Steele and others 
is not established. Mohler and Washburn seem to be the only 
investigators in this country who have carefully studied this 
affection. 

§ 57. Geographical Distribution. Takosis is reported 
from a number of localities in this country, more especially in 
the Northern States. 

§ 58. Etiology. Accord- 
ing to Mohler and Washburn 
this disease is caused by M. 
caprinus. It is pathogenic 
for goats, chickens, rabbits, 
guinea pigs and white mice, 
but not for sheep, dogs or 
rats. It usually appears in 
pairs. It has been isolated 
in pure culture from the 
heart's blood, spleen, kidneys 

and pericardial fluid. It ^ ,, ... ^ . 

^ Fig. 8. Micrococcus caprinus Jrom 

was not obtained in cultures ^/^^ ^^^^^^^ ,,y- ^„ ^„„.^^^, ^^^^ 

from the spinal cord. {Mohler). 

^5 59. Symptoms. The first observable symptom is a 
listless and languid appearance of the animal. The affected 
goats lag behind the flock. Frequently there is drooping of 
the ears and a drowsy appearance of the eyes. There is slight 
elevation of the temperature in the beginning, but later in the 
course of the disease it becomes subnormal. As the disease 
advances the goats move about in a desultory manner, the 
back arched, neck drawn down toward the sternum, and the 
gait staggeriug. Rumination is seldom impaired. The appe- 
tite is usually good but capricious. The exposed mucous 
membranes are pale. The respirations are accelerated and 
labored. The affected animals soon become so weak that they 
can stand with difficulty, and often they are knocked down 




MORBID ANATOMY 65 

and trampled by their companions. They shrink often to 
nearly half their normal weight. There is usually a fluid dis- 
charge from the bowels of a very offensive odor during the 
last few days. The goat groans occasionally and the head is 
usually bent around to one side. Death follows in from eight 
days to ten weeks. Recoveries have not been observed. The 
young are reported to be more susceptible to the disea.se than 
the older animals. 

§ 60. Morbid anatomy. Emaciation and anemia are 
the most striking lesions. The lungs usually contain areas of 
pneumonia. Their surface is mottled by areas of congestion 
and iron gray patches. On section these areas show a frothy 
mucus in the bronchioles. The heart mu.scle is pale, dull, soft 
and flabby. Inflamed hemorrhagic areas may appear on the 
epicardium. Sometimes they are present in the endocardium 
especially that lining the ventricles. The pericardium is 
slightly thickened and usually contains a small quantity of 
blood-stained fluid. The gall bladder is frequently distended 
with a pale-yellow watery bile. The liver appears to be unaf- 
fected. The kidneys are anemic and softened. The cortex is 
pale and contrasts strongly with the dark pyramids. The 
capsule is easily removed. The spleen appears to be atrophied 
and indurated, the fibrous portions exceeding the spleen pulp. 
The spleen may be attached to the diaphragm or neighboring 
organs by adhesions. The mucosa of the intestines gives the 
appearance of a chronic catarrh associated with necrosis of the 
mucosa. 

The microscopic study showed the terminal bronchioles 
and alveolar passages to have swollen walls and to contain 
various amounts of mucus and desquamated cells as a result 
ot the catarrhal inflammation. The blood vessels in the inter- 
alveolar tissue are distended and surrounded by migrated 
leucocytes. The kidneys show a catarrhal or parenchymatous 
nephritis with the most pronounced changes occurring in the 
cortex. The intercapsular space is dilated and contains an 
albuminous exudate. The convoluted tubules show the epi- 
thelium to be swollen and granular and occasionally desqua- 



66 TAKOSIS 

mated. The tubules may contain an albuminous deposit. As 
the specific micrococcus has not been found in the kidneys, 
Mohler and Washburn considered the lesions in this organ to 
be of toxic origin. 

The heart shows parenchymatous degeneration of isolated 
fibers or groups of fibers. The spleen shows an increase in 
fibrous tissue. Sections of the intestines, especially of the 
duodenum, show a productive inflammation with exudation. 
There is often desquamation of the mucosa. 

The blood count in experimental cases shows an increase 
in the number of red corpuscles. Mohler and Washburn report 
the examination of the blood in two such cases and one of nat- 
ural infection as follows : 

No. I. Red corpuscles 11,190,000, white corpuscles 20,560 
per cubic millimeter. 

No. 2. Red corpuscles 12, 160,000, white corpuscles 20,000 
per cubic millimeter. 

No. 3. (Natural infection) red corpuscles 10,208,000, 
white corpuscles 14,860 per cubic millimeter. 

They give the normal red corpuscles as 9,976,000, white 
corpuscles 9,200 per cubic millimeter. 

The increase in the white cells they state is due to an in- 
creased number of polymorphonuclear leucocytes and eosin- 
ophils. They found the specific "gravity of the blood to be 
1. 03 1 and hemoglobin 56. 

§ 61. Differential Diagnosis. Takosis is to be differen- 
tiated from the morbid condition resulting from various animal 
parasites, anemia caused by some previously existing disease 
such as chronic pneumonia, or poor food and starvation ; 
watery cachexia and hydremia, and contagious pneumonia. 

The positive diagnosis is made from the infectious nature 
of takosis, and by finding the specific organism, M. caprinus 
in the tissues. The symptoms caused by parasites -frequently 
resemble quite closely those of takosis. In takosis symptoms 
of pneumonia will frequently be noted, especially the labored 
breathing or rapid respiration. The luster of the fleece is less 



PREVENTION 07 

affected in takosis, while diarrhea is more frequently noted. 
Continuous coughing and snuffling, while diagnostic of the 
presence of lung worms, are not characteristic of takosis. 

The anemia due to other causes is not common. Hy- 
dremia usually results from poor feeding or pasturing on low 
ground. The symptoms are weakness, exhaustion, rapid 
respiration and palpitating heart. The mucosa of the eyes, 
nose and mouth are pale and swollen. The edema about the 
head, neck and abdomen will differentiate this condition from 
takosis. 

Hutcheou writes concerning the contagious pneumonia of 
goats as follows : 

" It was a specific infectious form of pleuro-pneumonia, 
affecting goats only. Cattle and sheep remaining free from 
infection although constantly exposed to it. The disease was 
introduced into Cape Colony by a shipload of angora goats 
from Asia Minor, where the disease is represented as being 
indigenous." 

§62. Prevention. The study of this disease by Mohler 
and Washburn brought out very clearly certain preventive 
measures that should be carefully noted. 

1. The most destructive outbreaks have occurred among 
goats that had recently been shipped from a Southern locality 
to a Northern latitude. Sudden climatic changes should be 
avoided. Hob.son states that the natives of Asia Minor assert 
that the goat cannot be transported from one village to another 
of higher altitude without suffering some deterioration. 

2. Angora goats should be provided with stables that 
are perfectly dry. These should be accessible to them at all 
times, as rains are very injurious to them. So averse are they 
to wetting that they will seldom be caught out in a shower if 
shelter is within reach. 

3. Careful feeding. 

4. When the disease appears, remove all well animals 
from the sick ones. 

Immunity seems to have been established by the injection 



68 TAKOSIS 

subcutaneously of sterilized cultures of the specific organism. 
The method, however, is still in the experimental stage. 

REFERENCES. 

1. HOBSON. Angora goat farming. Agricultural Journal, Cape 
Colony, Vol. VIII (1894), p. 81. 

2. H01.ZENDORFF. Lungen-Brustfellentziindung bei Ziegen. 
Archivfiir Thierheilk., Bd. XXII (1896), p. 345. 

3. HuTCHEON. Contagious pleuro-pneumonia in Angora goats. 
The Veterinary Journal, Vol. XIII (1881), p. 171. 

4. HuTCHEON. Contagious pleuro-pneumonia in goats at Cape 
Colony, South Africa. Ibid. Vol. XXIX (1889), p. 399. 

5. MoHLER and Washburn. Takosis, a contagious disease of 
goats. Bulletin No. 45, U. S. Bureau of Animal Industry, Washing- 
ton, D. C, 1903. 

6. NicoL ET Refik-Bey. La pneumonic des chevres d'Anatolie. 
Ann. de Vhist. Pasteur, Vol. X (1886), p. 321. 

7. Pegler. The book of the goat. 1885. 



CHAPTER V. 

DISEASES CAUSED BY BACTERIA 
GENUS BACTERIUM. 



§ 63. General discussion of the genus bacterium. 
The genus Bacterium includes all the rod-shaped, non-motile 
bacteria. The absence of raotihty appears to be a logical, 
natural and sufficient reason to place these organisms in a 
genus by themselves. The only objection, that can be reason- 
ably urged against it from the pathologist's point of view, is 
the changing of the generic name of a number of important 
pathogenic bacteria, such as those of anthrax, glanders, tuber- 
culosis and others, from Bacillus to Bacterium/> This, how- 
ever, is not serious but should be gladly welcomed if it enables 
us to bring into groups for study diseases that are etiologically 
more closely related. It is for this reason that the classifica- 
tion is adopted. The further subdivision of the non- motile, 
rod-shaped bacteria into several genera, as found in more 
recent classifications, suggests the possible desirability of a 
more restricted grouping of diseases for study and comparison, 
than Migula's classification permits. Several writers have 
already proposed a more limited grouping, such as is found in 
the Pasteur el loses. 

^ 64. Pasteurelloses. Lignieresv has introduced the 
term Pasteurelloses to include a group of diseases in different 
species of animals caused by the bacteria represented by the 

* It is important not to confuse the genus bacterium as revived by 
Migula with the same genus of earlier writers who characterized it as 
composed of non-spore bearing, rod-shaped organisms. 

T Lignieres. Contribution a I'etude et a la classification des septi- 
cemics hemorrhagiques les " Pasteurelloses." Ami. de Vlnstit. Pasteur, 
Vol. XV (1901), p. 734- 



70 



PASTEURELLOSES 



bacterium of fowl cholera, first described by Pasteur. Trevisan 
gave the generic name Pasteiirella to this group of organisms. 
Hueppe designated them under the heading of Bacillus septi- 
cetniac hemorrhagicac. He seems to have taken for his type 
the bacillus of schweineseuche of Loeffler and Schiitz. 

In order to simplify the nomenclature, Lignieres has 
grouped the diseases caused by the Pastcurella Trev. as indi- 
cated below. This plan was adopted by Nocard and Leclainche. 

1. Pastenrellose of birds. Fowl cholera. 

2. Pastenrellose of rabbits. Rabbit septicemia. 

3. Pasteurello.se of guinea-pigs. 

4. Pasteurellose of wild animals. Wildseuche. 

5. Pasteurellose of sheep. Pneumo-enteritis of sheep. 

6. Pasteurellose of goats. Infectious pneumonia. 

7. Pasteurellose of cattle. Septicemia hemorrhagica, 

septic pleuro-pneumonia of calves, 
diarrhea of calves (white scours) and 
enteque ( a disease of cattle in Argen- 
tine Republic, characterized by a state 
of progressive cachexia. ) 

8. Pasteurellose of buffalo. Barbone, an infectious dis- 

ease of buffalo characterized by acute 
fever and edematous engorgement of 
various organs. 

9. Pasteurellose of swine. Swine plague. 

10. Pasteurellose of horses. Infectious pneumonia or 

typhoid fever of horses. 

11. Pasteurellose of dogs. Maladie des chiefis {(Msiem^&r) 

and typhus du chien (malady of Stutt- 
gart, hemorrhagic gastro-enteritis. ) 
The very interesting and far reaching findings of Lig- 
nieres relative to the distribution of this genus of bacteria and 
the diseases produced by its different species are worthy of 
careful consideration. If his results are verified, this grouping 
will do much to simplify both the nomenclature and the de- 



SWINE PLAGUE 71 

scriptions of the various maladies caused by this group of bac- 
teria. We already have a similar grouping in tuberculosis, 
where the disease bears the name of its cause, no matter in 
what species of animals it exists or in what form it manifests 
itself. Such a simplying process is hoped for but at present 
it seems desirable to retain the names of the diseases that are 
now recognized. 



SWINE PLAGI'R* 

Sy>nniy»is. Infectious pneumo-enteritis. Pasteurellose 
of swine ; sepficeuiic du pore : p)ieumonii contagieuse ; Schwein- 
cseiuhe. 

>^ 65. Characterization. Swine plague is an infectious 
disease of swine occurring sporadically and in epizootics. It 
appears usually as a septicemia, or a pneumonia in which there 
is marked consolidation of the ventral and cephalic lobes and 
the cephalic portion of the principal lobe of one or both lungs. 
There may or may not be pleuritis. There may be marked 
changes in the intestine, consisting of superficial necrosis of 
the mucosa especially in the ileum and cecum. On this 
account it has been considered an infectious pneumo-enteritis. 

§ 66. History. In 1886, Smith found in a pig in the 
state of Illinois a disease which differed from hog cholera, and 
from the lesions he isolated an organism which differed from 
the bacillus of hog cholera. Later other cases of thisdisea.se 
were found in considerable numbers not only in the state of 
Illinois but in various places in the eastern part of the United 
States. Prior to this, Loeffler in Germany had described an 
organism which he had found to be the cause of an infectious 
pneumonia in swine {Schiveinesciiche ) and with which Smith 
was able to identify the organism he had discovered. The first 
publication on this disease in the United States is in the 

* For an explanation of the confusion existing concerning; llie 
nomenclature of swine plague and hog cholera see hog cholera. 



72 



SWINE PLAGUE 



Annual Report of the Bureau of Animal Industry for 1886. 
Smith described swine plague as an independent disease, 
although it is often associated with hog cholera in the same 
animal. On account of its frequent association with hog 
cholera, it has been thought by some investigators to be a 
secondary infection only. In 1895 the writer investigated 
several outbreaks of this disease in southern Minnesota where 
it occurred uncomplicated with hog cholera. More recently 
two epizootics of swine plague have been studied in New York 
State where no evidence was found of its being a secondary 
infection but where in every particular its independent nature 
was indicated. 



^ 67. Geographical distribution. Swine plague is a 
wide spread disease in this country. It seems to occur more 
or less frequently in every state in the Union. It is quite 

widely distributed in Ger- 
many, but to what extent it 
exists in other countries 
there is little or no available 
evidence. 

^ 68. Etiology. Swine 
plague is caused by a non- 
motile, elongated, oval bac- 
terium described by Smith in 
1886. It is identical with 
the bacillus of Schzveineseuche 
decribed by Loeffler in 1885. 
Fig. 9. Bacterium of swine plague Hueppe proposed the name 
from a cover-glass preparation of a Bacterium septicemiae hemor- 
rabbiVs liver. rhagicae for this organism. 

Hutyra has found a filterable virus in the blood and other 
parts of pigs suffering with Schiveincseuche. The possibility 
of a mixed infection in this case is not excluded. Other 
European observers have reported similar findings. 

The bacterium of swine plague and its varieties have not 
been systematically studied and classified. It has already 




ETIOLOGY 



73 



been noted that the bacteria of rabbit septicemia, fowl cholera 
and Wildseuche are closely related to it. 

Becker has described a pleuro-pneumonia in lambs and 
Evans has recently observed a septicemia hemorrhagica in 
elephants caused by this species of bacteria. The infection 
took place through wounds. 

The pathogenic organism associated with the lesions in 
certain forms of broncho-pneumonia in cattle diflfers very 
slightly from this. In human pathology, we find a striking 
resemblance in Micrococcus lanccolahis to the swine-plague bac- 
terium, especially in its manifold and varied pathogenic possi- 
bilities and its frequent presence in normal saliva. 

The fact should be recognized that experimentally the 
different varities or forms of this group {Bacterium septi- 
cemiae hemorragicae HxiQ-p^t, Paste urella Trev.)arenot inter- 
changeable in their pathogenesis except for the rabbit. Thus 
an epizootic form of fowl cholera has not been produced with 
the swine plague or rabbit septicemia organism. Further, it 
has been shown that in the upper air passages of healthy 
swine, cattle, horses, cats and dogs* there are bacteria not 
distinguishable in their cultural characters and their effect 
upon rabbits from the swine plague bacterium. The presence 
of this organism in the trachea of healthy pigs has been sug- 
gested as the source of the cause of sporadic cases of swine- 
plague. It explains the frequent association of this bacterium 
with hog cholera and other maladies. What the conditions 
are by which this organism is enabled to produce disease in its 
host have not been clearly pointed out. 

If the rabbit is taken as the animal on which to test the 
pathogenesis of the bacteria belonging to the swine plague 
group, we find that those from different sources are very simi- 
lar. In nature, the bacteria of swine plague, rabbit septi- 
cemia, fowl cholera, and those located in the normal upper air 
passages of the various species of animals mentioned exist, 

*The investigations thus far made show these bacteria to be present 
in 48 per cent of healthy swine, 80 per cent of cattle, 50 per cent of 
sheep, 16 per cent of horses, 90 per cent of cats, and 30 per cent of dogs. 



74 SWINE PLAGUE 

possessed of marked variation in virulence, that is, there are 
those that will kill a rabbit in from 1 6 to 24 hours when inoc- 
ulated subcutaneously with a pure culture and those that 
require from 3 to 10 days, or even weeks, to destroy life. 
With the variations in the time period, we have corresponding 
differences in lesions. The virulent forms produce septicemia 
while the attenuated varieties excite a severe purulent infiltra- 
tion about the place of inoculation and exudates on one or 
more of the serous membranes. Conversely, it has been shown 
that rabbits possessed of a certain amount of natural or artifi- 
cially produced resistance will, when inoculated with a viru- 
lent culture, die after the same period of time and with lesions 
similar to those produced by the attenuated virus in the sus- 
ceptible rabbit. 

■ The fact that this organism is not frequently described in 
our works on bacteriology and because of some confusion 
existing concerning it and the bacillus of hog cholera, it is 
deemed best to insert a short description of it here. 

^ 6g. Brief description of the bacterium of swine 
plague. 

Morphology. — A non-motile, rod-shaped organism varying from o.S 
to 2.0 microns in length and from 0.4 to 1.2 microns in breadth. The 
ends are oval, and the shorter forms resemble micrococci. The size 
depends upon the medium and the stage of development of the individ- 
ual bacteria. A capsule has not been demonstrated, although often 
there appears to be one in preparations made directly from tissues. It is 
not observed in cultures. Spores have not been seen. Involution forms 
are not uncommon in old cultures. They are especially numerous in 
the organs of a rabbit when it is allowed to lie for some hours after 
death before it is examined. It exhibits, when stained in cover-glass 
preparations made directly from animal tissues, a light center with 
deeply stained extremities (polar stain i. In preparations made directly 
from cultures this character is much less marked. It stains readily with, 
the basic aniline dyes. It does not retain the coloring matter when 
stained after Gram's method. 

Cultural and biochemic properties. — This organism is less hardy 
than the bacillus of hog cholera, and on certain of the media used it 
grows very feebly or not at all. It requires a temperature of above 37° 
C. although it develops very slowly at the room temperature. 



15ACTKRIUM 75 

Agar. — The growth on this medium is not vigorous. It is of a 
neutral grayish color, with a glistening, moist appearing surface. It is 
slightly viscid and adheres to the agar surface. Isolated colonies vary 
from I to 2 mm. in diameter, nearly round, convex, with smooth and 
sharply-defined margins. The condensation water becomes faintly 
clouded with a grayish sediment which becomes viscid. Within the 
agar the colonies appear as minute grayish dots. In agar, especially in 
plates (Petri dishes), it emits a peculiar, disagreeable, pungent odor. 

Gelatin. — Ordinarily it does not grow in gelatin. (Dr. Theobald 
Smith found that certain cultures grew in this medium.) 

Potato.— \i does not grow on potato. 

Bouillon. — Alkaline, peptonized bouillon becomes uniformly 
cloxided in 24 hours when kept at a temperature of 36° C. Occasionally 
cultures are obtained in which the growth appears in the form of floc- 
culent masses, but usually after a few generations these disappear and 
the liquid becomes uniformly cloudy. If the bouillon contains any 
dextrose or muscle sugar, its reaction becomes acid in 24 to 48 hours, 
owing to the fermentation of the carbohydrate. With the virulent cul- 
tures the liquid clears within a few days. The small amount of grayish 
sediment becomes viscid after some days, and upon agitation it is 
forced up, appearing as a somewhat twisted, tenacious cone, with its 
apex at or near the surface of the liquid. Frequently a thin, grayish, 
somewhat viscid band composed of bacteria is found on the sides of the 
tube at the surface of the liquid. It will not grow in acid bouillon. If 
the bouillon contains from i to 2 per cent, glucose, the growth is 
slightly more vigorous. 

Effects on sugars. — lnih.Qiexmenta.i\on tube, alkaline bouillon con- 
taining sugars becomes uniformly clouded in both branches, tras is 
not produced. In bouillon containing dextrose and saccharose the 
reaction becomes strongly acid in 24 hours, but the reaction of alkaline 
bouillon containing lactose is not changed. 

7I/i7/&.— Milk inoculated with this organism remains unchanged in 
appearance for several weeks. When boiled, after this period, the 
casein is not coagulated. 

Indol. — This organism grows feebly in Dunham's solution; some 
cultures have given a decided indol reaction, but others have not. The 
production of indol is reported to be one of the properties of the German 
swine plague. Smith* obtained only a trace of indol in one out of four 
cultures of swine-plague bacteria. 

/%,?«(7/.— This was found bv Lewandowski'st method in all of the 



*Special report on swine plague, 1891, p. 89. 
tDeutsche med. Wochenschrift, 1890, S. iiSb. 



76 SWINE PLAGUE 

cultures tested by Smith. I have failed to obtain the reaction in a few 
cultures, but usually it appears. 

Thermal death point. — This organism is destroyed in bouillon at 
58° C. in ten minutes. A temperature of 56° C. for this time did not 
destroy its vitality. 

Effect 0/ drying. — These bacteria cannot stand drying. The bacte- 
ria in a drop of bouillon dried on a cover-glass and kept at the room 
temperature are destroyed in 24 to 36 hours. In similar preparations 
made from agar cultures they resist drying from five to eight days. 
The difference in the time between the two cultures is probably due to 
the thicker layer in case of the agar preparations. 

Persistence of vitality in icater and .yo//.— Experiments to deter- 
mine the length of time this organism will live in water and in the soil 
show that it is destroyed in water in test tubes in from nine to eleven 
days. In the soil it was not found after eight days. Dr. Smith states 
that it is destroyed in the soil after four days. 

PoK'er to resist disinfectants. — The bacterium of swine plague is 
very sensitive to the action of disinfectants. A large number of these 
agents have been tested. The following are among the more important : 

Commercial sulphuric acid, "s per cent, kills in 30 minutes. 

Commercial hydrochloric acid, % per cent, kills in 10 minutes 

L/ime, lime water kills in i minute. 

Lime, 0.015 per cent, kills in 30 minutes. 

Carbolic acid, '4 per cent, kills in 60 minutes. 

Carbolic acid, i per cent, kills in 5 minutes. 

Carbolic acid, 2 per cent, kills in i minute. 

Formalin, solution 1:2000 kills in 5 minutes. 

Trikresol, ;/, per cent, kills in 5 minutes. 

Pathogenesis. — This organism is pathogenic for rabbits, guinea pigs 
and mice amongthe smaller experimental animals and for swine. With 
the virulent form rabbits inoculated either subcutaneously or in the 
vein with very small, o.ooi c. c. doses, die of septicemia in from 16 to 24 
hours. Guinea pigs are slightly less susceptible. When inoculated 
subcutaneously with o. I to 0.2 c. c. of a bouillon culture, they die in 
from 30 to 72 hours. Mice succumb in about 24 hours when inoculated 
with a drop of the culture. Pigs inoculated intravenously usually die 
from acute septicemia in from 18 to 36 hours. If they live longer there 
may be decided lung lesions. (See report on swine plague. Smith ) 

§ 70. Symptoms. It is frequently difficult to recognize 
symptoms distinctive of swine plague. The peculiarities of 
swine render it exceedingly difficult to obtain evidence on 
physical examination of lung disease. Sometimes this affec- 



MOKKID ANATOMY 



77 



tion runs a very rapid course, the animal dying of septicemia. 
Usually it is more protracted, lasting from a few days to a 
week or longer. Animals affected with the more chronic form, 
where there are lung lesions, eat very little or refu.se food 
altogether. They cough considerably, especially when forced 
to run. The back is usually arched and the groins sunken. 
The whites of the eyes are reddened. The skin over the 
ventral surface of the body, nose and ears is frequently flushed. 
The cough, however, is the most reliable indication we have 
of swine plague ; but in some cases of hog cholera the coexist- 
ence of broncho-pneumonia also causes the animal to cough 
when forced to move rapidly. 

§ 71. Morbid anatomy. There are many known varia- 
tions in the appearance of the internal organs of hogs which 
have died of swine plague. The characteristic lesions are. as 
previously stated, to be found in the lungs. Frequently the 
abdominal viscera appear to be normal, although a careful 
examination will usually reveal slight changes. In the lungs, 
however, the disease is ordinarily obvious. 

The variety of lesions produced by the inoculation of 
swine plague bacteria is not so great as that observed in the 
naturally contracted disease. While there are outbreaks in 
which considerable uniformity is observed, there are others in 
which each animal is a surprise to the pathologist. In general 
it may be stated that the lungs and the digestive tract are the 
chief seats of the disease, though other organs, notably the 
lymphatic glands, are secondarily involved. The disease is 
localized in the lungs and in the digestive tract probably 
because the bacteria gain entrance through the respiratory and 
digestive passages. 

The lungs have been found diseased in nearly every out- 
break which has been investigated. In some outbreaks the 
lung lesions predominated and pneumonia was the direct cause 
of death. In individual cases, pneumonia is absent but 
pleuritis and interlobular edema are generally present. In a 
few instances interlobular emphysema of the lungs has been 
observed. With pneumonia the seat of the le.sion varies : 



78 



SWINE PLAGUE 



usually the ventral lobes are first attacked, then the cephalic 
and azyffos, and lastly the principal lobes. This movement of 
the disease seems to depend on gravity, inasmuch as the dis- 
eased parts are marked off from the healthy portion by a nearly 

horizontal line. I n 
other words, the most 
dependent portions of 
the lungs are the ones 
affected first, and as 
the disease progresses 
upwards only a small 
portion of the princi- 
pal lobe directly un- 
der the back of the 
animal remains per- 
vious, provided the 
life of the animal is 
maintained up to this 
point. In cases where 
disease is caused by 
lung worms or by em- 
bolism, the pneu- 
monia involves por- 
tions of the principal lobes not contiguous to the ventral lobes. 
Two kinds of pneumonia are encountered, namely, lobar 
and catarrhal or broncho-pneumonia. In the former the vesi- 
cular portion of the lung substance is chiefly affected ; in the 
latter the smaller bronchioles are primarily attacked and the 
alveoli secondarily. In croupous- pneumonia, there is, follow- 
ing the stage of congestion, an emigration of red blood cor- 
puscles, some leucocytes, and an exudate of fibrin into the air 
spaces. These elements are firmly matted together by the 
coagulating fibrin, making the diseased lung firm to the touch. 
In broncho-pneumonia the catarrhal condition of the smaller 
air tubes makes them impervious to air. The lung tissue 
which they supply is gradually emptied of air and assumes the 
appearance of red flesh, owing to the collapse of the walls of 




Fig. 10. 



Portion of a pig's lung showii 
emphysema. 



ISrORBID ANATOMV 



79 



the alveoli and the distended condition of the capillary net- 
work. Subsequently the inflammation extends into the alveoli, 
which then become distended with cellular masses. 

The nature of the lung disease will depend more or less 
upon the mode of entrance of the virus. If it enters only 
by way of the air tubes it will appear perhaps as a broncho- 
pneumonia. If it enters the lung tissue through the circula- 
tion we may have more or less scattered centers of hepatiza- 




FiG. II. Right lung of pig. The stippled portion is usually 
involved in cases of infectious pneumonia or sivine plague. {/>) ventral 
lobe, {c) cephalic lobe, {a) principal lobe. The ventral lobe is usually 
the seat of the more advanced disease and consequently the first to become 
hepafized. The cephalic portion of the principal lobe (.r) is usually 
hepatized and the reinaining portion deeply reddoied. 

tion (embolic pneumonia). If it enters by way of the pleura, 
the virus will creep along the interlobular and peribronchial 
tissue before it invades the parenchyma proper. 

In natural infection of swine plague, bacteria seem to 
enter the lung tissue chiefly by way of the air tubes. At the 
same time it is not improbable that occasionally they may 
enter the serous cavities first, /. e. , invade the pleural cavities 
and thence the lungs. This probability is shown by inocula- 



8o SWINE PLAGUE 

tion in which intravenous injections produced exudative pleu- 
ritis and pneumonia of the most dependent portions of the 
lungs covered by the pleural exudate. It is not improbable 
that even in the natural disease the bacteria which have 
gained access to a portion of the lung tissue by way of the air 
tubes reach the pleura covering this portion, and may then by 
this route invade other portions of the lungs. It may be that 
in this way a pneumonia originally single may become double. 
It has been observed that the first pneumonic infiltration of 
the principal lobe was at the point of contact with the dis- 
eased ventral lobe, and that the resting of a lobe against an 
inflamed serous surface, such as the pericardium, caused a 
pneumonic infiltration at the point of contact. 

The character and seat of the lung lesions are somewhat 
variable. It is difficult to find two lungs exactly alike so far 
as gross appearances go. This to be sure may be due largely 
to the fact that animals die in different stages of the disease. 
Yet there are differences evidently not dependent on this fact, 
which must be left for special pathological investigation. 

In general the cephalic (anterior) half of a swine-plague 
lung is hepatized, of a dark-red or grayish-red color and firm 
to the touch. The pleura is more or less thickened and 
opaque, and possibly covered with easily removable, friable, 
false membranes. In the more recently affected regions a 
faint but quite regular, delicate mottling with yellow is 
observed to shine through the pleura when not thickened. 
These minute hazy, yellowish dots usually occur in groups of 
four. Occasionally whitish or yellowish patches varying 
much in size are seen, perhaps more frequently in the ventral 
lobes. These correspond to homogeneous dead masses of lung 
tissue. 

When such lungs are cut open, the section presents much 
the same appearance, both as regards color and mottling, as 
when viewed from the surface, excepting that the details are 
less distinct. In some cases, in the most recently invaded 
territories in the principal lobe and nearer the dorsum in the 
other lobes, the dark or grayish-red cut surface shows grayish 



MORBID ANATOMY 3j 

lines usual]}' arranged in curves and circles. These, so far as 
determined, represent the cut outlines of the interlobular and 
peribronchial tissue infiltrated with cells. It has already been 
stated that these lines may represent the paths along which 
the swine- plague bacteria invade the lungs from the pleural 
surface. 

The cut ends of the bronchi of the ventral lobes are fre- 
quently occluded with thick, whitish pus ; in the other lobes 
a reddish froth is usually present. Rarely they also contain 
thick glairy mucus in which particles of dry pus and lung 
worms are imbedded. The contents of the air tubes in the 
ventral lobes may have been derived from the overdistended 
alveoli, or else a broncho-pneumonia may have preceded the 
swine-plague pneumonia. 

In microscopic sections of diseased lung tissue the alveoli 
and smallest air tubes are found distended with cell masses 
consisting chiefly of leucocytes. Usually there is very little 
fibrin and very few red corpuscles in the alveoli, even in cases 
in which the disease was quite recent. It may be that the 
stage represented in ordinary croupous-pneumonia by the pres- 
ence of fibrin in connection with the cellular elements is very 
brief, and that it is speedily replaced by large numbers of leu- 
cocytes. The large predorainence of these elements in some 
portions of the lungs, as well as beginning fatty degeneration, 
is probably the cause of the regular mottling of the lungs, as 
seen from the surface. The little yellowish hazy dots represent 
alveoli surrounded by the hyperemic walls. 

The necrotic and caseous changes so frequent in swine 
plague are most interesting. The latter are usually quite small 
and disseminated in large numbers over the diseased lobes. 
The former represent larger masses from a marble to a horse- 
chestnut in size. They represent tissue which has been 
destroyed by the rapid multiplication of .swine-plague bacteria 
in particular localities. Hence they are found in all stages of 
the pneumonia. The large caseous masses may be considered 
as the result of a slow death of larger areas of lung tissue, due 
primarily to the gradual overdistention of the tissue bv leuco- 



82 



SWINE PLAGUE 




cytes, and hence the gradual cutting off of the blood supply. 
One is a rapid death due directly to highly virulent bacteria, 
the other a slow death, or a kind of dry suppuration in the 
later stages of the pneumonia, characteristic of the pig, and 

due indirectly to the 
irritation of perhaps 
more attenuated races 
of bacteria. In some 
cases there are exten- 
sive hemorrhages in 
the interlobular con- 
nective tissue. 

The inflammation 
of the pleura fre- 
quently extends to the 
pericardium. This 
membrane is opaque, 
thickened and its ves- 
s e 1 s distended. It 
may be glued to the 
contiguous lobes of 
the lungs and covered 
by a false membrane, smooth or roughened, which extends 
upon the large vessels emerging at its base. 

Disease of the digestive tract in a considerable proportion 
of animals inoculated with swine-plague cultures consisted 
n a severe catarrhal inflammation of the lining membrane 
of the stomach. The hyperemia was very intense, bordering 
on hemorrhage. Occasionally the extension of the peritonitis, 
produced by intra-abdominal inoculation along the mesenterj'^, 
causes a severe inflammation, with exudation on the mucosa 
of the small intestine. A case is reported where all the Peyer's 
patches of the small intestine were in a hyperemic and partly 
hemorrhagic condition. 

In the naturally contracted disease extensive hyperemia 
of the mucosa of the large intestine, bordering on a hemor- 
rhagic condition, has been observed. In other cases a peculiar 



Fig. 12. Hemorrhage in the interlobular 
tissue of a sivine-plague king: (a) hemor- 
rhage, {b) hepatized lobules. 



MORBID ANATOMY 83 

croupous exudation appeared, which seemingly resulted from 
the effect of swiue-plague bacteria in the large intestine. 

The production of intestinal disease by swine-plague bac- 
teria may be supposed to go on as follows : the bacteria first 
attack the lung tissues and there produce more or less hepatiza- 
tion. The blood through the lungs finds its path partly ob- 
structed. This reacts on the blood in the right side of the 
heart and the venous blood entering it. Hence there may be 
more or less stasis of blood in the portal circulation which in 
turn impairs the digestive functions of the stomach. The 




Fig. 13. Kidney from a case of acute szvine plague, shozcing punc- 
ti for 111 hemorrhages. 

swine-plague bacteria in the lungs in the later stages of the 
pneumonia may be coughed up in the contents of the bronchial 
tubes, swallowed and passed through the impaired stomach 
unharmed into the intestines. The stagnation of the feces in 
the large intestine furnishes the bacteria an opportunity to 
cause inflammation with exudation on the mucous membrane. 
The tendency of swine-plague bacteria to cause fibrinous 
inflammatory deposits on serous membranes may serve to 
explain such action on mucous membranes. 

There is general congestion with resulting degeneration 
of the parenchyma of the spleen, kidneys and liver in the acute 
septicemic forms of the disease. In these cases the specific 



84 SWINE PLAGUE 

bacterium is easily obtained from the abdominal organs. In 
brief, the lesions of swine plague as they appear in various 
outbreaks may be summarized in four classes, namely : 

1. The acute septicemic form in which the lesions are 
characterized by a general hyperemic condition of the serous 
membranes and parenchymatous organs. Not infrequently 
hemorrhages, especially the punctiform variety, occur. No 
localized lesions. 

2. Cases of pneumonia with or without pleuritis. The 
other organs remained normal in appearance. 

3. Cases where either in addition to, or possibly in the 
absence of, the lung lesions there are marked anatomical 
changes in the mucosa of the digestive tract and possibly in 
the lymphatic glands. 

4. Cases of mixed infection, especially with hog cholera, 
where in addition to the swine-plague lesions which may be 
more or less modified, there are those, especially of the diges- 
tive tract, characteristic of the accompanying disease. 

In order to present as clear a picture as possible of the 
findings in a case of this disease, the published autopsy notes 
of one animal are appended. 

"Pig died yesterday, put on ice. Weight about 30 pounds. Skin 
on ventral aspect of body more or less reddened ; over the sternum a 
few excoriations. The enlarged inguinal glands show as lumps under 
the skin. On section they present a mottled gray and red surface, the 
red limited chiefly to the cortex. Edema of the subcutis over right 
knee. 

" False membrane covers the left half of the mass of intestines and 
the spleen ; consists of an elastic, rather firm yellowish white layer. 
Spleen firmly glued to the surrounding intestines, slightly enlarged, 
dark, softened. Liver firm, cut with considerable difficulty. Kidneys 
in condition of parenchymatous degeneration. One hemorrhagic spot 
in medullary portion of the kidney. Pelvis contains a whitish glairy 
liquid. 

" Digestive tract. Two superficial necroses on the inner surface of 
lower lip in front, one on the upper lip and on edge of tongue near tip. 
Stomach contains a little deeply bile-stained fluid. Mucosa sprinkled 
with red spots of a washed-out appearance, most numerous in fundus 
and near pyloric valve. Hyperemia of duodenum begins sharply at 



MORBID ANATOMY 85 

pyloric valve. From the opening of bile duct a few drops of thick bile 
can be expressed. Remainder of small intestine not markedly 
changed. The Peyer's patch in lower ileum has some of its follicles 
enlarged from which caseous masses can be expressed. 

"Large intestine contains much sand and gravel. Mucosa of 
caecum of a dark slate color. The summit of the folds of a puri)lish 
hue. Free edge of valve bordered by a thin slough. On Feyer's patch 
near valve areas of necrotic tissue of a yellowish color, resting on a 
firm, yellowish-white base three-sixteenths of an inch thick. Upper 
colon has its mucosa of the same dark slate color, merging into a wine 
red. Two ulcers one-eighth of an inch in diameter observed. In lower 
colon congestion slight and gradually disappearing towards rectum. A 
small number of circular whitish erosions, apparently associated with 
the solitary follicles. 

"Thorax. On the left lung, the ventral and cephalic lobes are in- 
terspersed with small regions of collapse. The remainder of the lobes 
very emphysematous and hyperemic. Of the right lung, the anterior 
half (/. e., including cephalic, ventral, and adjacent portion of principal 
lobes) hepatized, covered by a thin false membrane, gluing the various 
lobes lightly to each other and to chest wall. The diseased lobes show 
the regular mottling in the upper, dorsal portion. As we proceed to- 
wards the ventral portion the mottling is less distinct, the tissue firmer 
and interspersed with small, irregular, necrotic foci. The smaller 
bronchi contain a thick, whitish pus. In ventral lobe a portion of the 
parenchyma as large as a marble completely converted into a grayish- 
yellow homogeneous mass. Of the principal lobe about one-third or 
one-fourth hepatized. The mottling of surface very regular. On sec- 
tion grayish, circumscribed areas one-half an inch in diameter inter- 
spersed. Over tnese masses the pleura is converted into a wrinkled, 
roughened, hide-like membrane. 

" Trachea and bronchi contain small quantities of foamy liquid in- 
termingled with yellowish particles. Bronchial glands barely enlarged, 
firm ; some lobules pale, others reddened. 

"Bacteriological notes. At the autopsy an agar tube was inoculated 
with a platinum loop lightly rubbed over the pleural exudate. On the 
following day a thin grayish growth with condensation water clouded. 
Examination of hanging drop and stained cover-glass preparations shows 
only swine-plague germs. 

"In cover-glass preparations of hepatized lung tissue a large number 
of germs resembling swine-plague bacteria were seen. 

"With a bit of hepatized lung tissue, a rabbit was inoculated subcu- 
taneouslyat 2 p. m. The rabbit was dead next morning at 8 .\. m., /. e., 
in less than 18 hours. In spleen, liver, and blood preparations nunier- 



86 SWINE PLAGUE 

ous pular-stained swine-plague germs present. An agar culture from 
heart's blood contained only swine-plague germs. 

"From the peritoneal exudate of pig, consisting of cells and fibrin 
and numerous bacteria of several varieties, two agar plate cultures were 
made. On Plate A one large colony of spore-bearing bacilli and one 
small colony of swine-plague germs. Plate B, completely overgrown 
by the spore -bearing bacillus. 

"A bouillon culture from the exudate contains streptococci and 
swine-plague bacteria. Agar plate cultures were made therefrom and 
both germs isolated. 

"At the same time a large rabbit was inoculated subcutaneously 
with a bit of the exudate. Dead in 18 hours. Stained cover-glass pre- 
parations of blood from heart, spleen and liver tissue show polar- 
stained swine-plague germs. An agar culture from the blood contains 
only swine-plague germs. 

"From the spleen, after thoroughly scorching through the exudate, 
two agar plate cultures and a bouillon culture were made with bits of 
spleen pulp. The bouillon culture contained only swine-plague germs. 
"The swine-plague bacteria were thus obtained from lungs, pleura, 
spleen, and peritoneal exudate, while hog-cholera bacilli, which were 
looked for with the greatest care, could not be found." (Smith, 
Report on Swine Plague, p. 62. ) 

The course of the disease varies in acute cases from one to 

three weeks. In chronic or complicated cases it is indefinite. 

The prognosis in swine plague is very unfavorable. Most 

of the affected animals die. and tho.se that recover are usually 

not thrifty. 

§ 72. Differential diagnosis. In sporadic cases, swine 
plague is to be differentiated from broncho-pneumonia due to 
other causes than the swine-plague bacterium. Pneumonia of 
a non specific nature is often associated with deaths due to 
dietary or other causes. It frequently causes death in chronic 
cases of other diseases (terminal pneumonia). 

In epizootics or outbreaks, it is to be distinguished from 
hog cholera when there is accompanying catarrhal pneumonia. 
To make a positive diagnosis, it is usually necessary to depend 
upon the results of the bacteriological examination. 

Pneumonia resulting from lung worms {Strongylus para- 
doxus) can be distinguished by a careful examination of the 
contents of the bronchioles. 



PREVENTION 87 

In case of coexistence of hog cholera and swine plague a 
bacteriological examination is necessary to determine the pres- 
ence of the two diseases, owing to the possibility of an accom- 
panying or terminal pneumonia with hog cholera. 

The question has arisen as to whether the presence of Bad. 
septicemiae hcmorrhagicae in the hepatized lung constitutes a 
diagnosis of swine plague. As understood at the present time 
it would seem that the presence of this species of bacteria 
would indicate the nature of the disease. It must be remem- 
bered, however, that bacteria not readily distinguishable from 
swine-plague organism exists in the normal upper air passages, 
from whence it could be brought into the lung and in such a 
case it might appear as a secondary invader only, or it might 
have been primarily the cause of the lesions. It is not improb- 
able that epizootics may start from these sporadic cases, 
although conclusive proof of this is still wanting. It seems, 
however, that the presence of this organism in the lung tissue 
of a sporadic case should be considered in the light of the dis- 
tribution of these organisms and not necessarily as the starting 
of an epizootic. 

§73, Prevention. Recent investigations show that out- 
breaks of swine plague are much more extensive than hereto- 
fore supposed. The present knowledge of this disease indi- 
cates that the adoption of measures for its prevention is quite 
as important as for hog cholera. In general the measures to 
be adopted and followed and the rules to be observed in the 
prevention of epizootic swine plague are practically the same 
as those for the prevention of hog cholera. It will be seen 
from a comparison of the two species of bacteria that the 
bacillus of hog cholera is a more hardy organism than that of 
swine plague. Thus the swine-plague bacterium is destroyed 
more rapidly by drying and will live a much shorter time in 
the soil. However, the channels through which it may gain 
access to a herd are practically the same, and every precaution 
suggested in reference to hog cholera, is applicable to swine 
plague. It is believed that the time during which a field, hog 



88 SWINE PLAGUE 

3-ard or pen should be kept free from swine after the appear- 
ance of the disease can, with safety, be shorter after swine 
plague than after hog cholera. In any case several months 
should elapse before the yards or pens are reoccupied. If the 
disease appears, the well animals should be promptly separated 
from the sick and placed in suitable pens or yards, protected 
against subsequent infection, and given an abundance of 
wholesome food and water. It is well to remove the sick 
animals to other pens. The thorough disinfection of the 
infected pens should be insisted upon before they are again 
occupied. 

v^ 74. Specific treatment. For a number of years 
investigations were almost constantly under way in the United 
States Bureau of Animal Industry, for the purpose of finding 
some method by which the disease could be successfully and 
specifically treated. Drugs and medicines have been tried, 
preventive inoculations and injections of toxins have been 
made. The serum therapy which has effected relief in certain 
other diseases has been and is now being tested with some- 
what favorable results, by a few European workers, yet we do 
not see that a specific therapeutic agent has been demon- 
strated. In view of this, it becomes necessary to apply with 
renewed zeal our present knowledge of the nature of the 
malady and endeavor to prevent its occurrence or reappear- 
ance by keeping the animals under the best possible condi- 
tions. Prevention of this disease is more promising than its 
treatment. 

§ 75. The effect of swine-plague bacteria in rabbits. 
In 1894, Smith and Moore described the appearance of the 
effect of swine-plague bacteria in rabbits and also the effect of 
resistance on the part of the rabbit on the form of the resulting 
lesions. As this disease is caused by a bacterium belonging 
to the septicemia hemorrhagica group, it seems desirable that 
the results above referred to should be restated. The appended 
paragraphs are taken from the report of these investigations. 

Among the forms of disease observed after the subcu- 



EFFECT ON RABBITS 89 

taneous inoculation of rabbits with swine-plagne bacteria from 
different sources (epizootics) are the following : 

1. Septicemia. 

2. Peritonitis. 

3. Pleuritis (usually with pericarditis). 

4. Pleuritis (usually with pericarditis and peritonitis). 

5. Local lesion onh'. 

In septicemia, death ensues within eighteen or twenty- 
four hours. The local lesion produced at the seat of inocula- 
tion is slight. Bacteria are abundant in the parenchyma 
(blood ve.ssels) of the various organs. In the form character- 
ized by peritonitis death ensues in three to seven days. The 
local lesion, which in all these forms of diseases increases in 
extent with the prolongation of the life of the animal, is here 
characterized by more or less suppurative infiltration of the 
skin and the subcutis. The peritonitis in its earlier stages is 
characterized by punctiform hemorrhages on the cecum 'and 
a fibrinous or cellular exudate. It always contains immense 
numbers of bacteria. When pleuritis is also present the exu- 
date usually involves the pericardium as well. It varies in 
amount according to the duration of the disease and is essen- 
tially the same as the peritoneal exudate. 

The form characterized by pleuritis and pericarditis with- 
out peritonitis is interesting in so far as the seat of inoculation 
does not explain the localization, for, in every case, the inocu- 
lation was made in the region of the abdomen. The lungs 
may become hepatized secondarily through invasion from the 
pleura if the animal lives long enough. 

Lastly, the form of disease in which the only localization 
is a very extensive suppurative infiltration associated with 
hemorrhage and edema of the subcutaneous tissue is not 
common. 

It should be stated that the cultures from the same out- 
break continued to produce the same form of disease in rab- 
bits until modified by age. The maintenance of a certain uni- 



go SWINE PLAGUE 

form virulence for years is well exemplified by a variety iso- 
lated in the summer of 1890. This variety was fatal to 
rabbits within twenty hours when first isolated and this 
degree of virulence maintained itself for a period of nearly 
four years. 

§ 76. Modifications of the septicemic type by in- 
creasing the resistance of rabbits. By the injection of steril- 
ized cultures which increase the resistance of rabbits, Smith 
and Moore were able to produce nearly all the pathological 
variations which follow the inoculation of natural races of 
swine-plague bacteria as isolated from outbreaks. This modi- 
fication of the septicemic type is not fortuitous, for among the 
large number of rabbits inoculated during three and one- 
half years with the culture employed, none survived 
twenty to twenty-four hours. Whenever the course of the 
inoculation disease in rabbits departed from this rapidly fatal 
type, it was due to some preliminary treatment of the rabbit. 

The degree of resistance determined quite regularly 
though not invariably the form of the disease. This degree 
was measured by the relative quantity of the protective ma- 
terial (sterilized cultures, sterilized blood, and blood serum) 
injected. The grades of disease induced range themselves in. 
the following order : 

No resistance — acute septicemia. 
Slight resistance — peritonitis. 

Increased resistance — pleuritis and pericarditis with or with 
out secondary pneumonia. 

4. Higher degree of resistance— pleuritis and peritonitis. 

5. Still greater resistance — irregular lesions in the form of ab- 
scesses, subcutaneous and subperitoneal. 

Nearly complete immunity. Very slight reaction at the 
point of inoculation. 

Most of the cases cited below as illustrating these modified 
forms of the septicemic type belong to the series of immuniz- 
ing experiments of the preceding article. To this the reader 
is referred for additional illustrations. 



MODIFICATIONS 



91 



First degree 0/ resistatia— peritonitis. — Rabbit No. 12 re- 
ceived 7 cc. of bouillon culture of swine-plague bacteria steril- 
ized b)' heat. Subsequently with a control rabbit it was in- 
oculated with a minute dose of swine-plague bacteria under 
the skin. The control died within eighteen hours, the treated 
rabbit in three days. The macroscopic changes were limited 
to the point of inoculation and the peritoneum. At the former 
there was a purulent infiltration of the subcutis, 1.5 cm. in 
diameter, with a dilation of surrounding blood vessels. The 
peritonitis was characterized by an exudate of a slightly viscid 
character covering liver, spleen, and cecum, and made up of 
fibrin, leucocytes and immense numbers of bacteria. 

Second degree of resistance— pleiiritis and pericarditis. — Rab- 
bit No. 38 was treated before inoculation with 4.5 cc. of a 
sterilized suspension of agar cultures of swine-plague bacteria 
in 3 doses. Together with a control rabbit, it received under 
the skin the equivalent of o.ooi cc. of a fresh bouillon culture 
of swine-plague bacteria. The control died in twenty hours. 
The treated rabbit died six days after inoculation. At the 
point of inoculation there was a purulent infiltration of the sub- 
cutis 3 cm. in diameter. The abdomen and abdominal viscera 
were free from macroscopic changes. In the thorax, the pleural 
cavity was lined with a grayish, friable exudate consisting of 
round cells and bacteria. Lungs hyperemic and only partly 
collapsed. Pericardium also covered with a slight exudate. 

Tliird degree of resistance — pleuritis (^pericarditis) a7id peri- 
tonitis. — Rabbit No. 15 received in the ear vein a total of 12 cc. 
of a sterilized bouillon culture of swine-plague bacteria. It was 
inoculated subcutaneously with virulent swine-plague bacteria 
May 26, and died June 3, eight days later. The control rabbit 
died within eighteen hours. The following changes were 
observed : 

A purulent infiltration into the subcutaneous tissue at the point of 
inoculation extending over an area 6 cm. in diameter. The superficial 
layer of the subjacent muscle discolored. Surrounding the area of 
infiltration the blood vessels were injected. The cecum and liver 
were covered with a very thin grayish exudate, which also ap- 



92 SWINE PLAGUE 

peared on and between the coils of the intestine. vSpleen not enlarged. 

The right lung and chest wall covered with a thin grayish exudate. 
In the cephalic lobe, two small areas of consolidation ; principal lobe 
hyperemic. The left pleural cavity lined with a quite thick membran- 
ous exudate, which covered the entire surface of the lung. On the dor- 
sal surface of the principal lobe a mass of lung tissue 2 cm. in diameter, 
firm and of a yellowish-gray color. The remaining portion of the prin- 
cipal lobe hyperemic ; cephalic lobe in a state of collapse. 

Pericardium covered with a thin cellular exudate. 

Higher degrees of resistance. — None of the treated animals 
which have come under our observation have succumbed to a 
mere extension of the lesion produced at the point of inocula- 
tion as is occasionally observed after inoculation with certain 
varities of swine-plague bacteria found in nature. There have 
been noticed, however, certain peculiar localizations resem- 
bling those produced in the subcutis after inoculation, and in 
a few cases the local lesion persisted a considerable length of 
time. It was quite severe in all fatal cases in which the disease 
was prolonged several weeks after inoculation, although the 
real cause of death was due in all such cases to localizations on 
one or more of the serous membranes. The peculiar forms of 
disease may be grouped as follows : 

(a) Persistence of local lesiofis. — Rabbit No. 50 received in the 
abdominal cavity 3.5 cc. of the sterilized suspension of agar cultures in 3 
doses. It was subsequently inoculated beneath the skin with o.ooi cc. 
of a bouillon culture of swine-plague bacteria which produced a large 
local swelling. On February 25, 1892, nearly eight months after its 
inoculation, it was chloroformed. The only lesion found was in the 
subcutaneous tissue. At the point of inoculation the skin was sloughed 
over an area 3 cm. in diameter. The denuded surface was covered with 
a thick scab. The subcutis beneath the scab and surrounding the ulcer 
was infiltrated with pus. A stained cover-glass preparation showed 
swine-plague bacteria. No other lesions were found. 

{b) Sub-peritoneal abscess.— ^ahhit No. 16 was injected intraven- 
ously with 16 cc. of sterilized bouillon cultures of swine-plague bacteria. 
After some days it was inoculated beneath the skin with o 001 cc. of a 
fresh bouillon culture of virulent swine-plague bacteria. The control 
rabbit died within twenty hours. Rabbit No. 16 showed no ill effect 
from the inoculation for several months, when it was noticed that it was 
becoming emaciated. It died June 11, 1892, one year and six davs after 
its inoculation, with a subperitoneal abscess. 



RESISTANCE IN RAB15ITS 



93 



(c) Mjiltiple abscesses under the skin. —Rabbit No. 439 received into 
the ear vein in three injections 4 cc. of sterilized blood from a swine 
plague rabbit. Later it was inoculated subcutaneously with o.ooi cc. of 
a bouillon culture of virulent swine-plague bacteria. The control rabbit 
died within twenty hours. Two months after the inoculation it was 
noticed that this rabbit with others was suffering from a large number 
of subcutaneous abscesses. 

REFERENCES. 

1. DE vSCHWEiNiTz. vSerum therapy. Proceedings Society /or the 
Promotion 0/ Agricultural Science, 1896, p. 47. 

2. DE ScHWEiNiTz. The serum treatment of swine plague and 
hog cholera. Bulletin No. 23, U. S. Bureau 0/ Aniinal Industry, 1899. 

.V Evans. Hamorrhagische septikjimie des elephanten. The 
Jour, of Tropical Vet. Science, Vol. i, p. 283. 

4. JOEST. Schweineseuche und Schweinepest. Jena, 1906. 

5. IvOEFFLER. Arbeiten a. d. Kaiserlichen Gesundheitsainte, Bd. 
I (1885), S. 51. 

6. Moore, Pathogenic and toxicogenic bacteria in the upper air 
passages of domesticated animals. Bulletin No. j. U. S. Bureau of 
Animal Industry, 1893. 

7. Moore. Concerning the nature of infectious swine diseases in 
the State of New York with practical suggestions for their prevention 
and treatment. Report of the Neiv York State Commissioner of 
Agriculture, 1897. 

8. Smith. Preliminary investigations concerning infectious pneu- 
monia in swine (Swine plague). Ann. Rpt. Bureau of Animal In- 
dustry, U. S. Dept. of Agriculture, 1886, p. 76. 

9. Smith. Special report on swine plague. Bureau of Animal 
Industry, (J. S. Dept. of Agriculture, 1891. 

10. Smith and Moore. Experiments on the production of im- 
munity in rabbits and guinea pigs with reference to hog-cholera and 
swine-plague bacteria. Bulletin No. 6, Bureau of Animal Industry, 
U. S. Dept. of Agriculture, 1894, p. 65. 

11. Welch and Clements. Remarks on hog cholera and swine 
plague. First International Congress of America. Chicago. 1893. 



94 HEMORRHAGIC SEPTICEMIA 

HEMORRHAGIC SEPTICEMIA IN CATTLE. 

Synonyms. Wild zind Rinderseuche; Pasteurellosis bovuni; 
Septicemie hemorrliagique du boeuf. 

§ 77. Characterization. Hemorrhagic septicemia in 
cattle is determined b}' an acute attack usually running a 
rapid course and terminating fatally. The lesions consist 
largely of hemorrhagic areas more or less widely distributed 
throughout the body and due to the presence ot a specific 
microorganism. 

§ 78. History. In 1878, Bollinger described under the 
name of Wild und Rinderseuche an epizootic disease which 
killed a large number of wild boars and deer in the Royal 
game preserves of Munich. After the disease in these animals 
had died out, the domestic cattle in the neighborhood began 
to die of the same or a ver)^ similar affection. He reports it to 
be sudden in its onset and rapidly fatal in its course, with a 
mortality of 90 per cent. Death occurred in from 12 hours to 
a few days after the appearance of symptoms. 

An exanthematous and a pectoral form are described. In 
the exanthematous form there are large and small hemorrhages 
disseminated throughout the muscles and viscera. The intes- 
tines exhibit large numbers of ecchj^motic areas, while the 
submucous tissue is infiltrated with a serous exudate. Large 
hemorrhagic tumors infiltrated with serum are abundant in 
the subcutaneous tissue, often extending into the muscles. The 
mucous membranes of the tongue, larynx and phar5'nx, and the 
lymphatic glands of these regions, are swollen and infiltrated 
with more or less bloody serum. In the pectoral form, there is 
a hemorrhagic lobular pneumonia, with considerable infiltra- 
tion into the interlobular tissue of a serofibrinous exudate. 
The pleura is infiltrated and inflamed and covered with a 
fibrinous exudate. The pleural cavities contain from two to 
twenty-five litres of liquid. At the same time there exist a 
certain degree of hemorrhagic enteritis and the widely dissem- 
inated hemorrhagic lesions common to the preceding form. 



HISTORY 



95 



In 1885, Kitt studied an epizootic disease in cattle and 
swine in Sincbach. From this disease he isolated a short, 
polar staining, non-motile, rod-shaped organism, fatal to cattle, 
horses, pigs, sheep, goats, dogs and rabbits. In the following 
year Oreste and Armanni reported a destructive disease of 
young buffaloes in Italy with symptoms and lesions similar to 
those reported by Bollinger and Kitt. This disease had been 
known in Italy for a century or more, where in certain dis- 
tricts it is reported to have recurred with great regularity, 
destroying both old and young animals. In the same year 
(1885) Poels described a septic pleuro-pneumonia in calves 
which prevailed in the vicinity of Rotterdam. It was of a 
septicemic nature. From the organs he obtained an organism 
belonging to the Bacillus septicemiae hcmorrhagicae group of 
bacteria. In 1889, Jensen described a similar disease affecting 
calves in Jutland. In the same year Piot reported the presence 
of " barbone " in the buffaloes and domestic cattle in Egypt. 
In some districts 40 per cent, of the horned cattle are said to 
have died in a single year. It is reported as being more preva- 
lent in the wet season. 

In 1890, Van Ecke described a hemorrhagic septicemia 
in cattle in Dutch India, particularly in Java, the lesions of 
which were similar to those first described by Bollinger. The 
specific organism was virulent for rabbits, mice, turtle doves, 
calves, horses and swine ; sheep and asses were almost 
immune. In the following year Galtier described the same 
disease imported from Algiers to Lyons. A number of other 
investigators have studied and reported cases of this disease. 
In 1890, Nocard isolated from cases of broncho-pneumonia in 
American cattle landed at La Villette, France, an organism 
similar to that described as the cause of septicemia hemor- 
rhagica. In 1896, Smith called attention to a similar organism 
which he found in cases of sporadic pneumonia in cattle ; he 
does not think, however, that this organism was primarily the 
cause of the disease, giving it a secondary place in the eti- 
ology. As early as 1891, Smith published the discovery of the 
presence of an organism morphologically and in its cultural 



96 HEMORRHAGIC SEPTICEMIA 

characters identical with that of swine plague in the upper air 
passages of healthy swine. The same year Moore reported the 
presence of a like organism in the upper air passages of cattle, 
horses, sheep, dogs and cats. The following year. Fiocca de- 
scribed a pathogenic bacterium resembling that of rabbit septi- 
cemia in the saliva of healthy cats and dogs. 

Hueppe proposed the name Bacillus septicemiae henior- 
rhagicae for this group of organisms and septicemia hemor- 
rhagica for the disease they produce. Lignieres has designated 
the diseases caused by this group as Pasteurelloses. While 
there may be objections to this unifying name, there seems to 
be no serious reason for not accepting it as a working hypoth- 
esis. In 1898, Fennimore described under the name of "Wild 
and Cattle Disease " a malady occurring in Eastern Tennessee. 
Its serious nature caused an investigation to be made by the 
Tennessee Agricultural Experiment Station. Norgaard, who 
assisted in this investigation, recognized it as the same disease 
as that described by Bollinger in 1878. Fennimore states 
that it has occurred to a considerable extent in his practice. 
In 1 901, it was carefully studied by Wilson and Brimhall for 
the Minnesota State Board of Health. They report 64 cases 
of this affection which they have examined in cattle in the 
state of Minnesota. In 1903, Reynolds described an investi- 
gation into several outbreaks of this disease in the same state. 
It is from the two latter reports that we draw very largely for 
the symptoms and morbid anatomy of this disease in cattle. 

§ 79. Geographical distribution. It will be seen from 
the history that this disease is a wide .spread malady occurring 
in nearly every country. It appears to be quite prevalent in 
the western and northern parts of the Mississippi valley. 
It occurs in other localities more rarely. 

§ 80. Etiology. Septicemia hemorrhagica in cattle is 
caused by an organism belonging to the group of bacteria 
designated by Hueppe as the hemorrhagic septicemia group 
and specifically named Bacillus boviseplicjis by Kruse. This, 
according to Migula's classification, should be Bacterium 



SYMPTOMS 97 

bovisepticuvi. A brief description of the organism as given by 
Wilson and Brimhall is appended. 

"The organism has a strong tendenc}' to show polar staining in tis- 
sues and to form chains of much shortened individuals in liquid media, 
which causes it to be mistaken in examinations of a single specimen for 
a (liplococcusora streptococcus. Sometimes in cover-glass preparation^ 
from solid organs and very frequently in those from body fluids and 
liquid cultures, the bacteria were found in chains of three to twelve 
individuals. In cover-glass preparations the bacteria are from 0.6/7 to 
0.8// broad and from i.o to 1.5// in length. In tissues which have been 
fixed in 96 per cent, alcohol, they are somewhat smaller. In cultures, 
especially in fluid media, they are apt to be much smaller and approach 
diplococci in appearance. The ends are rounded. In stained prepara- 
tions directly from the tissues most of the bacteria have the ends 
intensely stained and the central portion but faintly so. In some chains 
in rapidly growing broth cultures this is not the case, many of the indi- 
vidual bacteria being evenly stained throughout and somewhat pointed 
at the ends. They do not retain the stain by Gram's method. The 
organism is non-motile. It is aerobic, but prefers the depths rather 
than the surfaces of the media. It grows best at the body temperature 
and more slowly at room temperature. In plain and dextrose broth a 
growth appears in 24 hours. In Dunham's solution a small amount of 
indol is formed in 4S hours. No coagulation of milk. On Liiffler's 
blood serum, direct from the diseased tissues, it failed to grow well. On 
potato no appreciable growth has been obtained. In gelatin plates 
small, granular, white to slightly yello%vish colonies appear after 48 
hours. In gelatin stab cultures a light growth occurs on the surface, 
while along the needle tract numerous colonies like those in the deep 
portions of the plate cultures develop. The bacteria are destroyed in 
fluids at 58° C. in 7 or 8 minutes, by i to 5,000 mercuric chloride in one 
minute, and by a solution of lime water as weak as 0.04 per cent, 
almost immediately." 

The period of incubation is supposed to be very short. 
The method of infection is not known. 

§ 81. Symptoms. There is little opportunity to deter- 
mine the symptoms. The animals observed at the onset of the 
disease by Wilson and Brimhall appeared to be dumpish and 
out of sorts. There is sudden stopping of the milk secretion in 
milch cows. As a rule the affected animals refuse food. Of 
the few that make an attempt to eat, those with affected throats 
are unable to swallow except with much difficulty. These 



98 HEMORRHAGIC SEPTICEMIA 

cases also breathe ver)' heavily. The animals show marked 
disinclination to move and when incited to do so, exhibit stiff- 
ness, and in some instances actual lameness. Animals have 
been observed to drop to the ground and die in a short time, 
apparently without pain. Other animals live for several hours 
in great pain as indicated by groans and spasms of the muscles. 
The paroxysms of pain are apparently intermittent. There is 
extremely rapid loss of flesh in the animals that are sick for 
any length of time. 

Reynolds has observed the symptoms in a few cases. He 
describes three .stages. First (24-36 hours) general dullness 
and checking of milk secretion. Second, diarrheal discharge 
dark in color, and of disagreeable odor. The breath was 
noticed to be offensive. In some cases nervous symptoms 
developed. The temperature remained about normal during 
this period. Third, in this stage the eyes are wild, there is 
grinding of the jaws, convulsions of the face and neck muscles 
followed by a period of intense restlessness and activity. 

He also records the observation that the cases that ap- 
peared to be the worst in the beginning lived longer than 
those that appeared to be mild. 

Opportunities for the accurate determination of tempera- 
ture at the beginning of the disease have been very few. An 
initial temperature of 105.6° F. followed by a rapid decline 
has been observed. Painful edematous swellings about the 
legs, shoulders and under the throat are noted as early symp- 
toms. The intestinal discharges are often streaked with 
blood. In other cases the feces are black, tarry or of a bloody, 
serous nature. Bloody urine and a bloody serous discharge 
from the nose have been present in some cases. The vaginal 
and rectal mucous membranes are intensely congested. 

The marked sweUing of the face, stomatitis, glossitis, and 
convulsive movements of the jaws in the pneumonic form of 
the disease, described by European writers, more especially 
Bollinger, were not observed by Wilson and Brimhall or by 
Reynolds. 



MORBID ANATOMY 99 

The duration of the disease is short. Often the animals 
are found dead. 

The prognosis is unfavorable. The mortality is placed at 
from 80 to 90 per cent of the animals affected. 

^ 82. Morbid anatomy. The characteristic lesions of 
the disease are widely distributed areas of hemorrhage, vary- 
ing in size from a pin point to several centimeters in diameter. 
They vary in color from light red to almost black. They are 
frequently accompanied with a sero-fibrinous exudate, u.sually 
yellow, but occasionally dark red in color. The hemorrhagic 
areas in the animals just dead are not so dark as those in 
animals that have been dead for some hours. The large areas, 
some centimeters in diameter, are apparently due, in some 
instances at least, to single hemorrhages, infiltrating an exten- 
sive mass of tissue, and in others to a number of minute hem- 
orrhages closely placed and partially coalescing. Gas is not 
present in the subcutaneous connective tissue except in cases 
where extensive post-mortem changes have occurred. 

There is extensive fullness of the vessels of the subcu- 
taneous connective tissue in the acute cases, especially in 
those animals which are not killed by bleeding. In animals 
which live until emaciation is marked, there is no engorgement 
of the vessels. 

Reynolds reports one outbreak in which meningitis 
involving the spinal cord, brain or both of these organs were 
invariably present. 

All cases show some hemorrhagic areas in the subcutane- 
ous tissue, though the number and size of these vary greatly 
in the different cases. Some animals show not over a dozen 
areas between two and three centimeters in diameter, though 
many minute ones are present. In other animals, on remov- 
ing the skin, hemorrhagic areas are found in great numbers 
and so extensive that a large fraction, possibly one-eighth, 
of the body surface appears to be involved. The large hemor- 
rhages in the subcutaneous connective tissue appear to be of 
the composite type noted above. 



HEMORRHAGIC SEPTICEMIA 



The location of the superficial lesions varies in different 
animals. In most cases the parts about the shoulder are most 
affected. A few animals show marked lesions in the gluteal 
and inguinal regions. 

At first sight the muscle tissue in some cases seems to be 




Fig. 14. Photograph sho~iOing hcDiorrhages beneath the eiidocardiu-tn 
of the right , ventricle (Reynolds). 

much involved. A closer examination, however, usually 
shows that while some of the minute hemorrhages are in the 



MORHin ANATOMY lOI 

muscle proper, the larger ones are in the intermuscular con- 
nective tissue. They are usualh' accompanied by a consider- 
able quantity of yellowish or blood-stained serous exudate. 
The intermuscular connective tissue appears to be quite as 
much involved as the subcutaneous connective tissues. 

The lymphatic glands are frequently though not uniformly 
nor constantly enlarged. Those that are enlarged are edema- 
tous and often hemorrhagic. The cervical and prescapular 
glands are most seriously affected. 

The nasal mucous membrane in some cases is congested, 
and a bloody serous discharge from the nostrils is present. 
The tissues around the larynx are hemorrhagic and infiltrated 
with blood-stained serum. The mucous membranes of the 
larynx and trachea are more or less congested and covered 
with a frothy mucus, sometimes streaked with blood. In some 
instances no lesions are observable in these organs. The lungs 
are in general almost fere from evidence of disease. Occasion- 
ally there are a small number of hemorrhagic areas, pyramidal 
in shape with their base on the pleura. In most cattle the 
parietal pleura is studded with small hemorrhages. The 
diaphragm sometimes contains very large hemorrhagic areas. 

The pericardial sac usually shows small, sometimes very 
numerous, hemorrhages in the walls, and in man^v instances 
contains a blood-stained serum. 

The heart walls, with but few exceptions, contain ecchy- 
moses and petechiae. These sometimes extend deep into the 
muscle. Similar areas of hemorrhage are also visible in the 
endocardium. The heart usually contains post-mortem blood 
clots. 

The blood, in animals just dead, is said to be somewhat 
lighter than normal in color. When post-mortem changes 
set in, the blood is darker in color, but reddens on exposure 
to the air. 

The spleen shows on its surface a few small hemorrhagic 
areas. It is usually normal in size, color and consistency, 
except where post-mortem changes have taken place. 



I02 HEMORRHAGIC SEPTICEMIA 

Stomatitis and glossitis are rarely observed. The pharynx 
is usually congested. 

The stomach walls contain a few or many hemorrhagic 
areas. These are sometimes extremely large, especially on 
the third stomach. As a rule the larger hemorrhages pene- 
trate the entire thickness of the walls The smaller ones are 
confined to the subserous or mucous coats. The stomach con- 
tents are apparently normal. 

The intestinal walls are constantly affected. Hemorrhagic 
areas involving all the coats are frequently present. Smaller 
ones, visible only from the inner or outer surface, are always 
present. General enteritis and peritonitis are constantly 
observed. lyOcalized enteritis is frequent. 

The bowel contents are in some cases dark and tarry : in 
others the feces are apparently normal in color and consistency 
but streaked with bloody mucous. 

The kidneys are usually but slightly affected. When 
lesions are present they are hemorrhages but pin point in size 
and mostly confined to the cortical substance, though a few 
are found in the walls of the pelvis and ureters. The urine is 
bloody in some instances. 

The vaginal mucous membrane is congested in many 
cases. Wilson and Brimhall saw one animal that was four 
months pregnant which exhibited small hemorrhagic areas in 
the placental membranes. 

The udder is congested in some cases. It may be 
hemorrhagic. 

The central nervous system occasionally shows hemor- 
rhages in the dura. A few cases are reported of hemorrhages 
on all of the joint surfaces. Brimhall recently reported an 
outbreak where the autopsies showed very few hemorrhagic 
areas in the subcutis and internal organs. There were lesions 
in its spinal cord. The spleens were enlarged. In nine out- 
breaks Bad. boviscptiaiyn was present. 

Wilson and Brimhall fixed portions of the subcutaneous 
tissue, skeletal muscles, lymphatic glands, lung, heart wall, 
stomach wall, and spleen in 95 per cent, alcohol and in 4 per 



DIFFERENTIAL DIAGNOSIS IO3 

cent formaldehyde solution and stained by various methods. 
In general the lesions found were enormous extravasations of 
blood, some recent and some showing coagulation of fibrin. 
In the areas of less recent hemorrhage, the surrounding tissues 
showed varying degrees of ordinary coagulation necrosis. 
This was particularly marked in the affected muscles, lymph 
glands and portions of the lungs. In the borders of such 
necrosed areas leucocytic infiltration was not infrequent. In 
the spleen, in which the hemorrhagic areas were neither num- 
erous nor large, there was in some instances an apparent 
destruction or shrinkage of the parenchyma. 

A very important feature in this disease has been brought 
out, namely, that it is necessary, in order to obtain cultures of 
the bacterium producing it, that the media should be inocu- 
lated at once. It is evident from the literature, that with this 
precaution cultures should invariably be obtained. 

§ 83. Differential diagnosis. Septicemia hemorrhagica 
in cattle must be differentiated from anthrax, symptomatic 
anthrax, and the affection known as "corn-stalk disease." 
Death from this disease must also be distinguished from those 
due to certain accidental causes, poisoning, or the effect of 
over eating of grain or green fodder (hoven). The sudden- 
ness with which the animals may die from all of these causes 
renders the symptoms, should they be observed, of very little 
value in making a diagnosis. It is necessary, therefore, that 
in all cases, especially with the first animals to die, careful 
post-mortem and bacteriological examinations should be made. 

In case of septicemia hemorrhagica, the cultures will 
usually reveal the presence oi Bad. boviscptiaim. The le.sions 
will be hemorrhagic in nature. 

In case of the "cornstalk disease " the lesions may consist 
of small hemorrhages (petechias) especially of the serous mem- 
branes and heart. The cultures will be negative. 

With anthrax and symptomatic anthrax, their specific 
bacteria will be found. 

^ 84. Prevention. When this di.sease occurs it is im- 



I04 HEMORRHAGIC SEPTICEMIA 

portant to remove the unaifected animals to other fields or 
enclosures. It is well to divide them into small groups if 
possible. The carcasses of animals that die should be burned 
or buried deeply with a good covering of a disinfectant, such 
for example, as quick lime. Should death occur in a stable, 
all contaminated litter should be burned and the floors, man- 
gers and walls thoroughly disinfected. 

Experiments directed towards protective inoculation have 
been made, but thus far the results have not been sufficiently 
satisfactory to warrant the recommendation of the methods. 

REFERENCES. 

1. Bollinger. Ueber eine neue Wild und Rinderseuche. 
IVIiinchen. 1878. 

2. Brimhall. Haemorrhagic septicemia in cattle. A)ne>-. Vet. 
Rev., Vol. XXVII I 1903-4), p. 103. 

3. Fennimore. Wild and cattle disease. Jonr. of Comp. Med. 
ami Vet. Arcliiv., Vol. XIX ^l89S), p. 625. 

4. Galtier. Nouveaux faits tendant a etablir que la pneumo- 
enterite infectieuse existe sur les grands et les petits ruminants en 
algerie. Rectieil de Med. Vet.. 7 serie, Vol. VIII (1891 ), p. 97. 

5. HuEPPE. Ueber die Wildseuche. Berlin klinisclie Wocfieii- 
sc/iri/i, 18S6, S. 753. 

6. KiTT. Ueber eine Experimentelle,derRinderseuche(Bollinger) 
ahnliche Infectionskrankheit. Sitzungsberic/ite der Geseilscliaft fiir 
Morphologic und Physiologie in Miinehen, I. 1885, S. 240. 

7. PioT. Le Barbone du Ruffle. Bulletin d V Instut. Egyptien, 
1889. 

8. PoELS. Septische Pleuropneumonie der Kalber. Fortschr. d. 
Med., 1S86, S. 388. 

9. Reynolds. Htemorrhagic Septicaemia. Am. Vet. Review. 
Vol. XXVI (1902), p. 819. 

10. Reynolds. Htemorrhagic Septicaemia. Bulletin No. S2, Minn. 
Agric. Experiment Station, 1903. 

If. Wilson and Brimhall. Sixty-four cases of hemorrhagic 
septicemia in cattle due to bacillus bovisepticus. Report .State Board 
0/ Health 0/ Minnesota, i<^oi. (Very full bibliography, i 

12. WooLSEV .\ND Job LING. A report on hemorrhagic septicemia 
in animals in the Philippine Islands. 1903. No. 9. Bureau of Gov- 
ern>nent Laboratories, Manila, P. I. 



FOWL CHOLERA IO5 

FOWI< CHOLERA. 

Synonyms. Chicken cholera; cholera gallhiarmn; Hi/lmer 
cholera: Pastcurellosis avium; cholera dcs ponies. 

% 85. Characterization. This is au infectious disease 
of fowls caused by bacteria, and transmissable by cohabitation 
and inoculation. It is determined by a high fever, great weak- 
ness and prostration, and usually terminates in the death of 
the affected bird. It is reported that it attacks all varieties of 
domesticated poultry (chickens, ducks, geese, pigeons, tur- 
keys), and caged birds such as parrots and canaries. It also 
attacks some species of wild birds. It is communicable by 
inoculation to rabbits and mice. Guinea pigs are not very 
susceptible. 

i^ 86. History. This disease is mentioned in some of 
the oldest works treating of the diseases of animals. Fowl 
cholera was studied b}^ Chabert in 1782, who regarded it as a 
form of anthrax. Since 1825, it has been frequently observed 
in France where it caused enormous losses in 1830, in 1850 and 
in i860. About 1830, it became known in Russia, Bohemia 
and Austria. In 1851, Benjamin considered it to be a con- 
tagious disease but remarked that people and dogs might con- 
sume with impunity the meat of affected fowls. Delafond 
observed that it might be transmitted to birds and rabbits by 
using blood, secretions, and portions of the flesh. It was also 
recognized that the excrement plays an important part in the 
dissemination of the virus. 

During recent years it has been observed in nearly all of 
the countries of Europe as well as in the United States. It 
has been reported from many places in the United States, but 
its presence seems to have been determined by scientific 
investigation in but a very few of these. Salmon investigated 
it in South Carolina in 1879-80, and Higgins in 1898 reported 
it from Canada. Salmon gave special attention to vaccination 
and the effect of disinfectants in destroying the virus. In 
1904, Ward reported an outbreak in California. 



I06 FOWL CHOLERA 

Perroncito was among the first to describe the specific 
cause of the disease. This was followed by the contributions 
of Pasteur, who, in 1880, cultivated the bacterium in chicken 
broth and showed that its virulence might be reduced to such 
an extent that it could safely be used for vaccination. This 
is the first case in which a virulent organism was successfully 
modified in a laboratory and made to act as a vaccine. It was 
the forerunner of the preparation of vaccines for a number of 
diseases, more particularly for anthrax, black quarter, and 
rabies. 

§ 87. Geographical distribution. Fowl cholera seems 
to be widely distributed in Europe and it has been found in a 
few localities in the United States and in Canada. In Ger- 
many it is the cause of heavy losses among poultry. In 1903 
it is reported to have killed over 48,000 fowls and 23,000 geese 
besides other poultry. 

§ 88. Etiology. Fowl cholera is caused by a specific 
bacterium {Bacillus {bipolaris) avisepticus, Pasteurella avium^ 
which is not distinguishable morphologically or in its cultural 
manifestations from the other members of the group of bacteria 
of which Bad. septicemiae hemorrhagicae is the type. In this 
group are the bacteria of rabbit septicemia, swine plague, and 
Wildseicche. It is a small, slightly elongated organism with 
rounded ends. In stained preparations from the tissues it 
exhibits a pronounced polar stain. 

The period of incubalion is placed by European writers at 
from 18 to 48 hours. In the case of 40 fowls inoculated by 
Salmon, it varied from 4 to 20 days, the average period being 
8 days. Ward fed viscera of dead fowls to 10 healthy ones. 
They died in from 24 hours to 6 days. 

§ 89. Symptoms. The symptoms described for this 
disease in Europe differ somewhat from those reported by 
Salmon. Usually the appetite is lessened. Occasionally they 
continue to eat almost to the time of death. The earliest indi- 
cation of the disease is a yellow coloration of the urates. In 



MORBID ANATOMY IO7 

health, these are a pure white though they are frequently 
tinted with yellow as the result of disorders other than cholera. 

Occasionally the first symptom is a diarrhea in which the 
excrement is passed in large quantities and consists almost 
entirely of white urates mixed with colorless mucus. 

Very soon after the first symptoms appear the bird sepa- 
rates itself from the flock, it no longer stands erect, the 
feathers are roughened, the wings droop, the head is drawn 
down towards the body and the general outline of the bird 
becomes spherical or ball-shaped. At this period there is 
great weakness, the affected bird becomes drowsy and may 
sink into a sleep which lasts during the last daj- or two of its 
life, and from which it is almost impossible to arouse it. 

The crop is nearly always distended with food and appar- 
ently paralyzed. There is in most cases intense thirst. If 
the birds are aroused and caused to walk, there is at first an 
abundent discharge of excrement followed at short intervals 
by scanty evacuation. 

With the beginning of diarrhea the body temperature 
rises to 109 to rio° F. Ward states that in advanced stages it 
ranges from 109 to 112° F. The comb loses its bright hue 
and becomes pale and bloodless. European writers describe 
the comb as dark blue, purple, or black, and some writers in 
the United States have referred to it in the same terms. Sal- 
mon reports that he never observed it. 

Di.seased birds rapidly lose in weight. They become so 
weak that they walk with great difficulty, a slight touch causes 
them to fall over. The fowls become very much emaciated. 
Death may occur without a struggle or there may be convul- 
sive movements and cries. 

This disease may run rapidly through a flock destroying 
the greater part of the birds in a week, or it may assume a 
more chronic form, spreading slowly, and remain upon the 
premises for several weeks or months. 

i^; 90. Morbid anatomy. The comb is pale and blood- 
less. The superficial blood vessels usually contain but little 
blood. 



I08 FOWL CHOLERA 

The liver is usually enormously enlarged, softened, and 
the blood vessels are engorged. The gall bladder is distended 
with thick, dark bile. 

The crop is usually distended with food. The stomach 
often presents externally a number of circular discolorations, 
about three millimeters in diameter, which on section are 
found to be extravasated blood. The small intestines are 
congested. 

The rectum and cloaca usually present deep, red lines 
upon their mucous membrane, evidently the first stage of 
inflammation, which results, in chronic cases, in thickening of 
the walls, especially of the rectum, the desquamation of the 
mucous membrane and the formation of large ulcerated 
surfaces. 

The mesenter}' is generally congested, often greatly 
thickened and reddened, and rendered opaque by inflamma- 
tion. The ureters are distended with yellow urates ; the 
kidneys seem engorged, and on section accumulations of the 
tenacious, yellow urates are frequently seen. The spleen is 
generally normal in size and appearance, though frequently 
enlarged and softened. 

The pericardium is sometimes distended with effusions, in 
which case there is noticeable hyperemia of the surface of the 
heart. The lungs are often, though not generally, engorged 
with dark blood ; they are seldom, if ever, hepatized. 

The blood vessels are sometimes filled with a firm clot, 
and contain but little liquid ; at other times the blood does 
not coagulate at all. It seems to be those cases in which the 
duration of the disease is the longest, that the blood loses its 
power to coagulate. 

Ward has summarized the morbid anatomy in the fowls 
examined by him as follows : 

" At death, or some hours previous, the comb frequently takes on a 
dark purple color, but this does not always occur. Very often the comb 
is pale and bloodless. The skin of the breast and abdomen is frequently 
reddened. 

" In post-mortem examinations a congestion of the blood vessels of 
the liver, kidney, mesentery, or intestines is noticeable to some degree 



MOKHII) ANATOMY IO9 

in all cases Punctiform hemorrhages are found upon the heart with 
almost absolute uniformity. The liver is very fre(|uently marked with 
punctiform whitish areas of necrosis. Stained sections show these 
necrotic foci throughout the substance of the liver, and besides reveal a 
congestion of the blood vessels of that organ. The next most striking 
lesions occur in the first and second duodenal flexures. The mucosa is 
deeply reddened and studded with hemorrhages varying in size, but 
seldom exceeding one millimeter in diameter. These involve the 
intestinal coats to an extent that makes them distinctly visible on the 
peritoneal surface. The contents of the duodenum consist of a pasty 
mass, more or less thickly intermingled with blood clots. The intes- 
tinal contents sometimes consist of a cream-colored pasty mass, or may 
be brownish red or even green in color. Lesions are very rarely 
observed in other portions of the intestines. The ureters are noticeable 
in practically all cases by reason of the yellow-colored urates that they 
contain. The nasal cavity, pharynx and oral cavity frequently contain 
a viscous mucous fluid, probably regurgitated from the crop. 

" The field notes on twenty-one post-mortem examinations refer to 
hemorrhages in the heart in twenty-one cases ; punctiform necroses in 
the liver, fifteen cases ; hemorrhages in duodenum, seven cases ; the 
discoloration of the skin in six cases. The presence of a gelatinous 
exudate within the pericardium was noted twice. A fibrinous exudate 
in the pericardium occurred the same number of times. Hemorrhages 
in the peritoneum other than those visible through the mucosa of the 
duodenum occurred but twice. In one case hemorrhages were abund- 
antly scattered tliroughout the muscles of the trunk and legs. 

" Fowls inoculated subcutaneously with cultures exhibit on post- 
mortem examination the punctiform hemorrhages on the heart and the 
hemorrhages in the mucosa of the duodenum exactly as incases infected 
naturally." 

BI^OOI) COUNTS 0\- FOWLS INFECTKD HV INC,]-,STION AND 
INFECTED NATrRAl.I.V. 



;posure to infection 44.8'^ C. 

— - 43-7° C. 

-— 43-3° C. 

42.8° C. 

.... 42.2° C. 

cted - 42.S°C. 



Fowl. 


White 


Red 


R. 




Corpuscles 


Covpuscle.s. 




No. 3 


23,000 


2.290 000 per cnnn. 


3 days al 


No. 3 


20,000 


2,Soo,ooo ■' " 




No. 6 


37,000 


3,930,000 " 




No. 8 


87,000 


4,490,000 •• 




No. 8 


101,000 


2,960,000 •' •• 




A -- 


.=i8.ooo 


1,710,000 " 


Natnrall 


B... 


4.S.000 


1.925,000 " 





FOWL CHOLERA 
BLOOD COUNTS OF APPARENTLY HEALTHY FOWLS. 



Red Corpuscles. 


2,980,000 per cmm. 


2,987 


000 " 


3.115 


000 " 


3.980 


000 " 


3,920 


000 " " 


2,380 


000 " 


2,620 


000 " 



Fowl. White Corpuscle 

No. II - 24,000 

No. 12.. 26,300 

No. 14 36-000 

No. 15 52,000 

No. 16 61,000 

No. 17 30,000 

No. iS -_- 24,000 

The duration of the disease varies from a few hours to 
several days. 

The prognosis is unfavorable. The mortality is very high, 
often 100 per cent. 

§ 91. Differential diagnosis. Fowl cholera is to be 
differentiated from : 

1. A number of dietary disorders which cause the death 
of a large number of fowls. Such cases are often thought to 
be chicken cholera and so reported by the owners. A diagno- 
sis is to be made from the bacteriological findings. 

2. It is to be differentiated from fowl typhoid. There 
There are a number of resemblances in the clinical history of 
the two diseases but there are marked differences in both the 
morbid anatomy and etiology. For a comparison of the lesions 
and specific bacteria of these two diseases see fowl typhoid. 

§ 92. Prevention. Pasteur introduced a preventive 
inoculation or vaccine for this disease. Kitt has found that 
the eggs of fowls unknown to this disease possessed a sub- 
stance somewhat similar to antitoxin. He immunized fowls 
by injecting them simultaneously with from four to eight 
cubic centimeters of the whites of such eggs. While exceed- 
ingly interesting this method does not seem practicable. More 
recently he has obtained a horse serum that promises to be of 
immunizing value. Good sanitary conditions, isolation of the 
well from the sick fowls and thorough disinfection seems to 
be the most satisfactory procedure. It is important not to 
introduce the disease with newly purchased fowls or to expose 
healthy ones to the disease either at or in transportation to 
various poultry exhibits. 



GOOSE SEPTICEMIA HI 

REFKRENCKS. 



1. HiGGiNS. Notes oil an epidemic of fowl cholera and upon the 
comparative production of acid by allied bacteria. Jour, of Experi- 
mental Medicine, Vol. Ill (1898). p. 651. 

2. KiTT. DievSerumimpfunggegenGefliigelcholera. Monatshefte 
fitr praktische Tierheilk., Vol. XVI (1904), S- i- 

-. PERRONCiTO. Arch.fih-iviss. u.prackt. Thierheilk., 1879, S. 4- 

4. Pasteur. De I'attenuation du virus du cholera des poules. 
Comptes rendus des Seances de V Academic des Sciences, \o\. XCI 
(1880), p. 673. 

5. Pasteur. Sur les maladies virulentes, et en particulier sur la 
maladie appalee vulgairement cholera des ponies. Ibid. Vol. XC 
(1880), p. 239. 

6. Salmon. Annual Reports of the U. S. Commissioner of Agri- 
culture, 1880-82. 

7. Salmon. The diseases of poultry. Washington, D. C. 1889, 

p. 232. . ^ . 

8. Ward. Fowl cholera. Bulletin No. 136. College oj Agrtc, 
Calif. Agric. Exp. Station, 1904. 



GOOSE SEPTICEMIA. 

§ 93. Characterization. The disease is an acute sep- 
ticemia causing the death of the infected goose in a few hours 
after there are evidences of sickness. 

§ 94 History. In 1902, Curtice described this disease 
as causing considerable loss in Rhode Island. The following 
note by T. Smith, dated October 31, 1900, quoted by Curtice, 
is significant in explaning the condition under which the 
disease disappeared. 

" Geese born in April and May and collected during the summer 
and fall for fattening, kept in open yards, crowded together but able to 
move about ; about 500 in a pen. Fed on a mixture of corn meal and 
meat and beef scraps. Epidemic began in midsummer. Deaths up to 
twenty a day (one workman says sixty one day); about 3,000 lost to 
date." 

§ 95. Etiology. The cause of this disease is a bacterium 
belonging to the septicemia hemorrhagica group. It is stated 



112 GOOSE SEPTICEMIA 

to have " the characters of the fowl cholera type." It killed 
rabbits when they were inoculated with 0.2 cc. of a bouillon 
culture. 

i^ 96. Symptoms. The symptoms are indefinite. In 
the outbreak described the geese were often found dead. The 
description of the disease by Curtice is appended. 

" Few symptoms of disease were seen, those noted pertain- 
ing mainly to the death struggles. Very few that died were 
noticed to be sick more than an hour or two before death, 
and, as the experimental investigation demonstrated, the dis- 
ease could not have lasted, in the majority of the geese, more 
than thirty-six hours. An uncertain gait, a burrowing of the 
head in the dirt, twisting it around, or actions indicating 
spasms of the throat, were the earliest symptoms. Some 
geese were observed to die within five minutes or after the 
first seizure." There are few chronic cases and recoveries 
are not recorded. Some show no other symptom than being 
slower in action, and separating themselves somewhat from 
the flock. However, this sign is quite important when the 
wild nature and gregarious habit of the goose are taken into 
account. 

jj 97. Morbid anatomy. The tissue changes, as given 
by Curtice, are as follows : 

" There was considerable mucus in the throat and mouth, 
and a very tenacious mucus in the nose. The veins of the 
head were usually congested, as though the animal had died 
of asphyxia. This, together with spasm of the throat, indi- 
cates a spasmodic closure of the glottis. The digestive tract 
was found to be full of food in nearly all stages of digestion. 
In some cases the catarrhal products of the intestines contained 
petechiae. Sometimes these points were collected in more or 
less extensive patches. Perhaps more than half of the livers 
showed yellow spots of from a pin point to a pin head in size. 
These discolorations were found on section to extend into the 
substance of the liver, and were evidently dead tissue, or 
necroses. In one example the heart di.sclosed severe inflam- 



DIFFERENTIAL DIAGNOSIS I 13 

mation, botli epicarditis and pericarditis being present. In one 
case the lungs were affected. In all, fifteen cases were ex- 
amined, and from these this composite description of the post- 
mortem appearances is drawn." 

Hemorrhages on the serous membranes and punctate ne- 
croses in the liver seem to be cjuite characteristic lesions. 

Post })iorlei)i ;/(?/«.— These are a few taken from Curtice's 
publication. 

" Goose No. I. Died last night ; quite fat. Right lung, ventral por- 
tion quite firm, whitish. Some flocculi of exudate in peritoneal cavity. 
Liver shows numerous point-like necrotic foci. Blood thick, blackish 
and tarry. Mucus glassy on dusky mucosae of nose and throat. 

" Goose No. 2. Died last night. Somewhat thinner than No. i. 
Ecchymoses on fat in abdomen and gizzard and on heart muscle ;, 
necrosis in liver. Blood thick, tarry. Mucus in nasal passages. 

" Gander No. 7. Died last night ; now cold. No well marked hem- 
orrhagic lesion in pleuroperitoneal cavity. Whitish points in liver. 
Hemorrhagic or extremely hyperemic condition of duodenum. Jeju- 
num, or second coil of intestine, filled with a glairy mucous fluid in 
which are suspended shreds and patches of food (?). Few if any necroses 



§ 98. Differential diagnosis. The disease here described 
is caused by Badermm septicemiae hemorrhagicae which re- 
sembles that of fowl cholera and other members of that group 
of bacteria. A diagnosis, therefore, is made positive by finding 
this organism in the tissue of the sick and dead geese. 

M'Fadyean has described a di.sease undei: this title causing 
the death of many geese in which he found the blood swarm- 
ing with bacteria suggesting Bad. septicemiae hemorrhagicae 
but morphologically different, but which he could not induce 
to grow on any of several media in cultures under both aerobic 
and anaerobic conditions. It appears that this is a different 
disease from that described by Curtice. 

§ gg. Prevention. The procedure that can be suggested 
at present is isolation of the well from the sick, repeating the 
separations as often as new cases appear. The infected pens 
should be thoroughly disinfected before being reoccupied. 



114 FOWL TYPHOID 

REFERFNCES. 

1. Curtice. Goose septicemia. Bulletin No. S6, J\. I . Agr. E\p. 
Station. 1902. 

2. M'Fadyean. a remarkable outbreak of goose septicemia. 
lour. Conipar. Path, and Tlierap., Vol. XV (1902), p. 162. 



FOWL TYPHOID. 



§ 100. Characterization. A specific disease of fowls 
caused by Bacterium saiiguinarizim. It is not known whether 
or not other species of domesticated birds are susceptible. 

§ loi. History. This disease was briefly described by 
Moore in 1895. At that time it had been studied in but a few 
fowls and these the last to die in their respective flocks. In 
the following year other fowls were examined very carefully 
from two outbreaks of the disease and it is upon the data 
obtained in their investigation together with those procured 
from many produced cases that the description of the disease 
is based. It was described as an infectious leukemia. Further 
investigation, however, has shown that the excess of white 
corpuscles was due to a leucocytosis brought about by the in- 
fecting organism and that the disease is not a true leukemia. 

It was found by Smith in 1894, on Block Island, R. I. 
In 1898, Dawson found it to be the cause of very serious losses 
among poultry near Baltimore, Md. In all of the outbreaks 
studied, the owners of the fowls first reported the disease as 
-chicken cholera. In 1902, Curtice investigated an outbreak in 
Rhode Island. 

§ 102. Geographical distribution. It was first studied 
in fowls taken from an outbreak in Virginia. Since then, it 
has been identified in Maryland, the District of Columbia, and 
the State of Rhode Island. There is good evidence in the 
numerous reports of destructive fowl diseases to believe that it 
is quite widespread in the United States. Thus far, there 
seems to be no reports of its extent in other countries. 



ETIOLOGY 115 

ji 103. Etiology. Moore isolated and described a patho- 
genic bacterium which he designated Bacterium sanguinarhim . 
With this organism the disease has been produced in healthy 
fowls both by feeding cultures and l)y 
intravenous injections. Its etiological ^ -, 

relation to the disease is, therefore, r- •j^/3 

quite clearly established. It is possi- - l^^^*^ 

ble that certain accompanying condi- '^ . 

tions may be necessary in conjunction ^ V 

with the organism to cause the dis- 
ease to spread rapidly in a flock. 

Experimentally it did not spread from ^^^ ^^ ^ ^^^^^ ^^^^^. 
diseased (inoculated or fed) to healthy terhmi safiguinarium hi 
fowls when kept in the same yard. a blood space in the liver 

{much enlarged). 
^ 104. Symptoms. From the 
statement of the owners of the diseased fowls in the different 
outbreaks and from the appearance of those in which the dis- 
ease was artificially produced, little can be positively stated 
concerning the early symptoms. There is a pronounced anemic 
condition of the mucosa of the head. An examination of the 
blood shows a marked diminution in the number of red corpus- 
cles and an increase in the number of white ones. In the dis- 
ease produced artificially by feeding cultures of the specific 
organism there are, in most cases, a marked drowsiness and 
general debility manifested from one to four days before death 
occurs. The period during which the prostration continues 
varies from a few hours to two days. The mucous membranes 
and skin about the head become pale. There is an elevation of 
from I to 4 degrees in temperature. The fever is of a contin- 
uous type, as shown in the appended temperature chart of two 
fowls in which the disease was produced artificially. 

Although the course of the disease in different fowls is 
usually constant, there are many variations. The time 
required for fatal results is from three to fifteen days, but ordi- 
narily death occurs in about eight days after feeding the cul- 
tures. The rise in temperature can be detected about the third 



i6 



FOWL TYPHOID 



day and external symptoms about the fifth or sixth, occa- 
sionally not until a few hours before death. The symptoms 
observed in the cases produced by feeding correspond with 
those described by the owners of affected flocks. 

As indicated in the inoculation experiments, the symp- 
toms following the intravenous injection of the virus were, as 























































^ 










^^ 


^ 








1 ,D. 


ad. 






















/r- 






'"-'' 


^-^ 


o^ 


^^- 


--' 


f/O. 






















V'' 














^ 


-^ 




















/ 


r 










r^ 


- ^. 


















^ 








-■'/ 






■^ \ 


\ 


/ 






^ 


■^^ 


, y 




^^ 




f— 


, 


f>~- 


■-:.-_l- 










'/ 







































Fkv. i6. Temperature chart of trvo fatal cases artificially 
produced in foTcls. 



would be expected, considerably modified from those fowls 
which contracted the disease by the ingestion of cultures of the 
specific bacterium. 

i^ 105. Morbid anatomy. The only constant lesions 
found in the fowls which contract the disease naturally, as 
well as in those fed upon the virus, are in the liver and blood. 
The liver is somewhat enlarged and dark colored. A close 
inspection shows the surface to be sprinkled with minute 
grayish areas. The microscopic examination shows the blood 
spaces to be distended. The hepatic cells often stain very 
feebly. Not infrequently the cells are isolated and their out- 
lines indistinct. Occasionally foci are observed in which the 
liver cells appear to be dead and the intervening spaces infil- 
trated with round cells. The changes in the hepatic tissues 
are presumably secondary to the engorgement of the organ 
with blood. 

The rareness with which the intestinal tract is affected in 
both the natural and artificially produced cases is exceedingly 



MORBID ANATOMY "7 

interesting and important for the differential diagnosis. There 
is in most cases a hyperemia of the mucous membrane of the 
colon, but this condition is not uncommon in the healthy indi- 
vidual. The kidneys are generally but not uniformly pale. 
Thev are streaked with reddish lines, due to the injection of 
blood vessels. In section the tubular epithelium appears to be 
normal. The kidneys seem to be, from the number of bacteria 
in the cover-glass preparations, especially favorable for the 
localization of the specific organism. The spleen is rarely dis- 
colored or engorged with blood. The lymphatic glands were 
not appreciably enlarged in any individual examined. The 
lungs except in chronic cases are normal. The brain and 
spinal cord are unaffected. 

The heart muscle is usually pale and sprinkled with gray- 
ish points, due to cell infiltration and necrosis. These lesions 
are so common that it seems safe to consider them character- 
istic manifestations. Death usually occurs in systole, the 
auricles containing very thin, unclotted blood. 

The most important alterations are found in the blood. 
These consist, in the progress of the disease, of the gradual 
disappearance of the red corpuscles and increase in the number 
of white ones, as determined by blood counts made daily or 
every other day, from the time of inoculation, or of feeding 
the virus, until the day of death. 

The diminution in the number of red corpuscles and the 
increase in the number of white ones are illustrated in the 
blood count of two cases of artificially produced disease. 

In carefully heated cover-glass preparations of healthy 
fowl's blood stained with methylene-blue and eosin, the nuclei 
are colored a deep blue, and the cellular protoplasm surround- 
ing the nucleus is stained by the eosin. In similar prepara- 
tions made from the blood of the affected fowls there are a 
greater or less number of cells which do not take the eosm 
stain. These were called spindle cells by Van Reckling- 
hausen, blood plates by Bizzozero, and hematoblasts by 
Hayem. More recently Dekhuyzen has called them throm- 
bocytes. In these the portion of the cell body surrounding 



i8 



FOWL TYPHOID 



the nucleus remains unstained or becomes slightly tinted with 
blue. Occasionally they contain one or more vacuoles, and 
the margin is frequently broken. The apparent dissolving 

away of the red corpuscles 
has been frequently ob- 
served and corpuscles 
showing the intermediate 
stages are readily detected 
in carefully prepared speci- 
mens. These must be dif- 
ferentiated from the blood 
plates. 

The cause of the de- 
struction of the red cor- 
puscles is not satisfactorily 
explained. In his report 
on fowl cholera, Salmon il- 
lustrates leucocytes sur- 
rounding the red corpus- 
cles, but the marked di- 
minution of the red cells 
was not determined. He 
speaks, however, of the 
pale color of the blood. In fresh preparations of the blood, 
portions of red cells may be seen within the leucocytes, those 
containing spindle shaped granules. The determination of 
the extent of this mode of destruction of the red corpuscles 
necessitates further investigation. 

tabi^e; showing changes in the number of corpusci^es. 

Fowl No. 82, inoculated in the wing vein, February 6. 




Fig. 17. Blood from a iv ell advanced 
case of fowl typhoid showing red 
corpuscles^ blood plates and increase 
in the number of leucocytes. 







Number of 


Number of 




Date 


Tempera- 
ture (F°.) 


red cor- 
puscles, 
per c. mm. 


white cor- 
puscles 
per c. mm. 


Remarks 


Feb. 6 


107.4 


3.744.444 


21,222 


Well. 


7 : 109 


3.417,391 


26,087 


Apparently' well. 


8 1 108.2 


2,784.700 


55,000 


Do. 


9 I 108.4 


2,807,692 


76,925 


Do. 


11 1 107.4 


3.481,818 


90,909 


Feathers ruffled ; refuses food. 


13 1 110.2 


2,133,333 


100 000 


Very quiet ; comb pale. 


14 1 108 


2,530,000 


140,000 


Fowl died later in the day. 



MORBID ANATOMY 



119 



Fowl No. 501, fed culture March 26. 



Mar. 26 

28 

Apr. 2 

3 



Xumber of! Number of 
red cor- white cor- 
puscles I puscles 

per c. mm. per c. mm. 



166.2 



3,53500° 
no 2,430,000 

110.6 I 684,210 

106 I 1,745.000 



1^,940 
70.000 
80,000 
245.000 



Well. 

Fowl eats very little. 
Blood verv pale: fowl weak; refuses food. 
Verv weak; many red corpuscles at- 
tacked by leucocytes. 
Found dead. 



In fresh preparations of the blood of affected fowls exam- 
ined in Toisson's fluid, red corpu.scles which take the violet 
stain more or less intensely 
throughout are frequently 
observed. 

In the blood of poultry 
two distinct classes of white 
corpuscles are conspicuous. 
The first which predomin- 
ates in numbers, contains 
nuclei with from one to 
four lobes, and the cyto- 
plasm is sprinkled with a 
variable number of round, 
elongated, or spider- shaped 
bodies. In the fresh con- 
dition they are highly re- 
fractory. They stain with 
eosin, and if the prepara- 
tions are heated sufficiently 
thev will retain certain of 
the' aniline dyes. The other class consists of round or nearly 
round cells which takes the blue stain feebly. Usually it is 
difficult to detect the nucleus, although it is occasionally dis- 
tinct Between these two types there are many varieties. 
The leucocytes containing the spindle-shaped bodies appear to 
be the phagocytes, as they were the only ones which were 
observed to engulf the red corpuscles. Bacteria have not been 
demonstrated in these cells, although their presence has, in 




.s7/o: 



Section of chicken's liver 
'inq; blood engorgement. 



FOWL TYPHOID 



several cases, been suspected. From the appearances observed 
in the red blood corpuscles it seems highly probable that 
phagocytosis plays a comparatively large part in their destruc- 
tion. Another hypothesis is also suggested, namely, that a 
toxin produced during the multiplication of the specific organ- 
ism has this effect 
on the red corpus- 
cles. In the fresh 
preparations w e 
can observe the 
phagocytes attack- 
ing the red cells. 
In the stained ones 
mutilated red cor- 
puscles and free 
nuclei are present. 
The hypothesis is 
suggested that the 
leucocytes partially 
digest certain of 
the red corpuscles 
in their attack up- 
on them. Whether 
to the phagocytes 




Fig. 19. The phagocytic action of the white 
blood corpuscles upon the red ones in advanced 
cases. The changes represented fron i to g 
took place in jj minutes. 

ittributable 



these changes are entirely 
is an open question. 

In the blood from healthy fowls it is comparatively rare 
to see one of the white corpuscles engulfing a red one. As the 
disease progresses, however, this warfare becomes very con- 
spicuous, owing perhaps to the increased number of the color- 
less cells. Up to the present the study of these corpuscles has 
not been extended beyond the observations of the general ap 
pearance of these structures, and no attempt is made to explain 
the apparently marvelous increase in the number of the leuco- 
cytes. It is an interesting and as yet unexplained fact that 
the increase in the corpuscles is apparently restricted to those 
containing the spindle shaped bodies. 

§ 106. Differential diagnosis. Intestinal disturbances, 



DIFFKRENTIAI. DIAGNOSIS 



especially diarrhea and fowl cholera, are the diseases liable to 
be mistaken for fowl typhoid. 

A comparison of the important changes in the morbid 
anatomy in fowl cholera, as described by European writers, 
and in the disease under consideration, can be made from the 
appended columns, in which their more characteristic lesions 
are contrasted : 



Lesions in fowl cholera. 

Duration of the disease from a 
few hours to several days. 

Elevation of temperature. 

Diarrhea. 

Intestines deeply reddened. 

Intestinal contents liquid, mu- 
copurulent, or blood stained. 

Heart dotted with ecchymoses. 



7. Lungs affected, hyperemic or 

pneumonic. 

8. Specific organisms appear in 

large numbers in the blood 
and organs. 

9. Blood pale (cause not deter- 

mined). 

10. Condition of leucocytes not 

determined. 



Lesions in foivl typhoid. 

1. Duration of the disease from a 

few hours to several days. 

2. Elevation of temperature. 

3. Diarrhea not common. 

4. Intestines pale. 

5. Intestinal contents normal in 

consistency. 

6. Heart usually pale and dotted 

with grayish points, due to 
cell infiltration. 

7. Lungs normal, excepting in 

modified cases. 

8. Specific organisms compara- 

tively few in the blood and 
organs. 

9. Blood pale, marked diminu- 

tion in the number of red 
corpuscles. 

10. Increase in the number of 

leucocvtes. 



Attention should be called to the fact that as yet there 
seems not to have been a careful study of the condition of the 
blood in fowl cholera. Salmon observed many changes which 
may have been similar to or identical with those herein 
recorded. Ward found an increase in the number of white 
corpuscles and in some cases a decrease in the number of red 
ones in cases of fowl cholera. 

The difference between the specific organism of these two 
diseases can be readily appreciated by a comparison of the 



FOWL TYPHOID 



more diagnostic properties of each 
parallel columns, as follows : 



they are arranged 



BacteriiDit of foivl cholera. 

Bacterium short, with oval 
ends. 



It usually 
tissues. 



appears singly in 2. 



Ordinarily it exhibits a polar 
stain (from tissue). 



( Trows feebly or not at all on 
gelatin. 

It does not change milk. 

Resists drying from one to 
three days. 

Kills rabbits inoculated sub- 
cutaneously in from eigh- 
teen to twentv-four hours. 



It kills fowls when injected 
subcutaneously in small 
quantities. 



Bacterium sangu inariu ni . 

Bacterium short, with ends 
oval or more pointed. 

It usually appears in pairs 
united end to end or in 
clumps in tissues. 

It gives a light center, with 
uniformly stained periphery 
(from tissue). Rarely a 
polar stain is observable. 

Decided growth on alkaline 
gelatin. 

Saponifies milk. 

Resists drying from eight to 
twelve days. 

Kills rabbits inoculated intra- 
venously in from three to 
five days. Rabbits inocu- 
lated subcutaneously remain 
well or die in from six to 
ten days. 

It does not kill fowls when in- 
jected subcutaneous]}- in 
small quantities. 



While there are many similarities in the symptomatology 
of these two diseases, there are pronounced differences in the 
morbid anatomy and in the specific microorganisms. These 
facts render positive differentiation dependent upon a care- 
ful bacteriological and pathological examination. In fowl 
cholera the course of the disease is more rapid than in fowl 
typhoid. 

§ 107. Prevention. Prompt isolation of the well from 
the sick fowls and thorough disinfection of the houses and 
yards. 

In reference to preventing its introduction, Curtice makes 
the following observation ; 



SWINE ERYSIPELAS I 23 

" Inasmuch as one possible method of introducing the 
disease is through purchases, it will always be necessary for 
purchasers to enquire into the history of the flock from which 
additions are to be made, and especially to examine into the 
condition of the fowls. It is better in any case to keep new 
purchases by themselves for some weeks or until it is apparent 
that they are healthy." 

REFERENCES. 

1. Curtice. Fowl typhoid. Bulletin Sj. Agr. Exp. Station of 
the R. I. College of Agric. and Mech. Arts, 1902. 

2. Dawson. Infectious leukemia. Annual Report of the Bureau 
of Animal Industry, U. S. Dept. Agric., 1898. 

3 MooRE. A study of a bacillus obtained from three outbreaks of 
fowl cholera. Bulletin No. S, U. S. Bureau of Animal htdustry, 1895. 

4 Moore Infectious leukemia in fowls-A bacterial disease 
frequently mistaken for fowl cholera. Annual Report of the Bureau 
of Animal Industry, 1895-96. 



SWINE ERYSIPELAS. 
Synonyms. Red fever of swine ; rougcf ; Rotlatij. 
% 108. Characterization. This disease, peculiar to 
swine, is determined by a rise of temperature, cerebral distur- 
bances and pronounced reddening of areas of the skin. It is 
a disease of adult life. It is stated that pigs are rarely attacked 
under three months or over three years of age. Lydtm and 
Schottelius found some differences in the degree of suscepti- 
bility of certain breeds of swine. The common country pig 
was least susceptible. 

§ 109. History. This disease has been known in 
Europe for many years. Smith found a bacterium in rabbits 
inoculated with the organs of pigs that had died of an unde- 
termined disease in Minnesota, which was either the bacterium 
of swine erysipelas or of mouse septicemia. The latter organ- 
ism had been recorded on two previous occasions from pigs in 
this country. 



124 SWINE ERYSIPELAS 

§ 1 10. Geographical Distribution. Swine erysipelas 
is an infectious disease that occurs enzootically and in epi- 
zootics in most of the countries of Europe. It was formerly 
restricted in Bavaria to the districts along the Danube, and 
was entirely unknown in southern Bavaria (Kitt). It is 
stated that the disease tends to become enzootic chiefly in 
valleys and low-lying plains which have slow-flowing streams 
and heavy, damp, claj^ soil ; and that sandy and granite soils 
are comparatively free from it. It occurs chiefly during the 
months of July, August and September, although it appears 
sporadically during the winter m.onths. It has not been 
described from the United States. 

§111. Etiology. Loeffler and Schiitz 
'(^ ^'^^^/"^-^ pointed out in 1885 that swine erysipelas 

•V ^^•'^^f'^ / was caused bv a very slender bacterium 
-'■"" {Bad. erysipelatis suis) i to 2// long and 

0.3 to 0.4// broad, straight or slightly 
curved, ends not rounded and in cultures 
Fig. 20. Bacter- often appearing in filaments. It is very 
ium of swine ery- closely related to the bacterium of mouse 
sipelas, showing septicemia described bv Koch in 1878. In 
free organisms ^ .^^ere the bacterium of mouse 

a nd al so tn^j r '^ . . 

presence 'a' it h in septicemia is quite common, swine erysipe- 
the cells. las prevails. There is much uncertainty 

concerning the relationship of the bacter- 
ium of mouse septicemia to that of this disease. Smith has 
suggested that possibly the bacterium which has been found 
in this country may gain virulence sufficient to produce epi- 
zootics, if such is not already the case. It is exceedingly 
important that careful search be made for this organism in the 
outbreaks among swine where the nature of the disease is not 
clearly determined. House mice and pigeons are susceptible 
to the bacteria of swine erysipelas ; guinea pigs and fowls are 
immune. Rabbits suffer from erysipelatous swellings when 
inoculated subcutaneously in the ear. The bacterium of 
swine erysipelas is to be differentiated from that of mouse 
septicemia. 



SYMPTOMS ^25 

The period of incubation is stated to be at least three days. 
It is apparently longer than that in many cases. 

^ 112. Symptoms. The disease usually begins sud- 
denly and violently. The animal refuses food, makes efforts 
to vomit, has a rise of temperature, manifests severe nervous 
disturbance, is very weak, torpid and indifferent to its sur- 
roundings. When approached it tries to hide itself under its 
bedding. The hind quarters become weak and paralyzed. 
Muscul^ar spasms and grinding of the teeth are sometimes 
observed. At first there is constipation, the conjunctiva is of 
a dark red or brownish-red color, and the eyelids are some- 
times swollen. Usually a day or two after the first symptoms 
develop or, perhaps, from the first, reddish spots appear on 
the thin parts of the skin, such as the region of the navel, 
lower surface of the chest, perineum, inner surface of the 
thighs, ears and throat. These spots, which at first are bright 
red and about the size of a man's hand, become, later on, dark 
red or purple, and soon unite into large, irregularly-shaped 
patches. As a rule, they are neither painful to the touch nor 
prominent, but sometimes they show a slight inflammatory 
swelling. The skin of the red spots, especially of the ears, 
may suffer from an eruption of vesicles and may even slough. 
The reddening of the skin may be very slight in severe cases, 
or mav appear only immediately before, or even after, death. 
Death takes place usually on the third or fourth day. In the 
very severe form, the animal may die in twenty-four hours, 
otherwise the disease requires a week or longer to run its 
course. 

Jensen considers that this disease, instead of being uniform 
in its clinical aspects, manifests itself in the following forms, 
which differ from each other by well-marked peculiarities. 
The forms recognized as varieties of this disease but more 
generally considered as distinct maladies and known by differ- 
ent names are as follows : 



1. True erysipelas. 

2. Swine urticaria. 



126 SWINE ERYSIPELAS 

3. Erysipelas without redness of the skin. 

4. Diffuse necrotic erysipelas of the skin. 

5. Endocarditis of erysipelas. 

He also maintains that there may sometimes be transi- 
tional forms between the respective varieties which he enumer- 
ates. Different forms of epizootic erysipelas have also been 
described by Cornevin, Hess and others. 

§ 113. Morbid anatomy. In the ordinary form of epi- 
zootic erysipelas there is a septicemic condition without any 
well marked morbid changes of separate organs. In less acute 
cases the septicemia may give way to hemorrhagic and diph- 
theritic gastro-enteritis, considerable swelling of the lymphatic 
system, hemorrhagic or parenchymatous nephritis, and 
hepatitis, acute swelling of the spleen and myositis. The 
hemorrhagic gastro-enteritis consists at first of excessive 
inflammation of the mucous membrane of the stomach in the 
region of the fundus. The mucosa shows a dark-red discolor- 
ation which is partly diffuse and partly in spots. The cells 
suffer from cloudy swelling and the mucous membrane is 
covered with a viscid layer of mucus. The intestinal mucous 
membrane is swollen, especially on the top of the folds and in 
the neighborhood of Peyer's patches. It is infiltrated with 
blood and sometimes shows superficial scabs. Less frequently, 
circumscribed parts of the mucosa of the cecum and the anter- 
ior parts of the colon suffer from a diphtheritic affection. 

The solitary follicles and Peyer's patches appear as prom- 
inently raised patches. Sometimes they are infiltrated with 
blood and surrounded by a reddish band. There is ulceration 
and cicatrization of the solitary and agminated follicles. The 
mesenteric glands become more swollen than the other glands 
of the body, of a dark red color, and show softening. The 
surface of fresh sections is dun-colored with interspersed dark- 
red areas. The paraglandular tissue is hyperemic and infil- 
trated with blood. 

The kidneys are enlarged, the cortex of a grayish-red and 



DIFFERENTIAL DIAGNOSIS I 27 

the medullary portion of a very dark-red color. Frequently 
catarrhal nephritis occurs as a complication. 

The acute swelling of the spleen arises in consequence of 
an acute hyperemia, with an increase of the cellular constitu- 
ents of the pulp, in which case the organ is enlarged, but not 
softened as in anthrax. The pulp is of a purple color, moder- 
ately soft and free from hemorrhages. 

There is cloudy swelling and enlargement of the liver. 
The surface of sections has a grayish-brown color, and the 
acini are widened. The muscles are gray in color, soft, flac- 
cid, watery, glistening and sometimes they are sprinkled with 
hemorrhages. They give the general appearance of boiled 
flesh. The myocardium shows similar spotted changes, and 
punctiform hemorrhages beneath the endocardium. In the 
abdominal and thoracic cavities and pericardium, there may 
be found small quantities of an orange-colored, clear fluid, 
which may be mixed with a flaky coagulum. 

Many English veterinarians regard the occurrence of 
more or less luxuriant vegetations on the valves of the heart 
to be so common that it is to be considered almost diagnostic. 
It would appear from the literature that this endocarditis is 
not nearly so common in continental Europe. The lungs 
remain unchanged, or at most exhibit a post-mortem edema. 
By microscopic examination, the specific bacteria are found 
everywhere in the body, especially in the spleen and kidneys, 
and to a less extent in the blood. 

The duratio7i of the disease varies from i to 10 days. In 
types of moderate severity it runs from 3 to 4 weeks. 

The prognosis is unfavorable. There is from 20 to 80 per 
cent mortalit3\ 

§ 114. Differential diagnosis. Swine erysipelas is to 
be differentiated from : 

I. Hog cholera and swine plague. The frequent red- 
dening of the skin in these diseases together with the modified 
lesions so frequently observed may cause confusion. The 



128 SWINE ERYSIPELAS 

bacteriological examination will enable the positive diagnosis 
to be made. (See hog cholera and swine plague.) 

2. Anthrax, which is very rare in swine. Here, too, 
the bacteriological examination discloses the true nature of the 
disease. 

3. Er3'themata due to various dietary causes. 

The significance of a deep reddening of the skin about the 
head, abdomen and thighs of pigs is not fully determined. 
It is clear, however, that such a condition often occurs in the 
absence, so far as present knowledge goes, of a specific infec- 
tion. It is frequently found in pigs suffering from digestive 
troubles, or poisoning from eating decomposed offal. 

§ 115. Preventive inoculation. Pasteur's preventive 
inoculation was until recently the chief prophylactic means 
employed against epizootic erysipelas. Metchnikoff found 
that the blood of immunized rabbits was antitoxic, and L,orenz 
maintains that the serum of swine that have recovered from 
swine erysipelas is also antitoxic, and will produce immunity 
in other animals. The treatment introduced by Lorenz is to 
inject the immunizing serum in the proportion of i cc. to every 
10 kilograms of the body weight of the animal. Two days 
afterward o. 5 to i.o cc. of virulent culture is injected, and 
after twelve days the dose is doubled. The use of the 
immunizing serum is reported to be very successful. 

REFEREN'CKS. 

1. Bang. Ueber Rotlauf-Eudocarditis bei Schweinen. Deutsche 
Zeitschr.f. Thietmed., Bd. XVIII (1891), S. 27. 

2. Jensen. Die Aetiologie des Nesselfiebers und der diffusen 
Hautnekrose des Schweines. Deutsche Zeitschr. f. Thierined., 1892, 
S. 278. 

3. LOEFFLER. Experimentelle Untersuchutigen iiber Schweine- 
Rotlauf. Arbeiten aus d. Kaiserlichen Gesundheitsamte, Bd. i (1885), 
S. 46. 

4. LoRENZ. Die Schutzimpfung gegeii Schweinerotlaiif mit 
Anwendung eines aus Blutserum immunisirter Thiere hergestellten 
Impfstoffes. Deutsche Zeitschr./. Thierrned., Bd. XX (1894), S. i. 



ANTHRAX 129 

5. LoRENZ. Die Veterinarpolizeiliche Behandhmg des vSchwein- 
erothlaufes und die Schutzimpfung. Berliner thierarz. Wochen., 1897, 

s. 574. 

6. LoRENZ. Schut/.impfungeii gegen den Rotlauf der Schweine. 
Ibid, 1897, S. 109. 

7. Moore. Mouse septicemia bacilli in a pig's spleen with some 
observations on their pathogenic properties. Jour, of Comp. Med. and 
Vet. Archives, Vol. XIII (1892), p. 333. 

8. Pasteur ET Thuillier. La vaccination du rouget des pores a 
Paide du virus mortel attenue de cette maladie. Comp. rend us Acad, 
des Sciences, Vol. XCVII (1883), p. 1163. 

9. SCHUTZ. Ueber den Rotlauf der Schweine und die Impfung 
mil demselben. Arbeit a. d. Kaiserlichiu Ccsundlieistanitc, Bd. I 
(1885), S. 56. 

10. vSmith. An Kxamination of Pasteur's Vaccine for Rouget. 
Annual Report U. S Bureau of Animal Industry, 1885, p. 187. 

ir. Smith. Swine erysipelas or mouse septicemia bacilli from an 
outbreak of swine disease. A?inual Rept. U. S. Bureau of Animal 
Industry, 1895-96, p. 166. 



ANTHRAX. 



Synonyms. Splenic fever ; splenic apoplexy ; wool 
sorters' disease ; malignant pustule ; anthracemia ; mycosis 
iutestinalis ; charbon ; Milzbrand. 

§ 116. Characterization. Anthrax is an infectious 
disease occurring sporadically and in epizootics in herbivora 
and omnivora and communicable to nearly all warm-blooded 
animals, and to man. It is characterized by the presence in 
the diseased tissues or liquids of Bacterium anthracis, by an 
enlarged spleen, blood extravasations and by local gangrene. 
It usually occurs in the acute form. 

§ 117. History. Anthrax is among the oldest of the 
known infectious diseases of animals. Descriptions of epi- 
demics and epizootics of this disease are given by Homer, 
Plutarch, Livy and other writers before the Christian Era. 
The Arab physicians designated it as "Persian Fire." Exten- 
sive outbreaks are mentioned in the literature of the fifteenth, 
sixteenth, seventeenth, eighteenth and nineteenth centuries. 



T30 



ANTHRAX 



Chabert pointed out in 1780 that the various kinds or forms 
of the disease, which had previously been described as independ- 
ent affections, were all one disease. As late as 1805, Kausch 
gave a good description of anthrax but denied its contagious- 
ness. Delafond and Gerlach thoroughly investigated ovine 
anthrax in 1854 and its contagiousness was experimentally 
shown by Gerlach. In 1850, Heusinger published a very 
comprehensive treatise on anthrax which deals at length with 
its history and geographical distribution. 

Much new information concerning the nature of anthrax 
was acquired during the fifth decade of the last century. 

In 1S55, Pollander an- 
nounced the discovery, 
which he first made 
in 1849, of minute 
uubranched rod-shaped 
bodies in the blood of 
cattle dead of anthrax. 
Davaine observed simi- 
lar bodies in 1850. 
Then followed a long 
series of observations 
and somewhat contro- 
versial discussions on 
the bacterial origin of 
the disease, culminat- 
ing by Robert Koch's 
careful description of 
the morphology of its 
specific organism including the spore formation in 1876 
(1877 Pasteur). Cohn, however, seems to have been the first 
to have called the organism a Bacillus and to have suspected 
the existence of spores. Toussaint, in 1880, and Pasteur in 
188 1, published results of investigations directed toward pro- 
tective inoculation. Since that time, the literature on the 
cause, morbid anatomy and prevention of anthrax has become 
very extensive. 




Fig. 21. Anthrax bacteria in an im- 
pression preparation made from a colony 
on an agar plate culture. 



ETIOLOGY 131 

§ 118. Geographical distribution. Anthrax is a widel}- 
disseminated disease. The continent of Europe has perhaps 
suffered most from its ravages. It occurs, also, in Northern, 
Eastern and Central Africa, where in recent years it has 
become a great plague. In Siberia, it has caused fearful des- 
truction, and in that country it is still known as the "Siberian 
Plague." It has frequently appeared in England. Russia, 
India and Australia are also infected. South America is also 
reported to suffer much from its ravages. In the United States 
it has been reported from at least fifteen states. In fact there 
are very few, if any, countries where this disease has not been 
found. A knowledge of its specific cause, with the methods 
of properly disposing of dead animals, isolation and disinfec- 
tion, as well as the preventive inoculations now in vogue, have 
made it possible to prevent wide-spread epizootics. In 
America it is looked upon as a comparatively rare disease, 
excepting in certain infected districts. 

§ iig/ Etiology. Anthrax is due to the presence of a 
microorganism known as Badermm anthracis. This organism 
is found in the diseased tissues and organs of affected animals. 
On account of its spores, it is very resistant to the normal 
destructive agencies in nature. Consequently when it is once 
introduced into a locality it tends to remain there for many 
years, possibly causing from time to time a few cases of anthrax 
or serious epizootics or epidemics. The spores are also fre- 
quently carried in the wool, hair, hides, hoofs and horns taken 
from animals sick or dead of anthrax. Thus the affection has 
been introduced into far distant localities. 

Bacterium anthracis is a rod-shaped organism varying in 
length from i to 4 /i, but having a quite uniform breadth of 
about one micron. In a suitable medium it grows out in long 
flexible filaments which combine to form thread-like bundles. 
When examined, the ends of the rod seem to be square cut. 
In preparations from animal tissues there appear sometimes to 
be slight concavities in the ends of the segments when two of 
them are united. In cultures spores are formed. These are 



132 ANTHRAX 

oval, highly refractive bodies held within the cellular 
envelopes of the filaments, but later they are set free by the 




Fig. 22. Anthrax bacteria in a cover-glass preparation of blood 
sho-u'ing chains and capsules. 

dissolution of this membrane. They stain readily with the 
aniline dyes and also b}^ Gram's method. 

The bacterium of anthrax itself is not an especially hardy 
organism. On the contrary it is easily destroyed by weak 
disinfectants and it has a low thermal death point. Its spores, 
however, are among the most hardy of bacterial life to resist 
chemical and thermal agents. They resist drying for months 
or years and often boiling for a half-hour or longer does not 
destroy them. On this account it is very difiicult to eliminate 
the virus from infected pasture lands, especially if they are 
wet or marshy. 

As the spores may remain on the soil in a dormant condi- 
tion for many years, it sometimes happens that the disease 
does not appear until long after the introduction of the virus. 
Anthrax has been known to break out among cattle grazing 
on a field in which the carcasses or hides from affected animals 
were buried many years before. Through some means the 
spores seem to be able to get to the surface and contaminate 
the grass. The virus may be introduced with blood or bone 



CHANNELS OF INFECTION 133 

fertilizers, hides, hair or wool from infected countries. When 
the extent of this traffic is realized, it is easy to understand 
how anthrax has been brought to this country and whj' it 
occasionally appears here and there over a large part of the 
continent. Many outbreaks, as well as isolated cases, illustrat- 
ing this common method of dissemination are on record. 

The period of incubaf ion \s \Qry s\\or\.. In inoculated ani- 
mals it ranges from i to 5 days. 

§ 120. Animals attacked. Nearly all species of ani- 
mals suffer from anthrax. The herbivora and rodents are 
most susceptible. Horses and mules often suffer from it. 
M'Fadyean has reported outbreaks aggregating 54 cases, of 
which 49 were cattle, 4 horses and i pig. He states also that 
for a period of 5 years there had been reported 192 cases in 
horses and 3,390 in cattle. It is interesting to note that the 
Algerian race of sheep are immune. A satisfactorj' explana- 
tion for this striking exception has not been recorded. It has 
been stated that a single bacterium introduced into the subcu- 
taneous connective tissue of a guinea pig or mouse is sufficient 
to kill it. Cats, tame and wild rabbits and hares are the next 
most susceptible species. It is stated that dogs, pigs and foxes 
are very slightly susceptible. Rats, fowls and pigeons are 
reported to be immune. Fish and amphibia are rarely 
attacked. 

^ 121. Channels of infection. Three common modes 
of infection are recognized for anthrax, namely : through the 
digestive tract, by the skin and by the lungs. In cattle the 
infection seems to be largely through the alimentary canal ; 
in horses and sheep by the skin or digestive tract ; in men 
through wounds of the skin and the respiratory tract. 
Although these are the usual methods there are many excep- 
tions with each species. 

I. Infection througli t/ie alimentary canal. This is the 
more common mode of infection in cattle. The resulting 
disease has been designated by various names, among which 
are "intestinal anthrax," "fodder anthrax," "spontaneous 



134 ANTHRAX 

anthrax," internal anthrax," "anthrax fever," and anthrax 
without external manifestations. In these cases the infecting 
organisms, either the spores or the vegetating bacteria them- 
selves, are taken into the body with food or drinking water. 
M'Fadyean has recently shown that infected food stuffs are 
often responsible for the infection. It is stated that the 
infection takes place in most cases in the small intestine, the 
mucosa of which, it is stated, need not necessarily be injured. 
It is highh' probable that the gastric juice destroys most of the 
bacteria while the free spores are not injuriously affected by 
it. In the infected districts, the spores exist at or upon the 
surface of the soil and possibly on the blades of grass, from 
which they are easily taken up by grazing animals. In lands 
thus infected, the specific organism has been introduced at 
some previous time either by the burying of anthrax animals 
in these fields, by the use of infected tannery or slaughter 
house refuse as fertilizers, by flooding from infected streams, 
or by the bringing of the organism in the droppings of birds 
or other small animals which have fed upon anthrax carcasses. 
It is reported that the spores will find their way to the surface 
even when the dead animals have been buried at a considerable 
depth. There has been some controversy in the writings of 
Pasteur, Koch and Bollinger concerning the method by which 
the spores reach the surface. Pasteur supposed that they were 
brought by earth worms from the buried carcasses. Koch 
believed this impossible because of the low temperature of the 
ground at the depth at which the animals are buried. Bol- 
linger has shown experimentally the possibility of Pasteur's 
views. Karliniski and others have found that the spores of 
anthrax may be disseminated by slugs, insects and larvae 
which are found on untanned infected skins. 

2. Infection through the skin. In animals, this mode of 
infection occurs less frequently than in man. Anthrax pro- 
duced in this way is usually characterized by local manifesta- 
tions known as "carbuncle disease," or "malignant pustule." 
In this mode of infection the bacteria penetrate through 
wounds in the skin and exposed mucous membranes into the 



SYINIPTOMS 135 



living tissues by means of infected utensils, the use of infected 
instruments, and insects, especially the house fly {Miisca 
domestua.) Dalrymple has called attention to the spread of 
this disease among animals in the lower Mississippi Valley 
by means of the horse fly (^Tabanidae). In man many cases 
of the disease occur from the injuries or cuts made at the post- 
mortem of anthrax animals or by the infection of skin wounds 
while handling infected hides or wool. Malignant pustule is 
reported to be quite common among the employes of certain 
tanneries and upholstering establishments where hides and 
hair imported from infected districts or countries are used. 

3. Infection through the respiratory tract. Faser, Buch- 
ner, Lemke, and other writers have shown experimentally 
that the disease can be produced by the inhalation of spores. 
In man this form of infection is quite common among the wool 
sorters. In Great Britain, where much foreign wool is handled, 
it has been reported as causing as many as 500 deaths 
annually. It is known as "wool-sorters' disease." 

§ 122. Symptoms. In anthrax, the symptoms vary 
not only in different species of animals but also in diff"erent 
individuals according to the location of the disease. Again 
there is often considerable variation when the lesions are 
apparently the same. The most characteristic features of the 
disease are the suddenness of the attack, the grave general 
disturbances, high elevation of temperature, a tendency to 
ecchymosesofthe mucous membranes and local manifestations, 
such as carbuncles and edema of the skin, digestive disturb- 
ances, brain complications and difficult respiration. 

Anthrax has been classified according to its course as per- 
acute, acute and subacute. It has also been divided accord- 
ing to the site of its manifestations as anthrax with visible 
localization and anthrax without visible localization. 

Anthrax zvithout visible localization. This form is gener- 
ally due to ordinary infection presumably by spores. It 
includes the peracute, acute, and subacute. 

I. The peracute or apoplectic anthrax gives rise to 



136 ANTHRAX 

symptoms of cerebral apoplexy. The animal becomes sud- 
denly ill, staggers about for a brief period and falls. There is 
often a bloody discharge from the mouth, nostrils and anus. 
Death usually ensues in from a few minutes to an hour. 



/ 



<^ 



/ 






Fig. 23. A camera Iiicida drazcitig of a field in a preparation of 
blood from a case of acute anlhrax , much enlarged {Burnett). 

Usually there are convulsions. Sheep and cattle suffer most 
frequently with this form of the disease. They are often 
found dead. This is especially true in the beginning of an 
epizootic. 

2. In the acute form, the disease runs a somewhat slower 
course, lasting usually not to exceed twenty- four hours. The 
temperature rises rapidly to from 105 to 108° F. With this 
there are signs either of congestion of the brain or of the 
lungs. If the brain is affected the animal becomes restless, 
excited, stamps the ground, rears in the air, bellows, runs to 



SYMPTOMS 137 

and fro and finally goes into convulsions followed by stupor 
and death. If the lungs are congested there is difficulty in 
breathing, more or less wheezing, panting, groaning, palpita- 
tion of the heart, small and frequent pulse, cyanosis of the 
mucosaof the head, bloody discharges, hematuria, staggering 
and finally convulsions and death from suffocation. Occasion- 
ally there is a partial remission of the symptoms, followed by 
relapse. It has been observed that occasionally there are pre- 
monitory symptoms preceding the acute attack, consisting of 
slight digestive disturbances and diminished vivacity. Burnett 
found the anthrax bacteria in large numbers in the blood dur- 
ing this stage. He likewise found them to be present in the 
blood of the more chronic cases during the febrile period. 

3. The subacute form is known as anthrax fever or 
intermittent anthrax. The symptoms are the same as in the 
other forms, except that they are more sharply defined and the 
course is longer. The disease lasts from one to seven or eight 
days, the average being about forty-eight hours. The high 
temperature, the congestion of the lungs or brain complicated 
with intestinal disturbances, especially colic, are usually well 
marked. In epizootics where the peracute or acute form 
ushers in the disease, the later cases usually are of the sub- 
acute variety. 

Anthrax icith visible localisation. These forms usually 
result from infection of the skin and mucous membranes. 
The lesions are spoken of as carbuncles and often there is 
marked local edema of the skin. This form is common in 
manv horses and sometimes it occurs in cattle. It is reported 
to occur in other species. The carbuncles are circumscribed, 
cutaneous swellings which are at first hard, hot and painful. 
Later they become cold and painless, with a tendency to 
become gangrenous. The edematous tissue becomes doughy, 
cold to the touch and painless. Frequently fluctuating swell- 
ings of the skin occur. The duration of this form of the dis- 
ease varies from four to fifteen days. Ordinarily it is not so 
fatal as internal anthrax. 

When the infection is on the mucous membrane the 



138 ANTHRAX 

animal suffers from fever, dyspnea, difficulty in swallowing- 
and cyanosis, together with the immediate local effects. 
Death occurs much sooner than when the disease is located on 
the skin. It is stated that dogs and swine suffer from this 
form more than from the acute types. 

In horses, anthrax usually runs an acute or subacute 
course. The first symptom is rise of temperature with a rapid, 
feeble pulse. There may be chills and muscular spasms. 
The mucosa of the head becomes cyanotic and lacrymation is 
often present. The animal has a dull, stupid look, appears to 
be stunned and walks with a staggering gait. In some cases 
there are symptoms of cerebral congestion, such as restlessness 
or convulsions. Colic is a very characteristic symptom in the 
horse, otherwise the symptoms are the same as in cattle. 
Infection of the skin usually occurs on the hypogastrium, 
lower part of the breast, inner surface of the fore and hind 
quarters. Swelling of the hind quarters often causes lameness. 
Carbuncles of the mucous membrane of the tongue are said to 
be rare in this species. 

In sheep and goats the disease is usually of the acute or 
apoplectic form. The animals appear as if suddenly stricken 
with apoplexy. If death does not occur within a very short 
time, symptoms already described for this form of the disease 
may be recognized. Subacute anthrax is said to be very rare 
in sheep. 

In swine, anthrax is ordinarily characterized by local 
lesions on the mucous membrane of the larynx and pharynx. 
The animals have a rise of temperature and the intermaxillary 
space is generally swollen. The swelling may spread along 
the trachea, giving rise to difficulty in swallowing, hoarseness, 
cyanosis of the mucosa of the mouth, dyspnea and rapid 
breathing. The animal shows signs of paralysis. Death 
occurs from suffocation. Frequently the tongue becomes the 
seat of the disease. Carbuncles occurring on the skin, 
especially of the back, have been described in this species. 

In dogs and cats, the disease usually rans a very rapid 
course. The fact that they are usually infected by eating the 



MORBID ANATOMY ^39 

meat of animals dead of anthrax causes them to suffer largely 
from the intestinal form. It has been stated that probably 
much of the so-called anthrax in dogs is simply cases of 
ptomaine poisoning. 

It is reported that in birds anthrax usually runs a very 
rapid and usually fatal course. Toward the end they stagger, 
tremble or go into convulsions and die with bloody discharges 
from the mouth, nostrils and anus. From the first the birds 
are depressed, weak, and their feathers ruffled. There is 
evidence of dyspnea. Carbuncles are said to appear on the 
comb, wattles, conjunctiva, tongue and extremities. 

It has been stated that the milk from cows suffering with 
anthrax contains Bad. anthracis. The writer found in the 
examinations made in one epizootic that the anthrax bacteria 
were present in considerable numbers in the milk just before 
or immediately after death, but they were not found in the 
milk of animals in the earlier stages of the disease. 

§123. Morbid anatomy. The nature and extent of the 
tissue changes depend upon the course of the disease. When 
experimentally produced it is ordinarily a septicemia. This 
form often occurs in domesticated animals when they contract 
the disease naturally. The more common anatomical changes 
except in the most acute cases and in the strictly localized 
lesions or carbuncles, are : 

Hemorrhages varying in amount from petechiae to blood 
extravasations, with more or less .serous, gelatinous and hem- 
orrhagic infiltration of the submucous, subserous and subcuta- 
neous tissue. 

The capillaries are distended and frequently there are 
hemorrhages beneath the epidermis. The subcutis is spnnkled 
with ecchymoses. Frequently there are gelatinous effusions 
of a rather firm consistency and of varying size. The color 
also differs, ranging between a deep yellow and a yellowish 
brown. Often these edematous areas are spnnkled with hem- 
orrhagic foci. A simple serous edema may occur. 

The lymphatic glands may be hemorrhagic, edematous 



I40 ANTHRAX 

or both. An edema of the connective tissues of the neck or 
about the trachea is often ver}' marked. 

The muscles vary in color but usually they are darker 
than normal, and like the skin, they often become sprinkled 
with ecchymoses. The heart muscle suffers from parenchy- 
matous changes. 

In the larger cavities of the body, a sanguinolent fluid is 
found in moderate quantities. Blood extravasations of differ- 
ent sizes are seen under the serous membranes, particularly on 
the mesentery and mediastinum. The subserous connective 
tissue, especially on the mesentery, anterior mediastinum and 
in the neighborhood of the kidneys, is often infiltrated with a 
gelatinous substance. On this account the neighboring lymph 
glands are considerably swollen, filled with serum and 
sprinkled with hemorrhages. The internal organs contain a 
large quantity of blood. All the larger veins and the heart 
are filled, while the surrounding tissues show sanious 
imbibition. 

The spleen is usually considerably enlarged (two to five 
times its normal size), either uniformly or by prominent 
tumor-like protuberances. The pulp is soft, more or less fluid, 
and stained a dark red color. The capsule is always very 
tense. It is frequently sprinkled with ecchymoses. Occasion- 
ally this organ is slightly affected. 

The liver and kidneys are highly congested and some- 
what enlarged. The parenchyma contains areas of blood 
infiltration and the cells themselves manifest various kinds of 
degeneration. The portal lymph glands often appear to be 
enlarged, and the retroperitoneal tissue may be infiltrated with 
a serous, gelatinous fluid. The subperitoneal tissue of the 
intestines and of the abdominal walls may be similarly 
affected. 

The nature of the lesions of the intestinal canal varies 
according as the disease is intestinal anthrax, or anthrax 
caused by inoculation. In case of inoculation anthrax, the 
intestine is frequently normal. In other cases there may be 
submucous and subserous hemorrhages, or swelling of the 



MORBID ANATOMY I4I 

mesenteric glands. The principal changes in intestinal an- 
thrax are always found in the small intestine, chiefly in the 
duodenum. In the milder cases of intestinal anthrax the 
mucous membrane is affected by circumscribed or diffuse 
swellings. The bacteria are often found in very large num- 
bers on the surface of the raucous membrane. Necroses and 
ulcers appear in those parts where the bacteria are most 
thickly congregated. In very severe cases, the abomasum or 
the true stomach may be affected with a gelatinous and sanious 
infiltration of the mucous membrane. The mucosa of the 
abomasum, and especially of the duodenum, is, in consequence 
of excessive hyperemia, dark red or almost black, and is 
covered with ero.sions and ulcers or necroses, which may 
extend down to the submucosa. The contents of the intestine 
are bloody, and the submucosa is infiltrated with a serous, 
gelatinous, or hemorrhagic exudate, so that the mucous mem- 
brane often projects, in the form of large tumors, into the 
lumen of the intestine. On the site of Peyer's patches and the 
solitary follicles we may find flat or prominent nodules, the 
surface of which are covered with diphtheritic crusts. 

The lungs are greatly congested, edematous and show 
areas of ecchymoses. The entire respiratory mucous mem- 
brane is considerably reddened and ecchymotic. The mucous 
membrane of the pharynx and opening of the larynx is often 
so edematous that stenosis of the larynx takes place. The 
contents of the trachea and the bronchi consist mostly of 
bloody froth or mucus. 

The brain is often studded with ecchymoses. The sur- 
face of its membranes often exhibits hemorrhages with an 
accumulation of sanious serum in the ventricles. Extravasa- 
tions of blood sometimes occur in the anterior chamber of the 
eye and under the retina. All the other organs may contain 
hemorrhages, and the urine frequently contains blood. 

The blood is usually dark. It has a tarry or varnish- like 
lustre, and shows little tendency to coagulate. It does not 
assume its normal red color when exposed to the air. Burnett 
studied the blood ot a few cases of anthrax in 1904. The 
appended tables are taken from the results of his examinations. 



142 



ANTHRAX 



RESULT OF THE EXAMINATION OF THE BLOOD OF FIVE CASES OF 
ANTHRAX IN CATTLE. 



1 First Date of S^ 

Cow .symptom Exam- 2" = 

1 observed ination S s 


Hemo- 
globin 
per 
cent. 


Red 
Corpuscles 
per c. mm. 


Leuco- 
cytes 
per 
c. mm. 


Remarks 


No. 8 Ijuly 8 107.5° 








Anth. bact.i 
in blood 

I 


" 8 Jul.v 9 106.6 


60 


4,072,000 


20,000 


Died July 9 


" 4* July ID 106.2 








" 4 July II 


56 


5,471,000 


4,814 




" 4 " 13 103.0 


38 


3,400,000 


3,444 




" 4 " 19 


56 


2,086,000 


9,876 


Recovered 


" 6tJuly 7 










" 6 ' July 9 104.0 


50 


3,876,600 


8,222 


Anth. bact. 
in blood 


" 6 ; " II 




60 


3,954,000 


5,210 


," 6 '• 13 


101.8 










" 6 


" 14 


101.2 


47 


3,484,000 


5,666 


Apparently 

recovered. 

Died of 

Anthrax 

Nov. 4 


" 6 


" 19 




54 


I ,980,000 


8,777 


" 6 
" 3 


" 24 




63 


3.132,000 


11,888 


June 29 












July 14 


101.2 


57 


4,168,000 


5,222 


Recovered | 


" I July 15 




1 




July 16 


103.8 


53 


2,324,000 


8,111 1 




" 17 


lOI.O 


58 


2,632,000 


5,333 




" 18 102.0 






8,163 






" ^^i 




5,940,000 


11,000 






61 




10,767 


Recovered ' 

1 


1 ! 





*Teraperature July 8, 102.1°. 
iTemperature Julys, 107.4°. 



Temperature July 10, 100.0°. 
Temperature July 9, 103.0°. 



^lORBID ANATOMY 



143 



THE DIFFRRKNTIAf, COtTNT OF THE LEUCOCYTES IN FIVE CASKS 
ANTHRAX IN CATTI^E. 



COW 


Date 




I^ympho. 
cytes 


Large Mono 
nuclear 


Polynuc- 
lear 


Eos 
phi 


Ho- 
les 


Masst 
Cells 


No. 


0/ 


No. 


% 


No. % 


No. 

I 


No. 

.?! 

48 
7 
II 


0.4 
0.2 

I.O 

0.2 
0.2 

0.5 

°:! 
0.7 

I.I 

0.4 

0.7 

0.2 

0.8 
0.7 

0.5 


Soper 
No. 8 

1 " 4 


July 9 20000 


7080 


35-4 


2200 


II.O 


7120 35.6 


3520 

548 

75 

636 


17.6 

2.8 

II. 4 
2.2 

6.4 


" 11! 4S14 


1670 


27.4 




5-2 


|64.8 


1 ,, ,, 

t 

i " " 


34.7 


341 


7-1 


2200I 45-7 


" 13 


3444 


1432 


41.6 


261 


7.6 


i667| 48.4 




" 19 


9876 


4257 


43-1 


273 


2.7 


4696 47-5 


" ^ 


" 9 8222 
" ii; 5210 


3930 
2287 


47.8 
43 9 


296 


3-6 


3436 41.8 


518 


6.3 


41 
36 

62 

35 

I9 

10 

65 
36 

55 
86 


" " 


338 


65 


2115! 40.6 


432 i 8.3 


" " 


" 13 




40.1 


40 


47.2 




7.8 


.. <. 


" 14 5666 


2833 50.0 


119 


2.1 


2221 39.2 


430; 7-6 
[930 22 


~77~7r 


" 19 8777 
" 2411S88 


3747 42.7 


263 


3-0 


2800 31.9 


6033 50.7 


698 


5-8 


3120 26.2 


1946 
146 

1330 
640 
734 


16.3 
2.8 

16.4 
12.0 
9.0 


" 3 


" 14I 5222 


3352 64.2 


261 


5-0 


1451 27.8 


Bradish 
No. I 


1 
" 16 8rii 


35281 43-5 


154 


1-9 


3033' 37-4 


[ .< <. 


" 17 5333 
" 18, 8163 


2832 53-1 


256 


4.8 


1368: 29.4 


t ". " 


6375 78.1 


138 


1-7 


914 


II. 2 


" '« 


" i9|iiooo 


661 1 60.1 


253 


2.3 


2585 


23-5 


1496, 13.6 


1 " " 


" 2410767 


5911 54-9 


484 


4-5 


2186 


.0.3 


2099 


.9.5 



He found that the number of red corpuscles and the per- 
centage of hemoglobin are reduced. In the chronic cases 
they tend to return to the normal condition. There was an 
increase in the number of lymphocytes and a decrease in the 
number of polynuclear leucocytes. In some cases there was a 



144 ANTHRAX 

marked increased in the number of eosinophiles. No change 
from the normal was noted in the large mononuclear leuco- 
cytes or in the mast cells. 

The bodies of animals which have died from anthrax aie 
often well nourished. Rigor mortis is absent and they decom- 
pose quickly. Very frequently blood flows from the natural 
openings of the body, and the rectum is sometimes prolapsed. 

All the foregoing lesions may be absent in very acute 
apoplectic cases. The specific organism is, however, always 
present in the cadaver. It is important to note that occasion- 
ally the usual changes indicated by the symptoms and the dur- 
ation of the disease are not found on post-mortem examination. 
In one epizootic, the writer saw an animal dead from subacute 
anthrax in which the blood and tissues were teeming with 
anthrax bacteria, yet the organs examined macroscopically 
appeared to be normal. Other animals in the same outbreak 
exhibited the more usual anatomical changes. 

The period of dtiration varies from a few hours to a week 
or even longer. 

The prognosis is unfavorable. In some herds the mor- 
tality is ICO per cent while in others a number of animals 
may recover. The average mortality is placed at about 70 
per cent in animals. In the human species many persons 
recover from its local form (malignant pustule). 

M'Fadyean has reported this disease in 39 consecutive 
outbreaks in which a total of 54 animals died. In New York 
the disease existed in 1904 in 15 herds in one locality. There 
were more than 30 deaths. In one herd of 21 animals, 20 had 
the disea.se, 16 died and 4 recovered. In another dairy 4 out 
of 7 died, but in the others one or two animals in each was 
affected. In 1906 anthrax occurred on 84 different farms in 
the same county. There were 170 fatal cases of which 2>c> 
were in horses, 123 in cattle, 11 in sheep, and 3 in hogs 
(Burnett). These facts are interesting in showing that the 
disease does not always cause heavy losses in the infected 
herds. 



DIFFERENTIAL DIAGNOSIS I45 

§ 124. Differential diagnosis. It is important not to 
confuse anthrax with a number of non-specific disorders and 
accidental causes of death. The suddenness of the attack, and 
in very virulent cases, the short duration of the disease may 
tend to the mistaking of it for poisoning, cerebral apoplexy, 
pulmonary congestion, heat apoplexy, death from lightning, or 
acute gastro-intestinal inflammation. The affection known as 
corn-stalk disease is not infrequently taken for anthrax and 
vice versa. In all of these cases the doubt following the post- 
mortem can be easily settled by a bacteriological examination 
which, with genuine anthrax, will reveal the presence of Bac- 
terium anthracis. It is believed by those who have dealt most 
with anthrax, that the specific organisms are always in the 
circulating blood before death. The putrefactive organisms 
that resemble Bacterium anthracis morphologically do not 
appear in the cutaneous blood as quickly after death as they 
do in the organs. 

There are, however, certain specific diseases from which 
anthrax must be differentiated. The most important of these 
are symptomatic anthrax (black leg), malignant edema, and 
septicemia hemorrhagica. Rabies is not infrequently taken 
for anthrax. If the diagnosis cannot be determined by the 
anatomical changes (which can be relied upon only in some- 
what typical cases) the positive diagnosis can be made only 
with the finding of the anthrax bacteria. In animals just 
dead, where decomposition has not begun, these organisms can 
usually be found in properly stained cover-glass preparations 
made directly from the blood or ti.ssues. After decomposition 
begins to take place, a putrefactive organism, that is not easily 
distinguished from that of anthrax, often appears in the tissues. 
It is, therefore, necessary in such cases to resort to culture 
methods before a positive statement can be made. As the 
bacilli of malignant edema and symptomatic anthrax are 
anaerobes, they will not develop in aerobic cultures, such as 
on slant agar or in bouillon. The bacterium of .septicemia 
hemorrhagica, being a small oval organism, is easily told 
from that of anthrax. It is important to recognize the possi- 



146 ANTHRAX 

bility of error, if the conditions restrict the examination to the 
study of the microscopic preparations. 

Differential stain. M'Fadyean has described a peculiar 
staining reaction, first pointed out by Heins, which he con- 
siders of value for the microscopic diagnosis of this disease. 
The reaction is in evidence when films of blood, exudates, or 
tissue juice containing the bacteria are stained with a simple 
aqueous solution of methylene blue. The method as applied 
to blood is as follows : 

Place a drop of the blood on a clean slide. The size of 
the drop should be about 2 mm. in diameter. It is spread 
quickly with a platinum needle until it covers an area about 
12 mm. in diameter. Protect from dust and allow the slide to 
remain until all evidence of moisture has disappeared. When 
dry, heat the preparation by lowering it film upwards into the 
flame of a Bunsen burner or an alcohol lamp for a second. 
Repeat this three times or until the glass is too hot to be borne 
by the skin in the palm of the hand. Allow the slide to cool 
and then cover the film with i per cent aqueous solution of 
methylene blue. After a few seconds pour ofi^ the free stain 
and wash the slide thoroughly in tap water. Dry the slide by 
pressing it gently between two layers of bibulous paper, and 
then more thoroughly by holding it in the current of hot air 
above the Bunsen flame. Finally, mount in Canada balsam. 

The microscopic examinations (x 800 to 1000) will show 
an occasional leucocyte and the anthrax bacteria. There will 
appear no other visible formed elements. The nuclei of the 
corpuscles generally exhibit a greenish-blue tint, the anthrax 
rods are stained blue. The intensity of the stain depends upon 
the length of time after death before the films were made. 
Usually the segment character of all but the shortest rods will 
be apparent. If they are deeply stained this is not very dis- 
tinct. The peculiarity in the reaction lies in the color of the 
amorphous material which is present between and around the bac- 
teria. This material presents itself under the form of coarse 
or fine granules of a violet or reddish-purple color, which is in 
sharp contrast to the tint of the bacteria or cell nuclei, espec- 



PKOTKCTIVE INOCULATION I47 

ially with brilliant lamp or gas light. These violet granules 
differ a good deal in form and size ; sometimes they are very 
minute, and at others coarsely granular. When the bacteria 
are arranged in clumps the violet material is often in greatest 
amount about them. Free-lying anthrax rods will be sur- 
rounded by a thick envelope of the same substance. M' Fad- 
yean states that he has never found this reaction in animals 
dead from other diseases. The peculiar coloring, he states, 
in some cases may be observed without the aid of the 
microscope. 

cj 125. Protective inoculation. Toussaint was the fir.st 
to make use of protective inoculations in anthrax. He heated 
defibrinated anthrax blood to a temperature of 50 to 55° C. for 
from 15 to 20 minutes, then injected it as a protective agent. 
Pasteur, however, was the first to prove that immunity could 
be obtained by the use of cultures of attenuated bacteria. 
Several methods of attenuating the specific organisms have 
been proposed by Pasteur, Toussaint, Chaveau, Chamberland, 
Arloing and others. 

Pasteur's method consists in inoculating the animal with 
a small quantity of culture which has been grown at a high 
temperature— 42 to 43° C— for several days. This deprives 
the bacteria of their virulence. To strengthen the resistance, 
the animals are again inoculated with a stronger virus. After 
the two inoculations, they are said to be protected against the 
most virulent anthrax ; but the immunity is of short duration. 
Chamberland reported in 1894 that a total of 1,988,677 animals 
had been treated by this method in France, and that the loss 
from anthrax had diminished from 10 per cent in sheep and 5 
per cent in cattle to less than i per cent. Cope, in his report 
to the English Board of Agriculture, regards the conclusions 
of Chamberland as somewhat fallacious, because in order to 
prove that the animals inoculated received immunity, it should 
be shown that they were subsequently exposed to the ri.sks of 
natural infection. The excellent work which has been done 
bv Neal and Chester, at the Delaware College Experiment 



148 ANTHRAX 

Station, has shown the possible efficiency of this method. Of 
the 331 cows which they vaccinated against anthrax, two died 
of the disease, giving a death rate of less than i per cent and 
this in a territory so saturated with the virus that it was prac- 
tically impossible to keep cattle at all before its use. 

A more critical study of the reports on the use of this 
vaccine shows that while success can not be denied, failures 
must be admitted. It is reported both in England and Ger- 
many that the Pasteur vaccine has not been a marked success. 
In England, Klein, who tested the vaccine used in that coun- 
try, found that if the animals did not die from the effect of the 
vaccine, they did when exposed to the disease. The German 
veterinarians and agriculturalists agree that the first vaccine 
is mild and harmless, but that the second vaccine, even in the 
hands of experts, is dangerous and often fatal. In the state 
of Illinois a number of cattle died of anthrax immediately 
after receiving the second vaccine, and in Manitoba a large 
number (about 500) of sheep died after the second vaccination 
(Higgins). In these cases the vaccine used was not suffi- 
ciently attenuated. In a recent outbreak in the state of New 
York the animals that were vaccinated, but not carefully 
isolated from the infected pastures, continued to die of the 
disease after the second vaccination. This was due to the 
excessive attenuation of the vaccine. In the summer of 1907 
a large number of cattle in an infected territory were vaccin- 
ated with very good results. On a few farms, all of the unvac- 
cinated cattle died of anthrax, while the vaccinated ones 
remained well. It is reported to have been demonstrated by 
experiment that the virulence of the attenuated virus can be 
easily restored. Again, it has been shown by the investiga- 
tions of Chester and Neal, of the Delaware College Agri- 
cultural Experiment Station, that a vaccine which succeeded 
at one time subsequently proved fatal. The vital objection to 
this method is, that it requires the use of the living bacteria, 
which later may become virulent and consequently cause a 
subsequent outbreak. The scattering of pathogenic organisms, 
even in an attenuated condition, should be avoided if possible. 



THE SIMULTANEOUS METHOD I49 

It must be admitted, however, that Pasteur's method has done 
much good and helped to rob anthrax of much of its former 
terror, especially for the farmers of Europe. In America the 
spread of anthrax has been checked in many districts by its 
use. Dairy mple has pointed out its success in the lower Miss- 
issippi valley. Notwithstanding, it is highly probable that 
the spreading of a knowledge of the specific cause of this 
disease with that of the proper disposition of dead animals has 
also exerted much influence for good in checking its ravages. 
In Germany and England the stamping-out system is con- 
sidered superior to vaccination. According to Crookshank, 
in England it is regarded as the only reliable means of sup- 
pressing the disease. To this end rigid laws have been enac- 
ted. In this country as rigid measures as possible for its 
eradication seem infinitely better than the general adoption of 
methods for establishing a tolerance for its existence. 

vj 126. The simultaneous method. This method 
which consists in the injection of anthrax antitoxin or serum 
together with a small quantity of virulent anthrax bacteria, 
has proven to be very satisfactory. It has the advantage of 
being administered at one time. This method of protection 
against anthrax seems to have been first proposed by Sobern- 
heim in 1899. Since that time Sclavo in Italy and others 
have published on the method. Sobernheim reports excellent 
results by the use of this method in immunizing cattle against 
anthrax in South America. The serum is now produced in 
large quantities in Germany. In this country, it is just begin- 
ning to receive attention. 

§ 127. Prevention. In all cases the well animals should 
be removed from the barns or yards containing the sick ones 
and from pasture lands on which the sick became infected. 
The^emperature of healthy and uninfected animals should be 
taken morning and evening for from one to two weeks after 
they are removed and all of those showing an elevation- of 
temperature should be isolated. By careful isolation and safe 
disposition of the dead animals the spread of the disease can be 



150 ANTHRAX 

checked. Animals do not, as a rule, spread the virus when the 
first symptom (rise of temperature) can be detected. All 
infected stables and yards should be thoroughly disinfected. 

Tlie disposition of dead animals in an outbreak of anthrax 
is a matter of much importance. In all cases they should be 
burned if possible, if not, they should be buried deeply and 
covered with quick lime before the dirt is replaced. The 
ground over the place where they are buried should be fenced 
in to prevent other animals from grazing over it, and the sur- 
face should be burned annually for some years to destroy 
spores should they be brought to the surface. 

REFKRENCKS. 

1. Burnett. On the control of an outbreak of anthrax. Ant. 
Vet. Revieiv. 1908. 

2. Chester. Anthrax, bacteriological work. Report Del. Agr. 
E.vpt. Station, 1895, p. 64. 

3. Chester. Protective inoculation against anthrax. Proceed- 
ings of the Society for the ProDiotion of Agricultural Science, iS96,p. 52. 

4. Dalrympi^e. Anthrax and protective inoculation in Louisiana. 
Proceedings of the A))i. Vet. Med. Assn., 1901, p. 147. 

5. Davaine. Recherches sur les infusoires du sang dans la mal- 
adies connue sous le nom de sang de rate. Compt. Rend, de V Acad, 
des Sc. 1863, 1864, 1865. 

6. KoCH. Die Aetiologie der Milzbrand-Krankheit begriindet auf 
die Entwickelungsgeschichte des Bacillus Anthracis. Colin' s Beitr. 
ziir Biol, der Pflanzen, Bd. II (1876), vS. 277. 

7. M'Fadyean. Anthrax, four. Couipar. Bath, and Ther.. \'ol. 
XI (1898). p. 51. 

8. M'Fadvean. a peculiar staining reaction of the blood of ani- 
mals dead of anthrax, four, of Couipar. Path, and Ther., \o\. XVI 
(1903), p. 35. 

9. M'Fadvean. Extraneous sources of infection in outbreaks of 
anthrax, four. Conipar. Path, and Ther., Vol. XVI, p. 346. 

10. Moore. Report of an outbreak of anthrax. Annual Report, 
Comtnissioner of Agriculture of the State of New Yorl^. 1897. 

11. Pasteur, Chamberland et Roux. De Tattenuation des 
virus et de leur retour a la virulence. Coinp. Rend, de P Acad, des Sc, 
Vol. XCII (1881), p. 427. 



GLANDERS 15I 

12. PasTKIR. La vaccin du charbon. Ibid. p. 6b6. 

13. RiSSELL. Outbreak of anthrax fever traceable to tannery 
refuse. The ijth annual report of the Wis. Agric. Exp. Station, 1889. 

14. SoBERNHEiM. Ueber das Milzbrandserum und seine praktische 
Anwendung. Deut. med. IVochenschr., 1904. No. 26 u. 27. (First 
publication. Zeit.fi'ir Hygiene, 1899, Bd. 31). 



GLANDERS 
Sytumyms. Malleus; farcy; morve \ Rotzkrankheit. 

i^ 128. Characterization. Glanders is one of the most 
important diseases of horses, asses and mules and when trans- 
mitted to man, one of the most fatal diseases of the human 
species. It runs an acute or chronic course, attacking the lym- 
phatic system more especially in the upper air passages, lungs 
or skin. The disease is characterized by a strong tendency to 
the formation of small neoplasms or nodules which are likely 
to degenerate into ulcers from which exudes a peculiar .sticky 
di.scharge. In the very acute cases a considerable rise of tem- 
perature and general debility may accompany the formation of 
the lesions. Glanders of the skin is known as farcy. 

By direct inoculation several species of animals may be 
infected. Thus the disease has been reported in goats, rab- 
bits, sheep, guinea pigs, field mice, and several of the wild 
animals, especially those of the cat tribe. Swine and pigeons 
are very slightly susceptible. Cattle, white mice, rats and 
domestic fowls seem to be immune. 

^ 129. History. The theory of the contagiousness of 
glanders was much doubted at the beginning of this century. 
The view taken by the veterinarians at the Alfort Veterinary 
College was that glanders might arise spontaneously from an 
attack of strangles. This view was far more widely accepted 
than the theory of its contagiousness, which was stoutly sup- 
ported by the authorities at the Veterinary College of Lyons. 
It was not until Rayer (1837) had demonstrated the trans- 
missibility of glanders to man, and Chauveau (1868;) had 



152 GLANDERS 

shown that the virus was contained chiefly in the firm compo- 
nent parts of the infective material, that the fact of the infec- 
tious nature of the disease was accepted. 

The theory of the spontaneous origin of glanders was 
widely accepted in Germany. Sixty years ago it was believed 
that glanders could be produced by the injection of pus, and 
that strangles could develop into glanders. Glanders was 
looked upon as a tubercular disease, scrofula, pyemia, diph- 
theritis, general dyscrasia and cachexia respectively. Vir- 
chow was the first to declare that the nodules of glanders were 
independent, anatomical formations, which he placed under 
the heading of granulation tumors. Gerlach was the strong 
advocate for the exclusively infectious origin of the disease. 
Leisering appears to have been the first to give an accurate 
description of the lesions. 

The first biological researches into its nature were made 
in 1868 by Zurn and Hallier, who found a fungus which they 
believed to be its cause. In 1882, Loeffler and Schiitz suc- 
ceeded in finding the bacterium of glanders, in cultivating it, 
and in transmitting the disease to other animals by inoculating 
them with pure cultures of the organism. Their researches 
furnished the positive proof that glanders is a specific, infec- 
tious disease, produced exclusively by Bacterium mallei. 

§ 130. Geographical distribution. Glanders exists in 
the greater part of the civihzed world. It is more common in 
the temperate zones, where traffic in horses is active. In the 
United States it was largely confined to the Northern States 
before 1861, but it spread over the South in connection with 
the civil war. It is said to have entered Mexico with the 
American cavalry in 1847. Similarly, Portugal is said to have 
been exempt until the invasion by Napoleon in 1797. Central 
Hindoostan was said to be free from it until the war with 
Afghanistan in 1878. In all these cases, the movements of 
cavalry, artillery and of commissary trains were responsible 
for the introduction of the disease into new territory. In our 
own case the sale of horses and mules at the close of the civil 



ETIOLOGY 153 

war produced a very general diffusion of this disease, from 
which the country is still suiTering. 

Insular places, especially if far from the main land and 
free from importation of horses, usually escape. Thus glanders 
is very rare in Iceland and in the Faroe islands. In Australia, 
Tasmania and New Zealand it is reported to be unknown. 

^ 131. Etiology. Baderiiun mallei, the specific cause 
of glanders, was discovered and isolated in pure culture almost 
at the same time (1882) by Loeffier. Schiitz, Israel, Bouchard, 
Charrin. Weichselbaum, Kauzfeld and Kitt. It is found in 
the recent nodules, in the discharge from the nostrils, pus from 
the specific ulcers, and occasionally in the blood of animals 
affected with glanders. 

Morphologically it is a small organism with rounded or 
pointed ends. It varies in breadth from o.25/< to o.4/< and 
from i.5/< to 3// in length. It is usually single but pairs and 
long filaments, especially on potato cultures, are not rare. It 
frequently breaks into short, almost coccus-like elements. 
Galli-Valerio found great variations in its morphology when 
grown under certain different conditions. Branching forms 
were numerous. 

It stains with some difficulty. Of the aniline colors, the 
best results are obtained with the aqueous solutions, when they 
are made feebly alkaline. It is decolorized by Gram's method. 
It grows well, but slowly, at the body temperature on 
glycerin agar, in acid-glycerin bouillon, on blood-serum and 
on potato. 

Of the test animals, guinea pigs and field mice are the 
most .susceptible. In guinea pigs, subcutaneous injections are 
followed in four or five days by swelling at the point of inocu- 
lation and sloughing of the skin, which are followed by the 
formation of a chronic, purulent ulcer. The lymphatic glands 
become inflamed and symptoms of general infection develop 
in from two to four weeks ; the glands suppurate and in males 
the testicles are involved. A purulent inflammation of the 
joints may occur. The formation of the specific ulcers upon 



154 GLANDERS 

the nasal mucous membrane, which forms one of the charac- 
teristics of the disease in the horse, rareh' occurs in the guinea 
pig as a result of inoculation. The disease is often prolonged 
for several weeks or months. Guinea pigs succumb usually 
in from eight to ten days when injected into the peritoneal 
cavity with a virulent culture. In males, the testicles are 
invariably affected. 

The period of i7iciibation is not generally known. It evi- 
dently varies from a few to many days. 

§ 132. Symptoms. Two forms of glanders have been 
recognized, namely, acute and chronic. 

Acute glandtrs. Acute glanders is common in the ass and 
mule, but infrequent in the horse. After a short period of in- 
cubation the animal has a chill, elevation of temperature, a 
profuse muco-purulent, sticky discharge, sometimes mixed, 
with blood, from the nose. Particles of food arrested in the 
pharynx occasionally appear in the nasal discharge. If uni- 
lateral the margin of the nostril swells, the mucosa is dark 
red, infiltrated, marked with pea-like, yellowish elevations 
with red areolae, which in a few days become eroded, thus 
forming spreading ulcers. The submaxillary lymphatic 
glands on the affected side become enlarged. There may, 
however, be a uniform swelling of the intermaxillary space. 
The course is rapid and death ensues in from the sixth to the 
fifteenth da}'. The acute form rarelj' if ever becomes chronic. 

Chronic glanders. In the horse, this form of the disease 
may begin with a chill but usually the onset is very insidious. 
There may be a muco-purulent, sticky discharge, sometimes 
streaked with blood, from one or both nostrils. There may 
be intermittent or continued lameness, arthritis, edema of a 
limb, swelling of a testicle, cough, or epistaxis. There is 
usuall}' a nodular but comparatively painless swelling of the 
submaxillary lymph gland on the affected side. On palpation 
the swelling imparts a sensation suggestive of a number of 
peas. They are adherent to the adjacent structures. The 
nasal mucosa is congested, of a dark reddish color and 



MORBID ANATOMY 155 

sprinkled with superficial or deep ulcers either clean or 
covered with crusts. 

Rarely the submaxillary glands only are apparently dis- 
eased. In other cases, there is only a cough, the latent lesions 
being confined to the lungs. In still other cases, the lesions 
are restricted to one or both testicles, the spleen, or some other 
internal organ. Objective symptoms may or may not be 
present. Chronic glanders may terminate in the acute form. 

In chronic, cutaneous glanders, with or without edema of 
the limbs, there may be one or many nodules on the fetlock, 
or elsewhere on the line of the lymphatic vessels, with indura- 
tion of the lymphatics extending from it. The nodules may 
be suppurating and discharging, or they may be closed. 

?; 133. Morbid anatomy. In chronic glanders the most 
frequent locations of the lesions are on the respiratory mucous 
membrane, in the lungs, lymph glands and skin. M'Fadyean 
states that he has never seen a case of glanders in which the 
lungs were not affected if any lesions were found. Other 
organs are more rarely invaded. The mucous membrane of 
the upper respiratory passages is the usual seat of the lesions. 
Glanders occurs in two forms, (i) as circumscribed nodules 
with the formation of ulcers and cicatrices ; and (2) as diffuse 
or infiltrated lesions. 

In nodulaf glanders, which is the common form, the 
lesions are most frequently situated on the upper portion of 
the nasal septum and in the cavities of the turbinated bones. 
The affection begins with the appearance of nodules varying 
in size from a grain of sand to a millet seed. They are more 
or less translucent, of a roundish or oval shape, and of a dirty 
gray or grayish-red color. The nodules, which may attain to 
the maximum size of a pea, project somewhat above the sur- 
face of the mucous membrane. They are surrounded by a 
reddish ring. Some of them are isolated and others are 
arranged in groups. Microscopically they consist of a large 
number of lymphoid cells, which disintegrate in the centre of 
the nodule. In consequence of the central fatty and purulent 



156 



GLANDERS 



degeneration, the nodules become yellowish in color, dis- 
charge and form ulcers. These ulcers are sometimes super- 
ficial, sometimes deep, 
lenticular or crateri- 
form, surrounded by 
a hard, indurated 
edge, and frequently 
becoming confluent, 
with irregularly ser- 
rated and eroded 
edges. They are 
sometimes covered 
with a brownish crust. 
The ulcers may in- 
crease in area or in 
depth and may even 
involve the underly- 
ing cartilage or bone, 
causing perforation of 
the septum nasi, and 
distensions of the 
maxillary or exostoses 
on the turbinated 
bones. The shallow 
lenticular ulcers may 
heal without leaving 
any visible .changes ; 
but the deeper ones, 
after granulating, 
leave a radiating, 
star-shaped cicatrix 
which is either smooth 
or horny, and which, 
according to the shape 
of the ulcer, may be 
of an irregular or oblong form. The nasal septum is frequently 
covered with these scars. The ulcers and cicatrices are some- 




FiG. 24. Nasa/ septum atid portion of 
turbinated bone shouiing glanders ulcers 
'with tcvo perforations ( Williams). 



MORBID ANATOMY 



157 



times found in the maxillary and frontal sinuses, in the gut- 
tural pouches and in the eustachian tubes. They may also 
occur in the larynx, especially in the region of the vocal 




Fig. 25. Photograph of a portion of a tiasal septum shoivitig ulcers in 
advanced glanders: {a) perforations of septum, {h) conjluent ulcers and 
necrotic tissue. 



158 



GLANDERS 



chords. In the trachea and even in the bronchi, particularly 
on the anterior surface, numer- 
ous long, oval ulcers or long, 
pointed, serrated scars are fre- 
quently found. In addition to 
the ulcers, a catarrhal inflamma- 
tion of the mucous membrane is 
very apt to be present. 

Diffuse glanders manifests it- 
self as a diffuse catarrh of the 
mucous membrane of the nasal 
and neighboring cavities, with 
superficial ulceration, thrombosis 
of the veins, inflammatory in- 
filtration of the submucosa. con- 
siderable thickening of the mu- 
cous membrane and the forma- 
tion of a peculiar, radiating cica- 
trix. 

Both the nodular and infil- 
trated forms are found in the 
lungs. 

In the nodular form, the lungs 
contain nodules-'^ varying in size 
from a millet seed to a pea. 
They are gray by transmitted 



*Nocard showed that when glan- 
dered horses are treated with mallein, 
a certain proportion of them recover, 
in which case nodules that are pres- 
ent in the lungs cease to contain 
living bacteria, a fact he has fully 
proved by inoculation. On post- 
mortem examination the nodules 
may be readily felt by passing the 
hand with firm pressure over the sur- 
face of the lung, which, when badly diseased, will feel like a bag full 
of shot or peas. 



Fig. 26. A'asd/ Sifl/nn froii a 
slandered Iwrse slwiving two 
large scars and several smal- 
ler recent healing ulcers and 
scars {Williatns). 



MORBID ANATOMY 



159 



light, glassy and pearl gray by reflected light, and are sur- 
rounded by a congested or a hemorrhagic ring. The center of 
the nodules shows a pale yellow point in consequence of casea- 
tion and disintegration of the innermost cells. These nodules 
are of different sizes, of varying numbers, and of different 
ages. The formation of a capsule by a connective tissue mem- 
brane is induced by a reactive inflammation in the tissue sur- 
rounding the nodule. The nodules may be of an embolic 




Fig. 27. Drazving of a horse's lung containing glanders nodules (<?). 
They appear on both the pleural and cut surfaces. 

origin situated principally in the periphery of the lung, their 
structure being the same as that of the nodules in the nasal 
mucosa. Sometimes the lung nodules represent lobular pneu- 
monic foci, in which the alveoli are filled with red and white 
blood corpuscles and with desquamated epithelium of the 
lungs. Central disintegration occurs very early. These areas 
are surrounded bv a membrane resulting from a reactive in- 
flammation which manifests itself and out of which a connec- 
tive tissue capsule develops later on. There are two theories 
concerning the structure of the early nodules. One is, that 
the first cells are epithelial in nature, thus closely resembling 



l6o GLANDERS 

a tubercle. The other is that the first stage of the nodules 
consists of air cells filled with leucocytes. 

M'Fadyean has called attention to the structure of the 
lung nodules, in which he finds a central part composed of 
leucocytes that have filled the air spaces, the walls of which 
have disappeared as if by liquefaction. This is surrounded by 
a zone of epithelioid cells. A third zone surrounds this, in 
which the walls of the air vesicles are recognizable. The 
walls are thickened. The fourth zone is composed of air ves- 
icles filled with a fibrinous exudate, which entangles a few 
leucocytes. Frequently the exudate is free from red blood 
corpuscles, but at times it contains much blood. In older 
nodules the third and outermost zone is composed of cirrhotic 
lung tissue, in which can be distinguished the remains of the 
air cells. This zone passes gradually into the normal tissue. 
In the last stage the central area shrinks and becomes calcified, 
while the other zones become converted into a distinct fibrous 
capsule. Other observers have not reported the calcification. 
It has not occurred in the writer's observation. The cell 
necrosis in glanders has been designated by Unna as chroma- 
tolasis which consists in the disintegration of the nucleus before 
the destruction of the cell body and the retention of the stain- 
ing property of the broken, nuclear chromatin. This gives 
the dark color in the central part of a stained nodule. 

Besides these nodules, there are often chronic bronchitis, 
peribronchitis, parabronchitis, atelectasis, inflammation of the 
tissue of the lung and less frequently circumscribed or exuda- 
tive pleuritis. 

Infiltrated glanders of the lungs form tumors from the 
size of a walnut to that of a child's head, consisting of a diffuse 
glanderous infiltration of the alveoli and of the interstitial 
connective tissues. Frequently on section the infiltrated parts 
of the lungs resemble very closely a soft sarcoma. They are 
of a dirty white color, of a gelatinous, juicy consistency and 
irregular in shape. They may either become indurated so as 
to form hard, connective tissue-like new growths (fibroma-like 
tumors of glanders, according to Gerlach), or they may become 



MORBID ANATOMY 



l6l 



gangrenous. In nodular and in infiltrated glanders of the 

lungs, the bronchial glands and frequently the mediastinal 

glands become enlarged, indurated and studded with small 

foci of cell infiltration. 

In glanders of the skin (farcy) the nodules are found in 

the papillary layer, in the cutis and in the subcutaneous and 

superficial intermuscular 

tissue. The cutaneous 

nodules vary in size 

from a hemp seed up to 

a pea. They suppurate 

rapidly and form small 

ulcers. The nodules in 

the subcutis are inflam- 
matory (metastatic) tu- 
mors from the size of a 
pea to that of a hen's 
egg. They change into 
large abscesses and dis- 
charge externally. In 
the region of the nodules 
the lymphatic vessels 
are inflamed, swollen, 
and frequently resemble 
a rosary or knotted cord. 
Ulcers often develop 
from these secondary 
nodes. The neighbor- 
ing lymph glands are at 
first swollen and soft, 
but later they become indurated by the growth of connective 
tissue and studded with dirty white nodules about as large as 
a pin head, or with yellow foci of caseation. The capsule 
around the lymph glands becomes infiltrated with small cells 
and subsequently thickened. In rare cases secondary chronic 
farcy occurs. It is marked by a large, diff"use new growth of 
connective tissue with nodular thickening 



tiG. 2^. J>l'(lHm (>/ (I i; Ul/ntt: I J :n liiiU" 

in the lung of a horse: (a) necrotic center, 
{c) zone of giant cells, (d) capsule stir- 
ro II nding the nodii le ( Sch i'ltz ) . 



of the skin. This 



l62 GLANDERS 

condition is termed glanderous elephantiasis or pachyderma. 
It chieflv affects the limbs and head. 



r' 


^_i 




r ^i4VL 




l5 


^^^Hi^^ 'V ^^^^^^^^^^1 




K^-^^^^^H 


1 



Fig. 29. Photogyaph sho-wing cutaneous glanders or farcy buds. 
{Photograph by Kelly). 



GLANDERS IN MAN 



163 



Of the abdominal organs, the spleen is most frequently 
attacked. It then contains embolic uodules, which vary iu 
size and either suppurate or become calcareous. vSimilar 
nodules occur, though not so often, in the liver, kidneys, 
testicles, brain, muscles, heart and bones. In the bones, the 
lesions consist of a cellular infiltration of the medulla and 
purulent breaking down of the osseous tissue. Ulcers are 
very rare on the mucous membranes of the eyes, stomach and 
vagina. The blood shows signs of shght leucocytosis. The 
specific bacteria are found in the blood only in cases of acute 
general infection. 

The anatomical changes in acute glanders consist chiefly 
in a disintegration of the respiratory mucous membrane, in a 
serous infiltration of the submucosa, subcutis, and inter- 
muscular tissue, with inflammation and suppuration of the 
lymph vessels and lymph glands. There are also metastatic 
formations in the skin and lungs. The nasal mucous mem- 
branes are covered with rapidly spreading ulcers with consid- 
erable infiltration into the submucosa. The mucous membrane 
of the larynx and pharynx may be swollen and covered with 
ulcers. The lungs are studded with purulent metastatic foci 
or fresh nodules. The skin is excessively swollen and covered 
with glanderous nodes. Sometimes diffuse gangrene of the 
skin occurs. 

ji 134. Glanders in man. The symptoms of glanders 
in man are of much importance to the veterinarian. Although 
the susceptibility to the disease is usually not very great, cases 
of human glanders unfortunately occur, especially among 
veterinary surgeons and those having the care of horses. 
Human glanders is reported to be (juite common in Russia. 
The parts usually first affected are the hands, nasal mucous 
membrane, lips and conjunctiva. After a period of incubation 
of from three to five days the infected part becomes swollen 
and painful, with subsequent inflammation of the lymph ves- 
sels and swelling of the glands. Fever is often the first 
symptom, and it is nearlj' always followed by a nasal dis- 




164 GLANDERS 

charge, ulcers on the nasal mucous membrane, pustules and 
abscesses in the skin, ulcers in the oral cavity, larynx, and 
conjunctiva, articular swellings, and grave general distur- 
bances. Sometimes there is intense gastrointestinal trouble. 
Nodules occur in the lungs in some cases. As a rule, death 
takes place in from two to four weeks, and occasionally in a 
few days. In other instances, the disease becomes chronic, 
lasting for months or years. Bad. mallei has been found in 
the blood in cases of acute glanders. The positive diagnosis 
depends on the possibility of infection having taken place, on 
inoculation in guinea pigs, or the proof of the presence oi Bad. 
mallei. Treatment is usually of no avail. The only hopeful 
cases are those that are purely local in their manifestation. 
A few of these are reported to have been cured by applying 
deep cauterization. 

§ 135. Differential diagnosis. Glanders is to be differ- 
entiated from a variety of nasal and lymphatic disorders more 
or less common in the horse kino. Before the discovery of 
the specific bacterium of glanders or of mallein, it was neces- 
sary to determine as closely as possible the differential anato- 
mical characters between glanders and those of other affec- 
tions, such as chronic nasal catarrh, strangles, lymphangitis, 
follicular ulceration of the nasal mucosa, cancer, sarcoma, 
actinomycosis, melanosis and the like. Strong has described 
a disease in the Philippine Islands, which first appears in 
nodules, that resemble those of glanders very closely. It is 
caused by a blastomyces. It occasionally attacks cattle as 
well as horses. The disease most liable to be mistaken for 
farcy or skin glanders is epizootic lymphangitis caused by a 
yeast-like fungus {Saccharomyces farcimi?ios7is) . This disease 
has recently been discovered by Pearson in Pennsylvania. 

Since the discovery of practically positive means of diag- 
nosis, it does not seem wise to speculate upon the chances of 
a correct differential determination by obscure clinical evi- 
dences. If the diagnosis of glanders can not be made from the 
symptoms and lesions in evidence three reliable diagnostic 



MALLEIN 165 

procedures are available. These are animal inoculation, the 
use of mallein and the agglutination or serum test. 

Animal inoculation. Male guinea pigs should be used. 
The material for inoculation usually consists of the nasal dis- 
charge from the suspected glandered horse, bits of scrapings 
from the ulcers, or pieces of other diseased tissue. The 
method to be followed is precisely the same as with the sub- 
cutaneous inoculation of tuberculous material. In these cases 
there is liable to be a local swelling and abscess. The first 
symptom of glanders noticed is usually orchitis. The lym- 
phatic glands in the groin are also enlarged. After the 
orchitis becomes well advanced, the guinea pig may be chloro- 
formed and examined. Pure cultures of the specific organism 
can be obtained in most cases from the suppurating foci in the 
testicle. The spleen is usually enlarged and sprinkled with 
grayish nodules. Other organs may be involved. The diag- 
nosis by the inoculation of a male guinea pig is known as the 
Strauss method. 

Mallein. Mallein is prepared in the same way as tuber- 
culin. It consists of the glycerinated bouillon in which the 
glanders bacteria have grown and in which are the products 
resulting from their multiplication. It has a somewhat fetid 
odor. In applying the mallein test the horse is injected 
usually in the neck with the required amount (0.5 to 2 cc.) of 
mallein, the quantity depending upon the degree of concentra- 
tion. If a concentrated mallein is used it should be diluted 
with a I per cent carbolic acid solution to at least 2 cc. The 
reaction is as follows. In a few hours there forms at the place 
of injection a hot, inflammatory swelling. It is very painful 
and in case of glanders quite large. From all sides of the 
swelling there may radiate wavy lines consisting of swollen 
lymphatics, hot and painful when touched, extending toward 
the adjoining glands. When the mallein injection is made 
aseptically, this swelling never suppurates, but it increases in 
size during a period of from 24 to 36 hours and persists for 
several days, when it gradually diminishes and finally disap- 
pears at the end of eight or ten days. With the appearance 



1 66 GLANDERS 

of the local swelling the patient becomes dull and dejected, 
the eyes have an anxions expression, the coat is lusterless, the 
flanks contracted, the respiration hurried and the appetite is 
impaired. Frequent shudders are observed to pass through 
the muscles of the fore legs and sometimes the trunk is subject 
to violent convulsive movements. The most active and 
fractious horses become listless and indifferent to their sur- 
roundings. These general phenomena constitute what the 
French call the "organic reaction," but they are not always 
so clearly marked. Differences in their intensity are observed 
but they are never completely absent. 

The temperature reaction never fails to show itself. In 
about eight hours after the injection the temperature of a glan- 
dered horse gradually rises 1.5°, 2° or 2.5° F., and even more 
above the normal. The rise in temperature usually attains its 
maximum between the tenth and twelfth hour, occasionally 
not till the fifteenth, and more rarely not until about the 
eighteenth hour. An important fact to note is that the reac- 
tion called forth in glandered horses by the injection of mallein 
persists for from 24 to 48 hours and in some cases the temper- 
ature remains above the normal for even a longer time. In 
practice it is advisable to take the temperature of the suspected 
animals two or three times before the injection of the mallein, 
and every two hours, beginning at the eighth and going to the 
twentieth hour after the injection. It is often suflBcient for 
diagnostic purposes to take the temperature but four times, 
viz., at 9, 12, 15, and 18 hours after the injection. 

In healthy horses the injection of mallein, even in a much 
larger dose, produces no effect on the temperature or the gen- 
eral condition of the animal. There is produced, however, at 
the point of injection, a small edematous swelling, somewhat 
hot and painful to the touch, but the edema instead of increas- 
ing, diminishes rapidly and disappears in less than 24 hours. 

The reaction called forth by the injection of mallein in a 
glandered animal is quite specific. When it occurs one is 
enabled to state at once and with certainty that glanders exists, 
although the lesions may be quite minute or obscure. When 



MALLEI N 



167 



the reaction does not take place it is generally considered that 
the animal tested is not glandered, although the physical 
examination may suggest it. Notwithstanding the specific 
action of mallein, its administration can give really useful 





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FIG 30. Mallein reaction. Teviperature curves of six hordes for 24 
hours after injecting mallein. The horses 7cere in one stable Jrom 
zvhich a well developed case of glanders had been removed. 



l68 GLANDERS 

indications according to Nocard "only when, and as far as, we 
can remove the causes of error that have been pointed out by 
experience." For example, it would be imprudent to use 
mallein in case of animals already suffering with an abnormally 
high or low temperature. The further precautions should be 
taken that the animals subjected to the test are removed as far 
as possible from atmospheric variations and the influence of 
strong sunlight, fog. rain and currents of air. If it be true 
that the majority of horses are not susceptible or slightly so, 
to these influences, there are still some that are affected by 
them. A rise of 1.5 or 2 degrees in temperature would not 
necessarily indicate a reaction. Again, it must not be for- 
gotten that certain diseases, strangles for instance, frequently 
produce great daily variations in the temperature ; therefore, 
when there is reason to believe in the presence of a disease of 
this kind, it is necessary to make sure that the increase of 
temperature consequent on injection of mallein is persistent, 
and that the organic reaction is clearly present. 

Tlic agglutination method or serum diagnosis. Rabieaux 
found tliatthe difference which exists between the agglutinat- 
ing power of a serum from a glandered and from a healthy 
horse may be used as the basis of a method or diagnosing 
glanders. He collected the serum as pure as possible, diluted 
it with sterile, distilled water to i in 10, or to i in 500. The 
diluted serum was then mixed in a small sterile tube with 
an equal volume of a 24 to 72 hour culture of Bad. mallei in 
peptonized bouillon (without glycerine). The mixture was 
placed in an incubator at a temperature of 35° to 37° C. and 
examined at variable times under the microscope. In dilu- 
tions of from I in 10 to i in 50 the agglutination occurred in 
20 minutes to 3 hours. In serum of a non-glandered horse 
from 2 to 6 hours were required to produce the agglutination. 
In weaker dilutions the differences were more marked. The 
development of the method can be followed from the writings 
of M'Fadyean, Bourget and Mery, Arpad, Fedorowsky, 
Reinecke, Bonome, Schiitz and Miessner, Schniirer and 
Moore, Tavlor and Giltner. 



MALLEIN 169 

The method consists in the preparation of a test fluid from 
a suitable culture of Bad. mallei to which is added the diluted 
serum. 

The "test- fluid" is prepared by washing the growth 
from a 72 hour acid-agar culture by the aid of a sterile wire 
loop into distilled water containing 0.85 per cent sodium 
chloride and 0.5 per cent carbolic acid crystals. This suspen- 
sion is then placed in a thermostat at 60° C. for two hours, 
which kills the bacteria. Three cubic centimeters of the 
"test-fluid" are placed in each of several small test-tubes. 
With a sterile pipette, the diluted serum is added to the tubes 
of test-fluid and thoroughly mixed. In making the different 
dilutions, the amount of diluted serum to be used is readily 
ascertained by the following table : 



Dilution 


of Amount of Di-' 


Amount 


of 


Dilution 


Serum 


luted vSerum 


Test Fluid 


1-40 


1.2 c. c. 


3 c. c. 




I-IOO 


1-40 


0.6 


3 




1-200 


1-40 


0.405 


3 




1-300 


1-40 


0.3 


3 




1-400 


1-40 


24 


3 




1-500 


1-40 
1-40 


0.195 
015 


3 




I -boo 
1-800 


1-40 


0.12 


3 




1-1,000 


1-40 


0.105 


3 




1-1.200 


1-40 


0.09 







1-1,500 


1-40 


0.06 


3 




1-2,000 


1-40 


0.03 


3 




1-4,000 


1-40 


1 0.015 


1 3 







Where dilutions greater than i-iooo are made, a serum 
diluted 1-80 may be used to better advantage, unless the 
pipette employed is very finely graduated. In this case the 
amount of diluted serum for a certain dilution must be double 
that indicated in the table. 

The mixture thus prepared is placed in an incubator at 
-,7° C. for 24-30 hours. A temperature higher than 37° C. 
interferes with the agglutination. 

The reaction consists of a layer of the agglutinated bac- 
teria covering the entire convexity at the bottom of the ttibe. 



lyo GLANDERS 

This film-like sediment may become so dense that it rolls in at 
the periphery. The supernatant fluid becomes clear in the 
lower dilutions, but in the higher ones the clarification may 
not be complete, showing that all the bacteria have not 
become agglutinated. This is further evidenced by the fact 
that the layer is less dense in the higher dilutions. The 
reaction may begin in six hours, but cannot be considered 
complete until 24 to 36 hours have elapsed. If no reaction 
appears in 24 hours it cannot be considered negative, as it may 
occur in from 30 to 40 hours after setting. Often, however, a 
reaction appears in less than 24 hours. 

After the agglutination is completed, further standing 
produced no visible change in the test fluid. 

A negative result shows a small round concentrated spot 
of sediment in the center of the convexity at the bottom of the 
tube, the test fluid remaining apparently unchanged even after 
several weeks. Animals whose blood serum agglutinates in 
dilutions of 1-500 are suspicious and a reaction in dilutions of 
1-800 or higher indicates an infection with Bad. mallei. 

As pointed out by Bononie and confirmed by Taylor, 
there seems to be little or no change produced in the precipita- 
ting power of the serum of the blood taken before, during or 
after the mallein reaction but the agglutinating power as deter- 
mined microscopically is very much increased during the 
mallein reaction. 

This is shown by the appended table : 



MALLEIN 171 

Table showing both tnacroscopically and microscopially the ag^lulina- 

tion of dead glanders bacteria with blood serum from horses 

taken before, during and after the mallein reaction. 



Blood taken the day pre- Blood taken during Blood taken after the 
vious to malleination the reaction temperature had re- 

Feb. 21. Feb. 22. turned to normal 

.Mar. 2. 



V 1 


Macro- 


Micro- 1 


Macro- 


Micro- 


Macro- 


Micro- 


No. 1 


scopic 


scopic 


scopic 


scopic 


scopic 


scopic 


~T'\ 


1-800 


I-IOOO 


1-800 


1-1800 


1-800 




l-IOOO 


4 


1-800 


I - 1 200 


I-IOOO 


1-2000 


I-IOOO 


1-1500 


5 


1-1500 


I- J 600 


I-I500 


1-2500 


I-IOOO 


I-I200 


6 


I- 1 200 


1-1500 


I -1 200 


1-2000 


i-i8oo 


1-1800 


7 


I- 1000 


I- 1 200 


I - 1 000 


1-1800 


i-tooo 


I- I 400 


8 


1-500 


1-500 


I -800 


1-1600 


1-500 


1-600 


9 


1-800 


I-IOOO 


1-800 


1-1400 


1-500 


1-800 


10 


1-500 


1-600 


1-500 


I-IOOO 


1-500 


1-800 


12 


1-200 


1-300 


1-500 


1-800 


1-500 


1-750 


13 


I-IOOO 


I-I200 


1-500 


I-IOCO 


1-800 


I-IOOO 


14 


1-500 


1-600 


1-500 


1-800 


1-500 


1-800 


15 


1-1200 


I-I4OO 


1-1200 


1-2500 


1-1200 


I- I 800 


16 


I-IOOO 


I- I 200 


I-IOOO 


1-2400 


I-IOOO 


1-2200 


17 


1-500 


1-800 


1-800 


I -1500 


1-800 


I-I400 


18 


I-IOOO 


I-I400 


I-IOOO 


I-I800 


1-800 


I-I500 


19 


I-IOOO 


I-IOOO 


1-800 


1-1200 


I-IOOO 


I -I 200 


20 


1-500 


I-6GO 


1-500 


1-800 


1-500 


1-800 


21 


1-500 


1-750 


1-500 


I-IOOO 


1-800 


I-I200 


22 


I-IOOO 


I-I400 


I-IOOO 


1-2500 


1-800 


1-2200 


23 


1-200 


1-200 


1-200 


I-IOOO 


i~8oo 


I-IOOO 


24 


I-IOOO 


1-1200 


I-IOOO 


1-2200 


I- 1 200 


1-2000 


25 


1-800 


1-800 


1-500 


I- 1 200 


1-800 


I-IOOO 


26 


I- 1 200 


I-I500 


I-IOOO 


1-2200 


I- 1 200 


1-2000 


27 


1-500 


I-IOOO 


I-IOOO 


I-I800 


1-800 


1-2000 


28 


1-500 


1-600 


1-500 


I-I200 


I-IOOO 


1-1500 


29 


1-800 


I-IOOO 


1-500 


1-1200 


I-I200 


1-2000 


30 


I-IOOO 


I-I200 


1-800 


1-1800 


1-800 


1-1600 


31 


1-500 


1-600 


1-800 


1-1400 ' 


l-IOOO 


I-I500 



The agglutination in higher dilutions with the living 
organisms as determined microscopically was pointed out by 
Taylor. A comparison of the agglutination of the living and 
killed bacteria with, the serum from glandered horses, as 
shown by the mallein reaction, is given in the appended table : 



172 



GLANDERS 



Macroscopic and microscopic agglutination of Bacterium mallei ivitli 
horse serum by the use of killed atid living cultures. 



Number 

of 
Horse 


Macroscopic. 

Dead bacteria, 24 

hours at 37° C. 


Microscopic. 

Dead bacteria, 12 

hours at 37° C. 


Microscopic. 

Ivive bacteria, 12 

hours at 37° C. 


I 


1-8000 


1-12000 


1-30000 


2 


1-2000 


1-3000 


1-12000 


3 

4 


1-800 
1-1600 


I-IOOO 

1-1800 


I-IOOOO 

1-6000 


5 
6 

7 
8 

9 

lO 


1-500 

I-IOOO 

i-Soo 
1-800 
1-1600 
1-500 


1-600 
I- 1 250 

I-IOOO 
I-I200 
I- 1800 
T-800 


1-5000 

1-25000 

1-8000 

I -1 2000 

1-24000 

1-7500 



The method as pointed out by Schiitz and Miessner is a 
macroscopic one. It depends upon the precipitation ot the 
agglutinated masses of bacteria. Normal horse's serum 
agglutinates glanders organisms in high dilutions as deter- 
mined microscopically. This, however, does not appear to be 
of diagnostic value. 

Disposition of reacting horses. The question arises 
whether animals found by the help of mallein or the agglutin- 
ation test to be glanderedought tobe immediately slaughtered. 
Nocard said no. The experience of the last few years goes to 
prove that among the animals that react there are some which, 
when removed from the infected center and thereby withdrawn 
from all chance of new contamination, recover. "We ought 
therefore," he continues, "to confine ourselves to the destruc- 
tion of those which in addition to the reaction, present some 
clinical indication of the disease, such as ulceration of the nose, 
indurated glands, suppurative lymphatics or other pronounced 
manifestation of the disease. The animals showing physical 
signs of infection must simply be removed from among the 
healthy horses and subjected from time to time, say every two 
months, to the mallein test. If any of these should eventually 
show the clinical signs of glanders, it should be slaughtered 
at once. On the other hand, those animals which have stood 
two successive doses of mallein without reacting ought to be 



prevp:xtion 173 

considered definitely cured, restored to their places and put to 
the free disposal of the owners.'' 

The views advocated by Nocard are not universally enter- 
tained in this country. It has been shown repeatedly that a 
good reaction, following the injection of mallein, was a sure 
indication of glanders as revealed by post-mortem. The 
question, however, concerning the necessity of immediate 
slaughter for purposes of protection, where there are no evi- 
dences of lesions on physical examination, seems to be an open 
one. This question which pertains to sanitary police rests, 
until the results of conclusive investigations are recorded, with 
those entrusted with the protection of animals and men from 
this disease. However, the results of certain experiments in 
the use of mallein as a therapeutic agent and the fact that cer- 
tain animals recover when kept in quarantine are very sugges- 
tive. Certainly further investigations are needed to deter- 
mine the safe and equitable disposition of animals devoid of all 
symptoms and obvious lesions of glanders, but which give a 
reaction to the mallein or agglutination test. 

§ 136. Prevention. Isolation of the healthy animals 
from the infected ones and thorough disinfection of the stable 
are important. It is also desirable not to bring strange horses 
in close contact with home animals, until their freedom from 
this disease is determined. 

REFERENCES. 

1. Babes. Observations sur la morve. Arch, de Med. e.vpcr. et 
(/' Anal, path.. Vol. Ill (1891), p. 619. 

2. Berxs and Way. Practical Application and Results of the 
Agglutination Method of Diagnosing Glanders in One Hundred and 
Fifty-two Cases. Amer. Vet. Rev., Vol. XXX (1906), p. 822. 

3. BONOME. Leber die Schwankungen des Agglutinin und 
Prazipitingehaltes des Blutes wahrend der Rotzinfektion, Centralbl. f. 
Bakt., Bd. XXXVIII. (1905^ S. 601. 

4. BouRGET ET Mern'. Sur le seradiagnostique de la morve, La 
Semaine Med., 1898, p. 61. 



174 GLANDERS 

5. Butler. Glanders. Bulletin A^o. /6. J/tss. Agr. Exp. Sta- 
tion, iSgi. 

6. Carv. Glanders. Bulletin No. jj;. Ala. Agr. Expt. Station 
of the Agricultural and Jlechanical College, Jan. 1892. 

7. Dawson. Equine glanders and its eradication. Bulletin No. 
77. Florida Agric. Exp. Station, 1905. 

8. De Schweinitz and Kilbornh. The use of mallein for the 
diagnosis of glanders in horses and experiments with an albumose 
extracted from cultures of bacillus mallei. Am. Vet. Revieic, Vol. 
XVHiS92),p. 439. 

9. Francis. Glanders, tests with mallein. Bulletiti No. jo. 
Texas, Agri. Exp. Station, 1894. 

10. Frothingham. The diagnosis of glanders by the Strauss 
method. Jour, of ISIedical Research, Vol. VI ( 1901 ), p. 331. 

11. Galli-Valhrio. Contribution a 1' etude de la morphologic 
du Bacillus mallei. Centralb. fiir Bakt., Bd. XXVI (1899). S. 177. 

12. HiGGiNS. Glanders and mallein. Proceedings Atner. Vet 
Med. Asso., 1904, p. 135. 

13. LfANGER. Untersuchuug iiber die differential diagnostische 
Bedeutung der Rotzagglutination u. s. w. Afonatshefte fiir prak. 
Tierheilkunde, Bd. XVI (1905), vS. 241. 

14. Loeffler and Schutz. On the bacillus of glanders. Deutsche 
Med. Wochenschrift, Dec. 1882. Translated, Vol. CXV, New Sydenham 
Society. 

15. M'Fadvean. The pulmonary lesions of glanders. Jour, of 
Compar. Path, and Thera., Vol. VIII (1895), p. 50. 

16. M'Fadyean. Glanders. Jour. Compar. Path, and Thera., 
Vol. XVII (1904), p. 295. 

17. Moore, Taylor AND GiLTNER. The Agglutination Method 
for the Diagnosis of Glanders. Avier. Veter. Rev., Vol. XXX 
(1906), p. 803. 

18. NocARD. The value of mallein as a means of diagnosis in 
doubtful cases of glanders. Jour. Compar. Path, and Thera., Vol. VIII 
(1895), p. 227. 

19. Rabieacx. Serum diagnosis of glanders. Abstract Jour. 
Compar. Path, a ?id Thera., Vol. XVI (1903), p. 59. Orig. Jour, de 
Med. Vet., 1902. 

20. Reynolds. State control of glanders in Minnesota. Jour, of 
Compar. Med. and vet. Archives, Vol. XX (1899). 

21. Rutherford. Glanders. Proceedings Am. Vet. Med. Asso., 
1906, p. 215. 



TUBERCULOSIS 1 75 

22. SCHi'TZ. A contribution to the subject of jflaiulers. Jour, of 
Compar. Path, and Thrra , Vol. XI (1898), p. i. 

23. SCHUTz. Zur Lehre voni Rot/.e. .Iniiii.fur ?ciss. 11. prakt. 
T/iierheilkunke, Bd. XXIV (1898), S. i. 

24. SCHiJTZ UND MiESSNER. Zur Serodiagnose der Rolzkranklieit. 
Archiv.fih- K'iss. u. prakt. Ticrliielkunde, Bd. XXXI (1905), S. 353. 

25. Smith. On the influence of slight modifications of culture 
media on the growth of bacteria as illustrated by the glanders bacillus. 
Journal of Comparative Medicine, (1890), p. 158. 

26. Strong. Preliminary report of the appearance in the Philip- 
pine Islands of a disease clinically resembling glanders. 1902, No. /, 
Bureau of Government Laboratories, Manila. 

27. Strauss. Sur un moyen diagnostique rapide de la morve. 
Arch, de Med. e.vper. et de Anat. path., Vol. Ill ( 1889), p. 460. 

28. Way. The practical application of the agglutination method 
for the diagnosis of glanders. Am. I'ct. Revicxv, Vol. XXXI 
(1907), p. 709. 

29. Wherrv. Glanders : Its diagnosis and Prevention. Bulletin 
No. 24. Bureau of Government Laboratories. Manila. (1904). 

30. Williams. Glanders. Bui. No. 4. Mont. Agr. Exp. Stat., 1894. 

31. Wright. The histological lesions of acute glanders in man 
and of experimental glanders in the guinea pig. Jour, of Exp. Med., 
Vol. I (1896), p. 577. 



TUBERCULOSIS 



Synonyms. Consumption ; pearl disease ; grapes; phthisis ; 
scrofula ; tabes ; "The great white plague." 

§ 137, Characterization. Tuberculosis is an infectious 
disea.se from which the human .species, cattle and swine suffer 
very exten.sively and which, under favorable conditions, attacks 
nearly if not all species of animals including fish. It is a dis- 
ease of slow development, involving either primarily, or in 
association with other organs, the lymphatic system. It is 
characterized by the formation of nodules, or tubercles, in 
consequence of the activities of Bacterium tuberculosis. It does 
not destroy life by acute toxemia, but by a chronic and Umg 
continued systemic poisoning and by the morbid changes 
brought about through the localization of these lesions in 
organs necessary to life. 



176 TUBERCULOSIS 

§ 138. History. Tuberculosis is one of the oldest dis- 
eases affecting cattle of which there are identifying records. 
It seems to have been known to the Jewish people during their 
Egyptian captivity and the ecclesiastical laws for many cen- 
turies contained numerous enactments against the consump- 
tion of flesh from tuberculous animals. In 1370, it was for- 
bidden in Munich to have on sale the flesh of animals affected 
with tuberculosis. A number of other cities passed similar 
ordinances. In 1702, Florinus described the disease and 
emphasized the then existing opinion that it was identical with 
syphilis. This led to the practice of destroying all tubercu- 
lous animals. In 1783, the Berlin Board of Health rejected 
the theory of the connection of tuberculosis and syphilis and 
declared the flesh of affected animals to be fit for food. This 
led finally to the cancelling of all laws throughout Prussia 
against the use of flesh for food trom animals affected with the 
disease. Tscheulin, in 1816, recognized in reference to the 
infection of meat, three degrees of bovine tuberculosis, viz: 
I, in which the tubercles were to be removed ; 2, in which the 
diseased parts were to be destroyed and the meat sold at a low 
price ; and 3, those cases in which the lesions were so exten- 
sive that the whole carcass must be rejected. 

The study of the lesions themselves gave rise to a num- 
ber ot beliefs concerning their nature. Thus, Virchow, Schup- 
pel and others declared that the tubercles in cattle were lym- 
pho-sarcomata. L,eisering considered them simply as sarco- 
mata. Spinola and Haubner maintained that human and 
bovine tuberculosis were identical. 

In 1865, Villemin showed that tuberculosis was due to a 
specific infection. He produced the disease in rabbits by 
inoculating them with tuberculous material from human sub- 
jects. He also produced the disease by feeding experimental 
animals and by causing them to inhale tuberculous material. 
Chauveau, in the same year, produced the disease in cows. 
These results were soon confirmed by Klebs, Cohnheim and 
Gerlach. These experiments, in which the disease was pro- 
duced in one species with tuberculous material from another, 



HISTORY 177 

followed by the discovery by Koch of the specific bacterium of 
the disease, led to the view that tuberculosis in all species of 
mammals was identical. This generally accepted belief caused 
sanitarians to look upon tuberculosis in cattle as a great men- 
ace to public health. The result was that during the closing 
decade of the last century, this disease in cattle was treated 
more vigorously as a menace to the human species than as a 
destructive disease of animals. 

In 1896, Dr. Theobald Smith pointed out that for certain 
animals the tubercle bacteria from cattle were more virulent 
than those from man and further that there were certain 
morphological and cultural differences existing between them. 
In 1898, he published the results of a more extended series of 
investigations. Since that time a number of investigators 
have arrived at the same conclusion. The fact has come to be 
well known that certain differences exist between the bacteria 
of tuberculosis found in the human and in the bovine species. 
Koch's experiments reported at the tuberculosis congress in 
London in July, 1901, give additional evidence of a difference 
in virulence for experimental animals of the bacteria of human 
and of bovine tuberculosis. To what extent the human 
species becomes infected from the bovine kind cannot be 
stated, but the accumulating evidence tends to the conclusion 
that bovine tuberculosis is of less significance in its influence 
upon public health than has heretofore been thought, and ol 
more importance as a rapidly spreading and destructive dis- 
ease among cattle. It is not proven, however, that the human 
species is not affected with the bacteria of bovine tubercu- 
losis. The investigations of the last five years have shown 
that not infrequently human tubercle material will produce 
tuberculosis in cattle. The interim reports of the Royal Com- 
mission appointed in 1901 are important in this connection. 
Salmon has published an important paper on the relation of 
human and bovine tuberculosis in reply to Koch's paper of 
1 90 1. Concerning its transmission, the conclusion seems to be 
warranted, that the virus of tuberculosis spreads very largely 
among men and cattle from individual to individual of the 



178 TUBERCULOSIS 

same species rather than from one species to the other. A 
number of cases of tuberculosis in mau seems to have been 
caused by the bovine type of the tubercle bacterium. Accord- 
ing to Smith there are forty to fifty such cases on record. 

§ 139. Extent of tuberculosis especially among 
cattle and swine. The committee on cattle diseases and 
animal food of the American Public Health Association for 
1901 reported the appended statistics concerning the extent and 
increase of tuberculosis in cattle and swine in various countries. 

"The slaughter house statistics of Prussia show 14.6 per 
cent of the cattle and 2. 14 per cent of the swine to be tubercu- 
lous. In Saxony the percentage is 29.13 with cattle and 3.10 
with swine. In the city of Leipzig the figures are 36.4 for 
cattle and 2. 17 for swine (Siedamgrotzky). Of 20,850 animals 
in Belgium tested with tuberculin in 1896, 48.88 per cent 
reacted. Of 25,439 tested in Denmark from 1893 to 1895, 
49.3 per cent reacted ; and of 67,263 tested from 1896 to 1898, 
32.8 per cent reacted (Bang). An examination of 20,930 
cattle in Great Britain, either slaughtered and examined post- 
mortem or tested with tuberculin, showed 5,441 or 26 per cent 
affected with tuberculosis. M'Fadyean estimates that 30 per 
cent of the cows !n Great Britain are tuberculous. Figures 
available in the United States do not cover a sufficient area of 
our territory to allow us to make a reliable estimate of the 
extent of tuberculosis in milch cows. 

"Our beef cattle as they come to the large packing houses 
are as yet comparatively free from tuberculosis. Of 4,841,166 
cattle slaughtered in the year 1900, under Federal meat inspec- 
tion, but 5,279 or o. II per cent were sufficiently affected to 
cause the condemnation of any part of the carcass. Of 23,336,- 
884 hogs similarly inspected, 5,440 were sufficiently affected to 
cause a condemnation of some part of the carcass. This is 
equal to 0.023 per cent, or slightly more than one-fifth the 
proportion found in beef cattle. 

"The slaughter house statistics of all countries show that 
the percentage of affected hogs increases as the disease becomes 



GEOGRAPHICAL DISTRIHUTION 179 

more common in cattle, so that we must consider not only the 
effect of the disease upon beef and milk producing animals 
but also upon swine. Tuberculosis is more acute with hogs 
than with cattle, and there is a much greater tendency to gen- 
eralization, consequently the parts used for human food are 
more likely to be affected, and if there is a possibility of com- 
municating the virus through the meat the danger is increased 
by this peculiarity of the disease in swine." The statistics of 
the last few years show a rapid increase in the amount of 
tuberculosis in swine. In 1905 64,919 carcasses of hogs and 
142,105 parts were condemned for tuberculosis. 

Ji 140. Geographical distribution. Tuberculosis is an 
exceedingly wide spread disease. In earlier times it was quite 
prevalenramong cattle in Central Europe. It seems to have 
existed in Western Asia and Northern Africa at an early date. 
From these centers it has spread to nearly every cattle raising 
country of the world. Its rapid spread during the last fifty 
years is attributed to the increase in cattle exchange resulting 
in the introduction of tuberculous animals into healthy herds. 
It is stated that in many countries, and in large districts with- 
in others, tuberculosis did not exist until it was introduced 
within recent years by the importation of diseased animals. 

In countries where there has been little or no importation 
of cattle and in which the native breeds still exist unchanged, 
as in manv parts of Russia, Austria and Spain, in the north- 
ern part of Sweden and Norway, and in parts of Africa, tuber- 
culosis is practically unknown. This is true of the cattle on 
the island of Jersey, where for more than a hundred years for- 
eign cattle have not been introduced. 

In the United States, the disease is very widely distrib- 
uted It is found to a considerable extent in certain localities 
where the climatic conditions seem to be beneficial for tubercu- 
lous people. The explanation for this seems to be that tuber- 
culous animals have been introduced into certain herds in these 
districts There are, however, large areas in which it is prac- 
ticallv unknown. The Western steers that are killed in the 



i8o 



TUBERCULOSIS 



slaughter houses of Kansas Cit}^ Omaha, Sioux City and 
Chicago are practically free from this disease. Tuberculosis 
exists, however, in many places where beef cattle are raised, as 
the result of the introduction of affected breeding stock. In 
many localities, especially where there is an extensive inter- 
change of animals, a large percentage of the herds are more or 
less affected. 

§ 141. Etiology. Tuberculosis is caused by a rod- shaped 
organism known as Bacterium tuberculosis. It was discovered 
by Robert Koch in 1882. Schiil- 
ler and Toussaint had previously 
studied growths which seem, from 
the results of their inoculation ex- 
periments, to have been this organ- 
ism. The bacterium of tuberculosis 
is a slender, rod-shaped organism 
with rounded ends, from 2 to 5/< in 
length and from 0.3 to o.5/< broad. 
The rods are straight or slightly 
curved, and occur singly, in pairs 
or in small bundles. Frequently 
they cross one another. They do 
not produce spores, but vacuoles are often observed and 
branching forms have been described. 

The bacterium of tuberculosis is readily cultivated on 
artificial media such as blood serum, glycerinated agar and 
bouillon after it has been adapted to such artificial conditions.* 
It is, however, not easy to cultivate it directly from ordinary 




Fig. 30. 



Bacterium tuber- 
culosis. 



*To accomplish this necessitates a very special and careful proce- 
dure. Dr. Theobald Smith, of Harvard University (Jour of Exp. Med., 
Vol. III., 1898, p. 451), has the credit of formulating a method by com- 
bining details in such a manner that the procuring of cultures is, in 
most cases, possible. Dog serum is used. The method, as he gives it, 
is as follows : 

" The dog was bled under chloroform and the blood drawn from a 
femoral artery, under aseptic conditions, through sterile tubes directly 
into sterile flasks. The serum was drawn from the clots with sterile 
pipettes and either distributed at once into tubes or else stored with 0.25 



ETIOLOGY IS I 

tuberculous lesions. Although at the time of their discovery, 
the tubercle bacteria from man and from animals were believed 
to be identical, they have been found to possess slightly differ- 
ent characters and properties. Smith pointed out in 1898, 
that morphologically those from cattle wereshorter and thicker 
than those from man, that the growth was slightly different 
on blood serum, and that they were much more virulent for 
cattle and rabbits than those from the human species. Since 
that time his conclusions have been confirmed by a number of 
investigators. Koch obtained like results. At present, there- 
fore, we must look upon the tubercle bacteria coming from 
these different species as possessing races or varieties which, 
perhaps, are the result of their different conditions of life. 
The investigations which have been made with the decidedly 
different forms of this organism found in tuberculosis of fowls 
and of fish have led a few experimenters to believe that they 
are simply varieties of the organism first described by Koch. 
Further inquiries are necessary to fully satisfy bacteriologists 
that all of these forms are thus related to the one species. 

to 0.3 per cent chloroform added. Discontinued sterilization was ren- 
dered unnecessary. The temperature required to produce a sufficiently 
firm and yet not too hard and dry serum is for the dog 75° to 76° C. For 
horse serum it is from 4° to 5° lower. The serum was set in a thermo- 
stat into which a large dish of water was always placed to forestall any 
abstraction of moisture from the serum. About 3 hours suffice for the 
coagulation. When serum containing chloroform is to be coagulated, I 
am in the habit of placing the tubes for an hour or longer in a water 
bath at 55° to 60° C, or under the receiver of an air pump, to drive off 
the antiseptic. This procedure dispenses with all sterilization excepting 
that going on during the coagulation of the serum. It prevents the 
gradual formation of membranes of salts, which, remaining on the sur- 
face during coagulation, form a film uusuited for bacteria. Tubes of 
coagulated serum should be kept in a cold closed space where the 
opportunities for evaporation are slight. They should always be kept 
inclined. 

"The ordinary cotton-plugged test tubes I do not use, because of 
the rapid drying out permitted by them, as well as the opportunities for 
infection with fungi. Instead, a tube is used which has a ground glass 
cap fitted over it. This cap contracts into a narrow tu])e plugged with 
glass wool. This plug is not disturbed. The tube is cleaned, filled, and 



1 82 TUBERCULOSIS 

There seems to be no reason for doubting that the bovine and 
human forms are varieties or races of the same species. The 
diiTerence in the conditions of life under which they exist in 
the bodies of men and of cattle are quite enough to explain 
resulting differences in the bacteria. 

S 142. Symptoms. The symptoms vary according to 
the course of the disease. There is a chronic form, which is 
most common, and an acute form or miliary tuberculosis. 

The symptoms of chronic tuberculosis depend upon the 
location of the lesions and their extent. When the lesions are 
situated deeply and are not of great extent, they may not 
exhibit visible evidence of their presence. In such cases, the 
infected animal may present the picture of perfect health and 
show no disturbance of function. Indeed some animals, in 
which the lesions are both extensive and widely distributed 
and which have never presented noticeable signs of the disea.se, 
are slaughtered for beef without a suspicion of the presence of 
tuberculosis until they are examined post- mortem. 

inoculated by removing the cap. With sufficient opportunity for the 
interchange of air little evaporation takes place, and contamination of 
the culture is of very rare occurrence. In inoculating these tubes, bits 
of tissue, which include tuberculous foci, especially the most recent, 
are torn from the organs and transferred to the serum. Very little 
crushing, if any, is desirable or necessary. I think many failures are 
due to the often futile attempts to break up firm tubercles. Nor 
should the bits of tissue be rubbed into the surface, as is sometimes rec- 
ommended. After a stay of several weeks in the thermostat, I usually 
remove the tubes and stir about the bits of tissue. This frequently is 
the occasion for a prompt appearance of growth within a week, as it 
seems to put certain still microscopic colonies in or around the tissue 
into better condition for further development. The thermostat should 
be fairly constant, as urged by Koch in his classic monograph, but I 
look upon moisture as more important. If possible, a thermostat should 
be used which is opened only occasionally. Into this a large dish of 
water is placed, which keeps the space saturated. Ventilation should 
be restricted to a minimum. As a consequence, moulds grow luxuri- 
antly and even the gummed labels must be replaced by pieces of stiff 
manila paper fastened to the tube with a rubber band. By keeping the 
tubes inclined, no undue amount of condensation water can collect in 



SYMPTOMS 



183 



Since the lesions of tuberculosis vary so much in different 
cases it is not possible to give a description of what can be 
designated the characteristic or even the usual symptoms ot 
this disease. There 
are, however, certain 
general manifesta- 
tions that appear in 
most of the advanced 
cases, such as emacia- 
tion while the appe- 
tite continues good. 
This is always a sus- 
picious indication and 
especially if accom- 
panied by cough, 

rough coat and tight, 

harsh skin. Rough 

or loud respiratory 

sounds are suspicious, 

and, in advanced 

cases, it is often found 

that the animal groans 

when pressure is 

brought to bear upon 

the chest wall. Many 

cases bloat habitually. 

Hard, painless swel- 
lings (enlarged lymp- 
hatic glands) beneath 
the skin in the region 
of the escutcheon, 
flank, shoulder or throat are .suspicious 




Fig. 31. Right lateral aspect of posterior 
half of steer's head, {a) Lower jaw, {b) ear 
passage, {c) horn, [d) styloid process of 
occipital bo7ie, {e) parotid gland, {J) sub- 
ma villary gland. A . Right parotid lymph 
gland. B. Right post maxillary lymph 
gland. C. Right submaxillary lymph 
gland. These glands are often the seat oj 
'^tubercular deposits {Stnitli). 



thebotW^TI^ the upper portion of tl.e ,eru„, '"-^ ^ '^'^ 
only precaution to be applied .0 prevent ,n,ec„on "' ' "°"'^^ 'g° 
.Jo l,l,«a.^tbej^,.„.bet.ee„tu^ 

Llip'meTorenl^'th'rptu, into sterile .ol.eu para«in an.! .0 cover 



184 TUBERCULOSIS 

In tuberculosis of the luugs, it may be said that coughing 
is the most noticeable symptom. It is most common after 
feeding, drinking, or after rapid moving following a period ot 
repose, but sometimes it occurs without any apparent cause. 
The cough is usually strong, dry and frequently of a high 
pitch. Sometimes it is very violent, accompanied by protru- 
sion of the tongue. Auscultation reveals modified and abnor- 
mal sounds of different kinds in the lungs ; sibilant, sonorous 
and mucous rales are most common. A dull sound is often 
detected on percussion. It is also to be noted that this condi- 
tion is of slow development and long duration, thus aiding one 
to distinguish it, in many cases, from bronchitis or pneumonia. 

Where the mediastinal lymphatic glands are enlarged and 
press upon the esophagus, it is stated that the animal bloats 
habitually. Chronic or habitual bloating accompanied by a 
good appetite and no other evidence of disease of the digestive 
tract, especially if there is shortness of breath and cough, 
may be looked upon as strongly indicative of tuberculosis with 
enlarged mediastinal lymphatic glands. Enlarged tubercular 
glands along the esophagus may press upon that organ caus- 
ing obstructions and preventing the escape of gases from the 
stomach. This often gives rise to lymphangitis. 

vSometimes large tubercular masses develop on the pleura. 
In such cases the principal symptom is a friction sound that is 
heard most distinctly during inspiration. If the masses are 
large enough they give rise to a dull sound upon percussion. 
In tuberculosis of the stomach and intestines, digestion is 
interfered with. This gives rise to poor appetite, frequently 
to diarrhea and sometimes to alternation of diarrhea and con- 
stipation. In tuberculosis of the peritoneum or of the lin- 
ing of the abdominal cavity, the lymphatic glands of the 

the tube with a sterilized paper cap. The white bottle caps of the drug- 
gist aje very serviceable." 

While the tuberculous material is perfectly fresh (uncontaminated) 
and in the early stages of the disease, it is safer to inoculate a guinea 
pig, and after the lesions begin to develop to chloroform it and make 
the cultures from the recently affected liver or spleen. 



SYMPTOMS 



:85 



flank are often enlarged and hard. vSonietimes this condition 
can be diagnosed positively by a rectal examination and the 
discovery of the hard, nodular masses. Tuberculosis of the 
liver does not give rise to obvious symptoms unless the dis- 
ease is far advanc- 
ed, in which case 
jaundice may be 
observed. 

In animals in 
which the post- 
pharyngeal lym- 
phatic glands are 
enlarged from tu- 
berculosis, the 
breathing is harsh 
and noisy. In this 
condition there is 
sometimes difficul- 
ty i'n swallowing, 
and particles o f 
chewed up food are 
occasionally expel- 
led from the mouth, 
either voluntarily 
when it is found 
that they cannot be 
swallowed conven- 
iently, or by the 
coughing they oc- 
casion upon reach- 
ing the pharynx. 
These enlarged 
glands may some- 
times be detected 
by palpation accomplished by placin 
of the throat above the larynx and then pressing from op 
posite sides. 




Fig. 32. Dorsal aspect of bovine lungs, {a-a') 
right and left caudal lobes, (b-b') r. and I. ven- 
tral lobes, [c-C) first and second right cephalic 
lobes, {c^-) left cephalic lobe, {e) trachea, {x x) 
region most frequently involved in the earliest 
stages of pulmonary tuberculosis. The lesions 
at this stage are usually embedded in the lung 
tissue {Smith). 

one hand on each side 



i86 



TUBERCULOSIS 



Tuberculosis of the udder is detected by an enlargement 
and hardening of the affected part, usually by the absence of 
f. pain and the fact that the 

secretion is not altered un- 
til the part has been dis- 
eased for some time. In 
advanced cases, instead 
of milk, the udder se- 
cretes a yellowish, cloudy 
and sometimes flocculent 
liquid. In acute, 
rapidly developing cases, 
there may be pain and 
edema of the skin. In 
nearly all cases of udder 
tuberculosis the supra- 
mammary lymphatic glands 
situated above the udder in 
the middle of the escutch- 
eon, are enlarged and hard. 
If there is doubt as to the 
character of the disease of 
the udder, the milk, or 
possibly a piece of excised 
udder tissue, may be ex- 
amined bacteriologically. 

In tuberculosis of the 
brain, the animal is un- 
steady and uncertain in its 
movements. It lies down 
much of the time, is usuallj^ 
subject to occasional cramps 
and is apt to carry the head 
in an unusual position. 
Such cases are inclined to 
advance rapidly and termi- 
nate in death following coma or convulsions. 




Fig. 33. Trachea and bronchial tubes, 
of bovine lungs shoiving attached 
bronchial glands, (a-a') Supply right 
and left caudal lobes, {b.b') supply r. 
and I. ventral lobes, {c-c') branches of 
the right supernumerary bronchus, 
((C=) supply left cephalic lobe, {d) 
branch to azygous lobe, {e) trachea. 
A. Left bronchial lymph gland. B. 
Right bronchial lymph gland. C. 
Lymph gland base of supranumerary 
bronchus. D. gland often betiueen 
bronchi. The glands A. to D., are 
often involved {Smith). 



SYMPTOMS 



187 



In tuberculous disease of the bones and joints, the parts 
are enlarged, there is loss of motion, pain and usually abscess 
formation followed by the discharge of thick yellow pus. 
In tuberculosis of 

the uterus or ovar- 1 1 » / 

ies and sometimes 
in peritoneal tuber- 
culosis of the cow, 
the subject is al- 
most continually in 
heat. In tubercu- 
losis of the uterus, 
there is sometimes a 
discharge of thick, 
yellowish material 
mixed with mucus. 
In tuberculosis of 
the testicles the or- 
gans become en- 
larged and hard. 

In all advanced 
cases, the nutrition 
of the animal is in- 
terfered with and, 
sooner or later, the 
"tuberculous cach- 
exia" appears. It 
is, however, in 
many cases remark- 
able to note the ex- 
tent of lesions in 
animals that are 
well nourished and 




Fig. 34. Dorsal aspect of bovine lungs sho'cving 
position of the posterior mediastinal glands ; 
[a, h, c, c') caudal, ventral, cephalic lobes, (/) 
esophagus, (g) muscular pillars of diaphragm. 
(h) posterior aorta, (i) caudal margin of the 
ligamentof the lung. A. Left bronchial gland. 
Mediastinal glands are shown, most of them 
resting on the esophagus. The large caudal 
gland resting on the pillars of the diaphragm 
is most frequently diseased and often attains 
ail enormous size. The remaining medias- 
tinal glands are arranged in tioo sets on the 
right and left margins of the esophagus 
(Smith). 



ime condition by the 



present no external 

signs of disease. Animals killed in pni 

butcher are sometimes found to contain extensive and widely 

distributed lesions of tuberculosis. In general tuberculosis, 



I88 TUBERCULOSIS 

many of the symptoms described above may occur simultane- 
ously. The symptoms of acute miliary tuberculosis, "gal- 
loping consumption," are rapid loss of flesh, depression, poor 
appetite, cough, weakness, rapid breathing, harsh respiratory 
sounds, some elevation in temperature, increased pulse rate 
and, sometimes, enlarged lymphatic glands. The course of 
this form of tuberculosis is always rapid and terminates in 
death. Acute miliary tuberculosis occurs when large num- 
bers of tubercle bacteria are discharged into the blood or 
lymph currents. They are then carried to other parts of the 
body, filtered out in the capillaries of the lungs, liver, spleen, 
kidneys and elsewhere, causing tubercular lesions in each of 
these localities. The lesion from which the infectious material 
entered the circulation may have been a comparatively small 
nodule. This form of the disease is more likely to appear in 
young animals than in adults, and is more common among 
swine than in cattle. 

^ 143. Morbid anatomy. The usual direct anatomical 
changes following the invasion of tubercle bacteria are the for- 
mation of nodules or tubercles. A tubercle has been defined 
as, "a small nonvascular nodule composed of cells varying in 
form and size with some basement substance between them 
and with an inherent tendency to undergo central necrosis." 
In a large number of cases the individual tubercles are dis- 
tinct and easily recognizable, while in others they are coal- 
esced, forming a mass of necrotic tissue. The lesions vary, 
therefore, from well isolated minute or larger nodules to 
masses or cavities containing a purulent, caseous, or calcified 
substance. 

The location of the primary lesion depends upon the 
channel of infection. If the specific organisms are lodged in 
the oral cavity or pharynx they may, through an accidental 
abrasion of the mucosa, be taken to some of the lymphatic 
glands about the head; if they are taken directly through the 
respiratory passages into the lungs they either develop no- 
dules in the lung tissue proper, or they are carried through 



MORBID ANATOIMY 



189 



the lymphatic system to the lymph gjlands draining the lungs 
where the lesions first appear. If the specific bacteria are 
first lodged in the intestinal mucosa, primary tuberculous ulcers 
may develop or they may pass into the mesenteric lymphatics 
or the portal vein. It may happen that the bacteria may be 
carried by means of the lymph or blood stream and lodged in 
any part of the body, such as the brain, kidneys, spleen, 
testes, ovaries, bones, joints, and subcutaneous and intermus- 
cular glands and serous membranes. The evidence at hand, 




Fig. 35. A draiviuo- of a section ofveryyoniiix tubercles in spleen ( T/io>na). 

however, seems to show that in a large majority of ca.ses the 
primary lesions are located in one of the five following organs : 
(i) in the lungs or the lymphatic glands draining them, (2) 
in the lymphatic glands about the head, (3) in the mesenteric 
glands and intestines, (4) in the portal glands or liver sub- 
stance itself, and (5) in the generative organs and udder. 

It not infrequently happens that the apparent primary 
lesions occur on the pleura, peritoneum, meninges or synovial 
membranes while the organs remain free from disease. In 
such cases the lesions consist of many tubercles varying from 



I go 



TUBERCULOSIS 




Fig. 36. Section of a tuberculous heart of a cow. {a) tuberculous deposit 
surrounding tlie Iieart muscle and base of the larger blood vessels. 



:\[ORBID ANATOMY IQI 

one to ten or more millimeters in diameter or ot bunches of 
closely set tubercles which are more or less flattened or irregu- 
lar in shape, owing to their mutual pressure. Sometimes 
these tubercles are attached to the serous membrane by a small, 
tough, fibrous pedicle ; frequently, however, this is absent 
and the nodules rest bodily upon the membrane. 

The striuture of the tubercle consists in the beginning of a 
few cells surrounding the invading specific organisms. These 
are soon encased by a zone of epithelioid cells and giant cells 
which is soon surrounded by an outer layer of round or 
lymphoid cells. The central portion becomes necrosed and as 
the nodule enlarges the central necrotic portion becomes cor- 
respondingly large. 

This histological structure of the tubercle is typically illus- 
trated in the beginning avian tubercle. In cattle there is a 
strong tendency for the necrotic tissue to become infiltrated 
with hme salts and encapsulated. In certain species a deposit 
of fibrous tissue in the out,er zone of the tubercle has been 
observed. In the smaller and more susceptible experimental 
animals such as the guinea pig and rabbit and frequently in 
swine, the lesions are of a more diffuse nature infiltrating the 
interstitial tissue with the tuberculous mass and gradually 
encroaching upon the parenchyma. Circumscribed tubercles 
may also be present. 

In secondary or generalized tuberculosis one or more of 
the organs, such as the omentum, serous membranes, or lym- 
phatic system, may become more or less thickly sprinkled witK 
minute grayish nodules about the size of a millet seed. These 
tubercles are at first almost the color of mother-of-pearl but 
later as the central caseous degeneration begins they become 
grayish. Giant cells are usually numerous. 

In studying the lesions in a fatal case of tuberculosis one 
may find with varying modifications one or more of the follow- 
ing conditions : 

I . The primary lesion may be found in any one of the 
organs or membranes. Its comparative age is determined by 
the character of the anatomical changes. It may be entirely 



192 TUBERCULOSIS 

encysted, caseous or calcareous and dead. In addition to the 
primary focus, there may be a succession of tubercles of vari- 
ous ages distributed in one or more organs. 

2. The lesions may be restricted to one organ, as the 

liver, in which the primary focus has spread by continuity due 

to its infiltrating nature until the destruction of the tissues ot 

the organ has become so extensive that death results. Such 

cases do not seem to be common. 

3. The primary lesion may be 
well marked and accompanied by 
miliary tubercles sprinkled ex- 
tensively throughout the organs 
and tissues of the entire body. 

4. The lesions throughout 
the body may resemble each other 
very closely, so that difficulty 
may be experienced in determin- 
ing the primary focus. 

In the lungs, two distinct 
forms of lesions are observed, (i) 
The air cells may be infiltrated 
with the tuberculous mass spread- 
ing directly from the primary 
focus. This may be purulent, 
caseous or calcareous. The color 
may be whiti.sh, gray or of a yel- 
lowish tinge. (2) The lesions 
may consist of miliary tubercles. 
In later stages these nodules, 
more or less translucent, may be- 
come yellowish, caseated and 
Fig. 37. Tubcrcui ,^ :u calcareous in their centers. Large 




lung showing areas oJ\ {a) casea- 



tubercular nodules are frequently 



Hon, (b) calcification, and [c) 
liquefaction. formed by the massing of several 

of these minute tubercles. 
When the lungs are primarily attacked the caudal (prin- 
cipal) lobes are most frequently involved. Smith considers 





""VH^H 


* > ' 


i^B 




\ J^^^^l 


.'':■ '''/^- ^ 


1 


-' * 


'^M 


^^ jBH m- 


^H 


WH V 


m 






L . 


J| 



Fig. 



38. Pliotoi!:raph of a scciion from anterior lobe of a tuberculous lung 
C07U, sliowino- tuberculous infiltration and calcified areas. 



194 



TUBERCULO.SIS 



the seemiug predilection for the larger lobes to be due to 
mechanical conditions. The writer has found, however, that 
in certain herds that have been killed after the tuberculin test, 
thejprimary and only lung lesions were in the ventral and 
cephalic lobes. It is important to note that usually the bron- 
chial glands are also involved. When the pleurae are affected 
the lesions consist of nodules varying in size from that of a 
millet seed to a large pea, sprinkled more or less thickly on 
one or both of the visceral or parietal surfaces. These form 




Fig. 39. Plwloi::iapli of pleura slnncin<i small tuberculous nodules. 



the "pearl disease" Pcrlsucht of the German and the 
"grape disease" of the English writers. If they become 
confluent, large masses are found. 

Tuberculosis of the thoracic glands is very common and 
usually accompanies lesions in the lungs; but the lungs may 
be healthy and the glands involved. (See figures for location 
of glands.) The primary lesions may be and often are found 
in the lymphatic glands about the head. 



MORBID ANATOMY 



195 



In the abdominal cavity the organs most frequently in- 
volved are the peritoneum, mesenteric lymph glands, portal 
lymph glands and liver. The kidneys, spleen, ovaries and 
uterus are more rarelj^ the seat of tuberculous tumors. Ulcers 
in the intestine have not been common in the writer's observa- 
tion. The ulcers in the cases observed have been isolated 



Irv 






:^-v^. 



^ * ' *\ ; % £^ ^ .,.-"^ 



'/'*^:^i6:-r -'i-'.>\r: 



i^4' '- 



^,f 



'£, 






% 

Fig. 40. Tubercles on the mesentery of a eorc {Harding). 



with elevated borders and a depressed center. Sections show 
that the tuberculous infiltration extends outward and to a cer- 
tain extent undermines the mucosa. Tuberculosis of the testis 
is sometimes found. The udder becomes the seat of tuber- 
culous deposits in a small percentage of cases. It is 



IQD TUBERCULOSIS 

more often affected in cases of generalized tuberculosis. 

When the primary infection is restricted to a single focus 

the disease is said to be localized. When the specific bacteria 




41. A photograph of the tuberculous nodules on the o>ntntum 
from an advanced case of generalized tuberculosis. 



are spread from the primary' lesions through the agency of the 
Ijnnph and blood streams, sprinkling other organs with the 
infecting bacteria, each of which becomes the starting point 



MORHID ANATOMY 



197 



for the development of a new tubercle, the disease has become 
generalized. -■■ 

It was formerly considered that when the lesions existed 
in both of the large (abdominal and thoracic) cavities of the 
body the disease was generalized. It is possible, however, 
for it to be generalized when the lesions are restricted to the 
orcrans of one cavity, as the secondary seeding with the bac- 




FiG. 42. A p/iofooraph of several inbercHlous ulcers in the inlesline 
■ of a CO 70. 

teria that have escaped from a primary focus through the cir- 
culation may be restricted to the cavity in which the first 
lesion developed. It seems better, therefore, to accept 
Ostertag's views and classify local and generalized tuberculosis 

*The^ederal meat inspection regulations state that animals affected 
with -extensive or generalized tuberculosis " are to be condemned. 



TUBERCULOSIS IN SWINE 



in accordance with the nature of the lesions rather than their 
distribution in the body. 

The fact is worthy of consideration, that very often cattle 
killed after reacting to tuberculin do not show extensive dis- 




FiG. 43. A photoi^raph of a section of a tuberculous ulcer, from a 
corv's intestine, sho7c'in<rinfltration under the tnaroinal mucosa. 

tribution of lesions. Frequently animals are killed soon after 
infection has taken place, in which case the lesions are re- 
stricted to a single lymphatic gland or other organs. In other 
cases old lesions of considerable proportion are found as shown 
in Fig. 36, where the heart muscle is entirely encased in a 
thick calcareous tuberculous deposit. In this case, the animal 
was in good fle.sh and killed for beef without a suspicion that 
it was in any way diseased. 



TUBERCULOvSIS IN vSWINE 

§ 144. Channels of infection. It is stated that among 
swine young animals belonging to the precocious breeds seem 
to be more liable to tuberculosis than others. In nine eases 
out of ten the animals are infected by ingestion. The pig 
easily becomes tuberculous when fed on material rich in tuber- 
cle bacteria. If pigs are fed on the refuse from dairies and 
cheese manufactories in districts where there is much tubercu- 



SYMPTOMS 199 

losis in cattle or on tuberculous viscera they readily become 
infected. Mohler found that when hogs were fed on tubercu- 
lous milk for three days, and killed and examined post-mortem 
107 days later that 83.3 per cent were tuberculous. Hogs that 
received infected milk for 30 days and were allowed to live fifty 
days thereafter 100 per cent were affected. Infection through 
the respiratory tract, while it is certainly possible, seems to be 
rare. The piggeries where the refuse from butter and cheese 
factories is fed and those which join abattoirs supply the ma- 
jority of swine found on post-mortem to be tuberculous. 

Ostertag has called special attention to this disease as 
existing among swine in certain parts of northern Denmark 
and Germany, where there was much tuberculosis in cattle^ 
and where the swine were fed the slime from creamery separa- 
tors. Experiments show the possibility of infection by means 
of the sputvim of tuberculous people. 

In the cases which have come to notice there is ver}^ 
strong evidence that the swine were infected by being fed the 
milk from tuberculous cows. In one of these cases, the tuber- 
culin test showed that a large number of the cows from which 
the milk was obtained were affected. 

v? 145. Symptoms. In most cases tuberculosis of the 
pig is first recognized at the abattoir. Sometimes, however, it 
causes local and general troubles, which varj' according to the 
organ or system attacked. The following symptoms have 
been noted. 

Its localization in the abdominal organs causes the arrest 
of fattening and the progressive wasting of the subject. The 
mucous membranes become pale, the hide becomes dirty and 
there is usually either constipation or diarrhea. The animal 
is in low spirits, the corkscrew of its tail is straightened, the 
abdomen is pendulous and the eyes are sunken. Palpation of 
the abdomen is painful and may reveal more or less volumi- 
nous masses, due to the changes in the mesenteric glands. It 
is common to find glandular tumors in the submaxillary 
region or at the thoracic inlet. In this form, the malady may 



200 TUBERCULOSIS IX SWINE 

last several months, but death supervenes rapidly if the lesions 
become generalized by the scattering of the bacteria through 
the blood stream. Primary pulmonary tuberculosis is very 
rare but sooner or later lung lesions complicate abdominal 
tuberculosis. They betray themselves at the outset by a short, 
dry, abortive cough and by difficult respiration. The cough 
soon becomes paroxysmal and painful and is often followed by 
vomiting ; the respiration becomes hurried and gradually pain- 
ful and more difficult, wasting is very rapid, and death super- 
venes in a few weeks. 

The scrofula of swine (glandular tuberculosis) usually 
shows itself by a puffing up of the face, which a careful exam- 
ination shows to be lifted up by the subjacent glands, these 
being enlarged, indurated, still fairly mobile and free from 
heat or tenderness. The retropharyngeal, superior cervical 
and sublingual glands are usually affected, forming a kind of 
necklace of unequal and knotty tumors, reaching from ear to 
ear and becoming larger under the neck between the rami of 
the lower jaw. Similar tumors may be developed at the 
thoracic inlet, behind the shoulder or in the groin, which, as 
they increase in size, become harder and more adherent to the 
neighboring tissues. Sometimes, however, a slight fluctua- 
tion is perceptible. The tumor may suppurate and discharge 
a small quantity of a thick and gruraous pus, but the glandu- 
lar tumor does not disappear and the opening into the abscess 
remains for a long time as a fi.stula. 

There may be swellings of the bones, causing a true 
tuberculous arthritis when the lesions happen to be situated 
at the level of an epiphysis. Persistent lameness, fistulous 
wounds suppurating indefinitely, necrosis and caries, are the 
complications of the lesions of the bone, the development of 
which is always extremely slow. 

§ 146. Morbid anatomy. The manifestations of tu- 
berculosis in swine are exceedingly interesting. Nocard 
found the lesions to consist of miliary granulations which 
rapidly become caseous, as in cattle, but which more rarely 



Plate I. 




TUBERCULOUS LUNGS OF HOU 



MORBID ANATOMY 



contain calcareous salts. General- 
ization is common, in which case 
the viscera are thickly sprinkled 
with gray granulations which are 
translucent throughout, or opaque 
in their centers, and quite analo- 
gous to those found in tubercular 
lesions in other animals. 

As the disease most often re- 
sults from ingestion of the virus, 
the digestive apparatus and the cor- 
responding lymphatic glands (sub- 
maxillary, parotid, pharyngeal, su- 
perior cervical, mesenteric, sub- 
lumbar, etc.) may be decidedly 
diseased, while the other organs re- 
main practically intact. Lesions of 
the small intestine and of the 
cecum are common and take the 
form of ulcers of the mucous mem- 
brane, of miliary nodules or of 
tuberculous infiltrations, involving 
at once the mucous, the muscular, 
and subserous tissues. The lesions 
in the liver take the form either of 
miliar\' granulations, which are 
yellow and caseous and scattered in 
great numbers through the thick- 
ness of the organ, or else of rounded 
nodules which are yellowish white 
in color, varying in size from that 
of a pea to a hazel nut and of a 
tough consistency. On section 
they appear sometimes to be firm, 
homogeneous and fibrous ; some- 
times .softened in the center, 
often infiltrated with calcareous 
salts. The peritoneum and the 




Fig. 44. 



Tiibitculous spleen- 



irotit a pii: . 



202 TUBERCULOSIS IN SWINE 

pleura are sometimes the seat of an eruption of fine granula- 
tions which remain in a state of miliary nodules. Lesions like 
those in the liver may exist in the lungs, but generally there 
is found in these organs an innumerable number of minute, 
translucent, gray granulations, caused by the dissemination of 
tubercle bacteria through the blood stream, in which case the 
liver, the spleen, the kidneys, the medulla of the bones, and 
the mammae may be infiltrated with similar growths. 

Mohler has reported the results of the examination of 
120,000 infected hogs of which 93.3 per cent had tuberculous 
glands. 

It is common to find lesions localized in one or several 
lymphatic glands. The pharyngeal and submaxillary glands 
are the ones most often affected. They become voluminous, 
hard and knotty, as they have undergone a true fibrous trans- 
formation and, consequently, are difficult to cut. This is 
shown by the creaky sound under the cutting instrument. In 
section they have the appearance of old fibrous tissues; here and 
there small yellow foci are seen of a softer consistency, almost 
caseous; sometimes veritable purulent collections are found, 
either encysted or in communication with the exterior. If 
one submits the caseous or purulent matter to a bacteriological 
examination, tubercle bacilli are not usually found. The bac- 
terium, however, is present and if this matter is inoculated 
into the peritoneal cavity or the subcutaneous tissue of guinea 
pigs it will produce tuberculosis. 

These chronic glandular lesions, with their very slow pro- 
gress, have long been looked upon as constituting the scrofula 
of swine, and to scrofula was also assigned the tuberculous 
lesions of bones (ribs, vertebrae, articulations, shoulder blades, 
hip bones) which are common in pigs, both young and old. 

The older authors noted that the ancient scrofula was 
often accompanied by visceral tuberculosis, but they refused to- 
admit the identity and even the relationship of the two af- 
fections. 

The generalization of the disease, especially in the mus- 
cular tissue, is reported by several ob.servers. Moule called at- 



TUBERCULOSIS IX OTHER MAMMALS 203 

tention to this peculiarity of the disease. Stockman shows 
that while the disease is ordinarily generalized, muscular 
lesions may exist in swine in the absence of generalization. 
Zschokke has called special attention to the localization of 
tuberculous lesions in the head of swine, especially in the nares 
and brain. 



TUBERCULOSIS IX OTHER MAMMALS 

^ 147. Genera affected. It is stated that all species 
are sometimes attacked. Tuberculosis in the horse is rare, 
although a total of many cases have been reported. Bang has 
collected twenty-nine cases. In Saxony .oS per cent of the 
horses (3,500) that were slaughtered were tuberculous. In 
this and most countries there are no reliable statistics respect- 
ing the extent of the disease in this species. M'Fadyean has 
pointed out the fact that in a considerable number of cases of 
equine tuberculosis, where the horses have been fed milk from 
tuberculous cows, the morbid anatomy differs but slightly from 
that in tuberculous cattle. Recently several authors have 
reported isolated cases in Europe. In this country horses are 
practically free from it. 

Sheep and other domestic animals are reported to suffer 
more or less extensively from this disease. All of the so-called 
tuberculosis in sheep that I have examined proved not to be 
tuberculosis but the " nodular disease " caused by an animal 
parasite, {Oesopagostoiiia Cohimbianu))i) . A few cases, how- 
ever, have been reported. 

Tuberculosis in dogs and cats is quite rare but several 
cases in each genus are on record. 



AVIAN TUBERCIXOSIS 

§148. History. In America, tuberculosis in fowls was de- 
scribed by Pernot in Oregon in 1900. In 1903 Moore and Ward 
found the disease in California, where in certain flocks it was 



204 AVIAN TUBERCULOSIS 

very destructive. It was recognized by the owners as " spotted 
liver," going light, and rheumatism. In 1900 it was described 
by Burnett from northern New York. In Europe it has 

been known for a long time. 
.- rrr'^-'T^.i- i; 149. Symptoms. The 

V '• .^ •-• symptoms described as quite 

/ '»**", constant are emaciation, which 

*< in advanced cases becomes 

/^ ' extreme, and anemia. The 

J s * I - comb, the skin, and the visi- 

•i"^^, hie mucosa about the head 

\ '«' • y are usually pale. As the 

; course of the di.sease advances 

/ ^ the feathers become ruffled 

and the fowls are weak, dump- 
ish and move about very little. 
The eyes are bright in most 
cases until the end is near. 
' . The appetite is good, and the 

^' 'X 

V , • / temperature is in most cases 

• ' >-v . '^ "" ' 

.1 '^ ~f '^. ^ ^N rarely it is subnormal. The 

/I ^ , ,' V,, blood is pale. The hemo- 

( ' /^'• I / " ' globin varies from thirty-five 

* \ ■• . N to seventy per cent as tested 

• ' with Gowers' hemoglobino- 

meter. The red blood corpus- 
cles var}- from 1,010,000 to 
Fig. 45- Avian tubercle bacteria. 2,600,000 per cubic milli- 
(/ ) from /tver tissue of a fowl, {2) meter. There appears to be a 
a p/wtograph from a preparation slight increase in the number 
from a glycerine agar culture, x of white corpuscles, especially 

about 600. r ^^ ■ 1-1 

of the eosinophiles. 
Tuberculous fowls are often lame. Pernot mentions this 
as one of the important symptoms in the cases he observed. 



w V ' -^ \.^^ fowls eat ravenously until a 

"Vi"" . -^^ ^- ,f^ few days before death. The 

""si within the normal limits, 



AVIAN TrUERCLE 15ACTERIA 



'■^5 



It is due to joint lesions in some cases. In others it appears 

to be due to extensive lesions in the 

viscera. 



i^^ 150. The avian tubercle bac- 
teria. These organisms resemble quite 
closely those of the human and bovine 
varieties in their size and general mor- 
phology as they are found in the tissues 
of the fowl. A measurement of over two 
hundred individual organisms in cover 
glass preparations made directly from 
organs of fowls gave the following : In 
the liver the length varied from 1.2 to 
3.5 /<, in the spleen and in the skin they 
varied from i to 4 /( in length. A gen- 
eral average gave a length of 2.7 /<. They 
often appear in these preparations in 
dense masses. Chains made up of a 
number of short elements are rarely pres- 
ent. Granules are occasionally observed. 
In the preparations from the skin a con- 
.siderable number of them contain polar 
granules and not infrequently three such 
bodies were noticed in a single individual. 
Perhaps the most striking feature con- 
cerning these organisms in the tissues is 
their enofmousj numbers. Sibley has 
called attention to the similarity of avian 
tubercle bacteria [to those of leprosy in 
that thej^ nitiltiply to such enormous 
numbers without a pronounced breaking 
down of the tissues. 

This variety is more easily obtained 
in pure culture from the lesions than the 
human or bovine forms. Mooreobtained 
pure cultures in about 20 per cent of 




Fig. 46. ^ g/j'ii'rine 
ag^iir culture of avian 
tubercle bacteria. Cul- 
ture four Tl'CcA'S old. 



206 AVIAN TUBERCULOSIS 

serum tubes inoculated directly from tuberculous lesions in 
fowls. It grows readily on glycerin agar, Dorset's egg 
medium, potato and in glycerin bouillon. 

The colonies on glycerin agar vary from one to three 
millimeters in diameter. The central portion is raised and of 
a slightly yellowish tint as observed under a hand lens. This 
central part is surrounded by a flat expansion, about two- thirds 
the thickness of the center, varying from one-half to one milli- 
meter in width, with ray-like projections radiating from it and 
extending into the outer and very thin band of growth with a 
lobulated margin. On the egg medium of Dorset the growth 
is not more vigorous than that upon glycerin agar. Potato 
cultures are quite vigorous, wrinkled and of a yellowish- 
brown color. 

Fowls inoculated in the abdominal cavity or subcutane- 
ously with from one-half to one cubic centimeter of a glycerin 
bouillon culture develop either localized or generalized tuber- 
culosis in from six weeks to three months, but a much longer 
time is necessary to destroy them. 

Rabbits and guinea pigs are not readily infected by the 
inoculation of pure culture. Moore and Ward failed to pro- 
duce any tuberculous lesions in these species. 

i^ 151. Morbid anatomy. The lesions are widely dis- 
tributed, and vary much in their location in different individ- 
uals. The liver is most frequently involved. The spleen, 
intestines, mesentery, kidneys, lungs and skin are affected in 
order mentioned. The appended table gives the distribution 
of the lesions in 17 cases observed by Moore. 



MORBID ANATOMY 



207 



TABLE SHOWING THK, DISTRIHUTION OF I.RSIONS IN Tl'HER- 
/ CULOUS FOWLS. 



1 ^0^ 






C)KC,.\N 


r, INVOI. 


VKI).* 






Skin 


1,^^! 


Liver 


Spleen 


Intes- 
tine 


Mesen- 
tery 


Kidney Ovary 1 


Lungs 


Bones 


,k' 


XX 








1 




2 D 












1 




XXX 


^ K 




XXX 










._- __ 






4 K 107 

5 K 105 2- 

6 K 107.4 

-7 K" 107 2 


XX 
XXX 
XXX 

"xx 


_ 
XX X 
















XX 

X 


X 


























XXX 
X 


XXX 
X 


XX 








8 D 


X 
X 










9 I> 








XX 




108.4 

106.4 

107.4 

107 

107.6 

106.8 


XXX 
XXX 
XXX 
XXX 
XXX 
XXX 


X 

X 

XX 












11 K 

12 K 

13 K 

14 K 

15 K 

16 D 


X 
X 




i 










XXX 


XXX 


— - 
















XX 




1 


. 










XXX 
XXX 






■ 




17 K 

I 


105 


1 XXX 


XX 

1 






















*The relative numbers of tubercles are indicated by the number of Xs. XXX 
indicates an extensive invasion, XX a less number of tubercles, and X very few. 
Figures 47 and 48 show extent of lesions represented by X.XX. 

The tubercles, especiall}' in the liver, in the earlier stages 
of the disease, are small greyish points varying from 0.25 to 
i.o millimeter in diameter. In advanced cases they are larger. 
They have a cheesy con.sistency, and are easily removed from 



208 



AVIAN TUBERCULOSIS 



the surrounding tissue. The removed, necrotic nodules have 
a roughened surface. The color is greyish or whitish in the 
early stages, but in the later cues it changes to a yellowish 
tint. Occasionally there are two distinct crops of tubercles, 

one consisting of no- 
dules 4 to 6 milli- 
meters in diameter 
and separated by a 
centimeter or more, 
and the other of close- 
ly set grayish tuber- 
cles 0.25 to 0.5 mm. 
in diameter. In some 
cases the tubercles 
are few in number 
but larger i n size. 
The liver cells be- 
tween the tubercles 
are usually in a state 
of more or less degen- 
eration, and frequent- 
ly fat globules are 
numerous. The 
blood spaces are more 
than normally dis- 
tended with blood. 
The lesions in the spleen, like those in the liver, consist of 
minute or larger tubercles of a grayish or of a yellowish tint. 
The central portions of the larger tubercles are often homo- 
geneous, darker in color and more or less hyaline in appear- 
ance and consistency. 

The tubercular growths in the intestine start in the walls 
of the intestine. They present a glistening appearance, gray- 
ish in color and firm to the touch. Frequently they are 
confluent. When single they vary from i to 10 qim. in ' 
diameter. They are usually sessile on the intestine but on 
the mesentery they are frequently pedunculated, varying from 




Fig. 47. A p/io/ograph of a tuberculous 
liver from a foivl. 



MORBID ANATOMY 



209 



2 to 5 mm. in length. On section the young tubercles exhibit 
a grayish, glistening surface, but the more advanced nodules 
contain recognizable necrotic centers. In the larger tubercles 
on the intestines the necrotic centers frequently open into 

the lumen. 

The skin lesions consist of a cellular infiltration usually 
about the root of the feathers. Frequently the nodules be- 




FiG. 48. A photograpn ., . ...:..^^ ■ ^^ ,rle /,'0,najbwl s/wu',»g 
the necrotic center and surrounding zones. Enlarged. 

come confluent. They may or may not involve the subcuta-' 
neous connective tissue. 

The microscopic examination of the tubercles of the liver 
shows them to consist of a necrotic center surrounded by an 
irregular zone of epithelioid and giant cells. This is sur- 
rounded by a band of tissue consisting for the greater part of 
liver cells more or less disintegrated, free nuclei and a few 
infiltrated round cells. This zone is circumscribed by a nar- 



AVIAN TUBERCULOSIS 



row reactionary band consisting very largely of round cells. 
The structure is constant in both small and large tubercles, 
and not strikingly different from the structure of tubercles in 




Fig. 49. A photograph of a tuberculous mesentery of a foTcl. 
are a few small tubercles on the intestine. 



There 



certain of the mammals. The larger nodules seem in some 
instances to be the result of a contiuuous growth of a single 



)IFFEKKXTIAr, DIACXOSIS 



211 



tubercle, and in others to have resulted from the coalescence 
of a number of small ones. The necrotic center and reaction- 
ar\' zone of round cells are beautifully demonstrated by their 
reaction to nuclear stains. 

§ 152. Differential diagnosis. Tul)erculosis in cattle 




Fig. 50. A photoiiraph of the head and part of the neck of a 
tuberculous fowl. 

and swine is to be differentiated from actinomycosis, glanders, 
and various parasitisms resulting in nodules largely in the 
walls of the intestine. In cattle the nodules are produced by 
an Oesophagostoma. In sheep the nodules are caused by 



212 AVIAN TUBERCULOSIS 

O. Coluvibianum Curtice. In chickens a nodular taeniasis of 
the intestine is not infrequently mistaken for tuberculosis. 
Abscesses and necrotic foci due to various agencies must also 
be distinguished from tuberculous lesions. Enlargement of the 
lymphatic glands may be due to Hodgkin's disease. 

In cases of actinomycosis, the ray fungus can usually be 
detected on a microscopic examination. Bacteruun mallei can 
be found either in cultures or by guinea pig inoculations in 
cases of glanders, and in parasitic diseases the specific animal 
parasite can be found if diligently sought. A careful study of 
the recent lesions, especially in the nodules caused by the 
animal parasites, will show that they are not structurally like 
the tubercle as described above. 

From the symptoms and morbid anatomy it is clear that 
hard and fast lines for diagnosing tuberculosis cannot be laid 
down. As a rule the lesions are characteristic, although there 
are many exceptions. In making a positive diagnosis one 
must rely upon the discovery microscopically of the specific 
bacterium, the result of animal inoculation or the effect of 
tuberculin. 

The tubercle bacteria can be tound by making and prop- 
erly staining cover-glass preparations from the tuberculous 
tissues or discharges in a certain number of cases. When 
these tuberculous lesions open into the respiratory tract the 
specific bacteria can almost always be found in the expectora- 
tion. This is especially true in men, and Ravenel and others 
have shown that it is often true in cattle. In old and in the 
very recent tuberculous lesions, it is not so easy to detect these 
organisms microscopically. When there is doubt animal inoc- 
ulation gives quite prompt results. 

Tuberculosis in fowls is to be differentiated from certain 
other affections, such as lymphadenoma and sarcoma of the 
liver, asthenia, nodular taeniasis and excessive infestion with 
the air sac mite {Cytodites 7itidiis). Because of a close simi- 
larity in the general symptoms, and, in certain cases, of the 
gross lesions, between tuberculosis and certain other affections, 
the findings of a somewhat careful examination are necessary 



aSlTY ) 

DIFFERENTIAL DIAGNOSIS 2 1^ 

to warrant a positive diagnosis. In the living fowl it seems as 
yet to be impossible to fix upon any diagnostic symptoms. 
At post-mortem, however, properly stained cover-glass prepa- 
rations from the tubercles will reveal the presence of tubercle 
bacteria. This renders the positive diagnosis in the dead fowl 
a comparatively easy task. 

The positive diagnosis of tuberculosis rests in : 

1. Finding the tubercle bacterium on a microscopic 
examination of the lesions. 

2. The production of tuberculosis in experimental ani- 
mals by inoculating them with the suspected tuberculous 
material. 

3. Obtaining a typical reaction after the injection of 
tuberculin. 

§ 153. Microscopic examinations. The diagnosis by 
microscopic examinations is possible when one has the dis- 
charge from a lesion, such as the sputum when the lungs are 
involved. In case of tubercular abscesses, the examinations 
should be made from the scrapings of the walls of the abscess 
rather than from the purulent contents. It is often possible 
to find tubercle bacteria in sections of the diseased organs. 

A viethod for staining tiiberrlf hacteria. Stain the cover-glass with 
fresh carbol fuchsiii. Place a few drops of the stain on the film side of 
the cover-glass preparation and hold it over a flame with forceps nntil 
steam is given off. Allow the hot stain to act for from 3 to 5 minutes, 
or the preparation may be floated on the carbol fuchsin in a watch glass 
without heat. In this case it is allowed to act for from 10 to 15 minutes. 
The preparation is then rinsed in water and decolorized by treating it 
with a 10% solution of nitric or sulphuric acid for from V to i minute. 
It is again rinsed in water, when it is ready for examination. It can be 
dried and mounted permanently in balsam. The tubercle bacteria 
should be stained a deep reddish color. All other bacteria or animal 
tissue in the preparation should be nearly or quite decolorized. If 
desired, a counter-stain, such as alkaline methylene blue, may be used 
after decolorizing ; that is, the preparation should be again stained for 
about I minute in alkaline methylene blue, rinsed in water, and 
examined as before. In these preparations the tubercle bacteria are red 
and the other organiams and cells are blue. A counter-stain is of little 
value in preparations made for simple diagnostic purposes. When a 



214 TUBERCULOSIS 

counter-stain is desired Gabbett's decolorizing and counter-staining 
solution is very convenient. 

gabbett's solution 

Methylene blue (powder) 2 grams 

10% sulphuric acid 100 cc. 

After staining with the carbol fuchsin treat the preparations with 
this mixture until the film has a faintly bluish tint. This solution 
decolorizes and counter-stains at the same time. Care must be taken 
not to confuse the other acid fast bacteria with those of tuberculosis. 
The acid fast bacteria other than tubercle, are decolorized with acidulated 
alcohol (3 per cent hydrochloric acid in 95 per cent alcohol). 

§ 154. Animal inoculation for purposes of diagnosis. 
Guinea pigs are preferable, although rabbits may be used. 
With tuberculous tissue either of the two methods described 
below may be employed. 

1. A small piece (about the size of a pea or beau ) of the 
tissue may be inserted under the skin by first making an 
incision with a sharp scalpel through the .skin and superficial 
fascia, and then with a pair of fine forceps insert the bit of 
ti.ssue well under the skin and close the opening with one or 
more sutures. 

2. The tissue may be crushed in a mortar and thor- 
oughly mixed with a few cubic centimeters of sterile water or 
bouillon and then injected with a hypodermic syringe. The 
needle should be of large calibre. If it is suspected milk, it 
may be injected into the abdominal cavnty. If the material is 
tuberculous and contains living tubercle bacteria, the death of 
the animal follows in from three weeks to four months. 
Usually the lymphatic glands in the groin and axilla are en- 
larged and often caseous. If a guinea pig is used, the liver, 
spleen, lungs and kidneys are liable to be affected, in the 
order named ; if a rabbit, the lungs are often the first of the 
viscera to be attacked. 

In avian tuberculosis it is necessary to use chickens 
instead of guinea pigs. They may be inoculated subcutane- 
ously or into the abdominal cavity. Several weeks may be 
necessary for the di.sease to develop sufficiently to distingui.sh 



TUBERCULIN TEST 215 

the lesions or to enable one to find the bacteria micro- 
scopically. 

§ 155. Tuberculin test. The tuberculin test is the 
best '' and in a large majority of tuberculous cases among 
animals and in man, the only means of positively detecting 
the disease in the living individual. 

Tuberculin Tuberculin is the concentrated liquid, us- 
ually o-lvcerinated bouillon, on which tubercle bacteria have 
grown\;ntil the products resulting from their multiplication 
have become imparted to the medium in sufficient quantity to 
inhibit their funher development. It is not definitely deter- 
mined just what these products are or just how they are 
elaborated. Briefly stated, the preparation of tuberculin con- 
sists in the following procedure: 

I The preparation of the culture medium i glycerinated 
bouillon., distributing it m suitable flasks and inoculating it 
with the growth from a pure culture of tubercle bacteria. 

. The flasks are placed in an incubator at a temperature 
of about ^.7= C. where they remain until the growth ceases. 
The lenc^ih of time necessary to accomplish this depends upon 
the ac^e and condition of the culture from which the inocula- 
tions were made. From four to ten weeks are usually re- 

quired. 

^ \fter the maximum growth is attained, the cultures 
are sterilized by heat, either by boiling in a closed water bath 
or heating to a higher temperature in an autoclav. 

, \fter sterilization, the cultures are filtered to remove 
all of the dead bacteria, and then the filtrate is evaporated 
over a water bath to the desired degree. 

, The concentrated liquid is passed through a Pasteur 
or Berkefeld filter, standardized, bottled and labeled tor dis- 
Uibution It should be perfectly clear although its color may 
varv If it is cloudy it should be rejected. 

' It will be seen from the method of preparation that tviber- 
culin cannot possibly contain living tubercle bacteria. It is 



2l6 TUBERCULOSIS 

heated on two occasions to a temperature and for a length of 
time far in excess of that required to destroy them, besides be- 
ing passed through a filter capable of removing all bacteria. 

The original tuberculin or lymph of Koch was concen- 
trated to one-tenth of the volume of the saturated culture. 
This gave a thick, syrupy liquid owing to the presence of the 
glycerin. The diagnostic dose which came to be recom- 
mended for cattle of medium weight was 0.25 c.c. On ac- 
count of its consistency as well as the minuteness of the dose, 
it was found to be practicable to dilute this quantity with 
seven parts of a diluent. A weak solution of carbolic acid 
was ordinarily used. The difficulties and the danger of con- 
tamination involved in making the dilutions in the field led to 
the method of diluting the tuberculin in the laboratory before 
sending it out. This has been the practice of the Bureau of 
Animal Industry for a number of years. Equally as good re- 
sults are obtained by concentrating the saturated culture to 
the point where 2 c. c. contains an equivalent of the 0.25 c. c. 
of the highly concentrated lymph. This process avoids the 
necessity of dilutions and, with the addition of a few drops of 
carbolic acid, the weaker solution keeps perfectly. 

Tuberculin in the dose necessary to bring out its diag- 
nostic effect is harmless for healthy animals. Thousands of 
observations that have been reported assure us of this fact. 
Tuberculin is in daily use in every state in the Union, in 
Canada and in every country of Europe, yet so far as can be 
learned not a single case of injury following its use has been 
reported. In the tuberculous animal it produces a rise of tem- 
perature which, within certain limits, follows a definite course 
usually terminating in from 18 to 24 hours after the injection. 
Occasionally the temperature remains above the normal for a 
•longer time. The temperature usually begins to rise in about 
eight hours giving a steady but quite rapid elevation for from 
I to 3 hours, a continuous high elevation for from 2 to 4 hours, 
possibly longer, and a gradual decline. This is practically 
constant, be the raise moderate or extreme. In addition to 
the elevation in temperature there is sometimes a marked 



TUBERCULIN TEST 217 

nervous chill. Why we get this reaction-^- is not positively 
determined. 

Applying the tuberculin test. In brief, the method for 
applying the tuberculin test in cattle is as follows : 

1. The normal temperature of the animal to be tested 
must be determined. It is recommended that it be taken 
hourly or every two hours for the day preceding the test. In 
practice veterinarians usually take the temperature but once 
or twice before injecting the tuberculin. 

2. The tuberculin is injected subcutaneously in the side 
of the neck. Care must be taken that the syringe is sterile 
and the site of injection should be disinfected. The size of the 
dose depends upon the preparation of tuberculin, that is, the 
degree of concentration. 

*Trudeau {Johns Hof^khis Hospital BiiltetiH, July , 1S99) gives the 
following summary of the mechanism of the tuberculin reaction. "The 
most generally accepted theory at present in regard to it is, briefly, the 
small dose of tuberculin injected is a partly speciiic irritant both to 
tuberculous foci and to the susceptible organism in general. It pro- 
duces intense hyperemia of all tuberculous tissue in the body (local 
reaction), and as the result of this hyperemia much toxin stored up in 
the tubercles themselves is thrown into the general circulation and pro- 
duces fever and characteristic symptoms which go to make up what is 
termed 'a general reaction.' That these poisons stirred up in the tuber- 
cles are in part at least derived from the dead or weakened bacilli has 
been shown by the experiments of Babes and Proca, who found that if 
two sets of rabbits be injected with equal quantities of living and dead 
bacilli, the latter react to the tuberculin test at a much earlier period 
than those inoculated with living germs. This hypothesis that the gen- 
eral reaction is brought about by toxins already stored up in the tuber- 
culous lesions and exploded as it were by the hyperemia produced 
about these lesions as the result of the test of injection of tuberculin, is 
borne out by the fact that a greater amount of albumose can be recov- 
ered from the evaporated urine collected during the reaction than was 
contained in the test injection also by clinical observations which indi- 
cate that patients suffering from localized surgical tuberculous processes 
of limited extent, and where the vascular supply to the part is limited, 
required a larger test injection to produce the reaction than those who 
have extensive or scattered visceral lesions in highly vascular organs 
like the lungs." The reader is referred to this paper for a careful con- 
sideration of the vexed questions relating to tuberculin. 



2l8 TUBERCULOSIS 

3. Beginning 6 or S hours after the injection, the tem- 
perature should be taken hourly, or at least every two hours, 
for fully three-fourths of a day. 

4. During the time of testing, the cattle should be kept 
quiet and free from all exposure, and fed normally. 

5. In case of reaction, there should be a rise of at least 
1.5° F. above the maximum individual normal temperature as 
determined on the preceding day. The elevation should come 
on gradually, remaining practically at its fastigium for a few- 
hours and gradually subside. Erratic elevations of short dura- 
tion are to be excluded. In cases of doubt the animals should 
be retested. 

6. Animals advanced in pregnancy and those known to 
be suffering from any other disease or in oestrum should not be 
tested. All methods of treatment, including exposure to cold, 
or kind of food and drink which would tend to modify the 
temperature, should be avoided. Animals in which the disease 
is far advanced sometimes fail to react. 

7. The dose should vary to correspond with the weight 
of the animal. The dose for an adult cow of average weight is 
0.25 c.c. of the concentrated Koch tuberculin. In cases of a 
second test within a few days, the quantity of tuberculin 
injected should be larger than for the first test. 

Ward has pointed out the fact that fowls do not give a 
diagnostic reaction to tuberculin made from either the avian or 
mammalian varieties of the tubercle bacteria. 

In cattle there is a marked variation in the normal daily 
temperature. A fluctuation of two or even three degrees 
within 24 hours is frequently found. Cold water when drunk 
in considerable quantities lowers the temperature from two to 
four degrees. A temporary excitement usually causes an eleva- 
tion of from I to 1.5° F. There are also marked variations in 
the temperature of the same animal on consecutive days. The 
temperature at 12 noon and 12 midnight are often the same. 
In some cases the maximum elevation for the day occurs near 
midnight and on the following day the minimum temperature 
appears at that time. It is not uncommon for the maximum 



TrHP:RCULIN TEST 219 

temperature to occur twice in the same daj- and occasionally 
several times within the twenty-four hours. There are marked 
individual variations in the effect of ordinary conditions upon 
the temperature, such as food, excitement or temperature of 
the air. A hot spell causes a rise of two and in some cases 
four degrees. The average temperature of the animals in 
three herds tested by Howe and Ryder were 102.5°, 102.6°, 
and 101° F. respectively. 

In a well kept Government herd that was tested with 
tuberculin, the temperature of part of the animals was taken 
hourly for 24 and part of them for 16 hours preceding the 
Injection. An examination of the records-i^ shows the average 
daily variation of 20 animals in which the temperature was 
taken for 24 hours to be 2.31° F. The maximum individual 
variation in a single day was 4.3° F". , the minimum 0.5° F. 
In 25 other animals where the temperature was taken for 16 
hours, the average variation was 1.79° F. In these the maxi- 
mum variation was 3.2° F., the minimum 0.6° F. Ten 
healthy animals (did not react to tuberculin) in the same herd 
gave an average variation of 2.08° F. In these the maximum 
daily variation was 4.1° F., the minimum 1° F. The lowest 
temperature was usually, but not invariably, in the morning 
and the highest in the afternoon or evening. I have appended 
the records of the temperature of two of these animals. 



^Bulletin No. 7, Bureau of Animal Industry, U. S. Department of 
Agriculture, Washington, D. C. The tests were made by Drs. F. L. 
Kilborne and E. C. Schroeder, under the direction of Dr. Theobald 
Smith. 



TUBERCULOSIS 



THE INITIAI, TEMPERATURE OF TWO COWS, WITH RATE OF PUI.SE 
AND NUMBER OF RESPIRATIONS PER MINUTE. 



Cow No. I 



Cow No. 2 



Tempera- 
ture 



Pulse Resp. 

I 



Tempera- 
ture 



Pulse Resp. 



9 A. M. 


99.8 


48 


18 


98.6 


48 


15 


!0 " 


99-5 


66 


18 1 


98.6 


66 


15 


II " 


99.0 


60 


^5 


99.0 


60 


15 


12 " 


100.8 


54 


15 1 


99-4 


54 


15 


I P. M. 


101.4 


54 


15 


lOO.O 


54 


18 


2 " 


101.6 


48 


15 


100.2 


54 


18 


3 " 


102.0 


60 


24 


100.4 


72 


24 


4 " 


103.0 


66 


24 


102.7 


72 


24 


5 " 


103-3 


66 


24 


102.8 


72 


27 


6 " 


103.1 


57 


18 


103.0 


60 


27 


7 " 


102.2 


60 


20 


102.4 


60 


24 


8 " 


103.0 


56 


16 


102.0 


60 


24 


9 " 


103. 1 


52 


24 


102.2 


50 


24 


lO " 


102.5 


60 


20 


102.0 


50 


IS 


II " 


102.5 


60 


20 1 


102.0 


60 


20 


12 midnight 


102.4 


56 


16 


IOI.6 


54 


20 


I A. M. 


101.8 


60 


20 1 


101.4 


^8 


24 


2 " 


102.0 


64 


18 


102.2 


58 


18 


3 " 


102.0 


60 


18 


101.6 


38 


18 


4 " 


102.2 


54 


24 


101.5 


60 


24 


5 " 


101.6 


56 


24 


102.0 


60 


18 


6 " 


101.8 


60 


18 


102.2 


60 


20 


8 " 


102.5 


56 


16 1 


103.2 


60 


18 



In view of these normal temperature variations, which 
often exceed the tuberculin reaction, it is obvious that before 
applying the test the normal temperature of the animals should 
be approximate!}^ determined and that when thej- are being 
subjected to the test they should be cautiously protected, 
otherwise the comparativeh' slight elevation necessary to detect 
the disease may be disguised. 

As the reaction seems to be the result of an affinity exist- 
ing between the tuberculin and the living tuberculous lesion, 
it is natural to suppose that when the two are brought together 
in the same animal it would invariably take place. Experience 
has shown that it almost always does. It is important to 



TUBERCULIN TEST 221 

understand, as far as possible, the reason for the exceptions 
and the extent to which they occur. The reported failures of 
the tuberculin tests fall into two distinct classes. 







7/m/rs Aft 


r.r 1 yi 


' e.rfn c 


{ 




r 


? 


/C 




/^ 


/6' 


/r 


^r? 


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"-^ 










i5 


} 


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^ 








, 00' 


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/ o-^' 


3/y 












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/y 














. 03' 


^ 






























C^" 
















^ 


1 














.'O/^ 
















^ 

































.-^ teuipenxtuie curve of three cows after injecting tuberculin. 
I a healthy cozu, 2 and j tuberculous ones. 







■^.00 


s:io 


XSO 


.5: JO 


.S'.f-O 


s.so 


a./o 


■7.00 


S.Oo 




r 
























/03 
























lOZ 




.^^ 


i^^AN 


H rRi 


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or //a 


TCR 4 


T 39' F 
































100 










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^ 


— 


99 












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Fig. 52. Chart shoiviug the effect of drinking cold water upon the 
tetnperature of a coiv. 

I. There is a reaction and no disease is found. In 
explaining this alleged error, the records of the cases which 
have come to my attention have been so deficient in data con- 
cerning the normal temperature variation of the animals, and 



TUBERCULOSIS 



the incompleteness of the post-mortem examinations, that it 
seems possible for the error to rest with the observer quite as 
much as with the tuberculin. Unfortunatel}- we are as yet 
unable to determine by the reaction the extent of the disease, 
so that a beg^inning lesion no larger than a walnut may cause 
a pronounced rise of temperature and such a tubercle may be 





/ 


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.3 4 


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A.M 
9 /r 


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1 


































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y' 














































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AM 


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Fig. 53. Temperature curve of a hog. Dotted litie A represents temper- 
ature of a hog for 24 hours before the injection of tuberculin. The 
full line B represents the temperature of t/ie hog for .?/ 
hours after the injection of tuberculin {Schroeder). 

difficult to find, especially if located in the marrow of some 
bone or in the nervous system. 

2. There is no reaction and the disease exists. It is 
generally admitted that advanced cases often fail to react, but 
here the test itself is of little importance, as the disease can 
be detected by the clinician on physical examination. When, 
however, tuberculin is carefully prepared and scientifically 
administered, these exceptions are exceedingly rare. It seems 
to act always in active tuberculosis. 



TUHERCULIN TEST 



223 



Tuberculin does not give a reaction during the period of 
incubation. It does not cause a reaction in many, if not all, 
cases of temporary arrest or healing of the lesions. This ren- 
ders it difficult to interpret the negative results especially in 
herds where there are many positive reactions. In such cases 
there should be subsequent tests later. For this reason cattle 
bought on the tuberculin test can not be considered uninfected 



tiouRs ArrER Injection 




'Fig. 54. Irregular temperatures follozving tuberculin that arc >iot caused 
by tuberculosis [Curtice). 

as the result of the first test if they came from herds contain- 
ing reacting animals. 

The practical value of tuberculin lies in its efficiency in 
the arts of comparative and sanitary medicine. It is in the 
practical application that difficulties are encountered. The 
many details and precautions enumerated as absolutely essen- 
tial to the best results are often considered too tedious and 
time consuming, and consequently the practice has come too 
generally into vogue of neglecting or ignoring many of the 
precautions. In order that the test may be practicable, some 
practitioners resort to a shorter method of procedure even at 
the risk of an occasional error. 

§ 156. Prevention. Tuberculosis, like other infectious 
diseases, can be very largely prevented. To accomplish this 



224 



TUBERCULOSIS 



it is necessary to keep tuberculous animals from entering the 
healthy herds. If they are admitted and later the fact is dis- 
covered, it is necessary to remove them and to thoroughly dis- 
infect the stable. In eliminating the disease from a herd by 
means of the tuberculin test, it is necessary to retest the non- 
reacting animals after six months or a year have passed in 





A.M. 

9 00 




P.M. 
1 oo 








^oo 




A.M. 


^oc^ 




I0 6 






































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y' 






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/04- 












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.--^ 






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s 


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m 

Fig. 55. Temperature curve of a tuberculous cow for 48 hours. The line 
A. A. s/iozas temperature for 24 hours preceding- the injection of tuberculin, 
which ivas injected at g. A. M., March 16 ; b, b, b, shorvs the temperature 
for the 24 hours after the tuberculin injection. 

order to find any case that might have been infected, but in 
which the disease had not begun to develop, or cases that were 
temporarily healed at the time of the first test. 

§ 157. The control of tuberculosis in cattle. Several 
methods have been proposed to eliminate tuberculosis from 
cattle. The preventing of the spread of the virus from the 
diseased to the healthy animals is the most important precau- 
tions. The system introduced by Prof Bang of Copenhagen, 
Denmark, and generally known as the Bang method, has 



REFERKNCES 225 



proven to be most successful. It consists in the slaughter of 
the advanced cases and the isolation of the reacting animals, 
which are kept for breeding purposes. The calves are .sepa- 
rated from their dams immediately after birth and fed upon 
the milk of healthy cows or the sterilized milk of the reacting 
ones. This method has enabled many owners of infected 
animals to replenish their herds in from four to six years. In 
countries where it has been generally applied the percentage 
of tuberculous cattle has been wonderfully reduced. 

The vaccination of cattle against tuberculosis has been 
proposed as a prophylactic measure. The method has been 
extensively tried by Pearson in x\merica and von Behring in 
Germany. Its effectiveness can not be predicted at this time. 
The results of von Behring's experiments are promising but 
as yet the vaccinated animals (calves) have not attained to old 
age so that the length of the resistance that seems to be 
established by the vaccination is not determined. Several 
reports on the result of natural exposure to tuberculous cows, 
after a period of two years, show the vaccinated animals to 
be nearly as badly infected as the checks. The resul ts reported 
by Pearson indicate that the attainment of a bacterial immunity 
against tuberculosis in cattle is not likely to be an easy task. 
The experiments in this direction are most interesting and 
many investigators are hopeful for good results. At present 
it is in the experimental stage. 



REFERENCES. 



1 \DAMi On the significance of bovine tuberculosis and its 
eradication and prevention in Canada. Ca>iadia>, Jour, of Medicine 
and Surgery, Dec. 1899. 

2 Curtice. The detection of tuberculosis in cattle. Annual 
Report, Bureau of Animal Industry, U. S. Dept. Agric., 1895-96- 

3. Dorset. Experiments concerning tuberculosis. Bulletin 5.'. 
Bureau of Animal Industry, 1904. 

4 Eber Suggestions for a uniform system of interpreting the 
tuberculin reaction in cattle. The Jour. ComPr. Path, and Ihcra., 
Vol. XVIII (1905), P- 224. 



226 TUBERCULOSIS 

5. Koch. The etiology of tuberculosis. Mitt, aus dem. Kaiserl. 
GesiindhcUsamte, Vol. II ( 1884). Translated in Vol. CXV, New Syden- 
ham Society. 

6. Koch. The combating of tuberculosis in the light of the exper- 
ience that has been gained in the successful combating of other infec- 
tious diseases. Amer. Vet. Rev., Vol. XXV (1901), p. 44i- 

7. MoHLER. Infectiveness of milk of cows which have reacted to 
the tuberculin test. Bulletin 44. Bureau of Animal hidiistry, 1903. 

8. MOHLER AND Washburn. A comparative study of tubercle 
bacilli from varied sources. Bulletin 96. Bureau of Animal Indus- 
try, 1907. 

9. MOHLER. Tuberculosis in hogs, with special reference to its 
suppression. Amer. Vet. Rev., Vol. XXXII (1907), P- 176. 

ID. Moore and Dawson. Tuberculosis in swine, the nature of the 
disease with a report of three cases. Annual Report, Bureau of Ani- 
mal Industry, U. S. Dept. Agric, 1895-96. 

1 1. Moore. The preparation of tuberculin, its value as a diagnostic 
agent, and remarks on the human and bovine tubercle bacilli. Trans, 
of the Med. Society of the State ofN. Y., 1900. 

12. Moore, a report on bovine tuberculosis. Nezc York State 
Dept. of Agric., 1903. 

13. NOCARD. The animal tuberculosis. New York. 

14. Pearson. The Pennsylvania plan for controlling tuberculosis 
of cattle. Proc. Amer. Vet. Med. Assn., 1899. 

15. Pearson. Tuberculosis in cattle and the Penn. plan of its 
repression. Bulletin 75. Pemi. Dept. of Agric, 1901. 

16. Pearson. The repression of tuberculosis in cattle by sanita- 
tion. Bulletin J4. Penn. Dept. of Agric, 190 1. 

17. Pearson. The artificial immunization of cattle against tuber- 
culosis. Amer. Vet. Rev., Vol. XXIX (1905), p. 543- 

18. Ravenei,. The dissemination of tubercle bacilli by cows in 
coughing a possible source of contagion. Univ. of Penn. Med. Maga- 
zine, Nov. 1900. 

19. Ravenel. The comparative virulence of the tubercle bacillus 
from human and bovine sources. Univ. of Penn. Med. Bulletin 
Sept., 1901. 

20. Ravenel. The intercommunicability of human and bovine 
tuberculosis. The Univ. of Penn. Med. Bulletin May, 1902. 

21. Repp. Transmission of tuberculosis through meat and milk. 
American Medicine, Oct. 6, Nov. 2, 1901. 

22. Salmon. Legislation with reference to bovine tuberculosis. 



REFERENCES 227 

Bulletin 2S. Bureau of Animal Industry, U. S. Dcpl. of Agric, 1901. 

23. vSalmon. The tuberculin test of imported cattle. Bulletin ?.'. 
Bureau of Animal Industry, U. S. Dept. of .I'^ric, 1901. 

24. Salmon. Bovine and human tuberculosis. Procecdiiii^s 
.Inter. Vet. Med. .Isso., 1903, p. 436- 

25. Salmon. Tuberculosis of the food-producing animals. 
Bulletin jS. Bureau of Animal Industry, 1906. 

26. SCHROEDER AND CoTTON. The relation of tuberculous le- 
sions to the mode of infection. Bulletin gj. Bureau of Animal Indus- 
try, 1906. 

27. SCHROEDER AND CoTTON. Experiments with milk artificially 
infected with tubercle bacilli. Bulletin S6. Bureau of Animal Indus- 
try, 1906. 

28. SCHROEDER AND MOHLER. The tuberculin test of hogs. 
Bulletin 8S. Bureau of Animal Industry, 1906. 

29. vSmiTh. Investigations concerning bovine tuberculosis with 
special reference to diagnosis and prevention. (Pathological part). 
Bulletin No. 7, Bureau of Animal Industry, U. S. Dept. of Agric, 

1894. 

30. Smith. A comparative study of bovine tubercle bacilli and of 
human bacilli from sputum. The four, of Ex per. Med., Vol. Ill (J898). 

31. vSmiTh. The thermal death point of tubercle bacilli in milk 
and some other fluids. The four, of Exper. Med., Vol. IV (1899), 
p. 217. 

32. Smith. The channels of infection in tuberculosis, together 
with some remarks on the outlook concerning a specific therapy. 
Trans. Mass. Med. Soe.. 1907. 

REFERENCES TO AVIAN TIHERCULOSIS 

33. Burnett. Tuberculosis in chickens positively identified in 
New York. Am. Vet. Revieiv, XXX (1907), P- 1312. 

34. Brav. Tuberculosis in chickens, four. Compar. Med. and 
Vet. Archives, XVII (1896), p. 461. 

35. CadioT. Bur la tuberculose du cygne. Bui. de la Soe. Cen. et 
Med. Vet., Vol. XLIX (1895), P- 57°. 

36. CadioT, Gilbert and Roger. Inoculation of the tubercu- 
losis of gallinaceous to mammalia. Amer. Vet. Bevierc, XX (1896-7), 

p. 225. 

37 CADIOT Gilbert et Roger. Note sur la tuberculose des 
volailles. I^eeeuil de Med. Vet. Serie VII, Vol. VIII (1891), p. 22. 

38. CadioT, Gilbert and Roger. A contribution to the study of 



228 TUBERCULOSIS 

avian tuberculosis. vStudies in clinical veterinary medicine and surgery. 
(1900). (Translated by Dollar.) 

39. EbkrlEin. Die Tuberculose der Papageien. Monatshefte fi'ir 
Praktische Thierheilktmde, Bd. V (1894), S. 248. 

40. Froehner. Zur Statistik der Verbreitung der Tuberculose 
unter den kleinen Hausthieren. Monatshefte fur Praktische Tierheil- 
kunde, 1893, p. 51. 

41. LuCET. Sur un symptome de la tuberculose chez la poule. 
Rccueilde Med. Vet., Serie, VI f, Vol. VIII (1891), p. 172. 

42. Maffucci. Die Huhnertuberculose. Zeitschr.fiir Hygiene, 
Bd. XI (1892), p. 445- 

43. Moore and Warp. Avian tuberculosis. Proc. Auier. Vet. 
Med. Asso., 1903, p. 169. 

44. Moore. The morbid anatomy and etiology of avian tuber- 
culosis. Jour, of Med. Research, Vol. XI (1904), p. 5' 2 (Bibliography.) 

45. Nocard. Sur une tuberculose zoogleique des oiseaux de 
bassecour. But. et Memoires de la Sac. Centrale ct Med. Vet., 1885, 
p. 207. 

46. Nocard. Transmission de la tuberculose des poules et 
I'homme. Veterinaire, Vol. Ill (1886), p. 658. 

47. PernoT. Investigatiousof diseases of poultry. Bulletin No. 64. 
Oregon Agric. Expt. Sta., 1900. 

48. SiBivEY. Tuberculosis in birds. Jour, of Coinpar. Med. and 
Vet. Arch., Vol. XI (1890), p. 317- 

49. Straus et Gamaleia. La tuberculose humaine, sa distinc- 
tion de la tuberculose des oiseaux. Archiv. de Med. Exper., Bd. Ill 

(1891), p. 457. 

50. Straus et WurTz. Sur la resistance des poules a la tubercu- 
lose par ingestion. Congress pour V etude de la tuberculose, 1888, p. 28. 

51. Ward. Tuberculosis in Fowls. Bulletin No. 161 California 
Agr. Exper. Station, 1904. 

52. Weber. Review of the avian tuberculosis. Jour, of Compar. 
Med. and Vet. Arch.,\o\. XIII (1892), p. 429. 

THE FOLLOWING BULLETINS ON TUBERCULOSIS HAVE BEEN 

ISSUED FROM THE VARIOUS STATE AGRICULTURAL 

EXPERIMENT STATIONS. 

Bang. The application of tuberculin in the suppression of bovine 
tiiberculosis. Bulletin 41. Massachusetts. 1896. (A translation). 

Beach. The history of a tuberculous herd of cows. Bulletin 24. 
Storrs, Conn. 1902. 



BULI.KTINS 229 

Bitting. Bovine tuberculosis in Indiana. Bulletin 63. Ind. 1S96. 

Brewer. Tuberculosis. Bulletin 41. Utah. 1895. 

Carv. Bovine tuberculosis. Bulletin 67. Alabama. 1S95. 

CONX. The relation of bovine tuberculosis to that of man and its 
significance in the dairy herd. Bulletin 25. Storrs, Conn. 1902. 

DiNWiDDiE. The relation of virulence for the domestic animals of 
human and bovine tuberculosis. Bulletin 57. Kansas. 1S99. 

DixwiDDiE. The relative susceptibility of the domestic animals 
to the contagia of human and bovine tuberculosis. Bulletin 63. 
Kansas. 1900. 

Fischer. Bovine tuberculosis. Bulletin 69. Kansas. 1898. 

Glover. Relation of bovine to human tuberculosis. Bulletin 
66. Colorado. 1901. 

Grange. Tuberculosis. Bulletin 133. Michigan. 1896. 

Harding, Smith and Moore. The Bang method etc. Bulletin 
277. Geneva, N. Y. 1906. 

Hill and Rich. Bovine tuberculosis. Bulletin 42. Vermont. 1894. 

Law. Tuberculosis in relation to animal industry and public 
health. Bulletin 65. (Cornell) , New York. 1894. 

Law. Experiments with tuberculin on non-tuberculous cows. 
Bulletin 81. (Cornell), New York. 1894. 

Law. Tuberculosis in cattle and its control. Bulletin 150. 
(Cornell], New York. 1898. 

iVL\RSHALL. A study of normal temperatures and the tuberculin 
test. Bulletin 159. Michigan. 1898. 

M.\rshall. Killing the tubercle bacilli in milk. Bulletin 
173. Michigan. 1899. 

Mayo. Some diseases of cattle, Texas itch, blackleg, tuberculosis. 
Texas fever. Bulletin 69. Kansas. 1897. 

Moore. Bovine tuberculosis. Bulletin 225. (Cornell), N. Y. 1905. 

Nelson. On the use of Koch's lymph in the diagnosis of tubercu- 
losis. Report of the biologist. New Jersey. 1893. 

Nelson. Experimental studies of the Koch test for tuberculosis. 
New Jersey. 1895. 

Nelson. The suppression and prevention of tuberculosis of cattle 
and its relation to human consumption. Bulletin 118. New Jersey. 1896. 

Nf^om. Tuberculosis of cattle. Bulletin 50. S. C. 1900. 
Paige. History of tuberculosis in a college herd. Use of tubercu- 
lin in diagnosis. Bulletin 26. Massachusetts. 1S94. 



230 JOHNE S DISEASE 

Pearson. Tuberculosis of cattle. Bulletin 29. Penn. 1S94. 

REVNOtDS. Bovine tuberculosis. Bulletin 51. Univ. of Minn. 
Agric. Exp. Station. 1896. 

RisSELL. Tuberculosis and the tuberculin test. Bulletin 40. 
Wisconsin. 1S94. 

Russell. The history of a tuberculous herd of cows. Bulletin 
78. Wisconsin. 1899. 

Russell. a lesson in bovine tuberculosis. Bulletin 114. Wis- 
consin. J 904. 

Russell. Two ways of treating tuberculosis in herds. Bulletin 
136. Wisconsin. 1905. 

Russell and Hastings. Bovine tuberculosis in Wisconsin. 
Bulletin 84. Wisconsin. 1901. 

Stalker and NilES. Investigation of bovine tuberculosis with 
special reference to its existence in Iowa. Bulletin 108. Iowa. 1S95. 

Thorne. Bovine tuberculosis. Bulletin 108. Ohio. 1899. 

Van Es. Bovine tuberculosis. Bulletin 77. North Dakota Agri- 
cultural Experiment Station. 1907. 

Williamson and Emery. Tuberculosis and its prevention. 
Bulletin 117. N. C. 1895. 



johne's disease 

Synonyms. Pseudo-tuberculosis ; chronic bovine pseudo- 
tuberculous enteritis ; La diarrhee chronique du boeiif. 

§ 158. Characterization. Johne's disease is an intes- 
tinal disorder supposed to be due to acid-fast bacteria. It is 
characterized b}' a diarrhea, gradual emaciation and the pres- 
ence of large numbers of acid-fast bacteria on the surface of 
and in the mucous'membrane of the affected portions of the 
intestine. The distal part of the ileum is usually the most 
involved. 

§ 159. History. Johne and Frothingham described a 
disease in 1895 in which the intestinal mucosa contained large 
numbers of acid-fast bacteria. They thought it was a case of 
tuberculosis in a cow due to the avian tubercle bacterium. In 
1903 Markus called attention to its frequent occurrence in 
Holland. Since that time it has been recognized in Belgium, 



MORUID ANATOISIY 



231 



Switzerland, Denmark and England. A few cases have been 
observed in this country. Sir John M'Fadyean has proposed 
the name Johne's disease for this affection. 

j^ 160. Etiology. The cause of this disease is suppo.sed 
to be an acid-fast bacterium which is found in large numbers 
in the affected mucosa, and also in the mesenteric and colic 
lymphatic glands. Morphologically this organism closely re- 
sembles the tubercle bacterium. It varies in size from i to 2/.< 
in length and a few are said to attain to 4//. It stains uni- 
formly but occasionally the longer forms show alternating 
stained and unstained segments. It is remarkably acid-fast. 

According to M'Fadyean this organism is not inoculable 
to either guinea pig or rabbits. It has as yet not been culti- 
vated on artificial media. 

This bacterium apparently does not form a strong cell 
poison and hence the absence of necrosis. On the other hand 
the tissues appear to be almost powerless to restrain its multi- 
plication and invasion. 

The period of i7icubatioti is not known. 

§ 161. Symptoms. The first symptom to be observed 
is a loss of flesh, although the appetite remains normal. The 
hair becomes roughened and the animal presents an unthrifty 
appearance. Diarrhea soon sets in. As a rule, the diarrhea 
is profuse and persistent from the time it begins, although it 
may sometimes be checked temporarily by giving dry food 
and by the administration of astringents. 

S 162. Morbid anatomy. The lesions are primarily in 
the small intestines, but, as a rule, involving the large intes- 
tines, before death takes place. The distal part of the small 
intestines is most involved. The lesion is in the mucous 
membrane and even in seriously ill animals it is the only 
lesion that has been found. In some cases the acid fast bac- 
teria invade the submucosa in which ca.se the wall of the in- 
testine becomes thickened. In proportion to this thickening 
the mucosa shows more or less coarse wrinkling. I'lceratiou 
is not ob-served, and there is very little congestion. 



232 JOHNE S DISEASE 

The mesenteric lymphatic glands ma}- be slightly en- 
larged. When cut an appreciable amount of water-like liquid 
exudes from the surface. The absence of congestion has been 
noted. 

The most striking feature of the disease is the slight 
tissue changes even when the bacteria are exceedingly num- 
erous. In sections made at right angles to the mucous sur- 
face of the intestine an irregularity in the size and outline of 
the villi can be observed. Some of the villi may be partially 
denuded of epithelium. In the glandular layer the inter- 
stitial tissue between the tubular glands may be increased in 
amount and the glands may show evidence of atrophy. In 
sections stained by the Ziehl-Neelsen method, with Pappen- 
heim's stain for contrast, M'Fadyean states that those parts 
in which the bacilli are numerous have an appearance verj' 
similar to that of a genuine tuberculous lesion just before the 
onset of necrosis and caseation, that is, they appear to be 
mainly made up of the so-called epithelioid cells, with occa- 
sionally a well formed giant cell. Sometimes the outlines of 
these epithelioid cells are distinct, but, as a rule, wherever the 
bacilli are numerous there appears to have been a partial fusion 
of the cell bodies, and the appearance is that of a sort of matrix 
substance with imbedded nuclei. The majority of these 
nuclei are vesicular but shrivelled or distorted in appearance, 
and they stain lightly as compared with anj^ of the nuclei in 
the surrounding normal tissue. According to M'Fadyean, 
the important points to notice are that the diseased tissue is 
never sharply delimited and that there is no actual necrosis, 
although the appearance of the new tissue may be interpreted 
as indicating that the cells are on the point of losing their 
vitality. Within the parts which contain large numbers of 
bacilli there are also sometimes recognizable small round com- 
pact nuclei, apparently belonging to cells of the lymphocyte 
type, and at their margins there are numerous cells whose 
bodies stain red with Pappenheim's stain. 

The bacilli do not appear to be specially intra-cellular ; 
many of them seem to be lying free, and others appear to be 



PREVENTION 233 

situated within the fine reticulum of the villi. The structural 
alterations are everywhere proportional to the number of 
bacilli, which indicates that, contrary to what is the case in 
tuberculosis, the bacilli have little or no tendency to degener- 
ate and disappear from the older lesions. The bacilli when 
numerous are generally arranged in clumps or groups, and 
these often form a very large part of the epithelioid areas. 

The lesions in the lymphatic glands have a similar his- 
tology. They may be present either in the cortex or the 
medulla, but they are not tuberculous in the anatomical sense. 
A small number of giant cells may be present. 

The course of the disease varies from a few weeks to 
several months. It seems to be fatal in most cases. 

§ 163. Differential diagnosis. This affection is to be 
differentiated from tuberculosis and parasitic enteritis. The 
non-virulence of the organism for guinea pigs is the most 
reliable differential test between it and the bovine tubercle 
bacteria The finding of these acid- fast bacteria and the 
absence of distinct lesions and parasites would distinguish it 
from the other. As this disease is liable to occur in conjunc- 
tion with genuine tuberculosis, great care must be exercised 
in making the diagnosis. In some of these cases reported 
there appears to have been such a mixed infection. 

§ 164. Prevention. Johne's disease must be regarded as 
one which results from infection and from infection only. 
M'Fadyean states that in all the cases which have come under 
his observation there was a history of similar cases on the 
farm in several instances extending back over a period of 
many years. During the advanced stages of the disease large 
numbers of the bacilli must be voided with the feces, and m 
all ordinary circumstances there are ample opportunities tor 
infection from this source. In this way both pasture and 
other materials as well as drinking water may become seriously 
contaminated. At the present moment there is no knowledge 
with regard to the resistance of the bacilli outside the body. 



234 OVINE CASEOUS LYMPH-ADENITIS 

or the length of time that a contaminated pasture may be 
dangerous. 

In the present state of knowledge the question of preven- 
tion is an extremely difficult one in the case of farms on which 
the disease has existed for a number of years. The isolation or 
destruction of diseased and suspected animals should be prac- 
ticed. If in stables the feces passed by diseased or suspected 
animals ought to be burned. Cattle should be kept off from 
pastures in which such animals have run. As the time during 
which the bacteria remain alive outside of the body is not 
known, it is impossible to indicate the period during which 
infected pastures are dangerous to other cattle. 

REFERENCES. 

1. Bang. Chronische pseudotuberculose Darmentziindung beim 
Rinde. Berliner TieriirzUiche Wochenschrift, 1906, p. 759. 

2. BORGEAUD. Schweizer Archiv. f. Tierheilk., (1905), p. 221. 

3. JOHNE AND FroThixgham. Ein eigenthiimlicher Fall von 
Tuberkulose beim Rind. Zeitschrijt fur Thiermedicin, Vol. XXI 
(1894), p. 438. 

4. LiENAUX AND EeckhouT. Contribution a 1' ^tude d'une 
entente tuberculeuse speciale et de la diarrhee chronique du boeuf. 
Aniiales de Medecine Veterinaire, Vol. LIV (1905), p. 65. 

5. Markus. Zeitsch.f. Tiermediciv , Bd. VIII (1904), P- 68. 

b. M'Fadyean. Johne's disease ; a chronic bacterial enteritis of 
cattle. Jour, of Compar. Path, atid Thera., Vol. XX (1907), p. 48. 



OVINE CASEOUS I.YMPH-ADEXITIS (PSEUDO-TUBERCULOSIS 
IN SHEEP). 

Synonyms. Pseudo-tuberculosis ; ca.seous adenitis. 

§ 165. Characterization. Caseous lymph-adenitis is a 
disease of adult sheep which until recently was designated as 
pseudo-tuberculosis. It has been characterized by an enlarge- 
ment of one or more lymphatic glands, which contain foci of a 
greenish-yellow, caseous or purulent substance. It is rarely 
found in young animals. The mortality is very low, due 



ETIOLOGY 



235 



perhaps to the fact that the sheep are slaughtered before the 
disease has time to develop. It does not occur in epizootic 
form although it is more prevalent in certain localities than in 
others. 

sj 166. History. The name "ovine caseous lymph 
adenitis" was proposed by Norgaard and Mohler in 1899. 
These writers found the lesions and the accompanying micro- 
organism to correspond with those described by Preisz and 
Guinard in 1891 as pseudo- tuberculosis. The bacterium was 
fully described by Preisz in 1894. The organism has been 
found and identified from a large variety of lesions in a number 
of species of animals. It appears that at least many of the 
casesof lymphatic gland enlargement in sheep heretofore called 
pseudo-tuberculosis belong to this disease. Gilruth prefers the 
name pseudo-tuberculosis. Cherry and Bull describe it as 
caseous lymphatic glands and Sivori as caseous broncho-pneu- 
monia, the bacterium of Preisz being found as the probable 
cause in each case. 

§ 167. Geographical distribution. In the United 
States this disease is quite common in certain districts in the 
western and southwestern states. It exists in South America, 
New Zealand, Australia and Europe. 

Sivori found that 10 per cent of the old sheep killed in 
Buenos Ay res were affected. The prevalence of the disease in 
the United States is indicated by the reports of the federal 
meat inspectors, which show that of 16,000,000 sheep slaugh- 
tered in Chicago, Kansas City and South Omaha 3,236 were 
condemned for caseous lymph-adenitis or lesions which might 
be confounded with it. It is reported by an inspector from Los 
Angeles that of 950 sheep coming from a certain district, 82 
were suffering from lymph-adenitis. 

§ 168. Etiology. Caseous lymph-adenitis is caused by 
a specific microorganism first described by Preisz as the 
bacillus of pseudo- tuberculosis. Its description shows it to 
vary in size to such a degree that its polymorphism is said to 
be characteristic. It is non-motile and hence belongs to the 



236 



OVINE CASEOUS LVMPH-ADEXITI5 



genus Bacterium. It is aerobic, facultative anaerobic, stains 
readily and does not produce spores. It develops readily on 
ao-ar when this medium is inoculated from the caseous material 




Fig. 56. Bacterium of Preisz. Bacterium in pus cells 1-12 obj . 
4 ocular [Gilruth). 

from the affected glands. It is pathogenic for mice, guinea 
pigs and rabbits. The organism isolated by Gilruth seems to 
have been more virulent than the one isolated by Xorgaard 
and Mohler. 

§ 169. Symptoms. In the majority of cases no symp- 
toms of any importance are observed in the affected animals 
during life. The course of the disease is that of a chronic 
affection and the pathological changes develop so slowly that 
no general or local interference with the health of the affected 
animals is observed in lambs and sheep that are bred and 
raised for mutton and are marketed before they are two years 
old. Only in breeding ewes and wethers does the disease 
advance to a degree which makes it clinically recognizable 
without the aid of manipulation. The affected animals upon 



SYMPTOMS 237 

examination show an enlargement of one or more ot the 
superficial glands, the precrural and the sub-scapular glands 
being most often involved. The animals thus affected appear 
in every other respect to be in perfect health. In the older 
animals, the wethers and breeding ewes, the same glands may 
be enlarged to a considerable degree, reaching the size of a 
hen's egg or even larger. Some of these sheep may show a 
certain degree of unthriftiness or even emaciation. The 
disease is found in its most advanced stages in the older ewes, 
which is probably due to the fact that the wethers are gener- 
ally disposed of before they are three years old, while a good 
breeding ewe is frequently retained for seven or eight years. 
In such old animals the superficial lymphatic glands may be 
enlarged to such a degree as to interfere with locomotion, 
while the deeper seated glands and those of the body cavities 
are similarly affected. In the advanced cases the lesions often 
become disseminated by metastasis to the principal organs of 
the body. In such cases the disease may assume the appear- 
ance of chronic broncho-pneumonia or pleurisy, with occa- 
sional cough, slight dyspnea and increasing emaciation and 
anemia. The course of the disease is exceedingly slow. For 
this reason owners of affected flocks are often totally ignorant 
of the presence of the disease. This fact renders it very diffi- 
cult to obtain reliable information regarding its prevalence 
save from the statistics obtained from the slaughter houses. 
A majority of the inspectors have until recently classified the 
lesions either as tuberculosis, pyemia or abscesses. In 
response to inquiries it was found that the majority of cases 
which had been condemned under these headings were 
undoubtedly caseous lymph-adenitis. Several thousand cases 
are annually observed in the slaughter houses of the United 
States, but only a fraction of these are advanced to a degree 
that would warrant a total condemnation of the carcasses. 
Meat inspectors agree that lambs are very rarely aflfected, and 
that the progress of the morbid changes in the majority of 
cases is coordinate with the age of the animal. 



238 OVIXE CASEOUS LYMPH-ADENITIS 

§ 170. Morbid anatomy. The principal lesions are 
confined, according to the various descriptions, especiallj' that 
by Norgaard and Mohler, to the lymphatic glands. In many 
cases only a single gland is affected. The relative frequency 
with which the various glands become the seat of the lesions 




Fig. 57. The leg of a rabbit slio-unng enlarged glands after inoculation 
Ti'itli the Bacterium of Preisz {Norgaard and Mohler). 

may be given as follows : prescapular, precrural, superficial 
inguinal, bronchial, mediastinal, sub-lumbar, deep inguinal, 
and scrotal. Rarely the suprasternal and mesenteric glands 
are affected. Sivori mentions the mesenteric glands among 
those frequently affected. He fails, however, to mention the 
mesenteric glands as the seat of lesions in the detailed descrip- 
tion of twelve typical cases of caseous broncho pneumonia 
caused by the bacillus of Preisz. 

When first invaded by the bacterium, the adenoid tissue 
becomes hyperplastic and the gland enlarges to several times 
its original size. On section the surface is found to be watery, 
but otherwise the tissue retains its normal appearance. This 
is followed by the formation of various centers of degeneration 
which show concentric layers and gradually become confluent. 
Finally, the total volume of the gland is transformed into a 
homogeneous, caseous mass. At the same time the distended 
capsule increases in thickness and forms a sac which confines 
the semifluid, grumous inass. In rare instances the sac rup- 
tures and when close to the surface the contents will be dis- 
charged. Under ordinary circumstances, the caseous contents 



MORBID AXATO:\IV 239 

become cohesive and sticky and of the consistency of putty. 
In very old cases the mass becomes dry and mealy, with little 
or no tendency to calcification. The greenish yellow color oi 
the caseous mass, which is stated to be most characteristic, 
closely resembles the contents of the intestinal nodules pro- 
duced by Oesophagostoma Cohimbiaimtti. In very advanced 
cases, as for instance those of old breeding ewes, the internal 



) 



^ ' 

Fig. 58. Lung of sheep studded with nodules [Gilruth] . 

organs may contain lesions which microscopically resemble 
those of tuberculosis. The lungs may be studded with small 
nodulesthesizeof a pea, the spleen, liver and in rare instances 
the kidneys also may contain one or more foci of the same 
character, namely, a mass of greenish yellow material, sur- 
rounded by a firm, fibrous wall. There seems, however, to be 
a distinct line of demarcation between the affected and the 
healthy tissue. The bronchial and the mediastinal glands 
may be affected to a considerable extent without any lesions 
being found in the lungs. In some cases the lungs are ex- 
tensively involved. The lesions consist of nodules varying in 
size from that of a millet seed to that of a walnut. This con- 
dition is, as a rule, accompanied by a chronic pleurisy with 



240 OVINE CASEOUS LYMPH-ADENITIS 

extensive adhesions and also effusions into the pleural cavities. 

In the liver the lesions consist largely of nodules com- 
posed like those in the lymphatic glands, of a firm white 
fibrous sac containing a greenish-yellow, cheesy mass of vary- 
ing consistency. Cases have been reported, however, where 
the entire organ was filled with miliary nodules. 

The kidnej^s are rarely affected, but when they are the 
lesions assume the same characteristic appearance of a firm 
walled abscess protruding on the surface of the organ. As a 
rule, only one or two such foci are observed in each case. 

A histological examination of tissues containing miliary or 
sub-miliary nodules, shows them to be composed chiefly of 
leucocytes and nucleated round cells, the greater part of which 
are irregular in shape, especially toward the center where 
many of them are transformed into a granular detritus. 
Among the cells arranged singly or in clumps, are seen the 
short bacteria which stain irregularly. The shape varies con- 
siderably from oval or oblong to a dumb-bell shape. 

The bacteria are frequently seen within the degenerated 
leucocytes, the destruction of which is due, according to 
Preisz, to the specific chemical products elaborated by these 
microorganisms. 

The microscopic appearance is somewhat similar in all the 
lesions whether located in the lymph glands, lungs, liver, kid- 
neys or spleen. In the lungs the histological picture resem- 
bles that of broncho-pneumonia. In the liver the lesions 
originate in the portal capillaries, where the bacteria cause a 
proliferation of the endothelial cells, which, together with the 
accumulation of leucocytes and red corpuscles, cause the obli- 
teration of the vessels. In no case have giant cells been ob- 
served. The surrounding hepatic cells become swollen, then 
granular, and finally they undergo atrophy, leaving open 
spaces between them. Numerous round cells appear in the 
periphery of the nodules, which gradually undergo a connec- 
tive tissue metamorphosis and become organized into an en- 
capsulating membrane. 

When a miliary nodule from the liver of an experimental 



MORBID ANATOMY 24! 

animal, which has been destroyed three weeks after inoculation, 
is examined microsopically the following picture is observed : 
A caseous center composed of an amorphous material that does 
not take any of the ordinary stains. Surrounding the center 
may be seen numerous leucocytes more or less degenerated and 
frequently containing one or more bacteria, while clumps of 
these organisms are scattered among them. External to this 
is a dense round cell infiltration, the peripheral zone of which 
is undergoing connective-tissue formation, thus serving as a 
line of demarcation between the atrophied liver cells and the 
central cell mass. The process then repeats itself until a con- 
nective-tissue barrier strong enough to encapsulate the central 
part of the nodule and prevent its further growth is obtained. 
The nodules in the kidneys and lungs present a similar micros- 
copic appearance, excepting that the foci in the lungs are more 
regular on account of the catarrhal inflammation that accom- 
panies the reaction of the surrounding tissue. The center con- 
tains a dense mass of disintegrated cell structures composed of 
the desquamated and proliferated epithelial cells, degenerated 
leucocytes and round cells. In experimental animals which 
succumb quickly to an intravenous injection of virulent ma- 
terial, the lung tissue immediately surrounding the nodules is 
frequently seen to be hepatized. 

According to Gilruth the lesion commences by the arrest 
of the specific bacterium generally in a lymph-gland where one 
or more are surrou'nded by and included within the phagocytes. 
The micro-organisms multiply within the cell and ultimately 
cause the degeneration and death of the latter. Simultane- 
ously a slow chronic inflammation occurs around the focus of 
attack ; there is proliferation of connective tissue-cells and the 
formation of more or less new fibrous tissue. As the process 
spreads outwardly the centre degenerates, and the protecting 
wall increases in thickness. In fact, all the phenomena of the 
pathology of true tuberculosis in a gland occurs, with the ex- 
ception of the formation of giant cells. The degenerated centre 
of the nodule assumes a greenish tint, especially distinct at the 
time of exposure by the knife, but becoming gradually grayer 



242 



OVINE LYMPH-ADENITIS 



afterwards. In the centre of the older purulent or caseous 
mass (for the consistence varies from that of cream to that of 
cheese in different tumours) there are usually present no bacilli 
which can be demonstrated by the microscope or by cultural 
methods. 

§ 171. Differential diagnosis. This specific lymphatic 
affection is to be differentiated from : 

1. Infections of various kinds, not recognized as specific, 
which may cause enlargement or suppuration of lymph glands. 

2. The specific infectious diseases, such as tuberculosis. 

3. Lymphadenoma. 

If the diagnosis cannot be made from the gross appear- 
ance of the lesions a bacteriological examination will be neces- 
sary. The fact should be kept in mind that tuberculosis in 
sheep is very rare. In lymphadenitis, cultures in ordinary 
media will give a growth of the bacterium of Preisz. With 
tuberculosis the results would be negative (see tuberculosis). 
It is important not to confuse the nodular disease of .sheep's 
intestines with this affection. The location of the lesions in 
the walls of the intestine will be quite sufficient to determine 
the nodular disease. 

REFERENCES. 

1. Cherry AND Bull. Caseous lymphatic glands (pseudo -tuber 
culosis) in sheep. The Veterinarian, Vol. LXXII, p. 523. 

2. EberTH. Bacillare Nekrose der Leber. Virchow's Archiv, 
Bd. C (1885), p. 23. 

3. GiLRUTH. Pseudotuberculosis in sheep. (Lymphadenitis). 
Jour. Compar. Path, and Thera., Vol. XV (1902), p. 324. 

4. GiLRUTH. Pseudo-tuberculosis in sheep. (Lympho-adenitis). 
Bulletin No. i, New Zealand Dept. of Agriculture. 

5. NoRGAARD AND MoHLER. The nature, cause, and economic 
importance of ovine caseous lymph-adenitis. Sixteenth Annual 
Report, Bureau of Animal Industry, 1899, p. 638. (Full bibliography). 

6. Preisz AND Guinard. Pseudo-tuberculose chez le mouton. 
Jour, de mi'd. de vH. et de zootech, ser. 3, Vol. XVI (1891), p. 563. 

7. Preisz. Recherches comparatives sur les pseudotuberculoses 



SVMl'TOMS 243 

bacillaires et une nouvelle espece de pseudotuberctilose. ^hm. de l' Inst. 
Pasteur, Vol. VIII (1894), p. 231. 

8. vSivoRi. Sur une broncho-pneumonie caseouse du mouton, 
causee par le bacille de Nocard-Preisz. Rev. de mi'd. vet. ser. 8, Vol. 
VI (1899), p. 657. 



ASTHENIA IN FOWLS AND PIGEONS 

§ 172. Characterization. This is a disease especially 
of chickens and pigeons in which there is marked emaciation 
and a failure to take on flesh even when fed on the most 
nourishing food. Because of this, the disease has received the 
popular name of " going light." 

I 173. History. Although this condition or disease has 
been recognized for a long time, it seems to have been first 
described in 1898 by Dawson. He gives a brief account of the 
symptoms, morbid anatomy, etiology and a somewhat 
extended description of the specific organism which he isolated 
from the diseased chickens. The writer has studied this 
affection in pigeons but did not succeed in finding the organ- 
ism isolated by Dawson. 

§ 174. Etiology. Dawson found this disease to be due 
to the presence of a certain species of bacterium which he 
obtained in pure culture from the duodenal contents. He 
described it as Baderhim asthenice. This organism varies 
from I to 1.3// in length and about 0.5// in width with rounded 
ends. It is reported to possess the peculiarity of vegetating 
in temperatures varying from 50 to 120° F. It is fatal to rab- 
bits within 24 hours when inoculated into the abdominal 
cavity with 0.5 c. c. of a bouillon culture. Chickens inocu 
lated with this organism remained well. 

§ 175. Symptoms. The only symptoms which seem to 
be in evidence are the gradual loss of flesh and an exceedingly 
good appetite. It is reported by certain pigeon fanciers con- 
cerning pigeons and the fact is reiterated by Dawson, that the 



244 MISCELLANEOUS INFECTIONS 

disease is an exceedingly chronic one, often extending over a 
period of several months but usually terminating in death. 
In the cases reported, the fowls were well kept and given an 
abundance of nourishing food. There seems to be an inability 
on the part of the affected animal to assimilate nourishment. 

§ 176. Morbid anatomy. The most conspicuous lesion 
is extreme emaciation. According to Dawson the mucosa of 
the duodenum contains areas in which the walls are deeply 
reddened and in which the contents are of a mucoid substance. 
The writer made a number of post-mortems in pigeons suffer- 
ing from this disease without finding any gross tissue changes. 

The disease needs further investigation, but the fact that 
an organism has been found in the duodenum in large numbers, 
where it multiplies and apparently produces by-products that 
are absorbed and which interfere with the normal metabolism 
of the body, is of sufficient interest to call attention to the pre- 
liminary findings herein mentioned. It is not unlikely that if 
the present hypothesis concerning the nature of this disease is 
verified, a numberof disorders now attributed to general causes 
may be traced to some form of intestinal infection. 

REFERENCES 

I. Dawson. Asthenia (going light) in fowls. Annual Report 
of the Bureau of Animal Industry, U. S. Department of Agriculture, 
1898, p. 329. 



MISCELLANEOUS INFECTIONS 

§ 177. Diphtheria in calves and swine. Diphtheria 
of calves is an infectious disease of young calves characterized 
by the formation of a diphtheritic membrane (necrosis) on a 
greater or less portion of the mucous membrane of the mouth 
and throat. It often leads to septicemia and death. It is 
caused by the Bacterium of necrosis, described by Bang. 

The affection is quite common in Europe but it does not 
seem to be as well known in this country. 



MISCELLANEOUS INFECTIONS 



^45 



Loeffler, who investigated diphtheria of calves for the 
German Imperial Board of Health, believes that the specific 
cause of the disease is a bacillus, and not a micrococcus, as 
Daramann assumed. He found on the edges of the necrotic 
tissue large long bacteria which formed undulating threads, 
and which differed entirel}^ from the bacterium of diphtheria of 
man. Ritter confirmed the observations of Loeffler. On the 
other hand, Kitt regards the cause of diphtheria of calves to 
be the bacillus of necrosis. 

Swine suffer from a diphtheritic necrosis of the upper por- 
tions of the digestive canal and air passages. Johne seems to 
have been the first to point out the diphtheritic character of 
this necrosis. He was not able to demonstrate its cause 
although the bacillus of necrosis was found on the mucous 
membranes. Swine suffering from hog cholera frequentlj^ have 
areas of necrosis in the gums, tongue and other parts of the 
mouth. 

Kitt believes that there occurs sporadically an independent 
diphtheria of pigs which has no connection with swine fever. 
He believes its cause is the bacillus of necrosis, which occurs 
also in diphtheria in calves. The mucous membrane of the 
tongue, cheeks, phar3-nx and stomach shows yellow-white 
caseous deposits ; and that of the small intestine and colon, 
diphtheritic necrosis. 

The bacterium (bacillus) of necrosis has been found to be 
pathogenic for many species of animals. Mohler {Pro. Am. 
Vet. Med. Asso., 1905, p. 181) has pointed out the extent of the 
pathological activities of this organism in cattle, sheep, goats, 
antelope, several varieties of deer, horses, asses, hogs, kan- 
garoos, dogs, chickens, pigeons, rabbits, guinea pigs and mice. 
The extent and variety of the lesions it produces have sug- 
gested the term necrobacillosis for the lesions it initiates. 



CHAPTER VI. 



DISEASES CAUSED BY BACTERIA 
GENUS BACILLUS 



§ 178. General discussion of the genus bacillus. 
The genus Bacillus in Migula's classification includes all rod- 
shaped ynotile bacteria. In the older classifications it includes 
both non- motile and motile forms. The fixing upon motility 
as an essential generic character, and thus restricting the 
genus Bacillus to motile forms, is the occasion of some con- 
fusion between the genera Bacterium and Bacillus as applied 
to a number of important disease-producing bacteria. It is 
customary to speak of the Bacillus of anthrax, of tuberculosis 
and of glanders rather than of the Bacteritivi of these affections. 
As in the genus bacterium, there are a number of species of 
bacilli that are widely separated from each other. The 
diseases which they produce give very different pictures both 
clinically and in their morbid anatomy. 



HOG CHOLERA 



Syyiotiyms.'^ Swine fever ; pneumo-enteritis ; pig ty- 
phoid ; Svinpest. 

§ 179. Characterization. The distinguishing features 
of this disease are a continuous fever, ulceration of the intes- 



*This disease is known popularly by a large number of names and 
in some works on swine diseases many of them are employed. The 
more common of these are enteric fever, typhus carbuncular fever, 
carbuncular gastro-enteritis, carbuncular typhus, pig distemper, blue 
sick7iess, blue disease, purples, ted soldier, a>ithra.x fever, scarlatina, 
measles, diphtheria and erysipelas. Many of the terms appear to refer 
to some one or more of the observed symptoms or lesions. 



HISTORY 247 

tines, and more or less discoloration of the skin, especially 
over the ventral surface. 

>^ 180. History. The earliest outbreak in this countr\^ 
of which there is knowledge of a disease supposed to be hog 
cholera, occurred in the state of Ohio in 1833. It is presumed 
that it was brought from Europe with some of the animals 
imported from there for breeding purposes. After being intro- 
duced, it spread at first slowly, but later with increasing 
rapidity along the lines of commerce, until it invaded every 
part of this country where swine raising had become an 
industry. The disease was investigated and very carefully 
described by Dr. C. Sutton, of Aurora, Ind., from 1850 to 
1858. In 1861, Dr. Edwin M. Snow, of Providence, R. I., 
contributed an important paper on this disease to the U. S. 
Department of Agriculture. In 1875, Dr. James Law, of 
Ithaca, N. Y., 'furnished to the same Department a valuable 
paper setting forth the symptoms and morbid anatomy of this 
disease. He believed it to be contagious although the specific 
organism had not been found. The U. S. Commissioner of 
Agriculture appointed in 1878 nine men for a period of two 
months each to investigate the disease in various localities. 
In their report the symptoms and morbid anatomy formerly 
described were confirmed and two additional features set 
forth. Law showed that it was transmissible by inoculation to 
other animals, and Dr. Detmers described a microorganism 
which he called Bacillus suis and which he believed to be the 
specific cause of the trouble. Later, Detmers described his 
organism as a micrococcus. The work of investigation was 
continued under the direction of the Commissioner of Agricul- 
ture and finally, in 1885, the specific organism was discovered 
by Salmon and Smith, who described its essential characters 
and properties. It was called Bacterium of swine plague. 
Since that time the disease has been under investigation and 
the Bureau of Animal Industry has during the last few years 
been actively engaged in the efforts to produce a specific, 
therapeutic serum. 

In 1886, Dr. Theobald Smith discovered another bacterial 



240 HOG CHOLERA 

disease among swine. It was found to be similar to the 
German Schzveineseuche ho\.\i in the morbid anatomy and in 
the morphology and properties of its specific organism. In 
naming this disease the Bureau of Animal Industry called it, 
on account of its similarity to the German Sc/i-weiyieseiic/ic, 
swine plague and its organism the bacillus of swine plague, 
and changed the name of the disease described in 1885 to hog 
cholera and its organism to the bacterium"-^ of hog cholera. 
The changing of the name of the first disease described from 
swine plague to hog cholera has been the cause of some 
criticism and it has been credited with the responsibility of 
creating confusion. It has, perhaps, led hasty readers to a mis- 
interpretation of these diseases and their relation to those de- 
scribed in other lands under different names. While the names 
assigned may not have been especially happy ones, the trans- 
fer of the term swine plague from the intestinal to the lung 
disease must be considered as a fortunate occurrence and one 
which tended to simplify and not to confuse. 

Billings, of the Nebraska State Experiment Station, 
opposed this nomenclature. He not only refused to accept 
the change and to continue to write about hog cholera under 
the title of swine plague, but he denied the existence of the 
swine plague, as described in the reports of the Bureau of 
Animal Industry for 1886 and subsequently, as an indepen- 
dent disease. The wide dissemination of his publications on 
this subject has unquestionably been responsible for much of 
the haziness concerning the di.stinguishing features of these 
maladies. 

In 1893, Drs. Welch and Clements read a paper before the 
International Veterinary Congress in which they gave a very 
clear history of the nomenclature of these diseases and in 
which they adhered to the one of the Bureau of Animal In- 
dustry. 

§ 181. Geographical distribution. Hog cholera is 

*In 18SS the genus Bacterium was changed to Bacillus and this 
organism is spoken of since that time as the hog-cholera bacillus. 



ETIOLOGY 



249 



widely disseminated throughout the central part of the United 
States. It exists, however, to a certain degree in every state 
in the Union and in Canada. It has long been known in 
Great Britain. It prevails to a greater or less extent on the 
continent of Europe. The confusion that has arisen in the use 
of the terms swine plague and hog cholera renders it difficult 
to determine, from the brief description given in a number of 
reports, the nature of the disease in question. 

^ 182. Etiology. The specific disease, here described as 
hog cholera, is caused by Bacillus cholerae suis/^ A brief des- 
cription of its morphology, physiological properties and patho- 
genesis are appended. 



0, . • , ' 






>;-• 









Fig. 59. A photoo:rapli of ihc hacilliis 0/ /lo,^- cholera 7vith I hi' Jlagella 
slained. X aboiil loon diiunc/ers. 

*Moore described a bacterium found in a pii;, from which the swine 
plague organism was also obtained, that possessed the cultural and 
pathogenic properties of the hog-cholera bacillus. More recenlly. 
Smith has described a similar organism, which was isolated by Burrell 
in Illinois. 



250 



HOG CHOLERA 



Morphology.— .\ rod-shaped organism varying in size according to 
the medium in which it is developed. From agar cultures it is from 
1.2 to 1.8// long and from .5 to .8// broad. The ends are rounded. 

Spores have not been observed. It is actively motile. A variable 
number of flagella have been demonstrated but usually there are from 
3 to 5. The length of the flagella varies. The average seems to be 
about 7// although filaments 55// with an average length of 35 to 40/; are 
reported by Ferrier. It stains readily with the aniline dyes. Prepara- 
tions made from cultures usually stain uniformly ; while in the prepara- 
tions made from the tissue of inoculated animals there is frequently 
exhibited a light center with a deeply stained periphery. 

Cultural characters and biochcmic properties. — The bacillus is 
grown readily on all of the ordinary media used in bacteriological work 
at a temperature of 30 to 38° C. It is aerobic and facultative anaerobic. 

Agar.— On the surface of inclined agar after 24 hours at a tempera- 
ture 37° C. a grayish, glistening nonviscid growth appears. When 
isolated the colonies are nearlj- round, convex, 0.5 to 2.0 mm. in diame- 
ter. The edges are sharply defined and even. In stab cultures a grayish 
growth develops along the needle track with a more vigorous growth 
on the surface about the needle puncture. The growth reaches its max- 
imum in about 48 hours. 

Gelatin. — In this medium the growth is moderately feeble, the 
colonies appearing as grayish dots. When magnified they are finely 
granular and of a yellowish tint. The quantity and form of growth 
depend considerably upon the reaction of the gelatin. If decidedly 
alkaline there is often a tendency for the growth to spread. There is no 
softening or liquefaction of the medium. 

Potato. — The growth on potato takes the form of a very thin, glis- 
tening layer. It is usuall}- of a faintly yellowish color but this is sub- 
ject to variation on different potatoes. If the reaction is strongly acid 
no growth appears. 

Bouillon. — In alkaline bouillon it imparts in 24 hours a uniformly 
cloudy appearance to the liquid. Ordinarily there is no membrane on 
the surface. After some days' standing the growth begins to settle, 
forming a grayish, friable sediment. If the bouillon contains muscle 
sugar the reaction will be changed to acid, in from 24 to 48 hours, due 
to the fermentation of the sugar. Later, however, the liquid will 
become strongly alkaline, unless there was too much muscle sugar 
present. In acid bouillon the growth is less vigorous. It grows better 
in a bouillon containing peptone than in a simple beef broth. 

Milk. — When the milk is acid in the beginning it gradually 
becomes alkaline. There is no precipitation or coagulation of the 
casein, .\fter standing for from two to three weeks in an incubator a 



KTIOLOC.V 251 

gradually developing opalescence of the milk can be observed. Later 
it becomes clear, then light brownish in color. If allowed to stand 
longer in the incubator the volume of the culture shrinks by evaporation 
and the opalescent liquid becomes quite thick and dark-colored but not 
viscid. When the opalescence appears the milk is strongly alkaline. 
The process seems to be a form of saponification of the fat globules due 
to the presence of the alkali produced by the bacteria. 

I,uhil. — \n Dunham's solution the growth is quite feeble. Ordi- 
narily no indol reaction is obtained, although it has been observed in a 
few cultures obtained from different epizootics. 

Gas production.— In peptonized bouillon containing i per cent 
dextrose, gas appears within 24 hours and continues to form for from 
three to five days. During the first day from one-fourth to one-half of 
the total quantity is produced. By the end of the second day the gas 
formation is nearly at an end. The total amount which collects in the 
closed branch of the fermentation tube is equivalent to about one-half 
of the capacity of this branch. The gas set free is composed of CO._, and 
an explosive gas which consists largely of H. The ratio of CO., to H in 
the fermentation tube is approximately as 1:2. The reaction of the 
liquid becomes strongly acid, which condition checks the multiplication 
of the bacteria. 

Gas is not produced in bouillon containing lactose or saccharose. 
These sugars are not fermented. Alkaline cultures containing them 
become more strongly alkaline as the growth continues. 

Thermal reactions.— 1V\^ organism grows very feebly at a tempera- 
ture of 20° C. It will not thrive at a temperature above 43° C. It is 
destroyed when exposed to moist heat at 58^ C. for 10 minutes. 

Disinfectants.— This organism is destroyed after an exposure for 10 
minutes or less in the following solutions: 

Carbolic acid, i per cent. Hydrochloric acid, 1-5 of i per cent. 
Sulphuric acid, 1-20 of i per cent. Sulphate of copper, 1-4 of i per cent. 
Formalin, i to 2,000. Trikresol, 1-2 of i percent. 

Lime is also a good disinfectant when used in preparations contain- 
ing about I per cent CaO. 

Drying.— This bacillus resists drying for a variable length of time, 
according to the amount of protection it has. In a drop of a bouillon 
culture dried on a cover-glass and kept under bell jars, the vitality is 
retained for from 5 to 8 days. In bits of animal tissue containing the 
bacilli, the vitality is retained for from 20 to 40 days, according to the 
quantity of tissue taken. 

Pathogenesis.— ^nhcvit&we^ous injections of from i to 3 c. c. rarely 
produce fatal results in swine. An intravenous inoculation of 5 c. c. 
usually produces a septicemia. With smaller doses the "button ulcers" 



252 HOG CHOLERA 

characteristic of hog cholera have been produced (Welch). By feeding 
pigs with pure bouillon cultures the intestinal lesions typical of hog 
cholera have also been obtained (Smith). 

Rabbits inoculated subcutaneously with o.i c. c. of a bouillon cul- 
ture die in from 5 to 8 days. The essential lesions consist of necrotic 
foci in the liver and a very much enlarged and dark colored spleen. 
Guinea pigs are affected similarly to rabbits, but death does not usually 
occur until from 7 to 12 days. Pure cultures of the bacillus can be 
obtained from the blood, liver or spleen of the inoculated animals. 

While the above description applies to the form most 
frequently encountered, varieties are not uncon)mon. In 1894 
Smith called attention to several varieties of this species. It 
is interesting to add, that Reed and Carroll have found the 
bacillus isolated bj' Sanarelli, and thought by him to be the 
cause of yellow fever, to belong to this group of bacteria. 

In 1903, de Schweinitz and Dorset published the discovery 
of a disease practically identical in its manifestations with hog 
cholera of an acute type, but which was produced by a virus 
that passed through the finest porcelain filters. It is possible, 
therefore, that the disease now known as hog cholera may be 
differentiated into two maladies, one caused by B. cholerae suis 
and the other by the "invisible virus " McClintock, Boxraeyer 
and Siffer report like results in the production of a disease with 
the filtrate. These authors were unable to find the hog-cholera 
bacillus in the cases from which they obtained the invisible 
virus. This suggests that they are dealing with a new disease 
rather than with a new etiological factor for hog cholera. 
Until this infectious filtrate is obtained from animals from 
which pure cultures of B . cholerae suis were isolated from the 
organs, it seems unfortunate to consider it the cause of hog 
cholera. The experimental results obtained with ^. cholerae suis 
are too convincing to relegate it, without sufficient evidence, to 
the role of a secondary invader. 

More recently Dorset, Bolton and McBryde have con- 
firmed the earlier publication by de Schweinitz relative to the 
filterable virus. They state, however, that " it must be ad- 
mitted that a disease in hogs may exist which is due to 
B. cholerae sjiis, and which has no connection with the filterable 



SVlNIP'rOMS 



253 



virus found by us in the outbreaks we have studied." They 
believe, however, that such a disease " would be possessed of 
a low degree of contagiousness." 

Tin period of incubatiou varies from 7 to 14 days. Berry 
states that it varies from one to three weeks and perhaps 
longer. 

§ 183. Symptoms. The symptoms of hog cholera are 
by no means constant. The best informed writers on the sub- 
ject agree that hog cholera can not, with certain exceptions, 
be positively diagnosed from the symptoms. Animals suffering 
from various intestinal troubles frequently exhibit symptoms 
which very closely resemble those of this disease. 

There are two recognizable forms, namely, the acute, and 
the chronic or mild form. In the acute disease, the animals 
die very suddenly after a few hours' or at most a few days' 
sickness. In the other form, the disease runs a longer course. 
There is usually a rise of temperature of from i to 3° F. 

The sick animals act dumpish and spiritless and lie quietly 
in a corner or huddle together, usually concealing the head in 
the litter. They refuse to move when disturbed and are more 
or less oblivious to their suffering. The appetite varies. In 
acute cases the animals may eat quite heartily up to within a 
few hours before death. In more chronic forms they eat fairly 
well until the end. There may or may not be diarrhea. Fre- 
quently the bowels are costive. It is quite common in these 
cases to have an active diarrhea during the last few days. The 
color of the discharge depends largely on the food. Vomiting 
rarely occurs. The changes in the respiration and the pulse 
are difficult to determine. There is rarely any cough. Usually 
there is considerable reddening of the skin on the nose, ears, 
abdomen and on the inside of the thighs and public region. 
Occasionally this reddening is very marked. The redness is 
diffuse and becomes more intense as death approaches. In 
some cases there is a discharge from the eyes. In the chronic 
form the animal becomes emaciated. These symptoms vary 
to such an extent that it is .sometimes necessary to make a 



254 



HOG CHOLERA 



post-mortem examination and even the diagnosis must often 
be delayed until the results of a bacteriological examination 
have been obtained. It not infre- 
quently happens that swine suffering 
from hog cholera are attacked with 
swine plague, the two diseases co- 
existing in the same animal. 

§ 184. Morbid anatomy. The 
acute type. This might with equal 
propriety be called the hemorrhagic or 
septicemic type, inasmuch as the chief 
nd perhaps the only obvious changes 
are hemorrhagic in nature. They are 
more con.spicuous when an animal is 
examined immediately after death. 
The spleen is variably enlarged, soft, 
and gorged with blood. Sometimes 
it is twice as long as normal and the 
other dimensions are proportionately 
increased. It may extend across the 
median line to the right side. Next 
to the spleen, the lymphatic glands 
and the serous membranes are most 
^ti^^ r /V severely involved. The cortex of the 
glands appears on section as a hemor- 
rhagic line or band, according to the 
amount of extravasated blood, or the 
entire gland may be infiltrated with it. 
Among the glands most commonly 
hemorrhagic are those of the meso- 
colon, those at the root of the lungs, 
and on the posterior thoracic aorta. 
Besides these, the retro-peritoneal and 
the gastric glands may be involved. 
More rarely the mesenteric glands show slight blood extrava- 
sations. Hemorrhages are also quite frequent beneath the 
serous surfaces of the abdomen and thorax. They are most 




Fig. 60. Ulcers in the in- 
testine of a pig dead of 
hog cholera. 



MORHID ANATO-MV 



255 



abundant as petechiae and larger patches under the mucous 
membrane of the large and small intestines. They are occa- 
sionally found under the peri- 
toneum near the kidneys, the 
diaphragm and the costal pleura 
as extravasations nearly an inch 
in diameter. 

The lungs, in a small per- 
centage of cases, show subpleural 
ecchymoses in large numbers 
and on section small hemor- 
rhagic foci are observed through- 
out the lung tissue. In a feu- 
cases severe hemorrhages involv- 
ing one or more lobes have been 
observed. The kidneys are oc- 
casionalh^ the seat of extensive 
hemorrhagic changes. The 
glomeruli appear as blood red 
points; larger extravasations 
occur in the medullary substance 
and blood may collect around 
the apices of the papillae. The 
subcutaneous tissue over the 
ventral surface of the body may 
be dotted with petechiae and oc- 
casionally collections of blood 
(hematomata) are found in the 
superficial muscular tissue. The 
brain and spinal cord have not 
been generally examined. In 
one case, petechiae were ob- 
served on the cerebellum. 

The digestive tract usually 
is the seat of extensive lesions. 
The fundus of the stomach is as a rule deeply reddened ; there 
may be more or less hemorrhage on the surface, giving rise to 




Fig. 61. Spleens of pigs oj thc 
same age ; {a) dead from hog 
cholera, [d) normal {killed in 
health). 



256 HOG CHOLERA 

larger areas of blood clots. In some cases the small intestine 
has submucous ecchymoses throughout its entire length. In 
the large intestines these may be so numerous as to give the 
membrane a dark red appearance. The intestinal contents are 
now and then incased in a layer of blood clot. 

The chronic form is perhaps the most common, at least in 
those epizootics which have been reported. The acute hemor- 
rhagic cases usually die in the beginning of the outbreak and 
are apt to be overlooked. Following these are the more pro- 
tracted ones. In these animals the disease may be limited in 
its manifestations to the large intestine, although the other 
organs are not exempt from degenerative changes. These are 
due in part to the impairment of the functions of the large 
intestine, consequent fermentations and the absorption of the 
poisonous products elaborated by the specific bacilli in the 
spleen and other organs. 

The lesions of the large intestines are necrotic and ulcera- 
tive in character. The ulcers may be isolated and appear as 
circular, slightly projecting masses, stained yellowish or 
blackish or both in alternate rings, or they may be slightly 
depressed and somewhat ragged in outline. When the super- 
ficial slough is scraped away many ulcers show a grayish or 
white base. A vertical section reveals a rather firm neoplastic 
growth, extending usually to the inner muscular coat. When 
sections of such an ulcer are stained with aniline dyes and ex- 
amined under the microscope, the submucous tissue is very 
much thickened, infiltrated with rounds cells and containing a 
large number of dilated vessels. Resting upon this thickened 
submucosa, is a line of very deeply stained amorphous matter 
and upon this is situated the necrotic mass which fails to retain 
the coloring matter and which is permeated by a very large 
number of bacteria of various kinds. Frequently the eggs of 
trichocephalus are imbedded in the slough. 

The extent of the submucous infiltration depends upon 
the age of the ulcer. In old ulcers it contains many newly- 
formed capillaries, and evidences of the formation of connective 
tissue are present. The capillaries may extend to the very 



MORBID ANATOMY 257 

edge of the border where the slough begins. The latter may 
have been parti}' shed, leaving a smooth line bounding the 
cicatricial tissue. The submucous infiltration gradually disap- 
pears toward the periphery of the ulcer and slightly outside of 
the ulcer no inflammation of the membrane exists. Giant cells 
have been observed in the intertubular tissues at the edge of 
the ulcer. The depth to which the infiltration extends is not 
always limited to the submucosa ; it may extend into the 
muscular coats and cause inflammatory thickening and in- 
flammation and the formation of new vessels in the subjacent 
serosa. 

In some cases the necrosis, instead of appearing in circum- 
scribed ulcers from one-sixteenth to one-half inch or more 
across, involves the whole surface of the mucous membrane, 
giving it the appearance of a so-called diphtheritic membrane. 
In such cases the walls of the intestine are very much thick- 
ened and so friable as to be easily torn with the forceps in 
handling them. Such necroses are rare in epizootic cases, but 
they frequently appear in animals which have been fed with 
pure cultures of hog-cholera bacilli. 

The distribution of the ulcers varies but slightly. The}' 
appear most frequently in the cecum and on the ileo-cecal 
valve, as well as in the upper half of the colon. The lower 
half is implicated in severe cases only and then less extensively. 
The rectum is rarely ulcerated. The lower portion of the 
ileum is ulcerated in a small percentage of animals, especially 
when they have been fed with hog cholera viscera or cultures. 
The stomach is occasionally the seat of slight ulceration. 
The lymphatic glands of the affected intestine are usually 
much enlarged, pale, tough and whitish on sections. The 
spleen is rarely enlarged. The liver shows degenerative 
changes. The heart and lungs are usually normal. The 
broncho-pneumonia frequently found in young pigs in the 
winter months must be ascribed priniaril\- to exposure rather 
than to the presence of hog cholera. 

In some outbreaks the acute and the chronic types are 
not so clearly separated as indicated in the foregoing pages. 



258 HOG CHOLERA 

Frequently recent hemorrhagic lesions seem to be associated 
with cases presenting extensive ulcerations, which certainly 
are much older than the extravasations. It may be that the 
latter are the result of a secondary invasion of the hog-cholera 
virus, either from the ulcers in the intestine or from without. 
To illustrate more fully the difference in the lesions of the two 
forms of the disease, the published post-mortem notes of two 
cases are appended. 

(i) Acute fortn. Female, two years old, weight about 150 pounds. 
She had been known to be sick but a few hours. The examination was 
made two hours after death. A little blood was oozing from the nostrils. 
The skin was not discolored. Upon section the skin was normal in 
appearance. The liver was deeply reddened, due to engorgement of the 
blood vessels. Blood flowed freely upon section. The spleen was 
slightly enlarged and dark colored The kidneys were hyperemic, 
especially the medullary portion. In the pelvis of the right kidney 
there was a large blood clot. The mucous membrane of the intestines 
was normal with the exception of several irregular areas of hyperemia. 
In the fundus of the stomach was a large, dark blood clot. No ulcers. 
The mesenteric glands were enlarged and darker than normal In a few 
cases the cortex was hemorrhagic. The right lung was in a state of 
hyperemia. The heart contained very little liquid blood. 

Bacteriological examination. — A few bacteria were found in stained 
<;over-glass preparations from the spleen aud liver. Tubes of slant agar 
were inoculated with bits of the tissue from the hyperemic lung, liver, 
spleen and kidneys. These tubes developed cultures of the hog-cholera 
bacillus. A few of them were pure cultures ; the others contained, in 
addition to the hog-cholera organism, a quite large bacillus. (Report 
N. Y. State Com. Agric. 1887). 

(2) Chronic form. Small female, weight about 20 pounds, Con- 
siderable reddening of the skin over the ventral aspect of the body and 
limbs ; especially marked along the median line. Superficial inguinals 
enlarged, of a mottled, pale and deep red color on section. Spleen 
very large, 12 inches long, 2 inches broad, and five-eighths to three- 
fourths inches thick at the hilus ; gorged with blood, friable. A small 
number of punctiform hemorrhages in cortical portion of the kidneys. 
Glands of mesentery and colon enlarged and congested. Deep redden- 
ing of several square inches of mucosa fundus of stomach. Large intes- 
tine contains a semi-liquid mass chiefly earth. Four large ulcers in the 
cecum, one of them at least one inch across, covered by a yellowish 
slough ; the peritoneum covering it is thickened and inflamed. In 
upper colon there is considerable necrosis, involving the epithelium in 



DIFKKRHNTIAL DIACiNOSIS 259 

patches. Ivungs normal, excepting the right ventral lobe, which is 
solid. Bronchi and air cells of this lobe completely occluded by plugs ; 
surface bright red, mottled with yellowish points — the ultimate air cells 
filled with the cellular exudate. Subpleural ecchymoses over both 
lungs. From the spleen a liquid and a gelatin culture contained only 
hog-cholera bacteria. They were very numerous in cover-glass prepar- 
ations from this organ. 

A rabbit inoculated from the consolidated lung tissue died on the 
seventh day. At the point of inociilation a pasty mass extends to abdo- 
men, only subcutis involved. Spleen engorged. Single acini in the 
liver are completely necrosed, yellowish white. In both organs, hog 
cholera bacteria. Cultures from spleen pure. (Report on hog cholera, 
1889). 

The duration of the disease varies. In the acute septi- 
cemic type it ma}' not be more than a few hours or a day at the 
longest. In the chronic form it lasts from one to two weeks, 
sometimes longer. 

The prognosis is noi good. Berry states that recoveries 
are not rare. Although there are outbreaks where the mortality 
reaches from Soto loo per cent, there are others of a milder 
type where the fatalities do not exceed 50 per cent. 

§ 185. Differential diagnosis. Hog cholera is to be 
differentiated from a great variety of dietary disorders and 
poisoning from alkalies and possibly from other chemicals 
which may get into their food. * Powdered soap has been 
found to produce, when given in sufficient quantities, a series 
of symptoms quite similar to those of hog cholera. In addi- 
tion to the many as yet etiologically undetermined disorders 
often producing a high mortality and popularly called hog 
cholera, infectious pneumonia or swine plague and tuberculosis 
are to be distinguished. 

It sometimes happens that swine when kept under good 
hygienic conditions suffer from disorders which in their symp- 
toms resemble hog cholera, but anatomically the lesions are 
varied and irregular. A few such enzootics have been studied. 
A few have been described. In one instance B. coli communis 
seemed to stand in a casual relation to the trouble. Recently 
the writer has studied two similar enzootics where several 



26o HOG CHOLERA 

animals died and where the lesions were very few and exceed- 
ingly varied. .In some of them there were healing, intestinal 
ulcers. The bacillus isolated belonged to the paracolon 
group.* It may be supposed that possibly many of these 
mild cases (enzootics) are modified hog cholera. At present, 
however, such a conclusion does not seem to be fully justified. 

The dietary disorders are determined b}- their history, the 
irregularity of the lesions, and the failure to find the specific 
organism of hog cholera in the tissues of the dead animals. 
An important feature is the fact that the trouble does not 
extend beyond the herd or herds first attacked or animals fed 
and kept under like conditions. The amount of loss from 
these troubles is very large. They are very often confused 
with and mistaken for hog cholera. 

Hog cholera must also be differentiated from a new disease 
recently described by de Schweinitz, which resembles acute 
hog cholera symptomatically, but which is caused by an 
unknown organism that passes through a Chamberland filter. 

The differentiation of hog cholera from swine plague 
depends upon the specific bacteria. While in typical, chronic 
cases the intestinal lesions in hog cholera and the lung affec- 
tions in swine plague are sufficient to distinguish the nature of 
the disease, in many cases the variations of the lesions are such 
that diagnoses must depend upon the bacteriological findings. 
The essential differences between the two species of bacteria 
are brought out in the comparison appended. 

Bacillus of hog cholera. Bacterium of s-cvine plague. 

1. Rod-shaped organism with i. Elongated oval organism 
ends rounded, 1.2 to 2.0// in 0.8 to 1.5 /< in length, 0.6 to o.8/< 
length, 0.5 to 08// in width. The in thickness. The size varies ac- 
size varies according to the stage ^°''^\"-? ^o the stage of growth and 

p ,, J J- • • J .,., division and the culture media. 

ot growth and division and the , j , 

,^ ,. 2. From old cultures it usually 

culture media. . . ,. , ,.,. 

_ ... stains entirelv. when m process 

2. From cultures it stains en- ^^ division as found in the organs 
tirely . In tissues it usually stains of freshly dead rabbits the extrem- 
around the periphery leaving a ities stain leaving an unstained 
light centre. central band, "polar stain." 



*It differed from the hog-cholera bacillus in not saponifying milk. 



DIFFERENTIAL DIAGNOvSIS 



261 



3. Actively motile in liquids. 

4. From 3 to 9 flagella are 
demonstrable. 

5. Vis<orous growth in alkaline 
nutrient liquids. Less vigorous if 
liquids are acid in reaction. 

6. Moderate growth on potato. 
(Varies according to reaction). 

7. Distinct growth on gelatin. 

8. Saponifies milk in from 3 to 
4 weeks. 

9. Ferments dextrose with the 
formation of acids and gas. 

10. Does not ferment lactose. 
Bouillon containing it becomes 
strongly alkaline. No gas. 

11. Does not ferment saccha- 
rose. Bouillon containing it be- 
comes strongly alkaline. No gas. 

12. Destroyed by moist heat at 
58° C. in 15 minutes. 

13. Dies in water in from 2 to 4 
months. 

14. It dies in the soil in from 2 
to 3 months. 

15. Rabbits injected subcutane- 
ously with o.i cc. of a bouillon 
culture of a virulent bacillus will 
die in from 5 to 7 days. Enlarged 
spleen, necrotic foci in liver. 

16. Rabbits inoculated with cul- 
ture of an attenuated variety live 
from ID to 20 days or recover. The 
lesions are enlarged spleen and 
infiltration of the follicles in 
Peyer's patches. 

17. In guinea pigs the lesions 
are practically the same as in rab- 
bits. Death occurs in from 7 to 12 
days. 



3. Not motile in li(|uids. 

4. No flagella have been found. 

5. (rrowth moderate or feelile 
in alkaline nutrient liquids. No 
growth if liquids are acid. 

6. No growth on potato. 

7. Feeble or no growth on 
gelatin. 

8. Produces no apparent change 
in milk. 

9. Ferments dextrose with the 
formation of acids but no gas. 

10. Does not ferment lactose. 
No gas. 

XI. Ferments saccharose with 
the formation of acids. 

12. Destroyed by moist heat at 
58° C. in 7 minutes. 

13. Dies in water in from 10 to 
15 days. 

14. It dies in the soil in from 4 
to 6 days. 

15. Rabbits injected subcutane- 
ously with o.oi cc. of a bouillon 
culture of a virulent bacillus will 
die in from 16 to 20 hours. 
Septicemia. 

16. Rabbits inoculated with a 
culture of an attenuated variety 
will live from 4 to 10 days. The 
lesions are local infiltration of pus 
cells with pleuritis, pericarditis or 
peritonitis. 

17. Guinea pigs are slightly 
less susceptible than rabbits. There 
is more local reaction. Death oc- 
curs in from i to 4 days. 



262 HOG CHOLERA 

i8. Pigs are not usually af- iS. Pigs are not usually affected 

fected by subcutaneous injection by the subcutaneous injection of 

of small quantities of culture. If small quantities of culture. The 

the pigs are killed within i to 3 bacilli are not found except in the 

weeks the bacilli are found in the local lesion. In a few cases fatal 

local lesion and certain of the lyni- results are reported, 
phatic glands. Fatal results are 
reported in a few cases from these 
injections. 

19. Feeding cultures to pigs 19- Feeding cultures to pigs 
which have fasted for 24 hours pro- usually produces no effect. 
duces extensive intestinal lesions 

with fatal results. 

20. Intravenous inoculation in- 20. Intravenous inoculation in- 
to pigs causes either an acute sep- to pigs usually produces a septic 
ticemia or a chronic form of the form of the disease which kills in 
disease in which are produced from i to 2 days. Inoculation into 
quite typical round, firm, elevated the lungs causes pleuritis, usually 
ulcers. accompanied by pneumonia. 

Dawson pointed out the .serum reaction as a possible 
means of diagnosis. This test, however, seems of little value 
until the disea.se has run a course of many days. 

v^ 186. Prevention. As hog cholera is caused by a 
specific organism, the first fact to be determined is to find the 
channel or means by which it can be carried from an infected 
to a non- infected herd. The thorough investigations which 
have been made in the United States Bureau of Animal Indus- 
try have shed much light upon this subject. The observations 
of more recent years have confirmed the conclusion reached in 
the earlier reports of the Bureau concerning the means of 
spreading this disease. With these results, the pointing out 
of the ways by which the virus may be disseminated and the 
methods necessary for checking its spread is no longer ques- 
tionable and there is a certainty that it can be kept away from 
individual herds even in the midst of widespread epizootics. 
A few of the common means of its dissemination are worthy of 
note. 

I. The virus of hog cholera is frequently introduced into 
a non-infected locality by the purchase of animals, usually for 



PREVENTION 263 

breeding purposes, from herds in which this disease exists or 
has existed within the preceding few months. These animals 
are usually placed among the home raised swine without quar- 
antine, thus affording every possible facility for starting up a 
new outbreak. The reason for this is clear. 

2. The bacteria can be carried in the dirt on the animals 
or, as is most usually the case, the pigs may have been but 
recently infected and being transferred during the period of 
incubation they develop the disease later. It not infrequently 
happens that the purchased animals are actually suffering 
from a chronic form of the disease, to which they eventually 
succumb but meantime infect others. In purchasing swine, 
therefore, it is of the greatest importance that the history ot 
the herd should show that it had been free from infectious 
disease for at least one year. In addition to this, newly 
purchased swine should not be placed immediately after ship- 
ment in the pens with the home stock, but they should be kept 
in a separate enclosure until all danger of the disease has 
passed. 

3. Swine are often shipped in crates, boxes or in open 
cars in which hogs affected with hog cholera have previously 
been confined. The history of hog cholera contains many 
illustrations of this method of contracting the disease. 

4. The bacilli of hog cholera live for a considerable time 
in water. On this account the bacteria from outbreaks which 
start at or near the source of a creek or small river may be 
carried in the current and infect animals which wallow in the 
stream many miles below. By keeping swine in a small en- 
closure away from infected streams and fields the disease is 
often prevented. 

5. The bacilli of hog cholera can be carried in the dirt 
which adheres to one's shoes or to farming utensils. It not 
infrequently happens that the virus of this disease is carried 
from farm to farm on the tools taken from an infected place. 

6. The virus may be carried by buzzards, crows and 
other birds. There is no po.sitive proof that the virus has been 



264 HOG CHOLERA 

disseminated in this way although there is much evidence to 
support such a theory, particularly in the South. Several out- 
breaks have been attributed to this method of introducing the 
virus. The hypothesis emphasizes the necessit}'^ for promptly 
disposing of the dead animals instead of leaving them as prey 
for scavengers. If they cannot be burned it is best to cover 
the bodies with a liberal amount of lime and bury them. 

When healthy hogs are separated from those suffering 
with the disease it is a safe precaution to dip them in a disin- 
fectant to kill any hog-cholera bacteria that may be upon the 
exterior of the body. 

§ 187. Specific treatment. A large number of inves- 
tigations have been made to find a protective vaccine for this 
disease and also to find a specific serum treatment. Thus far 
satisfactory experimental results have not been obtained. In 
a number of instances, where the practical application of the 
"serum treatment" has been made, most satisfactory results 
followed, but the reports fail to give evidence of an accurate 
diagnosis of the disease treated. In these cases, the better 
management of the animals, in addition to the serum, would 
suffice to check the disease if the trouble was of a dietary 
nature. There is need for additional investigation along these 
lines. 

REFERENCES. 

1. Berry. Swine fever. Jour. Compar. Path, and Thera.,\o\. 
XV (1902), p. I. 

2. Billings. Bulletins Neb. Agric. Expt. Station, iSSS. Also 
many special publications and contributions to various veterinary 
journals. 

3. Dawson. The serum diagnosis of hog cholera. Nezv York 
Med. Jour., Feb. 20, 1897. 

4. DE SCHWEiNiTz. The production of immunity in guinea pigs 
from hog cholera by the use of blood serum f lom immunized animals. 
Annual Report of the Bureau of Animal Industry, U. S. Dept. of 
Agric, 1898. 

5. DE ScHWEiNiTz AND DORSET. A form of hog cholera not 
caused by the hog cholera bacillus. Circular No. 41, U. S. Bureau of 
Animal Industry, 1903. 



TKTANUS 265 

6. DoRSKT, Bolton and McBrvdh. The etiologj- of hog cholera. 
Bulletin No. j2. Bureau of Animal Industry^ U. S. Defii Agric 
1905- 

7. PETERS. Serum therapy in hog cholera Bulletin No. ^7, 
Uuir. of Neb. Agric. Exper. Station, 1897. 

S. Salmon AND vSmith. Annual Reports of the Bureau of Ani- 
mal Industry, 1885-1895. 

9. Salmon. Special report on hog cholera, its history, nature and 
treatment. U. S. Bureau of Animal Industry, iii8^. 

10. Smith. Zur Kenntniss des Hog-cholera Bacillus. Central- 
hlattfiir Bakter. u. Parasitenkunde, Bd. IX ( 1891), S. 253. 

11. Smith. Hog cholera group of bacteria. Bulletin No. 6, U. 
S. Bureau of Animal Industry, 1894, p. 9. 

12. Smith and Moore. Experiments on the production of 
immunity in rabbits and guinea pigs with reference to hog cholera and 
swine-plague bacteria. Ibid., -p. 41. 

13. Reed and Carroll. Bacillus icteroides and Bacillus cholerae 
suis. A preliminary note. The Medical News, Apr. 29, 1899. 

14- Welch. Report of investigations concerning the causation of 
hog cholera, fohns Hopkins Hospital Bulletin, Nov. i, 1889. 

15- Welch and Clements. Remarks on hog cholera and swine 
plague. First International Veterinary Congress of America held in 
Chicago. III.. October, 1893. 



TETANUS 

Synonyms. Lockjaw; trisnuis. 

?^ 188. Characterization. Tetanus is an infectious dis- 
ease (toxemia) is which the specific organisms are locahzed at 
the place of inoculation. It is characterized by spasmodic con- 
traction of the muscles referable to the nervous system and 
by the absence of obvious tissue changes. It is the result of a 
specific wound infection. All mammalia including man are 
susceptible. It occurs most frequently in horses, asses and 
mules ; next to them in the smaller ruminants such as the 
sheep and goat ; it appears least often in the dog. It is re- 
ported to occur rarely in birds and fowls are supposed to be 
immune. The human species is very susceptible. 



266 



§ iSg. History. Tetanus is one of the diseases that 
was recognized and described before the Christian era. It 
was not clearly differentiated until the discovery of its specific 
cause in 1884. 

§ igo. Geographical distribution. Tetanus is reported 
to be more prevalent in the hot climates than in the temperate 
ones, while in the very cold latitudes it is rarely if ever en- 
countered. It is more frequently met with in some districts 
than in others. Although very common in certain localities, 
it is, on the whole, a somewhat rare disease. There seem to 
be no statistics by which its frequency can be determined in 
this country, but in certain of the European armies this has 
been noted. In the Prussian army, it is reported to occur 
once in a thousand cases of sickness among horses. At 
Wiirtemberg, Hering reports it once in 3000 ca.ses of disease 
among the horses in the cavalry. It has also been noted that 
in some veterinary hospitals it does not occur for long periods, 
while at other times several cases may appear in rapid succes- 
sion. It is, however, a wide spread disease. 

§ igi. Etiology. Te- 
tanus is caused by a slender 
bacillus 2 to 5 // in length. 
It forms spores which are 
at the end of the organism 
giving it somewhat the ap- 
pearance of a pin. On 
account of this it has been 
designated the "pin bacil- 
lus." It is anaerobic. 
This organism was first ob- 
served by Nicolaier in 1885, 
although Carle and Rat- 
tone showed in 1884 that 
this disease could be transmitted from man to animals by inoc- 
ulation with the pus from the local lesion. In 1889, Kitasato 
isolated the bacillus and studied it in pure culture. This 




Fig. 62. Bacillus teiani. 



ETIOLOGY 267 

bacillus stains readily with the aniline dyes, especially with 
carbolfiichsin. It takes the Gram stain. It grows well in 
nutrient gelatin, agar or bouillon and on blood serum at the 
temperature of the body and in an atmosphere of hydrogen or 
in the absence of air as in deep agar cultures. The addition of 
a little grape sugar facilitates its growth. It has the distinc- 
tion of producing the most powerful (poisonous) toxin of any 
known bacteria, 0.23 of a milligram being estimated as a fatal 
dose for a man of 175 pounds weight. 

The fact that this bacillus is an anaerobe renders its culti- 
vation of little practical value in diagnosing the disease. Al- 
though it is not distributed in the body, it can usually be 
found in cover-glass preparations, made from the local lesion 
and stained with carbol fuchsin. 

Bacillus tctaiii is found in the soil. It has been found in 
hay dust, in the mortar of old masonry, in the dust in rooms, 
barracks and hospitals and in the arrow poison of certain 
savages in the New Hebrides. They obtain it by smearing 
their arrow heads with mud from crab holes in the swamps. 
It is reported that certain savages in Africa destroy their 
enemies by putting bits of broken glass mixed with certain 
soils in their shoes. The cause of death is tetanus. Mold 
rich in horse manure seems to be the most favorable abode for 
it. It has been stated that it exists in all soils. There are 
good reasons for believing that this is an over-estimate of the 
wideness of its distribution. It certainly is more numerous in 
some localities than in others. 

The tetanus bacillus is very resistant, especially in its 
spore form, to destructive agents such as drying and the 
ordinary disinfectants. Kitasato found that a 5 per cent solu- 
tion of carbolic acid applied for ten hours failed to kill the 
spores. Tizzoni and Cattani found that mineral and organic 
acids produced no effect upon the dried spores, von Behring 
found that iodine trichloride possesses a strong antiseptic effect 
upon them. They are not affected by the gastric fluids. It 
has been noted by Kitt that the dried spores in pus have 
retained their virulence for sixteen months. They are de- 



268 TETANUS 

stroyed when subjected to a temperature of ioo° C. in water or 
steam for ten minutes. The bacilli in the vegetative state are 
readily destroyed by the usual strong disinfectants, such as 5 
per cent carbolic acid. 

A number of bacilli closely resembling B. tetani have been 
described. This renders a careful study of the suspected 
organism necessary, as it is difficult in some cases to determine 
B. tetani microscopically. The guinea pig inoculation affords 
a ready means of differentiation whenever fresh material is 
available. 

§ 192. Mode of infection. As the bacillus of tetanus 
is widely distributed in the soil and consequently on articles 
contaminated with it, the most common modes of infection are 
punctures, scratches, and pricks made hy splinters, nails or 
infected instruments (traumatic tetanus). It may follow 
slight abrasions of the skin where infected earth comes in con- 
tact with the lacerated epidermis. Infection through wounds 
in the intestinal mucosa do not seem to have been clearly dem- 
onstrated. The most usual method seems to be by pricks 
and nail punctures, in which case the virus can be carried well 
into the living tissue and there is little or no bleeding to wash 
it out. Infection often occurs in young foals and lambs 
through the freshly broken umbilical cord (tetanus neon- 
atorum). 

The period of incubation. The shortest period which 
seems to be reported is a few hours and the longest is six 
weeks. In horses the period of incubation is usually from four 
to twenty days. After inoculation with pure cultures it is 
from four to five days and in sheep from two to four days. In 
guinea pigs inoculated with infected soil the incubation period 
is usually not over forty-eight hours and often less than that. 
Park has found that mice, guinea pigs, rabbits, rats, 
horses, goats and a few other animals inoculated with pure 
culture have a period of incubation of from one to three days. 
In man it varies from one to twenty days. There are, how- 
ever, a few exceptionally long periods reported. It has been 



SY:\ii"r()Ms 269 

noted by Richter and others that the shorter period of iucuba- 
tion the more severe the disease, tlie mortality being over 90 
per cent in the first and about 50 per cent when the symptoms 
were slow in appearing. 

§ 193. Symptoms. The first symptoms are often 
obscure and may be overlooked for several daj's or they may 
be ushered in suddenly with violent and extensive tonic 
spasms. The tetanic spasms usually begin in the muscles of 
the head and neck, extending from these to the muscles of the 
throat, trunk and extremities. It often happens that the 
spasms first appear in the hind quarters and extend forward. 
There is stiffness of the parts affected. If in the head, the 
muscles of mastication are first attacked with spasms, while if 
the hind quarters are first attacked, there are usually spasms 
of the muscles of the tail. The muscles at the site of inocula- 
tion are frequently the first to show spasms and, if the disease 
is of a mild type, they may be the only ones to exhibit symp- 
toms. Friedberger and Frohner have grouped the muscles 
which are attacked with the more obvious effects upon the 
appearance of the animal. They are as follows : 

1. The rmiscles of viastication. The contraction of these 
muscles is called trismus or "lockjaw." According to the 
degree of contraction, the jaws remain in more or less close 
contact, rendering prehension or mastication difficult or 
impossible. 

2. The other muscles of the head. These are spasmodi- 
cally contracted in different degrees. Spasms of the muscles 
of the ears cause the ears to be "pricked" and their tips to be 
drawn together ; of the recti muscles of the eyes, cause the 
eyes to be retracted in the orbit with protrusion of the nictitat- 
ing membrane ; of the nose, produce dilatation of the nostrils ; 
of the dilator of the upper lip, give an abnormal shape to the 
opening of the mouth. The muscles of the tongue, of degluti- 
tion and of the larynx are also usually attacked by spasms. 

3. The exteyisor muscles of the neck. Contraction of these 
muscles causes a stiff, outstretched carriage of the head and 



270 



TETANUS 



"ewe neck." The muscles of the neck become hard and tense 
to the touch. 

4. The extensor muscles of the back. Spasms of these 
muscles are manifested by an extremely hard condition of the 
muscles of the back, loins and croup. Several conditions may 
arise : orthotonous in which the neck is stretched out and the 
back and croup are carried horizontally, or opisthotonous in 
which the head is raised or drawn back and the vertebral 
column slightly depressed. This is the most common occur- 
rence. There may be a lateral curvature of the cervical verte- 
brae which is uncommon and also a convex curvature of the 
vertebrae which is very rarely observed. The tail, especially 
in horses, is often raised and occasionally said to be straight 
with the back. 

5. The jmiscles of the limbs. The spasms in these muscles 
make the limbs stiff and cause the animal to assume an attitude 
in which the fore legs are extended forward and laterally and 
the hind ones backward and laterally. They are bent at the 
joints only with difficulty. The contraction of the muscles of 
the abdomen gives the animal a tucked up appearance and the 
spasms of the muscles of respiration render breathing difficult. 

Besides the spasms the animal shows an increased reflex 
irritability and heightened sensibility. These manifest them- 
selves in excitement, timidity and intensified muscular con- 
tractions if irritated. Sweating is common, especially in severe 
cases. In mild cases it may be absent. There is usually 
little or no change in the internal temperature. In fatal cases 
the temperature is usually constantly high toward the last. 
The high temperature (104° to 106° F.) usually continues for 
some time after death. Bayer has observed in a horse. 24 
hours before death, a temperature of 102° F. ; one and a half 
hours before death, 105° F. ; at the moment of death, 111° F. ; 
and fifty minutes after death, 113° F. There is frequently no 
increase in the number of pulse beats until severe exacerba- 
tion sets in. The frequency of the pulse is much greater in 
animals which continue recumbent than in those which keep 
upon their feet. The pulse is often hard and small and the 



MORHID ANATOMY 27 I 

walls of the arteries are spasmodically tense. In many cases, 
however, it is full, soft and easily compressible. There is, as 
a rule, an increase in the number of respirations, which may 
become very high if the respiratory muscles are attacked. 
The number varies according to the excited condition of the 
animal. The respirations may increase four fold without a 
corresponding increase in the pulse beat. The breathing may 
reach from 80 to 100 per minute. In character the respirations 
are shallow on account of the fixed condition of the ribs and 
the spasms of the muscles which compress the abdomen. 
There may be cyanosis and catarrh of the nasal mucosa, 
coughing and in fatal cases symptoms of hyperemia and edema 
of the lungs and often pneumonia (usually aspiration in 
nature). There is constipation due to lack of peristalsis and 
the rigid condition of the muscles which compress the 
abdomen. Micturition becomes less frequent and more difii- 
cult. Complete retention of urine is said to occur in some 
cases. The urine has a high specific gravity and occasionally 
contains albumen. Some animals can eat readih' while others 
eat, if at all, with great difficulty. They like to play with 
drink set before them and often try to satisfy their thirst, 
which seems to increase as the disease advances. In fatal 
cases the animals seem to be perfectly conscious to the last. 
They seem to be possessed of a feeling of terror. 

v^ 194. Morbid anatomy. The gross examination of 
the tissues at post-mortem of animals dead from tetanus is 
usually negative. It has been pointed out by Goldscheider 
and Flatau that in experimental animals there are certain 
characteristic changes in the motor cells of the anterior horns 
of the spinal cord which in the order of their development 
depend upon the concentration of the toxin or virulence of the 
bacteria injected and upon the duration of the disease. The 
changes are primarily an enlargement of the nuclei, which at 
the same time become more distinct ; then follows an enlarge- 
ment and disintegration of Nissl's cell-granules with an 
enlargement of all of the nerve cells. These investigators also 



2^2 rHTAJNUS 

found that where antitoxin had been used it had a distinct 
retarding influence upon these changes. They found like 
lesions in the spinal cord of a human subject dead of tetanus. 
Very similar results have been obtained by Matthes, Westphal, 
Goebel and others. The lesions point to the anterior horns of 
the spinal cord as the primary seat or origin of the tetanic con- 
tractions. The changes pointed out above are said by 
Moschowitz to be characteristic of tetanus and constantly 
found. The motor ganglia cells of the anterior horns of the 
spinal cord seem at present, therefore, to be the most likely 
source of the spasms, due apparently to a specific affinity 
between those cells and the tetanus toxin. It is possible to 
explain also the local spasms on this hypothesis as the toxin 
elaborated by the nerves terminating in the affected region. 
The experiments of Tizzoni and Cattani suggest the possibility 
of such a theory. There is, however, need for further investi- 
gation on this subject. 

A considerable number of lesions may be found elsewhere 
in the body, none of which can be considered as characteristic 
of the disease, but which are secondary to the tonic contrac- 
tions. The blood, owing to lack of oxidation, may be dark 
colored, tarry, of a greasy appearance and tardy in coagula- 
ting. There may be numerous ecchymoses and sanious exu- 
dates in the subserous and mucous membranes. The lungs 
may be variously affected according to the extent of the trouble 
with the respiratory muscles. Thus congestion, edema, 
hemorrhages, pneumonia, emphysema and hypostatic conges- 
tions have been described. In the heart there are usually epi- 
and endocardial hemorrhages. The muscles may contain 
hemorrhages. The fibers of the muscles may show cloudy 
swelling, a loss of the transverse striae and changes 'in the 
nuclei. The liver may be swollen and abnormally yellow in 
color. The hepatic cells often show fatty degeneration. The 
spleen is often swollen, it may be engorged with blood or soft 
and flabby. The kidneys may or may not show degenerative 
changes. The bladder is usually distended with urine and its 
mucous membrane is often sprinkled with ecchymoses. The 



nil'l'KRKNTIAL DIAGNOSIS 



273 



digestive tract may show areas of cougestion and ecchymoses. 

The duration of the disease varies in different species and 
in different individuals of the same species. In the horse it 
may last for two or three days only or it may continue for 
several weeks. In cattle the course is usually less rapid, but 
it rarely runs longer than two weeks. In sheep it usually 
terminates fatally within a week and often in two or three 
days. 

i^ 195. Differential diagnosis. Tetanus, while possess- 
ing quite characteristic symptoms, may be mistaken for a 
number of other affections or specific diseases. Among those 
which should receive special attention are cerebro-spinal men- 
ingitis and rabies (for the symptoms and lesions see those dis- 
eases), rheumatism, eclampsia, catalepsy, convulsions in the 
newly born and pyemic polyarthritis in lambs and foals. 

The symptoms of tetanus which are perhaps the most 
diagnostic are (i) the continuous tonic spasms of different 
groups of muscles, (2) the apparent clearness of mind (if we 
may attribute such a quality to animals), and (3) the absence 
of fever in the beginning of the symptoms. The general atti- 
tude of the animal is also of much value. If the infected 
wound can be found, it is often possible to obtain cover-glass 
preparations in which the tetanus bacilli can be found. Nega- 
tive results are in this case not to be considered as final, for it 
is practically impossible to make these examinations suffi- 
ciently thorough to be sure of the absence of these bacilli, if 
they are not found. If they are found the diagnosis may be 
considered as positive. 

In poisoning with strychnine, there are symptoms which 
at first may be more confusing. This form of poisoning 
usually occurs in dogs where tetanus is rare, and again in 
strychnine poisoning the suddenness of the attack, the rapidity 
of the course and the increased reflex irritability are valuable 
diagnostic features. In differentiating tetanus from other 
affections in the newly born, the bacteriological examination 
of cover-glass preparations made from the end of the umbilicus 
may be of much a.ssistance. 



274 TETANUS 

§ 196. Prevention. Owing to the wide distribution of 
tetanus bacilli, precautions can consist only of the careful and 
thorough disinfection of all wounds. With animals at pas- 
ture, it is impossible often to know of the wounds until it is 
too late to apply this measure. In stables where the disease 
becomes prevalent, the floors and siding should be thoroughly 
disinfected and special watchfulness exercised to find at the 
earliest moment any injury by which infection could occur. 
The practitioner should learn as soon as possible the tetanus 
infected lands and stables in his community and, knowing 
these, give wise instruction to his clients to take such precau- 
tions as are possible. In case operations are to be performed 
on animals in such stables an immunizing dose of tetanus 
antitoxin may be administered. This practice is followed in 
many places in Europe. If the present knowledge of this 
disease is properly availed of, there should be only occasional 
cases which as yet there seems to be no way to avoid. 

§ 197. Tetanus antitoxin. It was first pointed out by 
von Behring and Kitasato that animals could be made immune 
to tetanus by using cultivations of the tetanus bacilli which 
had been attenuated with iodine trichloride. The blood serum 
of such immunized animals has the power to immunize healthy 
animals against the disease and to render the toxin in animals 
affected with tetanus inert. The antitoxin is prepared now, 
however, by injecting horses with the filtrate of bouillon 
cultures, either alone or with a quantity of antitoxin. After 
the first dose the animal becomes tolerant to a certain degree 
so that by repeated and constantly increasing doses complete 
resistance to the toxin is acquired. When this point is 
reached the serum usually possesses a strong antitoxic power. 
As a practical remedy for the disease in animals the recorded 
results from the use of this antitoxin are somewhat contradic- 
tory. In human practice the results are similar. Mosch- 
cowitz has collected 290 cases in man where it has been used 
subcutaneously, with 173 recoveries and 117 deaths or a 
mortality of 40.33 per cent. In a total ot 48 cases where the 



REFERENCES 275 

antitoxin was injected intracerebrally 23 recovered and 25 
died, a mortality of 52.08 per cent. 

Some interesting experiments suggested by Krokiewitz 
directed toward the finding of a specific treatment consist in 
the injection of an emulsion of brain substance. Primarily 
this method of treatment is based upon the hypothesis, set up 
by Goldscheider and Flatau, who, as a result of their research 
came to the conclusion that "The morphological changes in 
the nerve cells are the expression of a chemical process, i. e., 
of the chemical combination of the toxins with the nerve 
cells. Every nerve cell possesses atom groups which have a 
certain aflSnity for the atom groups of the tetanus toxin and 
are able to combine with them." Wassermann and Takaki 
substantiated this hypothesis experimentally. These observers 
injected into experimentally tetanized animals an emulsion of 
spinal cord, obtained from a freshly killed animal, to test, if 
possible, whether the nerve cells of the dead animal also have 
this affinity for the tetanus toxin, like the nerve cells of the 
living animal. By this experiment, they have come to the 
conclusion that every part of the nervous system, particularly 
the brain of the examined animals including man, has a 
definite and positive tetanus antitoxic power ; and that the 
injection of normal brain substance into experimentally 
tetanized animals has the power to save life. Further work in 
this direction is necessary to fully demonstrate the efficiency 
of this procedure. 

REFERENCES. 

1. vonBehring uxd KitasaTO. Ueber das Zustandekommeii 
der Diphtherie-Immunitat und der Tetanus-Immunitat bei Thieren. 
Deutsche Med. Wochenschrift, Bd. XVI (1890), S. 113. 

2. KiTASATo. Uber den Tetanusbacillus. Zeit. f. Hygiene, Bd. 
VII (18S9), S. 225. 

3. KiTASATO. Experimeutelle Untersuchuugen iiber das Tetanus- 
gift. Zeit. f. Hygiene, Bd. X (1891), S. 267. 

4. MoscHCowiTZ. Tetanus, a study of the nature, excitant, 
lesions, symptomatology, and treatment of the disease, with a critical 
summary of the results of serum therapy. Studies from the Depart- 



276 BLACK LEG 

merit of Pathology of the College of Physicians and Surgeons, Columbia 
Umversity, Vol. Vll (i8<)g-igoo}. (M. gives pathology and antitoxin 
treatment, summary of cases and full bibliography. ) 

5. McFari<and. Tetanus and vaccination. The Jo urua I of Med- 
ical Research, Vol. VII (1902), p. 474. (New Series Vol. II). 



BLACK LEG 



Synonyms. Black quarter; symptomatic anthrax; quar- 
ter ill; quarter evil; gangrenous emphysema; charbon sympto- 
matiqjie; Raiischbrauii. 

§ ig8. Characterization. Black quarter is an acute 
infectious disease of cattle characterized by the development 
of an emphysematous swelling of the subcutaneous tissues and 
mu.scles. These lesions are usually located upon and ordinarily 
extend over the greater part of a hind quarter or of a shoulder. 
The disease does not spread from animal to animal by simple 
contact but the infection takes place apparently from a com- 
mon source, the soil. The virus seems to exist in the soil in 
certain localities only. Like tetanus, it is a disease following 
a wound infection. 

Symptomatic anthrax is a disease of cattle, sheep and 
goats, although the two latter species are rarely attacked. 
Guinea pigs are very susceptible to inoculation. It is reported 
that horses, asses and white rats develop local lesions when 
inoculated subcutaneously with the virus. Other animals seem 
to be immune. In cattle, it rarely occurs in the very young, 
under six months, and in adults after the fourth year. 

§ 199. History. It is supposed that black quarter has 
existed for hundreds of years, although it was not until late in 
the last century that it was positively differentiated and recog- 
nized as a distinct and specific 'disease. The descriptions 
given to many of the earlier epizootics designated as anthrax 
correspond more exactly with the present knowledge of black 
quarter than they do of anthrax. 

In 1782, Chabert classified the various anthracoid dis- 



HISTORY 277 

eases recognized at that time into three groups, ( i) anthrax 
fever, where the disease manifested itself without external 
swelling, (2) true anthrax, where the lesions consisted at 
first of small, hard and very painful swellings followed or 
accompanied by fever and other general symptoms, and (3) 
symptomatic anthrax, where the swelling was preceded by a 
rise of temperature, loss of appetite and symptoms of general 
depression. This classification was held for nearly a century. 
BoutroUe, in 1797, refers to a disease which he called mal de 
adsse (quarter evil ) because it affected the animal in the thigh. 
Viborg described the disease in Denmark, where it has long 
been known to the laymen and designated by them as raslcsyge 
("rattle disease" ). Its clinical features were very accurately 
described by Walraff in 1856. In 1879, Arloing, Cornevin and 
Thomas proved the causal relations of a certain microorganism 
to this disease and thus established its specific nature. A 
year later (1880) they described the specific microorganism 
and demonstrated that the disease could be produced by inocu- 
lating susceptible animals with it. Since that time both the 
organism and the disease itself have been studied by many 
investigators. In this country, it has been under investiga- 
tion during the last few years by the Bureau of Animal 
Industry. 

§ 200. Geographical distribution. Black quarter ex- 
ists to some extent in nearly every country in the world. It 
is reported as occuring in the most northern latitudes in which 
cattle are kept, as well as in the temperate and tropical zones. 
In Europe, it occurs on the pastures on the Alps, where 
for five months in the year the ground is covered with snow 
and ice and in America it is quite common in certain northern 
districts. It has been reported from Asia and from Northern 
and Southern Africa. 

In the United States, it prevails to a greater extent than 
is generally supposed. The states and territories which, 
according to the reports of the Bureau of Animal Industry, 
suffer most from it are Texas, Oklahoma, Kansas, Nebraska, 
Colorado, North and South Dakota and Indian Territory; but 



278 



BLACK LEG 



a number of the other Western States are badly infected. 
Many of the states east of the Mississippi river have infected 
localities, but in a few of the Eastern and Southern states it 
seems not to exist. During the last few years infected locali- 
ties have been found in New York where there has been an 
annual loss from this disease, but where prior to recent inves- 
tigations the cause of death has been attributed to poisoning. 

§ 20I. Etiology. Black leg is caused by Bacillus chau- 
veaui. This organism varies from 3 to 6yw in length and from 
0.5 to i./< in width. The ends are rounded and it produces 
spores. It stains readily with ordinary aniline dyes and also 
after the gram method. In cultures long involution forms are 
often observed. It is anaerobic. In suitable culture media 
under anaerobic conditions or in animal tissues (other than 




\ \ 



\ 
^ 



^ 1 \ " 

o ' 






.\ 



Fig. 63. Bacillus of black leg ivith flagella and ivith spores 
{after Hutyra). 



blood) it multiplies rapidly with the evolution of gas. The 
presence of spores renders it very resistant to natural destruc- 
tive agencies and to the common disinfectants. The bacillus 
of black leg or its spores are supposed to gain entrance to the 
tissues of animals through abrasions of the skin or, possibly, 
the raucous membranes of the mouth or intestine. 

The period of incubation is not known in cattle but it is 
supposed to be very short. Guinea pigs inoculated with a 
culture of the organism die in from one to three days. 



SYMPTOMS 279 

§ 202. Symptoms. The first symptoms may be either 
general or local in character. Arloing, Cornevin and Thomas 
believe that general symptoms always precede the local mani- 
festations. Norgaard reports finding cattle with marked 
local lesions but few^ animals suffering from general symp- 
toms, although the latter may have preceded the former and 
have subsided. 

A general symptom is elevation of temperature, reaching 
in some^ cases 107° F. It usually falls to the normal or even 
subnormal before death. There is loss of appetite, loss of 
rumination and pronounced depression. Respiration becomes 
accelerated, reaching 140 per minute or even higher. The 
animal moves with difficulty and lies down frequently. At 
first the visible mucous membranes are congested and within 
twelve to fifteen hours they have a dirty leaden or purplish 
color. 

The local symptoms may appear on different parts of the 
body except below the knee or hock joints and on the tail. 
They are less frequently found about the head. They usually 
appear on the thighs, neck, shoulders and lower region of the 
chest. The swelling is at first small and painful. It spreads 
rapidly and may in a few hours attain to a large size, when it 
becomes characterized by a crackling and a gurgling sound 
when the hand is passed over it. On percussion it gives a 
clear, tympanic sound due to the collection of gas in the 
affected tissues. At the center of the larger swellings the 
skin becomes dry and parchment-like, cool to the touch and 
painless upon pressure. If lanced, a dark, reddish, frothy 
fluid flows from the wound. It emits a disagreeable odor. 
In some cases there is but one swelling but usually there are 
two or more which may become confluent. The lymph glands 
adjacent to the swellings are much enlarged. There is usually 
trembling of the muscles, which, as death approaches, may 
develop into violent convulsions. . 

Hun has pointed out the interesting fact that in a very 
large percentage of cases the sweUings appear on the right 
side. There seems to be no explanation given for this local- 



28o BLACK LEG 

ization. In this country, records are wanting of observations 
on this point. 

Arloing has called attention to a mild form of this disease 
in which the symptoms are slight debility, loss of appetite and 
slight local swelling. 

§ 203. Morbid anatomy. After death the carcasses of 
animals which have died of this disease soon become distended 
with gas. This is due in part to the fermentation in the 
digestive tract and in part to the formation of gas in the sub- 
cutaneous tissues due to the presence of the specific bacillus. 
The subcutaneous distension is especially marked in the region 
of the swellings but it extends for a considerable distance from 
these foci in the direction of least resistance. The tympanitic 
condition often causes the two legs on the upper side of the 
carcass to extend out straight without touching the ground. 
A dark, blood-colored, frothy discharge flows from the nostrils 
and anus. Decomposition takes place very rapidly except in 
the affected muscles, which retain a sweetish-sour odor for a 
considerable time after other parts of the carcass have become 
putrid. 

The skin covering the swelling is often affected with dry 
gangrene. The subcutaneous connective tissue is yellow, 
gelatinous, infiltrated with blood and bubbles of gas which 
escape if the tumor is incised. The muscles underneath the 
tumors are of a dirty brown or of a blackish color. At other 
places they are dark red or dark yellow and, when exposed for 
some time to the air, they may have a golden lustre. They are 
brittle, putrid and very rich in fluids. They crackle on palpa- 
tion. When incisions are made into them, blood of a frothy, 
greasy, tarry appearance and of a sickish, fetid odor issues 
from them when they are squeezed. The fibres of the muscles 
show extremely varied degenerative changes. The gases that 
are present in the muscles are inflammable and burn with a 
bluish flame on being ignited. They are said to have but 
little odor, on which account it is assumed that the}' consist of 
carburetted hydrogen. They are also said to contain carbonic 



MORBID ANATOMY 28 I 

acid but no oxygen. An exact chemical analysis of these 
gases seems not to have been made. The lymph glands near 
the tumors are enlarged and full of blood. They contain 
hemorrhages and are infiltrated with a serous fluid. The 
afferent lymph vessels are sometimes distended with gases, 
giving them the appearance of strings of beads. Changes 
similar to those of the external muscles appear in the muscles 
of the tongue and pharynx when the disease, as may happen 
in rare cases, is localized on the oral and pharyngeal mucous 
membranes. 

A large amount of blood-red exudate is frequently found 
in the abdominal cavity. In other cases only a small quantity 
of a serous fluid is present. In still others no changes at all 
appear. The abdominal changes seem to be determined by 
the swelling of the muscles, that is, whether it has or has not 
spread to the peritoneum. Yellow gelatinous and hemorrhagic 
infiltrations are often met with on the omentum, mesentery 
and in the neighborhood of the kidneys. The mucous mem- 
brane of the stomach and small intestines is frequently swollen, 
congested and infiltrated with hemorrhages, in which case the 
contents of the intestine are bloody. The liver is hyperemic, 
but the spleen is usually normal. 

In the thoracic cavity, the pleurae in the neighborhood of 
the swollen parts of the skin and mediastinum are sometimes 
hemorrhagic. The pleurae may ahso show large ecchymoses, 
in which case the thoracic cavity contains a sero-sanious exu- 
date. Hemorrhages are sometimes present in the lungs, peri- 
cardium, myocardium and under the endocardium. The 
muscular tissue of the heart is very soft, but the other muscles 
show only slight changes. The mucous membrane of the 
bronchi is sometimes hyperemic and sprinkled with hemor- 
rhages. 

The blood is of a normal color and coagulates readily. 
The fluids of the muscles have, according to Feser, an acid 
reaction, and the flesh becomes rapidly putrid. The bacilli of 
blackleg are found only in small numbers if at all in the 



282 BLACK LEG 

blood during life, but abundantly a few hours after death. 
They are numerous in the local lesions. 

The duration of the disease is from one to three days. 
Occasionally it is longer. The prognosis is grave. 

^ 204. Differential diagnosis. Black quarter is to be 
differentiated from anthrax, the "corn stalk" disease, septi- 
cemia hemorrhagica and various forms ot poisoning. Usually 
the localized subcutaneous lesions are sufficient to differentiate 
black quarter from these other affections. It often happens, 
however, that post-mortem changes have so modified the car- 
cass before it can be examined that the diagnosis is question- 
able. In this and all doubtful cases or where only small por- 
tions of tissue are sent for examination, it is necessary to 
resort to a more definite method or methods, such as the mi- 
croscopic examination, cultures and animal inoculation. 

1. Microscopic examination. Cover- glass preparations 
made from the fresh tissues will ordinarily exhibit the specific 
bacteria. They are easily distinguished in case of anthrax, 
black quarter and often with septicemia hemorrhagica, while 
in the "cornstalk" disease and cases of poisoning character- 
istic bacteria are not found. It is important to eliminate putre- 
factive bacteria, when the animals have been dead for some 
hours. 

2. Cultures. Ordinary culture media inoculated with 
the tissues from a case of anthrax will give growths of the 
anthrax bacterium, and from cases of septicemia hemorrha- 
gica that of Bad. bovisepticum, but with the other two dis- 
eases they will remain clear if uncontaminated. The black 
quarter bacillus will grow on these media only when placed in 
anaerobic conditions. In case of the "corn stalk" disease the 
media will continue to be clear. 

3. Atiifjial inociilatio7i. In guinea pigs inoculated in the 
deeper subcutaneous tissues with pure cultures of black leg 
bacteria or with bits of tissue from the affected area of another 
animal dead from the disease, death ensues in from one to two 
days. It is preceded by a raise of temperature, loss of appetite 



I'REVENTION 283 

and general indisposition. The site of inoculation is swollen 
and painful and drops of bloody serum maj^ sometimes be seen 
exuding from it. At autopsy the subcutaneous cellular tissues 
and underlying muscles present a condition of emphysema and 
extreme edema. The edematous fluid is often blood .stained 
and the muscles are of a blackish or blackish brown color. 
The lymphatic glands are markecily hyperemic. The internal 
viscera present but little alteration visible to the naked eye. 
In the blood stained serous fluid about the point of inoculation 
short bacilli are present in large numbers. These often present 
slight swellings at the middle or near the end. They are not 
.seen as threads but lie singly in the tissues. If the autopsy is 
made immediately after death, these organisms may not be 
detected in the internal organs, but if not made until after a 
few hours, they will be found there also. In early autop.sies 
only the vegetative forms of the bacilli may be found, but later 
(in from twenty to twenty-four hours) spore-bearing rods may 
be detected. With the " corn stalk " disease the inoculated 
animals will remain well. 

§205. Prevention. In checking the spread of the dis- 
ease it is very important wherever it is possible to remove the 
well animals from the infected field and to restrict the sick ones 
to a small one. The swellings should not be opened and the 
discharge scattered over the field. The dead animals should 
be burned if possible, otherwise buried deeply and covered well 
with lime as soon as possible after death. Birds and other 
animals should not be allowed to feed upon the carcasses and 
* the skin should not be removed. Every precaution to restrict 
the spread of the bacteria of this disease should be taken. It 
is very desirable to thoroughly disinfect the ground where the 
animal lay at the time of death. The spores are very resistant 
both to disinfectants and the natural destructive agencies such 
as sunlight and drying. It is not wise to use land upon which 
animals have contracted the disease for grazing purpo.ses for 
susceptible species. 

§ 206. Preventive inoculation. .Several methods of 



284 BLACK LEG 

fortifying exposed animals against the infection of sympto- 
matic anthrax virus have been proposed. In 1880, Arloing, 
Cornevin and Thomas demonstrated at Chaumont that animals 
injected with the filtrate of cultures of this virus into the jugu- 
lar vein were protected against inoculation with the strong 
virus. It was found, however, that this method was difiicult, 
as the vein had to be exposed and the greatest care was neces- 
sary to prevent infection of extra vascular tissue in introduc- 
ing and withdrawing the syringe. Later these investigators 
attenuated the virus by heating it to a temperature of 100 to 
104° C. and injecting it into the subcutis of the shoulder. This 
gave a partial immunity which was reinforced after eight or 
ten days by a second inoculation of a virus that had been 
heated from go to 94° C. for six hours. They injected the 
virus where the subcutis is quite dense, such as at the end of 
the tail where onlv local swellings would occur. This process 
is known as " the French method," Arloing" s or the " Lyons 
method." 

In 1888, Kitt of the Veterinary College in Munich, after 
a careful investigation of the subject, proposed a single injec- 
tion method using a virus attenuated by heating at a tempera- 
ture of from 85 to 90° C. for six hours. A single injection of 
this vaccine would usuall}' confer immunity. He further 
modified Arloing's method by making the injections in the 
shoulder regions where the skin is looser and the operation 
easier. Later, Kitt made further important investigations 
concerning preventive vaccines for this disease. 

In the fall of 1896, investigations looking to the 
preparation of a black quarter vaccine were begun in the 
Bureau of Animal Industr}' at Washington by Dr. Norgaard 
under the direction of Dr. Salmon. The various European 
methods were tried. The one finally adopted consists of a 
single vaccine, the Arloing principal with Kitt's modification. 

The material used for the vaccine is obtained from a fresh 
blackleg tumor, by pounding the muscle tissue in a mortar 
with the addition of a little water and squeezing the pulp 
through linen cloth. The juice is spread in layers on plates 



REFERKNCKS 285 

and dried quickly at a temperature of about 35° C. This 
temperature does not in the least affect the bacteria, and the 
dry virus obtained in this way retains a high degree of viru- 
lence for two years or longer. 

When vaccine is to be prepared, the dried material is pul- 
verized and mixed in a mortar with two parts water until it 
forms a semifluid homogeneous mass. This is spread in a thin 
layer on a suitable glass dish and placed in an oven, the 
temperature of which may be regulated with exactness. The 
reason for mixing the dried muscle with water is to insure a 
quicker and more uniform attenuation. The temperature of 
the oven is previously brought up to 95° to 99° C, and the 
virus is allowed to remain in it for six hours. When removed 
it appears as a brownish scale, which is easily detached from 
the dish. This scale is pulverized and put up in packages con- 
taining lo doses each. Before it is used, it is mixed with 
10 c. c. water, filtered and the filtrate injected in doses of one 
cubic centimeter. 

REFERENCES. 

1. Fisher. Blackleg in Kansas, and protective inoculation. 
Kan. State Agric. Exper. Station, 1901. 

2. Lewis. Symptomatic anthrax. Bulletin No. 27. Oklahoma 
State Agric. Exper. Station, 1897. 

3. Mayo. Blackleg. Bulletin No. 6y. k'an. State Agric. 
Exper. Station, 1S97, p. 108. 

4. NoRGAARD. Blackleg in the United States and the distribution 
of vaccine by the Bureau of Animal Industry. Annual Report of the 
Bureau 0/ Animal Industry U. S. Dept. Agric. 1898. 

5. NoRGAARD. Blackleg. Its nature, cause and prevention. 
Circular No. 23. U. S. Bureau of Animal Industry, 1S9S. 

6. Paouix. Blackleg. Bulletin No. 12. Mo. Agric. Exper. 
Station, 1890. 

7. Peters. Blackleg. Its nature, cause and prevention. Bulle- 
tin No. 65. Neb. State Agric. Exper. Station, 1900. 

8. SAI.MON. Black quarter. Annual Report Bureau of Animal 
Industry, U. S. Dept. of Agric. 1893-4. 



286 MALIGNANT EDEMA 

MALIGNANT EDEMA 

§ 207. Characterization. Malignant edema is an acute, 
wound infection disease of domesticated animals, which is es- 
pecially characterized b^' edematous, later crepitating tumors 
at the place of infection due to Bacillus oedematis nialigiii. 

% 208. History. Crepitating tumors following wounds, 
withdrawing of setons, castration, and the like have long been 
known. It was pointed out by Girard in 18 18, that creptita- 
ing tumors in sheep could be caused by subcutaneous injection 
of animal tissue taken from putrefying tissue. Chauveau 
(1873) showed by experiments performed on goats that the 
development of the disease stood in a close relation to living 
organisms present in injected putrescent blood. Pasteur, in 
1887, studied more closely the organism and named it Vibrio?i 
septiqtie. He obtained it in pure culture. Later Koch and 
Gaffky (1881) studied exhaustively the disease caused through 
contamination by contact with the ground, which they named 
malignant edema. Since then Kitt, Jensen, Sand and Leclainche 
have studied its bacteriology, while Jensen and Sand, v. Ratz, 
Frohner, Carl and others have made valuable contributions to 
the appearance of the malady among domesticated animals. 
Malignant edema is a wide spread but not a common disease. 

§ 2og. Etiology. Maligant edema is caused by 5a<rz7/z^^ 
vedetnaiis maligni Koch ( Vibrion septiqiic Pasteur). It is de- 
scribed as a bacillus resembling that of anthrax, but somewhat 
more slender, rod-shaped, and spore bearing. The ends are 
rounded. It is an anaerobe. In artificial cultures as well as 
in the animal body, after the death of the latter the bacilli 
grow into long filaments. Exceptionally, living animals contain 
the spore bearing bacilli in the edematous fluid (Jensen and 
Sand). The bacilli stain very readily with aqueous aniline 
dyes. In culture media containing sugar gases are formed, 
which have a characteristic disagreeable odor. The inocula- 
tion of a pure culture into the deep connective tissue of 
mammals and birds produces a tumor quickly spreading from 



MORHID ANATOMY 



287 



the place of inoculation and later crackling on account of the 
formation of gas. 

Of the domestic animals, the horse is the most susceptible 




Fig. 64. Bacillus oedematis rnaligni with flagella and spores ( Hutyra ) . 

to natural infection ; the cow, the sheep and the goat are less 
susceptible. The pig, dog and cat are rarely attacked. 

Infection sometimes follows contusions or lacerations, 
sometimes delivery, when in the latter help is given with hands 
or instruments not clean, while in other cases it occurs such as 
smallpox vaccination, castration, shearing, bleeding, drawing 
setons, subcutaneous injections where unclean syringes are 
used. 

§ 210. Morbid Anatomy. On the expansion of a 
tumor appearing in any part of the body, the connective tissue 
is distended and infiltrated with yellow or reddish fluid con- 
taining many small gas bubbles, which emits a characteristic 
odor. These gelatinous infiltrations of the connective tissue 
follow between the deeper layers of the muscle. The muscle 
itself is often sallow or dark red in color and is very brittle. 
The connective tissue in places seems to be strewn with larger 
or smaller hemorrhages. In the intestinal cavity there is a 
little reddish, serous fluid ; the peritoneum is deeply injected. 
In the cases in which malignant edema has developed in con- 
nection with parturition the uterus is insufficiently contracted, 
the subserous connective tissue of the true pelvis and the walls 
of the uterus are edematously infiltrated. 



288 MALIGNANT EDEMA 

The spleen is usually not affected. Occasioually acute 
tumors with gas formation are found in the pulp (Frohner). 
The liver may show tumefaction. The mucous membrane of 
the intestinal canal may show signs of acute catarrh. The 
lymph glands are swollen. The lungs are hyperemic and for 
the most part edematous. The muscular system of the heart 
shows usually a high degree of parenchymatous degeneration. 
The blood clots very little. The body quickly becomes putre- 
fied. The fluid pressed out of the crepitating tumor con- 
tains edema bacilli in great number, associated possibly with 
other bacteria. 

The presence of the bacilli of malignant edema in the 
tissues of a dead animal does not of itself prove that it died of 
this disease. These bacilli appear very often in the intestinal 
contents of animals which feed on plants in company with other 
bacteria and on that account are able after the death of the 
animal to multiply in its tissues, especially when the blood re- 
mains fluid for some time, as for example after a sudden death 
by suffocation. 

^ 211. Differential Diagnosis. Malignant edema, if 
it occurs in cattle, can be easily confused with symptomatic 
anthrax. As distinguishing malignant edema are the occur- 
rence of the disease in a region where symptomatic anthrax is 
not native, further the often very advanced age of the patient, 
the occasional localization of the tumor on parts of the body 
poor in muscle, and besides the insignificant affection of the 
muscular system in comparison to the severe affection of the 
connective tissue. 

In horses and sheep the development of a crepitating tu- 
mor with a fever indicates malignant edema. The crepitation 
distinguishes the disease from anthrax edema as well as from 
the inflammatory edemas often following wounds and caused 
by streptococci. In simple subcutaneous emphysema, follow- 
ing skin or lung wounds, fever rarely occurs. Finally care 
must be taken that on section a simple emphysema caused by 
putrefaction is not confused with a crepitating tumor formed 
during life. 



FOOT-ROT IN SHEEP 289 

^ 212. Prevention. In the prophylaxis of the disease 
the wounds of the skin and the mucous membrane are to be 
kept from infection with the soil, those which are already in- 
fected are to be disinfected, while after difficult delivery in 
which the genital passages have been injured a thorough 
cleansing of the latter and of the uterus check the development 
of the trouble. Test animals can be immunized against the 
virulent infection by injection of tissue juices containing spores 
after heating it to 92° C. for 7 hours (Leclainche and Vallee). 
These inoculations protect only against malignant edema and 
not at the same time against symptomatic anthrax, as Le- 
clainche and Vallee have proved in contradiction to the earlier 
experiences of Rouk and Duenschmann. 



FOOT-ROT IN SHEEP 

§213. Characterization. Foot- rot in sheep is an infec- 
tiotis disease characterized by a specific inflammation of the 
tissues just above the horny part of the cleft of the foot, which 
extends downward, undermining the horny portion. It 
appears in epizootic and enzootic forms. Sheep are most often 
attacked, although other species are reported to be susceptible. 

§ 214. History. Foot-rot has been recognized for more 
than a hundred years. It has been described from various 
parts of Europe by Chabert, Pictet and Gohier. It seems to 
have first appeared in this country late in the eighteenth cen- 
tury. It has recently been investigated by Mohler and Wash- 
burn. They found a specific organism, and thus differentiated 
it from the streptococcic infection. 

§ 215. Etiology. The cause of this form of foot-rot is, 
according to Mohler and Washburn, an anaerobic organism, 
Bacillus 7iecropJioriis. This organism is isolated with difficulty 
from these lesions because of the association with it of other 
bacteria. The most satisfactory method is by inoculating 
white mice or rabbits subcutaneouslv with the diseased tissue 



•290 



FOOT-ROT IN SHEEP 



from their organs 
time required to kil 



\ 



\ 

V 



vV \ 



\ 



V 



it can be obtained in pure culture. The 
1 these animals is usually from four to 
twelve days. 

The period of incuba- 

\. , tion in small animals is 

^\ N^ but a few days. In the 
--^ 1 naturally contracted dis- 

ease in sheep it is uncer- 
tain. In cases produced 
by inoculation of the 
I \ J -^ specific bacillus from 

\ " ^ / three to ten or more days 

elapse before symptoms 
appear. 

§ 216. Symptoms. 
Lameness is the first 
symptom noted. If ex- 
amined prior to this, 
Mohler reports a moist area of the skin just above the horny 
part of the cleft of the foot. The inflammatory condition 
extends rapidly to tissue beneath the horny part. There is 
often a discharge of a thin, purulent fluid. Mohler states that 
the discharge emits a pungent, dis- 
agreeable odor which is character- 
istic of this infection. There is 
emaciation which may be due quite 
as much to the inability of the lame 
^^f^'^ i^ '^^•^ sheep to procure food as from the 

^'^}Pf<fi<r'''^9. % Q- c specific action of the bacillus. 

The duration of tlie disease varies 
from a few weeks to several 
months. The cases are said usual- 
ly not to terminate fatally. 



Fig. 65. Bacillus iiecrophortis {after 
Mohler) . 




b 

Fig. 66. Necrotic area 
the liver of a rabbit ; 






liver cell, B, inflammatory 
zone. A, necrotic center 
{Mohler). 



§ 217, Morbid anatomy. The 
tissue changes are those of a purulent exudative inflammation. 
As the process undermines the horny portion of the hoof it 



•MISCELLLANEOUS INFECTIONS 



291 



may slough, and granulating tissue, commonly called "fungoid 
growths," develop. The invasion of the organism and the 
extending of the necrosis may continue until the tendons, liga- 
ments and even the bones may be attacked. There is going 
on at this time reparation processes which usually terminate in 
a peculiar growth composed of horny elements, dense epithelial 
cells, and granulation tissue (Mohler), 

§ 218. Differential diagnosis. Foot-rot in sheep is to 
be differentiated from inflammation of the feet caused by strep- 
tococcic infection, purulent inflammation of the interdigital 
space, the stoppage of the duct of the interungulate or biflex 
gland, and contagious foot-and-mouth disease. 

REFERKNCES 

1. Ernst. Ueber nekroses und den nekrosebacillus (streptothrix 
necrophora). Monatsheft f. prakt. Tier/ieilk., Bd. XIV (1902), S. 193. 

2. Mohler and Washburn. Foot-rot of sheep, its nature, 
causes, and treatment. Bulletin No. 63. U. S. Bureau of Animal 
Industry, 1904. 



MISCELLANKOUS INFECTIONS WITH BACILLI 

§ 219. Enzootic in cattle caused by a bacillus of the 
enteritidis group. In 1902, Mohler and Buckley=!^ described 
an outbreak caused by B. enteritidis among cattle in a stable of 
21 animals of which 8 contracted the disease and died. Three 
others exhibited the early symptoms. 

The symptoms were first refusal of food, suspension of 
urination and diminution in lactation. There was excessive 
salivation in some cases. The temperature varied from 102.7° 
to 104.1° F. The visible mucosae were congested. There 
was a wild expression in the eyes and the animals were very 



*MoHLER AND Buckley. Report on an enzootic among cattle 
caused by a bacillus of the enteritidis group. (Illustrated and bibli- 
ography). Annual Report of the Bureau of Ant ma I Industry, 1902. 



292 MISCELLANEOUS INFECTIONS 

excitable. The gait was irregular. Convulsions set in prior 
to death. 

The duration of the disease varied from two days to several 
weeks. 

The morbid anatomy varied. In the acute cases the 
anatomical changes were very slight. The most noticeable 
and characteristic lesion observed consisted of petechial hem- 
orrhages under the endocardium. These were present in every 
case. There were occasional blood extravasations in the 
intestinal mucosa. There was marked injection of the blood 
vessels of the meninges and blood tinted fluid in the cavity. 
The chronic cases presented a wider range of lesions in the 
organs. 

Cultures of the bacillus were obtained from the different 
organs. The bacilli were found in small numbers in cover- 
glass preparations made from the organs. The organism was 
fatal to experimental animals and to calves. It was more 
virulent than the bacillus of hog cholera obtained from hogs 
dead of that disease. 

Since Gaertner first discovered this organism in 1888 in 
the meat of a diseased cow, it has been isolated by others from 
both animals and man. It has been found to produce toxic 
properties that are pathogenic for animals, and several people 
have been reported to have become ill from eating broth made 
from meat containing this organism. During the last few 
years several bacilli differing slightly from Gaertner' s bacillus 
have been isolated from cases of meat poisoning. 

Bacilli of this group, or at least of closely related groups, 
have frequently been found to stand in a causal relation to the 
lesions with which they were associated. The more import- 
ant of these are Bacillus typhi mtirium obtained by Loeffler in 
1890 from an enzootic among mice, the bacillus isolated by 
Mereshkowsky in 1895 from the ground .squirrel, and Bacillus 
psittacosis isolated by Nocard in 1893 from the organs of 
parrots. 

In addition to these, other bacilli have been found appar- 
ently as the etiological factor in isolated cases among animals. 



GROUSE DISKASE 293 

S 220. Grouse disease. In 1887 Klein described a dis- 
ease of grouse characterized by congestion of the lungs, liver 
and kidneys with small necrotic areas in the liver and areas of 
redness in the intestines. The di.sease was found to be due to 
a bacillus which has been found to belong to the colon group. 
[The author has studied the bacillus of the Grouse disease a 
cultureof which was obtained from Krahl and found it to be 
B. coli cotnmiinis.'] Migula designates it B. scoticus. 

Quail disease ( Colibacillosis tetraonidaruni) . In May 1 907 , 
Morse {Circular No. 109, Bureau of Animal hidustry) described 
a disease of quail characterized by congestion of the lungs, 
focal necrosis of the liver, and intestinal ulceration. He found 
the cause to be a member of the colon group of bacteria. This 
seems to have several centers of infection in this country. 
Several species of quail and grouse are susceptible. While 
there are strong resemblances between this affection and the 
grouse disease described by Klein, Morse assumes that they 
are not identical. 



CHAPTER VII 

DISEASES CAUSED BY BACTERIA 
FAMILY SPIRILLACEiE. 



§ 221. General Consideration of Spirillaceae. This 
family of bacteria has thus far revealed very few species that 
are pathogenic for domesticated animals. 

§ 222. Diseases of fowls caused by spirillaceae. 
The disease of fowls reported to be caused by these organisms 
has not been found in this country. It is not unlikely that 
^ ^ some one or more of the many 

■'a» *^ ' - \ as yet mysterious diseases of 

\ poultry may be caused by 

members of this family. It is 
interesting to note that spirilla 
are not uncommon in the bac- 
terial contents of the intes- 
tines. It is believed that 
many of these are anaerobes, 
which would explain the diffi- 
culty encountered in trying to 
isolate them in pure culture. 

Sakharoff studied, in 1891, 
a peculiar disease of geese and 
showed it to be caused by a 
spirillum. It was designated 
spirochacte anserina. Cantacuzene has studied the mode of 
destruction of the spirilla. He found that they are destroyed 
by and within the macrophages of the spleen. 

The morbid anatomy in the affections caused by the 
spirilla appear to be largely engorgement of the spleen and 




Fig. 67. Spirochaete anserina fro'Di 

the blood of a goose {after 

Cantacuzene) . 



Sl'IRILLOSIS OF CATTLE 295 

swelling of the liver with fatty degeneration of the parenchy- 
matous tissue. The heart muscle is sometimes affected. 
Areas of necrosis have been described in the solid viscera. 

It is stated that the blood of the diseased fowl is not 
infectious 48 hours after it has been removed from the fowl 
but that if injected into a healthy fowl it will confer immunity 
against a virulent infection. Marchoux and Salimbeni found 
that if the fresh blood of the diseased fowl was heated for 5 
minutes at a temperature of 55° C. it would confer immunity 
but if it was heated for 10 minutes this property was lost. 

§ 223. Spirillosis of cattle. Theiler found spirilla in 
a few cattle in South Africa. The animals were suffering with 
" red water " with possibly one exception. He sent prepara- 
tions of these to Laveran who designated them Spirilhim 
Theileri. Theiler made a number of inoculations with the 
blood of animals infected with the spirilla with negative 
results. The following description of the spirillum is quoted 
from Theiler' s report : 

" The microorganism in question is a typical spirillum, 
and varies considerably in its length. The longest microbes 
measure from 20 to 30//. They are somewhat thinner at both 
ends, otherwise the thickness is about the same throughout 
the whole length — viz., about .25 to .\o }.i. The corkscrew-like 
forms are, as a rule, predominant, but there are other forms 
which are atypical in appearance and also shorter. For 
instance, the parasite may show itself as a simple curved line 
without any spiral curves, representing sometimes the shape 
of S ; it may also be completely doubled up, both ends may 
meet and take the shape of a ring, or both ends may cross each 
other and also form a loop. These loops may be of different 
shapes and sizes. Double loops may also be found. It is 
somewhat difficult to describe all the various forms, but they 
can be easily imagined, considering that the spirillum is a very 
flexible and agile parasite. 

" In preparations made by placing a cover-glass on a drop 
of fresh blood the microorganisms are easily detected. Some 



296 



DISEASES CAUSED BY SPIRILLACEAE 



of the red corpuscles show a slight irregular motion, and when 
closely watched it may be noticed that this disturbance may 
proceed in a certain direction, or again whirl round in the 
same place. When examined under a high power (i-i2th 
inch obj.) the agile spirillum is usually seen attached to one or 
more red corpuscles. Sometimes it is curled all round a red 
or white corpuscle. As soon as the organism becomes free 
and begins to travel through a clear space, a characteristic 
undulating movement is visible, which continues until it finally 
attaches itself to some other blood corpuscle. This motion 
may be noticed for some time ; it then becomes relaxed, and 
finally slackens down completely. I have observed the 
movements in preparations which were twentj'-four hours old. 
"Staining of the organism may be obtained with any of 
the aniline dyes used in bacteriology, viz., methylene-blue, 
fuchsin, thionin. Good preparations were obtained with 
Ivaveran's modification of Romanowsky's stain, and also with 
Azur II. In using the last two mentioned methods no chro- 
matic bod}' could be traced, such as is present in parasites 
belonging to the protozoa. 

"Cultivations on the 
usual artificial mecia were 
repeatedly tried, but al- 
ways with negative results. 
The same has been found 
to be the case with all the 
above-mentioned different 
spirilla found in men and 
birds. " 




u^ar^J^^ 







?^ 224. A disease of 
the pig due to spiro- 
chaetes. Dodd has recently 
described a spirochaete 
which he found in a pig 
sent to the government 
laboratory in Pretoria. The 
examination showed very few morbid changes in the tissues 



Spirochaetes from the lesions 
in the skin of a pig {after Dodd). 



OTIIKR SPIKOCHARTES FOUND IN ANIMALS 



297 



but the skin was sprinkled with dark hemorrhagic-like spots. 
From scrapings of these lesions he was able to find the organ- 
ism. It is described as long and very slender, its length vary- 
ing from 9 to 26 //. Both extremities are pointed. The spiral 
forms predominate but in the same preparation curved or 
simply long straight threads were observed. They appeared 
singly, in pairs and in clumps. It was difficult to distinguish 
It in the unstained preparation. It stains well with any of the 
ordinary aniline dyes but does not retain the coloring matter 
after being treated by the Gram method. 

S 225. Other spirochaetes found in animals. Bon- 
hoff (1905) described a .spirochaete found in the pustules of 
vaccinia of the calf. Martoglio and Carpano found a .spi- 
rochaete in the blood of the Abyssinian sheep. It exhibited 
from three to ten regular spirals and measured from 10 to 20// 
in length and from 2 to 4 // in breadth. The extremities were 
tapered and it did not stain by Gram's method. It could not 
be cultivated on any media used. Neither flagella, spores nor 
chromatin were discovered. Two spirochaetes were often 
seen attached throughout their length and apparently fused 
together at one extremity as through they had been produced 
by longitudinal fission. This parasite was present in the blood 
plasma. As in the case with the Sp. Theileri the disease could 
not be reproduced in any of the animals inoculated with the 
infected blood or even in sheep. This organism was de- 
scribed by Blanchard as Sp. ovma. 

According to Bizzozero the stomach of the dog always con- 
tains numbers of extremely slender spirochaetes formed of from 
three to seven turns and from 3 to 8 // in length lodged in the 
interior of the gastric cells. These were found in the Norway 
rat, cat and dog. In the latter they have been found to be 
constantly present. 

The principal species of the spirochaeta that have been 
described are the Sp. plicatilis Ehrenberg, in 1838. It is 
common in stagnant water and often attains a length of 100 to 
200 i.1. In 1875, Cohn described Sp. buccalis which is tapered 
at both extremities and common in the dental tartar and in the 



298 DISEASES CAUSED BY SPIRILLACEAE 

saliva. In the same year the Sp. Obertmieri was named by 
Cohn after its discoverer as the cause of recurrent fever in 
man. This organism varies from 15 to 30 // in length, is very 
thin and tapered at both extremities. In 1905 Schaudicn and 
Hoffmann described a spirochaete which is believed to be the 
cause of syphilis. It is known as Treponema pallidum. 

REFERENCES 

1. Cantacuzene. Recherches sur la spirillose des oies. Ann. 
de. V Inst. Pasteur, Vol. XIII (1S99), p 529. 

2. DoDD. A disease of the pig, due to spirochaeta. Jotir. Coinpar. 
Path, and Thera , Vol. XIX (1906), p. 216. 

3. Gabritschewskv. Beitrage zur Pathologic und Serotherapie 
der Spirochaten-Infektionen. Centratd.J. Bakter., Bd. XXIII( 189S), S. 
365, und 778. 

4. Levadite et Maxoxeliax. Xouvelles recherches sur la spi- 
rillose des poules. Ann. de /' Inst. Pasteur, Vol. XX (1906), p, 592. 

5. Sakharoff. Spirochaeta anserina et la septicemie des oies. 
Ann. deV Inst. Pasteur, Vol. V (1891), p. 564. 

6. Theiler. Spirillosis of cattle. Jour. Coinpar. Path, and 
Thera.. Vol. XVII (1904), p. 48. 



CHAPTER VIII 



DISEASES CAUSED BY FUNGI. 



ACTINOMYCOSIS. 

Syniptoins. Lumpy jaw ; wooden tongue; big head. 

^ 226. Characterization. Actinom3COsis belongs to 
the class of affections known as the infectious granulomata. It 
is a chronic disease determined by the presence of a specific 
cause — the ray fungus — which by irritation stimulates the for- 
mation of new growths consisting of round cells, epithelioid 
cells, giant cells and fibrous tissue. The neoplasms appear as 
tumors having either a tendency to develop into large and 
hard masses or to suppurate. It has been suggested that the 
suppuration was due to a secondary infection by pyogenic 
bacteria. 

Cattle (genus Bos) are most often attacked. Horses, 
dogs, pigs, sheep and elephants are slightly susceptible and a 
few cases have been reported in each. Men are susceptible 
but this disease is rarely found in the human subject. Other 
species seem to be immune. 

§ 227. History. The early history of this disease is 
quite obscure. Prior to the discovery of its specific cau.se, it 
was much confu.sed with other diseases resembling it more or 
less closely in certain gross appearances. It was designated 
by a variety of names, the more common of which are swelled 
head, lumpy jaw, big head, fibroma, sarcoma and osteosar- 
coma. It is popularly known in the United States as " lumpy 
jaw" and in Europe as "wooden tongue." The popular 
names were probably suggested by the character of the lesions, 
which differ to a marked degree. It was recognized as a 
specific disease by Rivolta in 1868, by Perroncito in 1875 and 



300 



ACTINOMYCOSIS 



by Bollinger in 1877. The ray fungus was undoubtedly ob- 
served prior to this by Lebert and Robin, both of whom failed 
to recognize it as a vegetable parasite. 

The fungus was carefully described by Dr. Harz, a botan- 
ist, who gave it the name actinomyces or ray fungus. Bolin- 
ger was the first to carefully study the disease in cattle and to 
demonstrate the power of the ray fungus to produce disease. 
With this discovery of Bollinger in 1877, actinomycosis be- 
came recognized as a definite, specific disease which could in 
most cases at least be differentiated from the other affections 
with which it had hitherto been confused. In 1845 von Lang- 
enbeck of Kiel observed and made drawings of peculiar bodies 
in a case of vertebral caries in man which it is now believed 
were rosettes of the ray fungus. In 1878, Israel demonstrated 
the disease in man. Since that time it has been carefully 
studied and described by a number of investigators. 

s5 228. Geographical distribution. Actinomycosis is 
quite widely distributed throughout North and South America 
and Europe. It is much more prevalent in certain countries 
and districts than in others. The observation has been made 
that animals pastured upon low lands and in river valleys are 
more liable to contract it than those feeding upon high and 
dry ground. It has also been noted that cattle fed upon rough 
or coarse forage are more prone to the disease on account of 
abrasions of the buccal mucosa than those kept upon less 
harsh food. 

It is very difficult to procure reliable statistics concerning 
the extent to which it occurs. The observations which have 
been made at the union stock yards, Chicago, show one case 
of actinomycosis in from 1600 to 1700 cattle. The statistics 
from the abattoirs in Berlin show one case to 4150 cattle and 
one in 8000 pigs. These figures do not, however, indicate the 
extent of the disease among the farm animals, as they are 
collected from those animals presented for slaughter only. At 
the clinic of the New York State Veterinary College there is 
presented for treatment a very few cases each year. In the 



ETIOLOGY 301 

Mississippi X'alley and in the South-west it seems to he more 
prevalent than it is east of the Allej^hany Mountains. 

§ 229. Etiology. Actinomycosis is produced by a 
fungus, Cladothrix acthio»iyccs, commonly known as the "ray 
fungus." ='^ The disease is the result of its multiplying in the 
tissues and not from the elaboration of a toxin. Undoubtedly 




Fig. 69. A rosette of the ray fungus together ivitlt different forms of 
tlic single club ends. X ^500. {After Crookshank) . 

the bacteria often associated with the fungus in suppurating 
lesions are of some significance. Wright states that he believes 
they play an important part in the extension of the disease. 
The fungus appears as minute, yellowish granules in the 
lesions. When examined microscopically, these granules are 

*The cladothrix is placed among the higher bacteria. There are 
many varieties of the actinomyces. Until they are better understood it 
seems better to group them with the fungi. 




Fig. 70. Photograph of a young actinoniycotic groivth under low 
power, showing clumps of the ray fungus. 







ic \ • 









.^ .•'••" •» 









Fig. 71. Photograph under higher magnification of one of the clumps 
of the ray fungus shoiving giant cells about the clump of fungi. 



ETIOLOGY 



303 



found to be made up of rosettes varying in size from 10 to 
200// in diameter, the average size ranging from 301040/^. 
This fungus can be cultivated on artificial media. It stains 
somewhat feebly with the aniline dyes. 

The rosettes are composed of a number of club-shaped 
structures (rays), radiating from the central mass which is 
composed of the mycelial part of the fungus. The club-shaped 
bodies vary in size but usually they are from i to 10 /< long. 
The rays are connected with the central portion by fine thread- 
like structures which are not readily demonstrated. In tear- 
ing or crushing the rosette, the clubs break off at or near their 
junction with the mycelial threads. Some investigators have 
mentioned a polymorphous form of actinomyces in which 
coccoid and rod-shaped structures are found. These are doubt- 
less the ends of the clubs which first appear in focusing on a 
rosette. 

The mycelial threads are wider in some portions than in 
others. In the narrowest places the walls seem to touch each 
other. Whether this irregularity is natural or the result of 
twisting the mycelial thread is not determined. The myce- 
lium is much more difficult to stain than the clubs. In some 
cases it seems to branch. The filaments can rarely be seen in 
the rosettes as thej' occur in the suppurating lesions. 

The natural habitat of this fungus is said to be on certain 
plants. According to Brazzola, they vegetate on the grasses, 
chiefly on Hordeinu murinum. He discovered quantities of 
the fungi between the vegetable fibres of barley which were 
imbedded in the gums of animals. Johne, Plana, Bostroem 
and others have found it on the awns of corn which were 
imbedded in the tonsils of pigs and in the tongues of cattle. 
Mayo, after making a careful study of this disease, states that 
the actinomyces are probably a degenerative form of some 
fungus which grows naturally upon food stuffs or grain. Bos- 
troem entertains the view that they develop exclusively on 
grains, particularly on the awns of barley. 

The period of incubation is not known. 



304 



ACTINOMYCOSIS 



§ 230. Infection. While actinomycosis is an infectious 
disease it does not seem to be transmitted directly from one 
animal to another. Numerous investigators have tried to pro- 
duce the disease by inoculating cattle, calves, sheep, goats, 
pigs, dogs, cats, rabbits and guinea pigs with actinomycotic 
lesions. The results have almost invariably been negative 
when pus was used, but the disease has developed after inocu- 




FiG. 72. Head of a steer with actinomycosis of the loiver jaw. 
( Photograph ed by Hopkins ). 



lating cattle with pieces of tissue containing the fungus in its 
vegetating state. 

It is believed that the infection occurs in susceptible 
species by the introduction of the fungus on food stuffs. The 
supposition is that the parasite gains entrance to the living 
tissues through slight wounds of the mucous membrane of the 
mouth or throat and perhaps the alveoli of diseased teeth or 
during the shedding of the milk teeth. It multiplies and 
extends from the points of entrance. After the infected awns 



SYMPTOMS 



305 



once gain lodgment, especially between the teeth, they are 
removed only with difficulty. The favorite points for the act- 
inomyces to enter the tongue is on the upper surface midway 
between the dorsum and the tip. The lungs may be the seat 
of primary infection due to the inhalation of the fungus. The 
disease has been rarely observed primarily in the udder but 
frequently in the subcutaneous tissue about the head. In man 
the source of infection is more obscure. Man}- cases have 
been reported where the individuals did not come in contact 
with diseased animals and were not occupied in agricultural 
pursuits or in handling grain but were glaziers, tailors and 
various shop tenders. There are a few cases reported, how- 
ever, where the circumstantial evidence points to direct infec- 
tion from diseased animals. 

The present knowledge of this fungus indicates that it 
must attain to a certain stage or period in its development 
before it will live and multiply in living animal tissues. It 
has been observed that, as a rule, cattle become infected when 
they are kept upon dry food. 

^ 231. Symptoms. Actinomycosis is manifested by a 
firm swelling or tumor usually situated in the region of the 
head or throat. It is first recognized as d slight swelling of 
the affected part resembling somewhat the result of a bruise. 
It is stated by those who have had much experience with the 
disease that many cases of actinomycosis seem to be caused by 
blows or injuries received while struggling in stanchions. 
The enlargement gradually increases in size. It is ordinarily 
sharply defined from the surrounding tissues. 

Upon manipulation the tumor feels hard and dense. In 
the region of the tliroat it may be fluctuating. After a 
variable length of time, the tumor-like mass may soften in one 
or more places, rupture and discharge a rather thick, yellow- 
ish and more or less sticky, purulent substance. The dis- 
charge may continue or, as often happens, the opening heals 
temporarily only to rupture again. The discharge often takes 
place into the cavity of the mouth or throat. Sometimes the 



3o6 



ACTINOMYCOSIS 



neoplastic tissue increases in amount until it gradually forces 
its way through the opening, resembling somewhat a cauli- 
flower in appearance. The actinomycotic growth frequently 
increases rapidly in size after it has discharged. In later 
stages the teeth may become ulcerated and loose. 

When the tongue is affected the animal finds it difficult to 
eat. The organ is swollen and in advanced cases hangs from 
the mouth. There is in these cases profuse salivation. When 

the pharynx is affected 
there is difficulty in swal- 
lowing and when the larynx 
is attacked there is difficul- 
ty in breathing. In this 
country the tumor is most 
frequently seen on the ex- 
ternal surface of the jaw. 
It is stated by Salmon that 
it usually begins in the 
connective tissue beneath 
the skin but soon extends 
to the bone, which it pene- 
trates. Actinomycosis of 
the cervical vertebrae may 
cause spinal paralysis. 
When the lungs are at- 
tacked the animal may present the appearance of one suffering 
from a chronic pulmonary disease such as tuberculosis. 

Actinomycosis is not a rapidly fatal disease. Animals 
rarely if ever die from its immediate effects. The length of 
time during which they survive depends very largely upon the 
location of the tumor and the rapidity of its development. If 
the tumor is situated where it does not interfere seriously with 
prehension, mastication or swallowing of food or where it does 
not occlude or press upon the respiratory passages the animal 
usually survives for several years. When death occurs it is 
usually due to inanition, the animal being unable to take 
sufficient food, although the drain upon the system by the 



^^ 


1 V^-'- •' 


'- u. ^ 



Fig. 73. A draiuing of a very young 
actinomycotic growth. A, actino- 
inyces ; B, giant cell ; C, surround- 
ing reactionary zone. 



MORBID ANATOMY 



307 



long continued discharge of pus must be severe. Mayo reports 
several cases where the disease was watched for five or six 
years and where it would possibly have continued several years 
more had not the animals been destroyed. Most animals which 
become affected with actinomycosis are either destroyed, treated 
or slaughtered for beef in the early stages of the disease. 



232. Morbid anatomy. The 



new actinomycotic 



> \, 



V 






v\ 








Fi(;. 74. A c/ra?i.'i/ij>' o/afi ac/ifi07nyrolzcjazi.'. 

growths have in or near their centers rosettes of the ray fungus 
surrounded usually by giant cells. These in turn are sur- 
rounded by tissue consisting principally of epithelioid and 
spindle shaped, connective tissue cells, among which giant 
cells may appear. As these cells increase in number they 
press against the surrounding tissues, thus producing the hard 
and dense tumor-like growths. This is especially true when 
they are located in the connective tissue. In certain other 
positions, such as the liver, the inflammatory cells are sur- 
rounded by a fibrous tissue framework which gives to the 
lesion a honeycomb appearance. On section a disagreeable 
"nutty" odor is given off which Mayo considers to be quite 
characteristic of the di.sease. The outside of the tumor is 



3o8 



ACTINOMYCOSIS 



usually composed of a dense layer of fibrous connective tissue. 
Extending from the periphery toward the center, the tissue 
becomes less dense and is composed largely of epithelioid cells. 
In the softer tissue there are often cavities of greater or less 
size filled with a viscid purulent substance in which the small, 
yellowish granules of the ray fungus can be found. If this 
pus is spread in a thin layer on a smooth surface granules com- 
posed of the "ray fungus" can often be seen with the unaided 











Fig. 75. Photograph of a section through an actinomycotic jaw : (a) 
tooth, (d) done, (c) actinomycotic tissue. 

eye. These pus cavities are usually connected with each other 
by small sinuses but sometimes they are separated by bands of 
fibrous tissue. 

If the disease is in the bone, usually in the head, as it is 
when the specific organism gains entrance and begins to grow 
in the interior of the jaw, the bone tissue about the organism 
becomes in places disintegrated and absorbed and pockets are 
formed containing the fungus. While the interior of the bone 
is being broken down and absorbed by the action of the acti- 



MORBID ANATONV 



309 



iiomycotic growth within, its diameter is being increased by 
the deposition of new tissue until it may become several times 
its normal size. 

The lesions spread in most cases by gradual invasion of 
the tissues surrounding the infected point. At the seat of 
infection, minute, inflammatory points appear, which extend at 
their periphery and unite to form larger areas of diseased 
tissue. These masses tend to extend in one direction and to 
heal in another, leaving behind bands of cicatricial tissue. 




Fig. 76. Actinomycosis of the upper ja7c. {Photoiiraphed by Hopkins) . 



The process usually differs widely from that of a simple 
inflammation. In its progress the disease shows no preference 
for structures but invades one tissue after another so that all 
may be involved alike. 

The lymphatics show no constant tendency to become 
involved. Metastasis occurs in a very small proportion of the 
cases. When it does, as reported by Ponfick, large areas may 
be simultaneously affected. He reports a case in the human 



3IO 



ACTINOMYCOSIS 



subject in which the left jugular vein was perforated by a mass 
of the fungi resulting in the formation of actinomycotic infarcts 
in the lungs, spleen, brain, and heart. 

In cattle, actinomycosis usually appears in one or more of 
the following locations. 

1. /;/ the inaxillary bones. Here it generally results in 
large tumor-like growths. Actinomycosis of the jaw usually 
commences with flat granulation of the gums and mucous 
membranes in the neighborhood of the teeth and spreads 
finally to the medullary tissues of the bone and to the perios- 
teum, soon giving rise to the osseous tumor. From the maxil- 
lary bone the disease may advance either to the subcutaneous 
connective tissue and the skin or to the oral cavity in the 
direction of the molar teeth, which become displaced. 

2. In the ton one. When the lesions appear in this organ 
the disease takes the form of an indurating glossitis. The 
tongue becomes thickly sprinkled with round or oval, hard, 




Fig. 77. Actinomycosis of the tongue, '^zuooden tongue 
by Hop/cins). 



[P/io tog rap tied 



fibrous nodules which finall}'^ become purulent or chalky at the 
center. Around these there is a considerable increase of con- 
nective tissue which leads to the atrophy of the muscle fibers. 



MORBID ANATOMY 31I 

Upon section the tongue is found to be hard and often gritty. 
The indurated tongue is often eroded from friction and various 
deformities of this organ are reported. 

3. 1)1 the pharynx. Here the disease usually takes the 
form of soft polypoid or fungoid nodules or lumps with a 
smooth surface and short peduncle. These nodules vary in 
size often reaching that of a goose's ^'g'g. These polypoid 
growths may cause great difficulty in swallowing and likewise 
interfere with respiration. Tumors of this kind may form in 
the esophagus or trachea. Rarely actinomycotic growths 
occur at other places in the alimentary tract. There are some 
cases in which the lesions are not restricted to the digestive 
tract. 

4. 1)1 the skin and subcutaneous tissue. The lesions of 
the skin and subcutis are found chiefly on the head and neck. 
They usually consist of firm nodules from the size of a hazel 
nut to that of a man's fist or even larger. Sometimes these 
nodules are pedunculated and at others they are attached to 
the skin by a broad base. Instead of the hard tumor there 
may occur soft granular fungoid proliferations covered with a 
brown crust or with a purulent secretion. At other times 
minute nodules appear in these proliferations and the .skin 
becomes thickened and indurated. However, the skin lesions 
may become very large. In this organ, the disease may be 
either primary or secondary. 

5. In the lymph glands. Actinomycosis often appears in 
the lymph glands of the head, larynx and pliarynx. The 
parotid and submaxillary glands are sometimes involved as 
secondary infections. It is reported that the sub-parotid 
glands are most frequently affected. 

6. hi the lu)io-s. The lesions in the lungs vary. They 
may consist of firm, .somewhat yellowish nodules which event- 
ually become calcareous in their center and vary in size from 
mere specks to that of a pea. This form is spoken of as 
miliary actinomycosis. In the second form the actinomycotic 
foci .soften and become filled with a gray mucopurulent fluid. 



312 



ACTINOMYCOSIS 



The lesion may spread to the pleurae and even reach to the 
surface of the bod}- by penetrating through the thoracic wall. 
The bronchial glands and the mucosa of the air passages may 
also become affected. 

7. hi other organs. Actinomycosis has been reported 
rarely as attacking the udder, spermatic cord, brain, spleen, 
liver, muscle, diaphragm, peritoneum, inguinal glands, vagina, 
uterus and cervical vertebrae. 

Assmann has recently summarized the literature on the 
dissemination of the lesions and has concluded that general- 




FiG. 78. r/iotograph 0/ a portion of a coic's tting, shoicing area of 
acti)wniycotic tissue surrounded by a wall of 
connective tissue. Natural size. 



ized actinomycosis is not rare in occurrence. He gives a de- 
tailed description of eleven cases in cattle and hogs. 

It is stated by Salmon that in England the disease ap- 
pears most often in the tongue, in Denmark the soft parts of 
the head are affected most frequently, while in some parts of 
Germany it is most frequently found in the pharynx. In the 
United States it usually appears in the lower jaw. In man as 
in cattle, the appearance of the lesions varies according to the 
part infected. In some cases the lesions closely resemble 
those of chronic inflammation but in others, such as the liver 



DIFFERENTIAL DIAGNOSIS 313 

or skin, they are often characteristic. In the lungs the lesions 
have frequently been mistaken for tubercle. Usually the dis- 
ease affects the head and if the maxillary bones are attacked 
the teeth are usually lost. 

Actinomycosis in swine. Actinomycosis appears in this 
species in the lower jaw, larynx, lungs, wounds caused by 
castration, in the mammary gland, muscles and bones. The 
character of the lesions does not differ to any marked extent 
in swine from those in cattle or man. In case of bone infection 
purulent cavities and sinuses are formed in which the yellow 
granules of the fungus occur. It is reported that occasionally 
pigs suffer from generalized actinomycosis. Duncker has 
found in the muscles of the pig a variety of the ray fungus 
which has been called Actinomycosis mnscolorum suis, to dis- 
tinguish it if possible from the bovine species. Its relation to 
the actinomycosis bovis has not been clearly determined. It 
is reported to have been found frequently. 

Actinomycosis in Iiorscs and sliccp. In the horse, acti- 
nomycosis of the bones, tongue, trachea, spermatic cord and 
submaxillary glands has been observed. The disease is re- 
ported to have been mistaken for glanders. The affection 
known as scirrhous cord seems to be due in rare cases to an 
infection by the ray fungus. One such case has occurred in 
the clinic of this institution. A very few cases of this disea.se 
have been reported in sheep, the lesions being restricted to the 
lungs or muscles. 

§ 233. Differential diagnosis. In cattle actinomycosis 
is to be differentiated (i) from tuberculosis, especially of the 
lungs, glands of the throat, head and the udder, (2) various 
forms of glossitis, polypoid growths in the pharynx, fibroma, 
.sarcoma and osteosarcoma of the jaw, parotitis and cellulitis. 
The writer has seen a few cases of bacterial infection of the 
maxillary glands giving rise to the formation of large quanti- 
ties of caseous matter which caused swelling and firmness 
suggestive of actinomycotic tumors. In one instance a speci- 
men reported to l)e actinomycosis was examined and found to 



314 ACTINOMYCOSIS 

contain a piece of bone about three inches long which had 
become wedged between the teeth and cheek and surrounded 
by inflammatory tissues. Frohner calls attention to conta- 
gious diseases as possibly being mistaken for this disease. 

The affection recently described by Lignieres as actitio- 
bacillosis is to be distinguished from actinomycosis of the skin. 
It is thought, however, by many workers that actinobacillosis 
is a variety of actinomycosis. 

In making a positive diagnosis of actinomycosis it is 
necessary to make a microscopic examxination of some of the 
diseased tissue or of the discharged pus in which the ray 
fungus may be found if the disease is actinomycosis. It is 
impossible to obtain this positive proof from the living animal 
when the disease is situated in the internal organs. With 
these it is necessary to depend largely upon the history and 
general condition of the animal. In preparing the discharged 
pus for a microscopic examination it is usually sufficient to 
crush one or more of the yellowish granules between a slide 
and cover-glass. It is of advantage to wash it with a dilute 
solution of caustic soda to clear away the pus cells. The 
rosettes are easily recognized with a low magnification. 

In man, actinomycosis is to be differentiated from certain 
forms of tuberculosis and the Madura foot disease which was 
described by Carter, in i860, as a " fungus disease. " This 
is a chronic, locally spreading inflammation of the foot, rarely 
of the hand, causing the destruction of the part involved and 
giving rise to a great overgrowth of connective tissue. My- 
cetoma almost invariably attacks the hand or foot and accord- 
ing to Carter there are no secondary deposits in the viscera. 
In actinomycosis the extremities are rarely attacked and the 
viscera are often the seat of the disease ; further the mycetoma 
is a disease of hot climates while actinomyco.sis is a disease of 
the temperate latitudes. The fungus of the two affections 
seem to be closely related but as yet their identity has not 
been established. 

^ 234. Specific treatment. The investigations of 
Thomas.sen, Nocard, and Norgaard and the experience of a 



SANITARY CONSIDERATIONS 315 

large number of veterinarians have proved verj^ conclusively 
the specific, curative effect of iodide of potassium. According 
to Salmon the iodide of potassium is given in doses of from 
1.5 to 2.5 drams dissolved in water and administered in a 
drench, once a day. The dose should var}' somewhat with the 
size of the animal and with the effects that are produced. If 
the dose is sufficiently large there appear signs of iodism in the 
course of a week or ten days. The skin becomes scurvy, and 
the eyes moistened. There is nasal catarrh and loss of appe- 
tite. When these symptoms appear the medicine may be 
suspended for a few days and afterwards resumed in the same 
dose. The cure requires from three to six weeks' treatment. 
Some animals do not improve with the administration of 
iodide of potassium and these are generally the ones which 
show no signs of iodism. 

If there is no sign of improvement after the animals have 
been treated four or five weeks and the medicine has been 
given in as large doses as appears desirable, it is an indication 
that the particular animal is not susceptible to the curative 
effects of the drug and the treatment should be abandoned. 

It is not, however, advisable to administer iodide of potas- 
sium to milch cows, as it will considerably reduce the milk 
secretion or stop it altogether. Furthermore, a great part 
of the drug is excreted through the milk making it unfit for 
use. It should not be given to animals in advanced pregnancy, 
as there is danger of producing abortion. 

v^ 235. Sanitary considerations. The literature upon 
this subject is largely to the effect that actinomycosis is rarely 
if ever either contagious or infectious in the sense that it can 
be transmitted from one animal to another or from one of the 
lower animals to man. There seems to be no indisputable case 
on record of such a transmission, although a few cases are 
very suggestive. It is the opinion of most pathologists that 
when the disease is restricted to small tumors and these are 
localized, that the affected parts should be destroyed but the 
remainder of the carcass may be used for human consumption. 

In Bulletin No. 2, of the Board of Live Stock Commis- 



31 6 ACTINOMYCOSIS 

sioners of Illinois, published in 1891, is the report of the some- 
what famous trial in the Peoria county circuit court of the case 
of J. B. Greenhut et al. vs. John M. Pearson et al. to recover 
damages for the rejection and destruction of certain actinomy- 
cotic cattle, in which is given the testimony of a large number 
of distinguished veterinarians and sanitarians concerning the 
wholesomeness of the meat of cattle affected with this disease. 
Although at that time there was a strong popular sentiment 
against the use of such animals, the jury after a forty hours' 
consideration reported their inability to agree and were dis- 
charged by the court. The most conspicuous feature of this 
evidence was the inability of the witnesses to produce satis- 
factory evidence of the communicability of the disease from 
animal to man. This evidence did much to show that the 
danger from this disease in eating meat of affected animals was 
after all a matter of opinion, fear or sentiment rather than a 
demonstrated fact. Mayo, in his bulletin upon the subject, 
states that there is no danger of persons contracting this dis- 
ease from eating the flesh of affected animals provided the 
visibly diseased portions are removed. 

RRFERKNCKS 

1. BOSTROEM. Untersuchungen iiber das Aktinomj^kose des Meu- 
schen. Beitrag. ziir path. Anat. 11. zur allge. Pathologic, Bd. IX 
(1891), S. I. 

2. Israel. Neue Beobachtungen auf den Gebeite des Mykosen 
des Menschen. Virchow's Archiv, Bd. LXXVI (1878), S. 11. 

3. Mavo. Actinomycosis bovis or "lumpy-jaw." Bulletin No. 
jS, Kansas State Agric. Exp. Station, 1892. 

4. Moore Actinomycosis mistaken for tuberculosis at post- 
mortem following the tuberculin test. A»i. I'et. Revicic, Vol. XXX 
(1906), p. 181. 

5. NocARD. Notes sur l'actinom3'cose des animaux. Rccueil de 
Med. VHer. Vol. LXIX (1892), p. 167. 

6. Salmon. Treatment of lumpy-jaw or actinomycosis in cattle. 
Bulletin No. 2, U. S. Bureau of Animal Industry , 1893. 

7. vSalmon. Actinomycosis or lumpy-jaw. Annual Report, 
Bureau of Aninial Industry, 1893-4, p. 88. 



INFKCTIOUS DISEASES 



317 



8. WoLFK UNI) IsRAKi.. UeberReinculturdes Actinomyces und 
seine Uebertrag1)arkeit auf Tliiere, Virc/i. Arch Bd' XXVI 

(1891), vS. II. 

9. Wright. The biology of the microorganism of actinomycosis. 
The Jour. 0/ Med. Research, Vol. XIII (1905), p. 349. 



ACTIXOBACILLOSIS. 

§236. Characterization. Actinobacillosis is described 
as an infectious disease of cattle, characterized by its clinical 
resemblance to actinomycosis. It is caused by an organism 
which "resembles, in marked degree, the bacterium of Fowl 
Cholera." It arranges itself in the tissues in "rosette" or 
ray-like forms. It is thought by some workers to be a variety 
of actinomycosis. It is described as an independent and dis- 
tinct disease. 

§237. History. Lignieres and Spitz described, in 1902, 
a disease in cattle resembling actinomycosis but which was 
caused by a bacterium. Until 1900-01 this affection was not 
differentiated from actinomycosis. Nocard, in 1902, identified 
the disease in France. In [904, Higgins described four cases 
in Canada. These appear to be the only records we have of 
this affection. 

§ 238. Geographical distribution. It is reported by 
Lignieres and Spitz to be epizootic in Argentine Republic. 
It has been described in France, and in Canada. 

§ 239. Etiology. This disease is caused, according to 
its investigators, by a bacterium which arranges itself in the 
tissues in a rosette or ray-like appearance. It is aerobic, 
facultative anaerobic, non-motile and of a variable size, rang- 
ing between i.o and 1.8 /< in length and from 0.4 to 0.6 // in 
breadth. According to Higgins, it has a distinct polar arrange- 
ment of the protoplasm as observed in the hanging drop prep- 



3l8 ACTINOBACILLOSIS 

aration. It stains with the ordinary aniUne dyes.^' It does 
not take the Gram stain. 

In the fresh tissues or in sections it appears in granules 
the same as in actinomycosis. 

The actinobacillose is virulent for guinea pigs and rab- 
bits. When inoculated into the abdominal cavity with pure 



% 




Fig. 79. A photograph of a section of a tuuior stained by Gram's 
tnethod but not fully decolorized. X about r, 000. [After Higgins). 



*Higgins recommends the Romanowsky stain as modified by Dut- 
ton'^and Todd for sections or preparations from pus. The formula for 
the stain and method for its use are as follows : 

Stain: Eosin, aqueous solution i part 

Borrell's Blue i " 

Water 8 parts 

Mix just before using and filter. Suspend the preparations (sections 
fixed to the slide) upside down on the stain to saturate them from 
below, to avoid precipitate. Stain in this solution for thirty minutes. 
Wash thoroughly in water, then in a 10% solution of tannic acid, which 
will^brighten the color, and again wash in water. Dehydrate in alcohol, 
clear and mount in xylol balsam. The stain as above prepared spoils 
quickly. 



MOkHID ANAT<)!\IY -^ig 

cultures guinea pigs die in from nineteen to thirty-one days 
( Higgins) of generalized actinobacillosis. These are reported 
to be characteristic and different from those of any of the 
other observed infective agents. According to Higgins, 
"Small pearly-white nodules appear just beneath the peri- 
toneal and pleural membranes, varying from i.o to 5.0 mm. in 
diameter. The liver presents lesions throughout its subtance, 
the surface being mottled. The spleen .shows, usually, a 
varying number of nodules. The great mesenteric fold of the 
omentum has in every instance been the seat of extensive 
lesions. The kidneys present nodules beneath their serous 
covering, but none have been observed in the substance of the 
organ. The stomach and intestines usually present nodules 
on their serous surfaces, varying from i.o to 0.5 mm. in dia- 
meter. ' ' There are other lesions such as ulcers in the stomach, 
nodules in the heart and pericardium. Subcutaneous inocula- 
tions are usually followed by similar lesions. 

Rabbits are said to react the same as guinea pigs. Nocard 
found an intravenous injection fatal to dogs in 24 hours. In 
horses a local abscess resulted which healed rapidly. 

The method of infection has not been fully explained, but 
it is supposed that the organisms are taken with food as in 
cases of actinomycosis. 

The organisms are .said to agglutinate in .serum of animals 
affected with actinobacillosis. 

It is destroyed in 10 minutes at 62° C. It grows best at 
incubator temperature (37° C). It is not rapidly destroyed 
by freezing. 

i^ 240. Symptoms. They do not appear, in cattle, to 
be differentiated from those of actinomycosis. 

§ 241. Morbid anatomy. The lesions are very similar 
to those of actinomycosis. The location of the affected parts 
varies. Lignieres describes it as attacking the skin, lymphatic 
glands, tongue, pharynx, mammary glands, the viscera and 
bones. The tissue changes appear to be an infiltration of puru- 
lent material, and the new formation of connective ti.ssue. 



320 ACTIONOBACILLOSIS 

The skin is often affected. In the single specimen which the 
writer has had an opportunity to study, the ray-like arrange- 
ment of the organism and the tissue immediately surrounding 
it, could not be easily distinguished from a section of actin- 
omycosis. 

ij 242. Differential diagnosis. Actinobacillosis is to be 
differentiated from actinomycosis, tuberculosis, perhaps cer- 
tain parasitic diseases of the skin, and localized bacterial 
infections. 

The diagnosis is made from the various locations of the 
lesions. The more important of these is the apparent selec- 
tion of the skin. The examination of the fresh pus does not 
reveal the yellow granules as observed in actinomycosis but 
when squeezed between two cover-glasses they are said to be 
distinct. The actinobacillosis does not take the gram stain, it is 
infectious for guinea pigs and rabbits, and it is readily cultiva- 
ted on artificial media. It appears to be transmitted more 
often in cattle by cohabitation than actinomycosis. 

The differentiation from any parasitic trouble is made by 
the finding of the animal parasite. The nature of the lesions 
and the finding of tubercle bacteria in the discharge by micro- 
scopic examination, or by producing tuberculosis in guinea 
pigs by inoculations, would differentiate it from tuberculosis. 

§ 243. Prevention. As the natural habitat of <?r/'/;z(?(^<3'- 
cillose is not known, the source of infection is undetermined 
and consequently effective preventive measure are not known. 
The fact that it seems to spread from infected to healthy cattle 
necessitates the isolation of the infected. It is more desirable 
when possible to separate the well from the infected animals. 

REFERENCES. 

1. HiGGiNS. Actinobacillosis. Bulletin No. /, Biological Lab- 
oratory, Department of Agriculture, Dominion of Canada, 1904. Also 
Proceedings Amer. Vet. Med. Asso., 1904. 

2. Lignib;res and Spitz. Actinobacillose. Contribution a 
V Hude des affections connues sous le nom d'actinomycose. Buenos Aires> 
1902. 



i.ep:ches 



32 r 



3. LiGNiKKics AND Spitz. Actinohacillose. Rccueil de IMedicine 
\''Hcrinaire, 1903. 

4- NoCARi). Actiiiobacillose der Znnj<e. A/Z/r. o'^.? Vet. Med. 
Berlin, Bd. I.VI (1903), p. 695, (abstract). 



LEECHES. 

Syjionyms. Summer sore ; leeching ; barsati, barsdti, bar- 
sattee, barsatti, baiisette, bursafi, bursatie, burusaltec, biirsatti, 
bursaidee, bursaiitie, bursautlie, bursotlee and bunisatitice. These 
names have been derived from the Indian word burns or 
bursaf, meaning rain or rain sore, it having been supposed that 
the malady was associated with the rainy season. 

§244. Characterization. " Leeches " or " leeching " 
is an infectious disease quite prevalent among the horse kind 
in Florida with lesions localized on the skin or the muco.sa of 
the head. It is thought by many that this affection is identical 
with the disease known as bursattee* in India. 

§ 245. History. Neal of Florida described this disease 
as affecting horses and cattle. He believes it to be peculiar to 
that section, where he states it is common and very fatal to 
horses and mules. There are hundreds of ponds in the central 
portion of the state around the margins of which there is 
usually a belt of grassy prairie, water grass and water lilies. 
Into these grassy places the horses, mules and cows often go 
during the summer and feed all day in the water. He adds, 
"after a varying exposure to the influence, or whatever it may 
be called, of the 'pond,' a slight lump or elevation of the skin 
may be found on some part of the body that has been sub- 
merged. To the touch it will feel as if a grain of shot were 
lodged beneath the skin. In eight or ten days the skin 
sloughs olT centrally over this hard spot, leaving a bloody, 

*It seems to be true that an entirely different affection is known by 
the same name in the northern portion of the United States. The term 
"Leeches" is also applied to the condition following the invasion of ths 
liver fluke [Fascio/a hef>atica). 



322 LEECHES 

bruised-like surface. This rapidly grows in size till in a few 
weeks there is a raw surface from four inches to a foot square. 
This oozes blood and serum and no pus. An examination 
will usually show a mass of yellow, gritty growth, coral-like 
in shape, embedded in a mass of bruised, bloody tissue, dark 
incolor with the edges roughened, elevated above the skin, and 
the skin decaying at the outside of the ulcer. The leech 
invades almost an}?^ tissue, but seems most common on the legs, 
abdomen and sides. Occasionally it is found in the head. 
The invaded tissues decay slowly and apparently without pain. 
I have seen hoofs cut off, the abdomen opened, the eyes eaten 
out and the teeth destroyed." 

In this country the disease has not attracted very much 
attention, nor has it been considered of much economic import- 
ance. An explanation for this may be offered on account of 
its seemingly non-contagious character and because it has been 
thought to be confined to comparatively limited areas, and 
because the animals, although infected, may be utilized for 
some purposes. On account of the chronic course of the dis- 
ease the affected animals are often killed from a sentiment of 
mercy before the disease can terminate fatally. 

Although this affection presents many points of similarity 
to the one found in India, the question of their complete iden- 
tity ought to be held in abeyance until a more thorough inves- 
tigation can be made. 

In a recent publication, Dawson, of the Florida Experi- 
ment Station, states "that 'leeches' or bursattee is a common 
disease in Florida, which manifests itself in the formation of 
tumor-growths which have some of the characters of actinomy- 
cotic tumors. Its structure is fibrous, and contains many 
sinuses, which discharge a bloody, 'honey-like' fluid. It is a 
fatal, infectious disease, which has its origin in the skin and 
finally penetrates all the tissues. Here and there in the tumor 
tissue yellow bodies with root-like projections may be found. 
These bodies are called 'leeches' by the natives. They consist 
of the mycelia of the fungus which causes the disease. The 
only remedy is the complete removal of the tumor and adja- 



HISTORY 323 

cent tissue at once. The application of caustics and disinfect- 
ants makes matters infinitely worse, as they stimulate the 
tissues to renewed growth-activity. In Florida the disea.se 
affects only the genus equinus." 

In 1896, some of the diseased tissue from cases of this 
affection in Florida, were sent to the Bureau of Animal Indus- 
try for investigation. They were studied by Fish, who made 
an extended report on the results of his findings. He also 
gave a very complete review of the literature. 

Hodgson, in 1853, referred to the sores as cancerous ulcers 
and Hart, in 1872, was strongly inclined to pronounce it 
cancer, although he could not confirm this view structurally 
by microscopic examination of the tissue. It seems to be 
generally accepted that the disease is peculiar to the Tropics, 
but cases have been reported in Kansas and Minnesota in the 
United States, not only during the summer months, but when 
the thermometer registered below zero. We might also expect 
that the disease would exist in Mexico and Central and South 
American countries, where the conditions of temperature and 
moisture are favorable. 

Reports show that a high temperature is essential for the 
development of the disease, although exceptional cases are 
noted as occurring during the cold season. Moisture does not 
seem to be necessary, since man}'^ cases develop when the sea- 
son is dry. It is, however, an important factor. Statistics 
show that cases are more numerous and that the disease 
assumes a more aggravated form during the wet season. 

In India, native as well as foreign bred horses are sus- 
ceptible, but according to some writers, none of the other 
equine species is affected. 

In the United States mules and cattle are said to develop 
it, but not so readily as the horse. Outbreaks among cattle 
are comparatively rare. Thin-skinned animals are more sus- 
ceptible than thick-skinned ones. Some discrepancy of 
opinion exists as to the kind of horses most likely to take the 
disease (assuming that bursattee and leeches are similar). 
Neal states that only horses of good blood leech, and the 



324 LEECHES 

Cuban and Texan ponies are as a rule exempt. Anderson 
states that it is the coarsely bred and hard-worked horses that 
are the most susceptible. The well-bred ones, having the ad- 
vantage of good hygienic surroundings, rarely contract it. 

§ 246. Geographical distribution. Bursattee has been 
reported from Bunnah and Hindoostan. It is thought that 
the prevalence of the disease is associated with the principal 
river systems of India. In the hilly, rocky and consequently 
drier districts there is a very noticeable diminution or absence 
of it. 

Outside of India there seem to have been no cases of this 
malady reported except in the United States, unless upon fur- 
ther investigation certain mycotic diseases which have been 
described in Europe should prove to be identical with it. 

Lyford (1866) reported it in Minnesota, Anderson, (1889) 
in Kansas and Alabama, and Neal ^1887) and Bitting (1894) 
in Florida. The latter writer states, that it is "now known 
all over the United States except in that region lying east of 
the Alleghany mountains and north of the Potomac river." A 
few cases have been presented for treatment in the clinic of the 
New York vState Veterinary College. 

-^ 247. Etiology. A summary of the literature shows 
that among the old theories "leeches" was believed to be a 
blood disease in many ways not unlike syphilis, scrofula and 
farcy. The "fly theory" of the causation and dissemination 
of bursattee was entertained by the natives of India as early as 
1820. Jackson, in 1842, seems to have been the first to 
believe that there was any connection between the disease and 
a fungus. 

Jackson suggested, in 1842, that the disease might be re- 
lated to a fungus or to a vegetable parasite. Collins, in 1874, 
expressed a similar belief, F. Smith, in 1879 and 1884, 
seems to have been the first to have worked along this line. 
He was able to find fungi in every fresh specimen of the 
sores that he examined. Steel, in 1 881, also found fungal ele- 
ments in these sores. T. Smith, in 1893, examined some 




MORBID ANATOMY 325 

alcoholic material and gave expression to the belief that the 
disease was caused by a fungus. Fish, in 1896, found a 
fungus embedded in the diseased tissue. He did not name it 
neither did he obtain it in pure cul- 
ture, but his illustrations are ver3' 
clear in showing the existence of 
the fungus. Fish gives in detail 
the methods he employed. It is to 
his work that we are indebted for 
the more careful description of the 
morbid changes. Fig. 80. A piece from the 

lip of an affected horse, shozv- 
§ 248. Morbid anatomy. As i"g' several diseased foci 
a rule the lesions are near the (-^"''^)- 
surface. Where the diseased portion has become well de- 
veloped there is usually a more or less complete detachment 
of the central inflammatory growth from the surrounding 
tissue. This nodular or "kunker" growth may vary in its 
density according to the stage of its development. During 
the early stages it is soft and easily cut ; later it becomes 
firmer and ultimately assumes a hard or "gritty" character. 

In cutting sections it is generally the exception to cut 
through the nodule or kunker evenly and to have it retain its 
proper relations with the other parts. Even if successful in 
cutting, the nodule drops out after some of the other processes. 
In the specimens examined the lesions were confined entirely 
to the skin and subcutaneous tis.sue ; no traces of muscular or 
glandular structure were observed. Around the central por- 
tion of the inflammatory growth there is a zone of leucocytes 
of the mononuclear and polynuclear varieties, the latter pre- 
dominating. They are embedded in an abundant stroma of 
connective tissue which is in a greater or less stage of degen- 
eration. The central portion of the zone is in some cases very 
closely packed with the leuococytes, while toward the peri- 
phery they are more loosely arranged and cause a marked 
irregularity of the margin from their uneven drifting into the 
tissue beyond. There is generally one and perhaps more 




Fungus. 
Fig. 8i. J^ai-ions forms of the fungus. 




MORBID ANATOMY 327 

points where this infiltration occurs quite extensively. In 
some of the preparations the wandering cells have been traced 
as far as the surface of the epidermis. 

Occasionally there may be found a narrow area at the 
periphery of the nodule, as seen /r— v 
in cross section, which is lighter h 
in color and less dense in text- 
ure than the central mass, evi- 
dently an extension of the 
growth. 

In the specimens examined 
the parts where the lesions 
abounded were not character- 
ized by a rich vascular supply. Fig 82. From the sa)ne lip, but 
The few vessels that were en- sho7ciiig a larger infected area 
countered were not of a normal V"^^'^)- 

character ; their walls were thickened, and the endothelium, 
instead of presenting the usual flattened appearance, was 
irregularly cylindrical. Although the condition was not ob- 
served, it is not impossible that the hyphse of the fungus may 
develop to such an extent as to compass or actually penetrate 
the walls of the vessels, causing inflammatory changes suffici- 
ent to permit, in the course of time, a disorganization or ab- 
sorption of a portion of the vessel itself, and that ultimately it 
may become incorporated in the nodule. 

DESCRIPTION OF FIO. 81. 

1. Shoiving a young fungus embedded in the tissues (/i/> \. 

2. Showing scale-like bodies embracing the filaments. 

3. Shoiving young branches of the fungus, and in one place the 
transparent sheath. Hematoxylin preparation. 

4. 3fycelium with scale-like bodies lying among the filaments. 
Hematoxylin. 

5. Vacuolated filaments. Hematoxylin. 

6. Branches shoiving a well developed, transparent sheath. In 
places the axis of the branch is disconnected and occasionally there is 
a faint sign of a septum. Hematoxylin. 

No. 4 ocular, 2 mm. objective. Camera lucida (.Ifter Fish). 



328 LEECHES 

The nodules are generally irregularly cone shaped and are 
of variable size. In section they reveal a very dense struc- 
ture, the framework of which forms a close reticulum. 

Within the meshes are what appear to be 

jKU^^^ leucocytes in various stages of disintegration, 

I ^^^T I and free nuclei. Among these, at places, 

1 there can be seen small bodies of nearly the 

Vi&.8:i.y4ntsolai- same size as the nuclei and taking the stains 
■ed nodtile show- •,. t,i.j-nr--r a^ 

,, , in the same way, but differing in form. At 

tug the charac- . . ' , ^ 

teristic rough- ^^^ portion of its circumference the substance 
e n e d , coral-like of the body is seen to draw itself toward a 
appearance of the point and in favorable preparations that point 
mass {Fish). ^^^ ^^^^^ followed some little distance as a 

delicate filament. In most cases the filament remains un- 
stained, or, as observed in a Gram-eosin preparation, the club 
end may stain blue and the filament red. Exceptionally one 
may find a clear area or vacuole in one of tlie clubs. From 
the fact that the filament is not usually traceable to its central 
connection a more or less flagellate appearance is given to the 
fungus, which represents a condition not believed to exist. 

Not infrequently small spherical bodies are found not far 
from the clubs, which take the stain readily and whose size is 
sufficiently small to admit of the possibility of their being 
spores. The free ends of many of the clubs point toward the 
periphery' of the nodule, but this is not a constant feature. 

The framework of the nodule stains very slightly or not 
at all and shows among the enmeshed corpuscles as a very 
irregular, distorted and somewhat glistening network. It is 
this portion of the nodule that gives the hard, gritty feeling, 
and is probably due to a greater or less deposition of lime salts 
along the reticulum. It appears that the framework of the 
nodule is composed of a mycelial net, which in the course of 
development has become more or less calcified. 

As a result of the treatment of the nodules with a lo per 
cent cold solution of caustic potash, a very profuse and intric- 
ately branched fungus became apparent. The branching is of 
an irregular order. In places there is seen in the filament a 



MORBID ANATOMY 



329 





















central axis, which takes the stain, and around this appears a 
transparent or hyaline sheath of varying size. 

In certain of the teased preparations (Bioudi-Ehilich 
stain) the wall of the filament, 
instead of being smooth and 
homogeneous, appears rough- 
ened, as if covered with very 
minute but numerous spinous 
processes. 

In the sections of the tis- 
sue in which the fungus ap- 
peared the substance of the 
filament was not uniform. In 
places it was drawn together 
in an irregular manner, with 
intervening clear spaces of 
greater or less area. 

In some places the fila- 
ments show distinct septa, but 
the latter are not common. 
Some of the club-like endings, 
especially those that are elon- 
gated, show a septum at the union with the filament proper. 
Scattered among and coiled around the ordinary filaments 
there have been observed much more slender ones apparently 
devoid of any external sheath. 

There have also been observed numerous small circular 
bodies of inconstant size. They have been seen lying freely 
in the meshes of the mycelium and also closely applied to the 
filaments. These bodies are not spherical, but thin and flat- 
tened, and some of them present a curved appearance, convex 
on the outer side and concave on the inner side. They sug- 
gest the possibility of having been closely applied to the fila- 
ments and have something of a scale-like arrangement. With 
possibly one exception, no trace of blood vessels has been 
found in the nodules. 



Fig. 84. The fungus. Toluidin 
blue preparation ( Fish ) . 



330 



In the circumnodular tissue pathologic conditions exist, 
consisting of certain areas of tissue necrosis. 







Fig. 85. A scclio7i through a nodule shocving its deuse texture, with 
a portion of its peripheral zone made up ofhyphic 'with leucocytes inter- 
spersed. Methylene blue and eosin stain. No. 4 ocular, Snun. objec- 
tive. Ca inera lucid a dra u • ing ( Fish ) . 

There is an infiltration of the connective tissue with a 
great number of wandering cells. In some places there are 



M OR HID ANATOMY 331 

well-defined nests in the stroma of the connective tissue, simu- 
lating, perhaps, a cancerous appearance. The character of the 
cells, which present a curiously vacuolated condition, would, 
however, tend to eliminate this view. The vacuoles very in 
number and size, the average number being i to 12 in a cell. 

In some preparations numerous leucocytes, of the mono- 
nuclear and polynuclear varieties, had drifted away from the 
nodule. They were for the most part elongated, and in all 
the nucleus or nuclei appeared to be in a healthy condition. 
The cells contained numerous eosinophiles, which took a deep 
orange color with the Biondi-Ehrlich stain. In places adjacent 
to these leucocytes there were frequently noticed a number of 
these small bodies apparently lying free in the tissue. No 
definite cell wall was distinguished in the leucocytes. 

The vacuolated cells are present in greater numbers than 
the heavily laden leucocytes. In the former nuclei were pre- 
sent and presented various phases of change. In some there 
is a single nucleus, which may be circular, crescentic, or in 
the form of a dumb-bell; in others there may be two or more 
nuclei which in advanced cases appear only as remnants. In 
extreme cases no nuclei at all are visible. The wall of the 
wandering cell differs from that of the leucocytes proper in 
possessing an appreciable thickness. This thickened bound- 
ary apparently gives considerable rigidity to the cells, as 
nearly all of them are approximately circular in form. Their 
average diameter is about 8 microns. In one specimen there 
appeared to be large giant cells, measuring from 1 2 to 18 
microns and apparently possessing quite a distinct cell wall. 
Within each giant cell there is some appearance of vacuolated 
cells, each with a single nucleus and fairly well-defined cell 
boundary. As many as eight or ten of these nuclei have been 
counted in a single giant cell. There is the possibility that 
these apparent giant cells are simply some of the vacuolated 
cells fused together, but the nuclei are well defined and take 
the stain very intensely, which is not coiniuDiily the case in 
the ordinary vacuolated cells. 

The connective-tissue cells surrounding the nodule show 



332 LEECHES 

marked signs of degeneration, their cytoplasm inmost cases 
being extremely vacuolated. Among these connective-tissue 
cells, which for the most part are quite branching and elon- 
gated, is another class of cells which are in general of an oval 
or elliptical form. The noteworthy appearance of these cells 
is the presence of numerous dots in the cytoplasm which take 
the methylene blue and toluidin blue stains very deeply. The 
appearance is, indeed, very much as if the cells were filled 
with micrococci. These are the granule cells of Waldeyer, or 
still further differentiated as the plasma cells, in contradis- 
tinction to the " mastzellen " or "food cells," which indicate 
an exalted degree of nutrition. The nucleus of the plasma 
cell takes the stain very slightly, or not at all, and is almost 
entirely obscured by the numerous " granules " in the cyto- 
plasm. These cells are well differentiated by the toluidin 
blue stain, as the}' take a deep purple color, while the sur- 
rounding cells are blue. 

Bitting has figured the jaw bone of a horse quite exten- 
sively affected with this disease. He believes that the lesions 
about the mouth result from the animal biting the affected 
areas on the body. 

Neyrick reports finding the inflammatory growths in the 
lungs of an affected subject, and Burke has reported them in 
the liver. There are no other lesions described in the internal 
organs although Neal writes that any tissue may be invaded. 

§ 249. Treatment. On the ground that the fungus sup- 
posed to be the cause of this disease may be closely related to 
the ray fungus of actinomycosis, the use of iodide of potas- 
sium has been recommended. It is reported to be fairly suc- 
cessful. The efficiency of this drug as a specific needs further 
confirmation. 

REFERENCES. 

1. Bitting. Leeches or leeching. Bullelin No. 25, Florida Agri- 
cultural Experiment Station, 1894. 

2. Fish. A histological investigation of two cases of an equine 
mycosis, with a historical account of a supposed similar disease called 
bursattee occurring in India. Atinual Report, Bureau of Animal In- 



PNEUMONOMYCOSIS 333 

djistry, U. S. Depl. of A^ricullure, 1895-6, p. 229. (This report con- 
tains a biblioi^raphy on Bursaitee. ) 

3. NiCAi,. I.eeching of horses and cattle. Annual Report, 
Bureau of Animal Industrv, U. S. Depl. of Agriculture, 1887-8. p. 
489. 



PNEUMONOMYCOSIS. 

^ 250. Species of fungi. The literature contains a num- 
ber of reports of cases of myco.sis in the lower animals as well 
as in man due to infection with different moulds. The genus 
Aspergillus seems to infect and to produce lesions in animals 
more frequentl}' than the members of other genera. In fact, 
Aspergillus fumigatus^^^\\\% to be the only important pathogenic 
species. The lesions encountered as a result of its invasion are 
largely restricted to the respiratory tract. Pneumonomycosis 
has been reported in a number of cases. Cadeac, Schneide- 
miihl, Friedberger and Frohuer, Ostertag and Kitt have all 
called attention to mycotic pneumonia. Renon considers the 
lesions resulting from aspergillus infection as a pseudo-tuber- 
culosis which he would designate as " Aspergillar tuberculo- 
sis." Aspergillar pneumonia is, however, quite rare. 

^ 251. Description and method of cultivation of the 
mould. The aspergillus fungus is readily cultivated artifi- 
cially. It grows on most of the ordinary culture media used 
in bacteriology if the reaction is acid ; it develops poorly in 
alkaline media. The well-known Raulin's fluid is reported to 
be the best medium for its cultivation, especially where the 
aspergillus must be isolated from mixed growths, as in the ex- 
amination of sputum. vSabourand's* solution of maltose also 
gives good results. 



*The formula recommended by Ravenel is as follows : 

Maltose, 3 70 grams. 

Peptone, 0.75 grams. 

Distilled water, loo.co c. c. 
To this may be addtd gelatin or agar to solidify it, the latter being 

preferable, as the aspergillus grows best, and forms fruit best at 37° to 
39° C. 



334 



PNEUMONOMVCOSIS 



For ordinary use potato, with or without glycerin, gives 
excellent results. A paste made by rubbing up crumbs of 
stale bread in water is also a good medium. Growth is said 
to be more rapid, however, in Raulin's fluid than in any other 
medium, the mycelium appearing in from five to twelve hours 
and spores forming in from twelve to fifteen hours. The 
growth is first a velvety white, soon becoming a delicate bluish 
green, which grows darker. On Raulin's fluid it changes 
after some days to a dark brown. Cultures on potato retain 
the green color for a long time, while those on bread paste 
become brown. 

The fungus retains its vitality in cultures for many 
months unimpaired. Its development has been reported when 
inoculated from cultures three or four years old. Spores do 
not form in a temperature below 20° C. and like the mycelium 
they require fresh access to oxygen for their best development. 
They measure 2.5 to 3// in diameter. In nature the spores are 
widely distributed but seem to be especially abundant in grain 
and vegetable matter. They have considerable power of re- 
sistance to heat and to chemical 
agents. They are killed by a tem- 
perature of 60° C. in five and one- 
half hours. In moist heat and in 
solution of bichloride of mercury i 
to 1,000 they are destroyed in 
fifteen minutes. 

Aspergilhis fumigatiis is dif- 
ferentiated from other species by its 
color in cultures, the high tempera- 
ture at which it grows, the size of 
the spores and by its pathogenesis. 
Aspergillus giaucus is the one most 
likely to be confounded with it. It 
may be differentiated from A. fumi- 
_gatus by its ability to grow at low temperature, its delicate 
green color, the large diameter of its spores — 9 to 15/^ — and its 
lack of pathogenic power. 




Fig. 86. Aspergillus fumi- 
gatus i?! fruit. 



cri/ri\'ATi()N 



335 



The mode of infection is through the respiratory tract. 
Only a small number of the spores inspired are able to reach 
the alveoli, the greater number of them being arrested in the 
tracheal and bronchial secretions. Hildebrant has shown that, 
having reached the alveoli, they penetrate the epithelial lining 
without difficulty. Both animals and man seem to possess 
immunity to intestinal infection. Renon has produced it only 
a few times experimentalh-. 

The aspergillus does not form toxin. Its pathogenic 
power is due entirely to lesions produced by the masses of 
mycelium which causes a necrosis of the cells and a leucocytic 
reaction which diminishes the functions of the organs, the 
final result being an enfeebled condition of the animal and a 
lessened resistance to hurtful influences. When fruit hyphae 
can form, the myriads of spores given off by them may be 
carried to other parts of the organ. In this way the foci 
rapidly multiply and practically the entire organ becomes 
invaded. The opinion held by some authors that in the mould 
myco.ses there is "no fructification or actual multiplication" of. 
the infected agent and that the "number of the diseased foci 
corresponds exactly with the number of spores introduced," 
is erroneous both for the disease naturally contracted as well as 
for the experimental form. In the produced lesions, fruit 
formation of the fungus is exceptional. It has been observed 
by Renon to take place only where there is full communication 
with the air. It has been observed only in the lung. It is 
extremely rare for aspergillosis to pass from one animal to 
another. The infection can onl)^ take place with the spores. 

Piieunionomycosis in cattle. Recently Pearson and Ravenel 
have described a very interesting case of pneumonomycosis in 
a cow due to A. fiunigatiis. As this seems to be the only care- 
fully described case in this species of animals listed in this 
country their description of the symptoms and lesions is very 
largely incorporated here. The case was in a Jersey cow six 
years old. She had been in poor condition for six months 
prior to bringing her to the Veterinary Hospital where she was 
tested with tuberculin with no reaction. At this time she did 



IE 



,1TY 



336 



PNEUMONOMVCOSIS 



not eat, was weak and depressed, respiration labored and from 
40 to go per minute. Pulse rapid. Percussion of the chest 
walls gave a sound that if anything was clearer and louder 




Fig. 87. Composite drazving of section of lung through nodule of 
aspergillus origin. F, fibrin in alveoli. S, fruit hyphae and spores 
of fungus (Ravenel). 

than the normal percussion sound. Upon auscultation it was 
found that the vesicular and bronchial murmurs were consider- 



MORBID ANATOMY ^o? 

ably increased in intensity and accompanied here and there by 
sibilant rales. She coughed violently at times. Six days 
after she came to the hospital the breathing became more rapid 
and difficult and the pulse very much accelerated. The animal 
did not eat, grew weak rapidly and died four days later, or 
ten days after admission to the hospital. 

§ 252. Morbid anatomy. The anatomical changes 
given here are restricted to the case of Pearson and Ravenel. 
The animal was much emaciated. The mucous membrane of 
the small intestine was catarrhal and showed a small amount 
of erosion. All the organs were normal except the lungs. 
The most striking feature on external examination was the 
extreme amount of emphysema. The lobules were separated 
from each other by 3 to 5 mm. and even at some distance from 
the borders one could see through the crevices by transmitted 
light. On the surface, the sub pleural connective tissue was 
distended by large blebs. Upon palpation the lung crackled 
and numerous hard nodules could be felt. On section numer- 
ous dark red nodules appeared in the surrounding normal 
tissue. In each lung there were from fifty to sixty of these 
nodules, from 5 to 12 ram. in diameter. Most of them were 
dark red and closely resembled partially organized blood clots. 
However, on crushing a portion in glycerin between two slides 
and examining it under the microscope, they were found to be 
made up almost entirely of a felted network of mycelial threads. 
Between these large nodules there were numberless smaller 
areas of much the same color, i to 2 mm. in diameter, not per- 
ceptible to the touch as nodules but which were of the same 
character and were no doubt foci of recent origin. These were 
seen especially well in portions of the lung which were pre- 
served by Pick's method, the slight bleaching of the tissue 
bringing them into relief. On opening some of the inter- 
lobular emphysematous spaces, small, whitish, mouldy look- 
ing patches were noticed which bordered the cavity. Scrap- 
ings of these patches were made up entirely of perfect fruit 
hyphae, with myriads of spo'-es. The diagnosis of a mould 
mycosis was in this way made at once and confirmed bv cul- 



338 PNEUMONOMVCOSIS 

tures and examination of sections. Cultures were made on 
gl3'cerinated potato, bouillon and plain agar, by opening a 
nodule with sterile instruments and tearing out a small portion 
of the center, which was transferred to the culture tubes and 
placed in an incubator at 39° C. Abundant growth was ob- 
tained on the potato by the end of thirty-six hours, white at 
first but soon changing to a yellowish and later to a dark green 
color. The growth in the bouillon and agar was slow. Plates 
and flasks of bread paste were made, and these with potato 
were employed for all subsequent cultures. The formation of 
the fruit hyphae was studied. The spores measured from 2.5 
to 3.5// in diameter. By these means the culture was identified 
as the aspergillus fumigatus. The experiments on other 
animals were limited to the inoculation of one rabbit, into the 
aural vein of which one-half cubic centimeter of a suspension 
of the spores was injected. The animal died in forty-four 
hours and from the liver and kidneys cultures were recovered. 
All of the organs were examined in sections, but the mycelium 
was detected in two only. 

Microscopic examination. The nodules were hardened and 
embedded, some in collodion and some in paraffin. Various 
staining methods were tried, hematoxylin and eosin, carbol- 
thionine. Gram and lithium carmine with Weigert's fibrin 
stain. Good results were obtained with all, but the carmine 
and Weigert gave the most beautiful picture and by this 
method the fungus was most perfectly demonstrated, the spores 
and mycelium taking on a deep purple color. The histology 
was studied largely in sections stained with hematoxylin and 
eosin. The bronchial epithelium was normal in places, but, 
for the most part, the columnar cells had been replaced by a 
sort of membrane, which appears to be made up almost entirely 
of a felt-work of mycelial threads. From this membrane 
hyphae grew out into the lumen of the bronchus, and here, 
owing no doubt to the supply of air, fruit hyphae arose, with 
perfect sterigmata and .spores. There was no cellular nor other 
exudate and very little debris. The under surface of this 
membrane was of looser texture and contained some cellular 



MORBID ANATOMY 



339 



infiltration made up of round cells, leucocytes, proliferated con- 
nective tissue cells and red blood corpuscles. The adjacent 
structures were closely filled with a cellular infiltration with a 
quantity of mycelium of the same description, this extended 
to the neighboring alveoli, which under low power appeared 
to have preserved their outline but with greater amplification 
were seen to have lost all their normal structure, showing 
clumps of homogeneous, irregular masses which stained faintly 
with eosin and were probably of connective tissue origin. 

In these areas the mycelium followed the alveolar wall as 
a trellis, the tissue seeming to afford no obstacle to its advance. 
Within the alveoli was a finely granular debris, with some 
coarser particles, probably the remains of cells. In sections 
stained with carbol-thionine large numbers of mast cells were 
seen in the alveolar walls. Bordering these degenerated areas 
were alveoli which had retained their normal structure and 
were filled with a network of fibrin holding in its meshes a few 
cells. In other parts of the sections were areas resembling 
those just described, but in which all anatomical landmarks 
had been destroyed, so that it was impossible to tell whether 
or not the spaces seen were bronchi. 

Some sections showed a widespread interstitial and alveolar 
hemorrhage, the blood showing a considerable increase in the 
number of leucocytes. The capillaries were congested and 
areas of edema with thickening of the alveolar walls were not 
uncommon. 

There were peribronchitis and arteritis, while in some sec- 
tions arterial thrombosis was seen, the thrombus being pene- 
trated by mycelium, though no fruit was found. Areas were 
also found in which the alveoli were filled with a cellular exu- 
date producing consolidation and thickening of the alveolar 
walls. 

Emphysema, both interstitial and vesicular, were marked 
and often extreme. Around the borders of the interstitial 
cavities was a distinct zone made up of red blood cells, leuco- 
cytes and homogeneous material, which was yellowish in fresh 
as well as stained sections. These areas contained very little 



340 



PNEUMONOMYCOSIS 



mycelium. All sections showed a small amount of anthracosis. 
The appearance of sections varied in different nodules as they 
were taken further and further away from the center. In 
general the fungus was thickest at the center, so thick in 
many instances that the lung tissue was hidden entirely, 
and grew less as we went outward. The tissue changes noted 
took place in a zone beyond the greatest growth of the fungus. 
In other nodules the fungus was evenly distributed throughout, 
following the alveolar walls. In these the tissue changes were 
slight. At times the fungus grew in dense, brush- like clusters, 
closely resembling actinomycosis under low amplification. 

This form was 
"" considered to show 

a marked reaction 
and resistance on the 
part of the animal 
and a lowered vital- 

L' im'^'V "< 'S^^m^ssmyst ^^^ ^° ^^^ fungus. 

r^8?^'*C^r >_j^^^^^^^S When found it indi- 

fV^M^' ' '^"'^"^^^^^^G^ - cated that the asper- 

mvHj'^ ' ^^^^^«^n gliosis was a pri- 

i^^)k*hl^ y^ ^^^^^§a rnary and not a sec- 

itt;«.-li«. -^tl :^2i^^^ ondary or terminal 

affection. No giant 
cells were found in 
any section. 

Fruit formation 
was not observed in 
the substance of the 
tissues at any time. 
It was observed most 
frequently in bronchi, which were for the most part denuded 
of their epithelium, and next in emphysematous cavities, 
where it could be detected in clusters by the naked eye. Fruit 
was found in sections, in spaces the nature of which it was 
impossible to determine accurately. Whenever the formation 
of fruit was seen, there were innumerable free spores as well 




Fig 88. Necrosis in the kidney of a rabbit 
due to A. funiigatus ; A., fmigus ; B and C, 
nuclei; D, tiecrotic tissue ; E, normal cells. 



MORRID AXATOMV 341 

as those still attached to the sterigmata, but in no case were 
spores detected in the substance of the tissues. 

In many sections, especially those from near the center of 
the nodules, the mass of mycelium was so dense that the struc- 
ture of the tissues was obscured. Besides the dense growths 
resembling actinomycosis already described, other brush-like 
clusters not unlike them were frequently seen. These differ 
from the former in being somewhat less compact, and that 
from their periphery numerous hyphae run out into the sur- 
rounding tissues, whereas in the actinomycotic form the masses 
are sharply defined and only here and there a few threads 
grow out beyond the cluster. Their appearance suggests that 
they mav be actinomycotic forms which have finally overcome 
the resistance of the tissues. Emphysema is less marked in 
the neighborhood of the latter. 

The cow was examined carefully for the lesions of tuber- 
culosis and in one lung some four or five caseous and calcare- 
ous nodules i cm. in diameter were found, in which tubercle 
bacteria were demonstrated, but no mycelium could be de- 
tected. In no part of the lung was there coexistence of the 
two infections. 

The fact that the animal did not react to tuberculin, 
although tuberculosis was present, is noteworthy and suggests 
that the mould infection may interfere with the test. It is 
probable that the tuberculous lesion was arrested in its 
progress. 

§ 253. Pulmonary mycosis in birds. Mohler and 
Buckley have recently described a case of this affection in the 
lung of a flamingo which died at the National Zoological Park 
in Washington. In this case the bird was very much ema- 
ciated. The lungs presented lesions suggesting those of tu- 
berculosis in their general appearance. The other organs 
(liver, spleen and kidneys) appeared to be normal. From the 
lung Aspergillus fumigatus was obtained. [The authors give 
a full description of the lesions with a historical sketch and 
results of experiments on the smaller animals.] 



342 EPIZOOTIC LYMPHANGITIS 

REFERENCES. 

1. Arwine and Lamb. A fifth case of " fungous foot " in America. 
The Anier. Jour.of Med. Sciences, Oct. 1899. 

2. DiNWiDDiE. On the toxic properties of moulds. Biilletiti No. 
JO, Arkansas A o-ric. Exp. Sta., May, 1896. 

3. Flexner. Pseudo-tuberculosis Hominis Streptothricha. The 
Jotcrnal of Experimental Medicine, Vol. Ill (1898). (Bibliography). 

4. MoHLER AND Buckley. Pulmonary mycosis in birds— with a 
report of a case in a flamingo. Annual Report of the Bureau of Animal 
Industry, igoj. {Also issued as circular No. j8. ) 

5. Ophuls and Moffitt. A new pathogenic mould. The Phila- 
delphia Med. fournal, June 30, 1900. 

6. Pearson and Ravenel. A case of pneumonomycosis due to 
the Aspergillus fumigatus. The (Jtiiversity Medical Magazine, Aug. 
1900. The Vet. Journal, New Series, Vol. II (1900), p. 229. 

7. Rknon. L'etude sur I'aspergillose chez les animaux et chez 
I'homme. 1897. 

8. Weis. Four pathogenic Toruhe (Blastomycetes). The Jour. 
of Med. Research, Vol. VII (1902), p. 280. 



EPIZOOTIC LYMPHANGITIS 

Symonyms. Japanese farcy ; pseudo-farcy ; equine pox ; 
equine syphilis ; inundation fever. 

§ 254. Characterization. Epizootic lymphangitis is 
described as a virulent infectious disease characterized by 
suppuration of the superficial lymphatic vessels, due to the 
presence of a specific organism. It is a disease of the solipeds, 
although Tokishige reports finding it in cattle in Japan. 

§ 255. History. This affection seems to have been 
known for a very long time and to have been confused with 
cutaneous glanders (farcy). French veterinarians have recog- 
nized the disease as river ic^rcy , farcin en ciil de poule, curable 
or benign farcy. In France these various forms were 
acknowledged to be identical, the "river farcy " being consid- 
ered as an attenuated form of glanders (farcy) until 1873, 
when Rivolta discovered the specific organism {^Saccharomycosis 



ETIOLOGY 



343 



farciminosus). This affection has been recognized at different 
times in Japan, China and India. It has been known in 
Algiers for many years and during the war in South Africa it 
seems to have been introduced there. From South Africa it 
has been imported into England and Ireland by government 
horses returning from the Cape. The first case in England 
appears to have been detected in 1902. In 1907, Pearson dis- 
covered it in western Pennsylvania. 

§ 256. Etiology. This disease is caused by an organism 
described by Rivolta as Saccharomyces farmninosns. It is also 
called a cryptococcus. According to Pallin, it is found in 
large numbers in the diseased tissues and products, partly 
free and partly enclosed in pus corpuscles, which often con- 
tain from ten to thirty or more of them. It is characterized 
by its clearly defined contour and its very refractile double 
outline. It measures from 3 to 4 // in diameter, and in the 
unstained preparations it is said to be best seen with an oil 
immersion and abbe condenser, under a magnification of not 
le.ss than 800 diameters. In stained preparations it can be 
recognized with a much lower magnification. 

The classification of this organism has been much dis- 
cussed by several workers. Canalis places it with the coccidia, 
Piana and Galli-Valerio consider it as belonging to the proto- 
zoa, and Formi and Aruch as a blastomycete. Tokishige 
and Marconi believe that it belongs with the saccharomyces. 
It is not easily stained by the aniline dyes, although Mettam 
has shown that by the Gram method, Nicolle's violet, Nicolle's 
thionine and others it is readily colored. It is cultivated with 
difficulty. Tokishige obtained cultures in bouillon, agar, 
gelatin and on potato. In bouillon it required seventeen days 
to obtain a growth. 

The infectious material may be transported by contact 
between the diseased and well horses, by stall bedding, by 
stable utensils and harnesses and possibly by insects. 

The period of inciibatio7i \'s> placed at from three weeks to 
three months and in certain cases it may extend to even eight 



344 EPIZOOTIC LYMPHANGITIS 

or ten months. In experimental cases symptoms have 
appeared after 32 days. 

§257. Symptoms. An infection takes place in wounds, 
the first symptom usually appearing at the seat of a pre-exist- 
ing wound. The lesions usually appear in the skin, but they 
may occur on a mucous membrane. They consist of swelling 
and suppuration of the lymph vessels and glands. These 
break and discharge a thick, yellow pus, stained with blood. 
Pearson states that the horses do not, as a rule, show any 
general disturbance except in very advanced cases. Pallin 
describes the opened sores as follows : 

" The buds, ulcers, or sores, by all of which names they 
are known, are characterized by their bright red exuberant 
granulations and their fungoid appearance, as well as by their 
indurated base and well-defined edges ; the adjoining skin, 
which is partially inverted, has a peculiar shiny appearance ; 
an opening exists in the center of the bud, from which the pus, 
at first creamy, and afterwards yellov^ish, oily, and curdled, is 
continually discharging."' 

These buds are quite different from those of glanders. 
The lesions are commonest in the limbs. The most usual 
location is on the fore-leg generally extending up along the 
fore- arm to the brachial region and point of the shoulder. 

The sores vary in size from that of a pea to a hen's egg. 
Pallin reports lesions on the mucous membranes in from 7 to 
10 per cent of the cases. When these occur on the nasal 
mucosae they are liable to be confounded with those of 
glanders. 

Usually the general symptoms are not conspicuous. The 
temperature remains normal and the appetite good. The 
disease seems to thrive best on animals in good condition. 

Pearson describes its symptoms as follows: "The most 
common manifestation consists in the presence of small, 
chronic, discharging ulcers in the vicinity of the hock 
joint of a thickened hind leg. In such a case, one may also 
find small scars showing where ulcers have healed and there 



MORBID ANATO:\IV 



345 



will probably be some firm nodules beneath the skin and, per- 
haps, one or more nodules that have softened, forming fluctu- 
ating abscesses. The regional lymphatic ducts are corded and 
the glands inside the thigh are hardened and nodulated. 

" The earliest observed symptom may be the occurrence of 
a firm nodule, from the size of a pea to that of a walnut, 
beneath the skin, anywhere on the body. Corded lymphatics 
extend from this lesion. In time, the nodule will soften and, 
at length, its purulent contents will break through the skin. 
The time required for these developments is most variable and 
may reach several weeks. Such pus is thick yellowish or 
greyish yellow and often it is mixed with blood. Sometimes 
it contains flakes. 

" In other cases, the first symptom observed is an indolent 
sore, covered with pus and scab, surrounded by a slightly 
swollen zone and from which one or more firm cords extend 
beneath the skin toward the lymphatic glands. This condition 
is, no doubt, the first to develop, but such a sore often escapes 
special notice until nodules occur. 

' ' Fresh ulcers may be surrounded by a slightly rai.sed 
zone of bright red granulation tissues ('proud flesh'). The 
ulcers occur irregularly and they disappear slowly ; some heal 
in a fortnight, others continue to discharge for months, and, 
after healing, may break out again. From this long continued 
irritation and from the formation of scar tissue, the skin thick- 
ens and the affected parts become indurated. 

" Ulceration sometimes occurs upon the conjunctiva and 
on the mucous membrane of the nostrils and upper respiratory 
act .'" 

§ 258. Morbid Anatomy. This disease consists in an 
inflammation of the lymphatics. On .section the walls of the 
vessels are thickened, their internal membrane is congested, 
and the ducts filled with thick-clotted lymph mixed with pus, 
which is followed by the formation of the abscesses (pustules) 
and granulating .sores. The affected parts become indurated 
as the result of the formation of fibrous tissue due to the 



346 MISCELLANEOUS FUNGOUS INFECTIONS 

inflammation set up by the disease. On the mucosa, the 
ulcers have a round, well defined raised border. They are at 
first isolated but later they become confluent. Nodules are 
occasionally found in the liver and spleen. A few horses 
appear to recover spontaneously. A few are apparently bene- 
fitted by proper treatment. It is said to be fatal in from lo to 
15 per cent of all cases. 

§ 259. Differential diagnosis. This affectibn is to be 
differentiated from glanders, ulcerative lymphangitis, tuber- 
cular lymphangitis, bursatti, and the so-called botryomycosis. 
The finding of the specific organism in case of epizootic lym- 
phangitis affords a positive means for its difi'erentiation and 
diagnosis. 

REFERENCES. 

1. MetTam. The staining of the organism of epizootic lymphan- 
gitis. The Vet. Record, Vol. XVI (1904), P- 834. 

2. Pallin. a treatise on epizootic lymphangitis. London, 1904. 
5. Pearson. Epizootic lymphangitis of horses and mules. Cir- 
cular No. S, Pennsylvania State Livestock Sanitary Board (1907). 



MISCELLANEOUS FUNGOUS INFECTIONS. 

^ 260. Farcy in cattle. This affection is described as 
being characterized by an inflammation tending to suppura- 
tion of the superficial lymphatic vessels and glands caused by 
a streptothrix. The descriptions of this affection, however, 
are not recent, those by Cruzel, 1869, and Nocard in 1888 
being among the latest, and consequently there is some ques- 
tion concerning its etiology. Nocard states that it is very 
closely related to actinomycosis. 

This affection is said to be chronic, attacking the lymph 
vessels and glands, which become hard and often caseous. 
Tokiskye has described cases in which the lesions extend into 
the respiratory passages. In some cases abscesses occur. 
They are reported to occur on the ventral surface of the bod}'. 



MYCOTIC STOMATITIS 347 

This disease does not appear to exist in this country. 
Until its differentiation from tuberculosis, actinomycosis and 
" botryomycosis" is made its real nature will remain in doubt. 

1. Cru/.ki-. Traite des maladies de I'espcce bovine. i.SSg. 

2. Mausis. M6moire sur le farcin. Ibid. 

3. NoCARD. Note sur la maladie des boeufs connue a la Guade- 
loupe sous le nom de farcin. Aiiiiales de V lust. Pasteur, Vol. II (18S8), 

p. 293- 

4. SoRiLLOX. Exemples de farcin dans le boeuf. Recueil de yned. 
vHer., 1829, p. 651. 

§ 261. Mycotic stomatitis in cattle. Cattle some- 
times suffer from stomatitis caused by fungi. The exact 
species that are involved in this form of infection are not 
clearly determined. A number have been incriminated. 
Mohler has recently described a stomatitis of this character. 
The symptoms are inability to eat, suspension of rumination, 
frequent movements of the lips, and in some cases dribbling of 
saliva. There is a desire to eat but prehension is difficult. 
The mouth is abnormally warm and the mucosa reddened, 
rarely small blisters will be seen which soon develop into 
ulcers. These vary in diameter from 3 to 25 mm. The 
erosions, which may become confluent, are found on the gums, 
dental pad, inside of the lips and on the end of the tongue. 
They also occur on the cheeks. The ulcers are hemorrhagic 
at the borders. The central necrotic portion soon sloughs, 
and the place is filled with granulating tissue. There are 
often erosions and exfoliation of the epithelium of the muzzle. 
There are at times swellings about the feet. 

The prognosis is good. 

The course of the disease varies from 7 to 15 days, the 
average being, according to Mohler, about 10 days. Ward 
has diagnosed a mycotic stomatitis in California. This infec- 
tion, which appears to occur in enzootics, resulting from the 
eating of food containing irritant fungi, is to be differentiated 
from foot-and-mouth disease, ergotism, and necrotic stomatitis 
caused bv B. necrosis. 



348 MISCELLANEOUS FUNGOUS INFECTIONS 

MoHLER. Mycotic stomatitis of cattle. Circular No. 51. Bureau 
of Atiimal Industry, U. S. Dept. of Agric. 1904. 

§ 262. Blastomycetes infection in horses. Fermi 
and Aruch described a disease in horses resembling glanders 
except that it did not affect the lungs, which was caused by a 
blastomycete. It is known as Farcin d' Afriqiie. Central- 
blattf. Bak., Bd. XVII (1895), p. 593. 

Frothingham has described a tumor-like lesion in the 
lungs of horses caused by a blastomycete. The growth was 
about ten inches in diameter and on section resembled in 
appearance a myxosarcoma. The central portion was easily 
removed, the outer zone forming a firm border wall composed 
of fibrous tissue. A microscopic examination of the central 
portion showed it to consist of a fine meshwork of fibrous 
tissue, in the meshes of which were many cells and blasto- 
myces. These were fatal to rabbits and guinea pigs. Jour. 
Compar. Med. and fW. Archives, Vol. XXIII (1902), p. 593. 



CHAPTER IX 

DISEASES CAUSED BY PROTOZOA 
GENUS PIROPLASMA. 



§ 263. General discussion of piroplasma. There are 
several species of piroplasma. Their life history is not known. 
In the infected animal they live within the blood, often enter- 
ing into and destroying the red blood corpuscles. They are 
transmitted from the infected to the uninfected animal by 
means of some insect usually a tick. The known species of 
this genus are parasitic and pathogenic in different species of 
animals. The term Piroplasmoses was introduced by Nocard 
to designate the diseases produced by these organisms. Ac- 
cording to his classification Piroplasmoses are diseases resulting 
from infection wuth any species belonging to the genus 
Piroplasma. Nocard recognizes four species, but others have 
been described more recently. 

Piroplasma bigemifium—iho. piroplasma of cattle. 

Piroplasma ^^z.s— the piroplasma of sheep. 

Piroplasma canis — the piroplasma of dogs. 

Piroplasma equi — the piroplasma of horses. 

To Americans, Piroplasma bigemiyium, the form infecting 
cattle, is the most important. 



TEXAS FEVER. 

Synonyms. Bovine malaria; red water; Spanish fever; 
splenic iever; " bloody murrain;" southern cattle fever; tick 
fever. 



350 TEXAS FEVER 

i^ 264. Characterization. Texas fever is an infectious 
blood disease of cattle, characterized by rise of temperature, 
hemoglobinuria, destruction of the red blood corpuscles and 
the presence in the blood of a protozoan parasite which is 
transmitted from animal to animal by means of the cattle tick. 

It is believed to be identical with the hemoglobinuria in 
Roumania, tick fever in Australia, and "La Tristeza " in 
South America. It has been named inalaria des bovides by 
Celli and Sentori and Malaria bovine by Lignieres. Although 
it dififers in many ways from human malaria, the analogy is so 
close respecting the specific cause, wide distribution and means 
of transmission, that bovine malaria seems to be a very suit- 
able name for this affection. At least it has the advantage of 
not stigmatizing any locality. 

The peculiar and interesting feature of this affection is 
the fact that cattle raised in the infected districts become im- 
munized so that they do not suffer from the disease but they 
carry its specific organism in their blood. When imported 
into non-infected districts, they transmit the virus, by means 
of the cattle tick, to susceptible animals, but remain them- 
selves perfectly well. 

§ 265. History, There is little knowledge concerning 
the early history of this disease. With the development of 
commerce, however, the shipping and interchange of animals 
gradually came into prominence and, with it all, this disease 
which had long been known in certain localities was more 
widely scattered until finally it came to be an important barrier 
to the cattle traffic. In 1868, this disease seems to have made 
its first important impression upon the American people. In 
June of that year, Texas cattle were shipped up the Mississippi 
river to Cairo and thence by rail into the states of Illinois and 
Indiana, where they caused during the summer enormous 
losses from this disease. Cattle from these states shipped east 
brought the disease with them. The cattle commissioners of 
New York and the Board of Health of New York City endeav- 
ored to check the importation of such cattle. The disease was 



GEOGRAPHICAL DISTRIBUTION 351 

careful!}' investigated at that time but nothing beyond a very 
accurate description of the gross lesions was obtained. Later, 
Salmon determined the boundary line between the non-infected 
and the permanently infected districts, or what is now known 
as the Texas fever line. (See Plate II). In 1889, the Bureau 
of Animal Industry undertook a systematic investigation into 
the nature of this disease, which resulted in the same year in 
the discover}^ of its specific cause by Dr. Theobald Smith and 
later the demonstration of the fact that the disease is trans- 
mitted from southern to northern cattle through the medium 
of the cattle tick. Prior to this (1888), v. Babes had found 
an intraglobular parasite in the blood of cattle suffering from 
an epizootic disease (hemoglobinuria ) in Roumania. While 
at first these diseases were thought to be diflferent in their 
etiology they are now believed to be identical. 

A number of investigations have been made by the Bureau 
of Animal Industry, the State Experiment Station and State 
Board of Agriculture of Missouri and Texas, the Louisiana 
Experiment Station and by the Queensland Government, 
Australia, for the purpose of obtaining a practical method for 
the production of immunity against Texas fever in susceptible 
cattle. The results that are being obtained are promising, as 
they have made it possible to take northern cattle into the 
infected territory of the south. 

j^ 266. Geographical distribution. In the United States 
the distribution of Texas Fever corresponds with that of the 
cattle tick {Boophihis annidatus) . This includes, with pos- 
sibly a few small exceptional areas, that portion of the country 
south of the "Texas fever line" which is shown by a red line 
on the accompanying map but which is changing constantly 
by virtue of the spread or elimination of the tick. It has been 
identified with the tick fever of Australia which has become 
a source of great loss to the cattle industry of that country. 
Lignieres has identified the disease in South America (Argen- 
tine Republic). It is also reported to be identical with a 
malady affecting cattle along the Danube river, in the Balkan 



352 TEXAS FEVER 

provinces and in South Africa (Rhodesia Rotwasser*). It is 
restricted, however, to those countries where the climate is not 
sufficiently severe to destroy the cattle tick during the winter 
season and where the animals are constantly infected. Cattle 
(genus Bos) are the only animals which suffer from it. 

§ 267. Etiology. Texas fever is caused by a microor- 
ganism belonging to the protozoa and named by Smith, the 
discoverer, Pyrosoma bigeniinum.-\ It is generally recognized 



*The Rhodesian redwater or East African coast fever is according to 
Stockman's report a very different disease from the tick fever in 
America. The conclusions from Stockman's report are as follows : 

1. That the disease is caused by a special blood parasite — a piro- 
plasma. 

2. That it is a disease peculiar to bovine animals. 

3. That it is only indirectly contagious ; that is to say, a sick 
animal will not infect another susceptible animal by contact, however 
intimate, or by any of the excretions or fluids of its body, as in the case 
of rinderpest and like diseases. 

4. That the indirect agents of infections are the nymphal and adult 
stages of the brown tick (Rhisicephalus Appendiculatus) and the black 
tick (R. Simus?). The former however is the more important factor. 

5. That only those ticks which in one of their intermediate stages 
have sucked on affected animals are capable of transmitting the disease 
to other oxen. 

6. That the infecting agent does not pass through the egg of the 
tick to the second generation, as was at first thought probable, by 
reasoning from analogy with what takes place in the blue tick in case of 
Texas fever. 

7. That the brown and black ticks existed in certain parts of the 
Transvaal long before the disease was imported and that the said ticks 
only become virulent after sucking sick animals recently introduced. 
These species of ticks exist to-day on many farms that are perfectly 
clean, and which will remain clean as long as sick animals are kept off 
them. 

8. That the blue tick is not a carrier of the disease. 

9. That the proportion of recoveries from the disease is five per 
cent, at the very most. 

tThe genus of the parasite has been changed to Piroplasma by Pat- 
ton, to Apiosomahj Wandelleck, to Accnibosporidies by Bouome, and 
Porteus virnlentissimus by Perroncito. vStarcovici has named the organ- 
ism described by Babes as Hematococcus, Babesia bigeminum bovis. 



\\ U ^\A 



-'-H^ 








ETIOLOGY 



353 



that Piroplasma is the proper generic term and this is used by 
writers on protozoa. 

If Texas fever in America and hemoglobinuria in Rou- 
mania are ident- 
ical, Babes was 

the first to call \^ ^^ ) \q ) ^^) 

attention to the 

existence of this ^^^^- ^9- P^'opiasma bt^euunnm in red blood 

corpHsdes. 
mtraglobular 

parasite. It seems that Dr. Stiles, in 1867, observed this or- 
ganism but failed to recognize its significance. It is found in 
the blood in cases of Texas fever and it also exists in the 
blood of immune animals in the tick infested districts. The 
life history of this parasite is not determined. In the blood 
of the diseased animals they appear in the unstained, fresh 
preparation, as minute or larger bright bodies which may be 
from 0.5 to 4.o/< in diameter according to the form of the 
disease. In the acute types of the disease certain of the red 
corpuscles contain pale or brighter pyriform shaped bodies. 
One end of each body is broad and rounded, the other tapering 
and pointed. Usually there are two of 
these bodies, both of the same size, in a 
corpuscle. More rarely there is but one, 
although four are occasionally observed 
(Fig. 91). When two are present the 
tapering ends approach each other and 
usually they are joined while the other 
ends may point in any direction. Several 

forms have been noted varying from a ^ ^ 

• 1 , ,. ^, ,, Fig. 90. Coccus 

round to a pyramidal outline. The small y^rw^ of Piroplas- 
and often the larger bodies have been ma bigeminum. 
observed to change their position within 
the red corpuscle. Smith has noted that the ameboid bodies 
observed were apparently single within the corpuscle. In 
dried and heated cover- glass preparations stained with alka- 
line methylene blue, these parasites are distinctly colored. 
They are also stained with carbol fuchsin and with heme- 




354 



TEXAS FEVER 




Fig. 91. Blood from 
kidney shoicing para- 
sites of Texas fever 
(Smith). 



toxylin. As a rule they stain more deeply in preparations 
made from internal organs than they do in those from the 
living blood. 

In the capillaries of the congested organs, the blood cor- 
puscles contain many more parasites. 
Smith has noted in one case from 2 to 3 
per cent of infected corpuscles in the 
^-^p=^r\^^ circulating blood but in cover- glass prep- 

'"'xv-=rik?^C^ arations made at the autopsy quite 

different results were obtained. In those 
from the skeletal muscles, blood of the 
right heart, and blood from the bone 
marrow (sixth rib) very few infected 
corpuscles were found ; in the blood 
from the left heart and lung tissue from 
2 to 3 per cent of infected corpuscles ; in 
the spleen 5 per cent ; in the liver and 
kidney tissue from 10 to 20 per cent ; 

and in the hyperemic fringes of the omentum and the heart 

muscle 50 per cent of the corpuscles 

were infected. In other cases the 

blood corpuscles in the capillaries 

were more and in still others less 

extensively infected. In the living 

blood the parasites were pyriform, but 

in the post-mortem specimens they 

were more nearly round. In the mild 

type of the disease from 5 to 50 per 

cent of the red corpuscles in the circu- 
lation are infected for a period of from 

one to five weeks. The parasite is 

round (coccus form). In the fresh 

preparations it is seldom seen : rarely 

it can be detected as a pale spot about 

0.5/1 in diameter at the periphery of 

the corpuscle. In stained (alkaline methylene blue) prepara- 
tions, the parasites appear as round coccus-like bodies from 




Fig. 92. Cover -glass prep 
a ra tionfro m k idn ey '. Cor- 
puscles sfiocving Piroplas- 
tna, coccus form (Smith). 



INl'KCTION 



355 




Fig. 93. Blood 
in capillary of 
heart s/iorcj- 
ing Piroplas- 
ma {Siiiilh). 



0.2 to 0.5// in diameter. They are situated within the cor 
puscle on its border. As a rule only one is found in i 
corpuscle. Sometimes a division was evident 
separating the parasite into two parts. They 
must be differentiated from somewhat similar 
looking bright bodies which are seen in the cor- 
puscles of healthy blood during different seasons 
of the year. 

Concerning the life history of this parasite, 
Smith considered the intraglobular stage hypo- 
thetically the swarming stage, which precedes 
the peripheral coccus-like bodies and the pyri- 
form and spindle shaped bodies which develop 
from the divided coccus-like peripheral forms. 
The free bodies are the parasites set free after 
they have reached the preceding stage by disintegration of 
the infected corpuscles. They are most commonly found in 
the kidney. The reproduc- 
tive stage has not been recog- 
nized. 

§ 268. Infection. Al- 
though practical stockmen 
had long looked upon the 
tick as a source of infection, 
it remained for Smith and 
Kilborne to experimentally 
demonstrate that so far as 
known the cattle tick {Bo'dphi- 
lus annulatusY^ is the sole carrier of the parasite. It was 
pointed out by them that when southern cattle were freed 

*This tick was first described by C.V. Riley in 1868 as Ixodes hovis. 
Later, Cooper Curtice investigated this parasite (Biology of the Cattle 
Tick, Journ. Comp. Med. and Veterinary Archives, July, 1891, Jan., 
1892) and'gave it the generic name of Boophilus {o^ loving). This 
seems to be the only genus of cattle ticks which transmits the parasite 
of Texas fever. Recently Karsch's genus Margaropiis has been pro- 
posed as the correct name instead of Boriphilus. 




Fig. 94. Sexually mature male 
tick after the last moult, dorsal 
vieiv (S)nith). 



356 



TEXAS FEVER 



from ticks they would not when kept together in small 
enclosures transfer the disease to susceptible animals, but that 
when susceptible cattle become infested with the ticks either 
by grazing in infested pastures or by having placed upon them 
young ticks hatched in the laboratory the disease appeared. 
The infection of northern cattle with Texas fever bv 




Fig. 95. Photograph of animal sick with Texas fever. {Photo- 
graphed by Connaway). 

southern animals consists therefore in first infesting them with 
the cattle tick.-'- The number of ticks necessary to carr}' the 
disease is small so that frequently they will not be observ^ed 
unless the sick animals are carefully examined. The life 

*It is interesting to add the results of an experiment conducted by 
Dr. Cooper Curtice in the Bureau of Animal Industry which shows the 
necessity of the tick in inoculating cattle. In a tick infested district in 
the south, a field was cleared of ticks by fencing and keeping cattle off 
for a year. Susceptible northern cattle were transported to and placed 
in this field where they thrived for a season. The second year they 
were placed in a second cleared pasture where they kept well for an- 
other year. The third year they were placed in a tick infested pasture 
where they died promptly of Texas fever. 



INFECTION 



357 



cj'cle of the tick will, therefore, explain the variation in the 
time elapsing between the exposure of northern to southern 
cattle and the appearance of the disease. Starting with tick 
infested animals placed with native cattle in a northern pasture 
the adult female ticks drop to the ground almost daily, so that 
the following life cycle may be assumed to begin at once. 

1. Adult ticks drop to the ground in from i to 3 days 
after the infested cattle are placed in the field. 

2. Adult ticks lay their eggs in about 7 days after drop- 
ping to the ground. 

3. Eggs are hatched in about 20 days after they are laid.-'^ 

4. Young ticks 
crawl upon cattle from 
I to several days after 
they are hatched. 

5. In about ten 
days from the time the 
young ticks crawl upon 
the susceptible cattle the 
rise of temperature ap- 
pears. 

The length of time 
that must elapse (period 
of incubation) from the 
exposure of susceptible cattle to the development of the 
disease depends on whether or not the whole life cycle of the 
tick must be passed or part of it has already gone by. If 
susceptible animals are placed in a pasture where the young 
ticks are just ready to crawl upon them the infection of the 
cattle is accomplished at once and the high fever appears in 
about ten days, practically the minimum time. It has been 
experimentally demonstrated that the young ticks are able to 
travel for a considerable distance in a pa.sture. In pastures 
where tick infested cattle are grazing, young ticks are very 

*Mohler states that the time required for the hatching varies from 
13 days to six weeks, depending upon temperature, moisture, soil, etc. 
He states further that the eggs may remain dormant for several months. 




Fig. 96. Sc.vHally Dialure fcina/e after 
the last Dioitlt , dorsal viezv {Siiiit/i). 



,58 



TEXAS FEVER 



liable to be on the ground continuously. In estimating the 
time to elapse after the exposure to the tick infested field, 
before the disease will appear, it is necessary, therefore, to 
determine the exact stage in the life cycle of the ticks at the 
time when the animals come in contact with them. 

Small quantities of the blood from immunized cattle in 
the tick infested district, when injected into susceptible 
animals either intravenously or beneath the skin, will produce 
the disease. While this mode of infection rarely if ever 
occurs in the natural order^of events, it may happen that in 

case of certain 







Fig. 97. 




Eggs and you Jig tick 
(Smit/i). 



/Ksi liatclied 



operations bits of 
blood may be car- 
ried directly from 
a southern to a 
northern animal 
thus inoculating 
the latter with the 
disease. 

In the fall of 

1898 two cases occurred in the practice of Dr. Ambler of 
Chatham, N. Y. The owner had his animals dehorned in 
December and soon afterward two fatal cases of Texas fever 
developed. The Piroplasma and the characteristic lesions 
were present. Inquiry revealed the interesting fact that the 
two animals which .sickened and died were dehorned immedi- 
ately after two imported southern cattle. The owner was not 
aware of the fact at the time that these were southern bred 
cattle, as he had bought them of a dealer in Vermont. More 
recently another case of this disease produced in the same way 
has been reported. 

§ 269. Symptoms. In the acute type of the disease 
which occurs during the hot summer months, the onset is sud- 
den and usually all animals exposed to the same infection 
together come down at the same time. The first indication of 
the disease is a rise of temperature, at first higher in the after- 



SYMPTOMS 359 

noon than morning, but this oscillation is minimized later in 
the course of the disease when the temperature remains high. 
The temperature rarely rises above 107° F. With a clinical 
thermometer the temperature can be detected two or more 
days before there are other symptoms. The respiration may 
rise to between 60 and 100 and the pulse may range between 
80 and 1 10 per minute. Late in the disease there may be 
hemoglobinuria. Smith and Kilborne found it in 33 out of 46 
fatal cases in which urine was found in the bladder. The 
passing ot the colored urine before death was noted in but four 
of their cases. In one of these which showed hemoglobinuria 
four days before death, the urine in the bladder was clear at 
post-mortem. As this condition seems to depend upon the ra- 
pidity of the destruction of the red blood corpuscles, a slow dis- 
integration may enable other organs to dispose of the coloring 
matter, while in rapid destruction of the blood much of it may 
be thrown into the urine. The urine contains small quantities 
of albumin. At first the specific gravity may be high but 
later it ranges from loio to 1020 and fails to effervesce with 
acids. The color varies according to the quantity of 
hemoglobin. As a rule there is marked constipation during 
the high fever. There is loss of appetite and usually cessation 
of rumination with the high fever. The blood is thin and 
pale. The high temperature, hemoglobinuria and thinness of 
the blood are quite diagnostic symptoms of the acute type. 

The course of the disease may vary, but the continuous 
high temperature does not usually last for more than ten days. 
Death often intervenes in from five to eight days. In the 
mild, nonfatal or chronic type which was first pointed out by 
Smith and Kilbourne and which occurs in the late summer or 
autumn, the general symptoms are similar to those of the 
acute type except they are not so severe and are prolonged for 
a greater length of time. The parasite is of the .spherical or 
coccus form. The general symptoms are not manifested unless 
the temperature goes above 103° F. Hemoglobinuria is not 
observed in this type. Cattle which have passed through an 
acute type owing to the heated season may have a relapse in 



360 TEXAS FEVER 

the form of a mild type in the fall. The essential difference 
between the two types is found in the different stages of the 
parasite circulating in the blood. Unless the temperature is 
taken and the blood carefully examined, mild types of Texas 
fever would be either overlooked or mistaken for any one of a 
variety of disorders common among cattle. 

§ 270. Morbid anatomy. Cattle which die of Texas 
fever undergo post-mortem changes very rapidly. For this 
reason the description of lesions made some hours after death 
may be misleading. 

Externally the animal presents nothing abnormal or char- 
acteristic of the disease. Rarely dried bits of blood may be 
found and also some small slightly elevated areas of a bluish 
color. The skin between the thighs, upon and about the 
udder and possibly elsewhere may have cattle ticks attached. 
It is important under ordinary circumstances to look for this 
parasite. The subcutaneous tissue may be more or less yellow 
in color. Edema of the subcutis over the ventral portion of 
the body has been observed. The muscles are usually normal 
in appearance although frequently they are pale. 

Very slight if any lesions have been recorded as occurring 
in the central nervous system and lungs. Blood extravasa- 
tions usually occur beneath the skin and endocardium, espe- 
cially of the left ventricle. On the external surface the 
petechiae occur for the greater part along the intraventricular 
"groove near the base. The capillaries of the heart muscle are 
packed with corpuscles. Parenchymatous and fatty degene- 
ration of the muscular fibers sometimes exists. The right ven- 
tricle is distended with blood either fluid or clotted and the 
left one firmly contracted. 

In the abdominal cavity there are frequent edematous 
areas about the kidneys and in the portal regions between the 
duodenum and liver. The omentum is often sprinkled with 
peculiar hyperemic patches consisting of delicate shreds of 
vascular tissue. This condition, however, is not characteristic 
of Texas fever. 



MORBID ANATOMY 36 1 

Usually the most conspicuous changes are in the spleen. 
This organ is much enlarged and increased from two to four 
times its normal weight. The normal markings, Malpighian 
bodies and trabeculae, are hidden in the dark brownish -red, 
glistening pulp which distends the capsule. The pulp may be 
firm or it may be in a semi-fluid condition so that it oozes out 
if the surface is cut. The enlargement and color of the spleen 
are due to an engorgement of red blood cells. There may 
also be present a greater or less number of large cells contain- 
ing granules, red corpuscles or clumps of 3'ellowish pigment. 
Free pigment is much more abundant than it is in healthy 
spleens. 

The liver is extensively affected. It is enlarged, con- 
gested, edges rounded, the bile ducts more or less distended 
and the parenchyma is usually in a state of fatty degenera- 
tion. The color is paler than normal and usually the surface 
is somewhat mottled. On section the color of the cut surface 
is brownish-yellow or it may be mottled like the surface. The 
mottling is due to a discoloration owing to degeneration of a 
zone bordering the intralobular vein. This zone varies in 
width and its peculiar color seems to be due to a tendency to 
necrosis. It is characterized b\' parenchymatous degeneration 
and the loss of the nucleus. It may involve a third or more of 
the lobule. This portion stains very feebly or not at all. The 
explanation for the necrosis of the liver cells is suggested by 
Smith as being due to the plugging up of the ultimate bile 
ca.nals with solid bile which may interfere in some way with 
the nutrition of the adjacent liver cells. The bile stasis he 
considers as a result of the breaking up in the capillaries of 
the liver of enormous numbers of infected corpuscles. This 
results in an abnormal fluid containing an excess of solids 
which the bile ducts are unable to carry away. When 
examined in fresh condition or in sections of tissue fixed in 
Miiller's fluid the engorgement of the bile canaliculi is seen. 
The bile stasis may occur over a portion or a whole of the 
lobule. The gall bladder contains usually an abnormal quan- 
tity of changed bile. It is thick and often semi-solid in con- 



362 TEXAS FEVER 

sistency, holding in suspension many flocculi. It imparts a 
deep yellowish tinge to all articles coming in contact with it. 
Owing to the mucus which is present it is quite viscid. 

The changes in the kidneys vary. If death occurs early 
they are usually enlarged and uniformly darker than normal 
throughout. The capillaries are distended with red corpus- 
cles. Parenchymatous and fatty degenerations are not com- 
mon, although occasionally present in the epithelium of the 
tubules. The pelvis is often sprinkled with ecchymoses. 

The bladder may contain ecchymoses. 

It is important to note that throughout the kidneys, liver 
and spleen pigment may be more or less abundant. 

In the digestive tract the lesions of this disease consist 
largely of congestion of the mucosa especially in lines corre- 
sponding to the summits of the folds of the mucous membrane. 
It is more marked in the cecum and rectum than in the colon. 
The cecum and less often the rectum contain dry, hard fecal 
balls. In some cases in the intestines lesions are not observable. 
In the older writings much emphasis is placed on certain 
lesions, mostly nodular or abrasions, in the digestive tract. 
Smith has shown, however, that most of these are due to 
animal parasites and have no relation to Texas fever. 

As already stated, Texas fever is a disease of the blood 
and consequently it is in this fluid that the most constant and 
morbid changes occur. They are characterized by the blood 
becoming thin and watery with a destruction of the red blood 
corpuscles. In some of the cases the loss of corpuscles is rapid 
and continuous until death or convalescence, while in others 
there is a marked oscillation between destruction and regenera- 
tion. In some animals the loss is not continuous, but the 
course of the disease is marked by the periods of rapid blood 
destruction and periods of rest, or, as it were, where the blood 
destruction was holding its own. These points are best illus- 
trated from actual cases, three of which are taken from the 
report by Smith and Kilborne. 



MORBID ANATOMY 



363 



(No 


. 129) 




(No. 


142) 




(No, 


•56) 


Date. 


No. of 
Corpuscles. 


Date. 




No. of 
Corpuscles. 


Date. 




No. of 
Corpuscles. 


Axig. II, 


6,125,000 


Sept. 


16, 


6,890,000 


Sept. 


20, 


6,844,000 


13. 


7,171,000 




22, 


5,430,900 




22, 


5,640,000 


16, 


5,370,000 




24, 


4,562,000 




29. 


2,307,0.0 


27, 


3,310.000 




29- 


5,274,000 


Oct. 


9, 


5,436,000 


29. 


1,675,000 


Oct. 


4, 


3,902,000 




22, 


4,666,000 


30, 


Died 8 p.m. 


1 


8. 


5,983,000 




25, 


2,754,000 






1 


22, 


4,333,000 




30, 


2,720,000 


First hi.ii 


^h a.:m. temp 


Nov. 


4. 


5,586,000 


Nov. 


6, 


2,344,000 


Aug. 24. 




\ 






1 


8, 
13, 


1 ,984,000 
1,183,000 



As evidence of the diminution of the number of corpuscles 
within the body these authors point ( i ) to the loss of hemo- 
globin through the kidneys, (2) to the overproduction of bile 
which is abnormal in the abundance of pigment and (3) to the 
actual observation of their destruction by the micro-parasite 
under the microscope. 

The regeneration of blood corpuscles is indicated perhaps 
by the count, but more surely by the forms of the corpuscles 
themselves. The abnormal forms are the very large corpus- 
cle.s, "punctate" forms and lastly the diffuse stained or 
"tinted" forms and the erythroblasts. The first of these 
may appear when the blood count reaches 3,000,000 and the 
other forms when it is still lower. These various forms, how- 
ever, are probably embryonic or immature corpuscles, which 
are forced prematurely into the circulation by the blood pro- 
ducing organs in trying to overcome the rapid destruction of 
corpuscles by the parasite. The action of the disease upon 
the leucocytes or the defensive activities of the white corpus- 
cles in combating the parasite of Texas fever have not been 
determined. In the work thus far performed and reported, 
they have received little attention. Suffice it to say that they 
have not been in evidence in this conflict and probabl>- take 
little or no part in the morbid changes of Texas fever. 

§ 271. Differential diagnosis. Texas fever is easih^ 



364 TEXAS FEVER 

differentiated from other disorders of infectious diseases by 
the presence of its specific parasite. 

In the absence of a suitable microscope the differentiation 
can in most cases be made from the character of the lesions, 
the history of the animals, the presence of the cattle tick and 
the course of the disease. The lesions are not simulated by 
any other disease of cattle, although the enlarged, dark spleen 
may suggest anthrax and in a hasty diagnosis the two may be 
contused. From the fact that all animals exposed together us- 
ually come down with the disease together poisoning may be 
suggested, but here again a study of the symptoms and lesions 
are sufficient to eliminate toxic disorders. 

§ 272. Prevention. Thediscoveryofthespecificcau.se 
of Texas fever and of the cattle tick as the common means of 
its transmission has reduced the preventive measures to a 
direct warfare against the tick. The National government 
has determined the territory in which the tick naturally exists 
and from which cattle, on account of the parasite, cannot be 
shipped to uninfected districts, except under certain very re- 
stricted conditions. (See regulations for transmission of cattle, 
p. 618, Report of the Bureau of Animal Industry for 1898). 
Likewise susceptible northern cattle cannot be transported to 
the infested districts (.south of Texas fever line) unless they 
can be placed in fields that have been freed from ticks. The 
elimination of the disease depends therefore upon the elimina- 
tion of Boophilus ammlatus. Recently the government has 
undertaken to eliminate the ticks. Thus far the reports are 
most encouraging. There seems to be no reason why in the 
dairy districts of the South their eradication cannot be accom- 
plished. 

^ 273. Immunizing susceptible cattle. A number of 
investigations have been undertaken directed toward the de- 
velopment of methods for immunizing northern cattle against 
Texas fever in order to enable the shipment, especially of 
breeding stock, into the South. In 1895, the writer in con- 
junction with Schroeder, began an immunizing experiment 
which was continued and reported by Schroeder in 1898. 



IMMUNIZING CATTLE 



365 



Young animals were selected and injected with blood 
taken directly from the jugular veins of southern animals. 
The injections were made in the fall and winter and in the 
spring the animals were placed in a highly infected field at 
Manchester, Va., where they remained for the summer. Dur- 
ing this time they were under the immediate observation of 
Curtice, who made a careful study of the blood, temperature 
and extent of tick invasion. The results of this experiment 
are shown in Schroeder's tabulation, which is appended. The 
animals were again exposed the following season without the 
development of Texas fever. 



Animal 


Effect of 


Effect of the 


No. 


blood injection. 


exposure to cattle ticks. 


I 


Severe. 


Very mild disease. 


2 


" 


Well marked but mild. 


3 


Very severe. 


Very mild. 


4 


" 


No disease. 


5 


Mild. 


" " 


6 


" 


Very mild. 


7 


Severe. 


No disease. 


8 


" 


" 


9 


Control Animals. 


" " 


10 




Died June 20. 


II 




" July 9. 


12 




" June 26. 


13 




" July 9- 


14 




Very severe disease, recovered. 



The inoculation disease appears in from eight to ten days 
after the injection of the blood. It lasts from one to two 
weeks. The symptoms are occasionally of a still shorter dura- 
tion, but the altered condition of the blood persists in some 
cases for a much longer period. 

Dairy mple, Dod.son and Morgan, of the Louisiana Ex- 
periment Station, conducted experiments along this line. 
They showed that immunity against a fatal attack of Texas 
fever can be conferred on susceptible cattle by inoculation with 
the blood of a native vSouthern animal or one which has recentlj^ 
been rendered immune. 



366 TEXAS FEVHR 

The Experiment Station of that state offers to immunize 
(free of charge) northern cattle, if they are shipped to the 
state, for its stock raisers. 

In Missouri, Counaway has immunized a few animals with 
the blood serum from immune (southern) cattle. In Missis- 
sippi, Robert has tried the serum for both prevention and 
treatment with somewhat similar results. In Virginia and 
Oklahoma the disease and its prevention have been studied. 
In Texas, Francis is immunizing cattle with most excellent 
results. He has pointed out the value of immunizing young 
(2 to 6 weeks old) calves by artificially infesting with ticks. 
In Australia the problem of immunizing cattle against the 
effects of the spreading of the cattle tick in order to save their 
stock from "tick fever" has become a matter of serious con- 
sideration. Certain European writers claim that immunity 
can not be permanently induced by artificial injections. 
Schroeder has shown that the parasite remains virulent in the 
blood of naturally immunized cattle for from 10 to 12 years. 

The very limited knowledge of the life cycle of the para- 
site of Texas fever precludes a satisfactory explanation ot the 
modus operandi in the production of immunity by these various 
procedures. On this point there is need for much extended 
investigation. 

REFERENCES. 

1. Babes. Die Aetiologie der seucheuhaften Haemoglobiuurie 
des Rindes. Virc/iozv's Arcliiv, Jan. 1889, .S. 81. 

2. CONNAWAY. Texas fever or acclimation fever. Bullet in No. 
37. Mo. State Board of Agriculture, 1897. 

3. Dalrymple, Morgan and Dodson. Texas or southern cattle 
fever. Bulletin 5/. Louisiana Agric. Expt. Station, 1898. 

4. DiNWiDDiE. Some Texas fever experiments. Bulletin No. 20 
Ark. Agric. Exper. Station, 1893. 

5. Francis and Connawav. Texas fever. Bulletin No. jj. 
Texas Agric. Expt. Station, 1899. 

6. Gamgee, Dodge, Bii,r.iNGS AND Curtis. Diseases of cattle in 
the United States. Report of the Commissioner of Agriculture, Wash- 
ington, D. C, 1871. 



RKKERKNCKS 367 

7. Hughes. The fi^ht against Texas Fever. A review of the 
work being attempted in the south for the control and eradication of 
the disease. Am. Vet. Review, Vol. XXIX ( 1906), p. 1309. 

8. Hunt .\nd Coi^mns. Report on lick fever. Brisbane. (Jueens- 
land, Australia, 1899. 

9. Koch. Vorlaufiger Bericht iiber das Rhodesische Rotwasser 
oder " Afrikanische Kustenfieber." Archiv. fi'ir wiss. u. praktische 
Tier/ieilkundc, Bd. XXX (1904) S. 281. 

10. Lewis. Texas fever. Bulletin No. S9- Oklahoma Agric. 
Exper. Station, 1899. 

11. LiGNlKRES. La "Tristeza" on Malarie Bovine dans la Repub- 
liqne .\rgentina. Buenos Aires, 1890. (Full bibliography). 

12. Mavo. Texas fever. Bulletin No. dc). Kan. Agric. Exper. 
Station, 1897. 

13. McCuLLOCH. The prevention of Texas feverand the amended 
laws controlling contagious disease. Bulletin No. 104. Virginia Agric. 
Exper. Station, 1899. 

14. MOHLER. Texas Fever. Bulletin No. jS. Bureau 0/ Animal 
Industry, 1905. 

15. NiLES. Splenetic or Texas cattle fever. Bulletin No. 61,. 
Virginia Agric. Exper. Station, 1896. 

16. NoRGAARD. Dipping cattle for the destruction of ticks. 
Annual Report, Bureau of Animal Industry, 1895-6, p. 109. 

17. Paouin. Texas Fever. Bulletin No. 11. Mo. Agric. Exper. 
Station, 1890. 

18. S.4lLMOX. Contagious diseases of animals. Special report No. 
22, Washington, D. C. 

19. Salmon. Report Commissioner of Agriculture. 1881-2. 

20. Salmon. Annual Reports, Bureau of Animal Industry. 
1884-5. 

21. SCHROEDER. Inoculation to produce immunity from Texas 
fever in Northern cattle. Ibid. 1898, p. 273. 

22. vSCHROEDER. Notes on cattle tick and Texas fever. Annual 
Report of the Bureau of Animal Industry, 1905. p. 49. 

23. SCHROEDER AND CoTTON. Persistence of Texas fever or- 
ganism in blood of southern cattle. Ibid., p. 71. 

24. Smith. Preliminary observations on the microiirganism of 
Texas fever. The Medical News. Dec. 21, 18S9. 

25. Smith and Kilborne. Texas fever. Bulletin No. i. 
Bureau of Animal Industry, U. S. Dept. Agriculture, 1893. 



368 ICTERO-PIEMATURIA 

26. vSmith and Kilborne. Annual Report, Bureau of Aniutal 
Industry, 1891-2. {Issued iSg^). 

27. Stiles. Report New York State Board of Health, 1868. 

28. Stockman. Some points to be considered in connection with 
Rhodesian redwater. Jour. Comp. Path, and Thera., Vol. XVIII 
(1905), p. 64. 

29. TheilER and Stockman. Some observations and experi- 
ments in connection with Tropical bovine piroplasmosis (East-coast- 
fever or Rhodesian Redwater). Jour. Comp. Path, and Thera. ,Vo\. 
XVII (1904), p. 193. 



ICTERO-HEMATURIA IN SHEEP 

Synonyms. Carceag ; hemaglobinuria in sheep ; Piro- 
plasmosis in sheep. 

§ 274. Characterization. This is an enzootic disease 
characterized by a rise of temperature with chill, and later 
icterus and marked changes in the blood due to a specific para- 
site invading its red blood corpuscles. 

§ 275. History. In 1892, Babes pointed out the con- 
stant presence of an intraglobular parasite in the blood of 
sheep suffering from an enzootic hemoglobinuria in Roumania. 
Bonome studied the same affection in Italy in 1895. Williams 
described this disease in Montana in the same year. He did 
not, however, report the finding of the parasite or record its 
description. 

§ 276. Geographical distributions. The piroplasma 
infection of sheep has been found in several places in Europe. 
Its existence in the United States is in question, although the 
description given by Williams of the disease he found suggests 
very strongly a Piroplasma origin. 

§ 277. Etiology. Pii'oplasma avis is the specific cause. 
This organism is very clo.sely related to Piroplasma bigemimini 
of Texas fever. 

§ 278. Symptoms. At the beginning the symptoms 



EOUINE MALARIA 369 

are said to be severe. There is a rise of temperature usually 
with a chill. After one or two days icterus appears. The 
urine is occasionally of a reddish brown color, due to the 
presence of hemoglobin. Death is preceded by a collapse in 
which the temperature is subnormal. The duration of the 
disease is usually but a few days. 

§ 279. Morbid anatomy. The subcutaneous tissues 
are infiltrated with a yellowish colored liquid. The blood is 
thin and watery. The muscles are pale and edematous. The 
mucous membranes of the pharynx and intestines are often 
hemorrhagic. The liver is small, soft and yellowish in color. 
The spleen is usually slightly enlarged. The kidneys are soft 
and friable. There usually occurs a parenchymatous nephritis. 

§ 280. Differential diagnosis. This disease is posi- 
tively diagnosed by finding the piroplasma in the blood. It is 
to be differentiated from anthrax, in which the specific organ- 
ism is readily found in the blood and organs. 

REFERENCES 

1. Babes. L'etiologie d'une enzootic des moutons denommee 
Carceag en Roumanie. Comp. R. del' Acad, dcs Sciences, Vol. CXV 
(1892), p. 359. 

2. BoNOME. Uber parasitiire Ictero-Haeniaturie der Schafe, Ein 
Beitrag zum Studium der Amobo-Sporidien. Archiv. fiir. path. 
Atiatomie, Bd. CXXXIX, S. i. 

3. Williams. The parasitic Ictero-Haematuria of Sheep. Bulletin 
No. S, 3/oH. Agric. Exp. Station, iSg^, also Anier. />/. Reviezv, 1897, 
P- 377- 



EQUINE MALARIA 

Syiiottyms. Piroplasmosis in horses ; South African 
horse sickness ; "Biliary fever." 

§ 281. Characterization. This affection of horses is 
characterized by a high temperature and a yellowish tint of the 
mucous membranes. The spleen is enlarged and the blood 
contains a Piroplasma eqiii. 



370 EQUINE oNIALARlA 

§ 282. History. The disease appears to have been first 
described by Wiltshire in 18S3. Guglielmi discovered the 
parasite of this affection in 1S99, and Rickmann found it in a 
large number of horses that died of "horse sickness." A 
good description of this affection was given by Theiler in 1901. 

^ 283. Geographical distribution. This disease 

appears to be very largely restricted to Southern Africa and 
Europe. The disease known as malarial fever in the United 
States has not been demonstrated to be due to a piroplasma. 
Peters describes this disease in horses in the West but he did 
not find its specific parasite. 

§ 284. Etiology. Laveran w^ho has studied this affection 
states that its cause is Piroplasma equi. It is closeh' related 
to P. bigeminum. It measures from 0.5 to 2.0 //. During the 
invasion and multiplication of the parasites there is a high 
temperature. In the blood corpuscle the parasite is single, in 
pairs or in rosette form. The disease was believed not to be 
transmitted directly with the blood containing the parasite. 
Theiler, however, succeeded in proving that equine piroplas- 
mosis is inoculable with the blood of immune horses into sus- 
ceptible ones. The natural method of infection is not known, 
but it is believed by many to be by means of a tick. 

Theiler's conclusions relative to the transmissibility of 
this parasite are as follows : 

(i) The piroplasma found in the mule and the donkey 
is identical with the piroplasma equi first found in the horse. 

(2) The disease caused by this piroplasma is inoculable 
with blood of immune animals into susceptible ones belonging 
to the domesticated species of the genus eqiuis. 

(3) The horse shows the greatest susceptibility for this 
piroplasma ; the donkey is less, and the mule the least, 
susceptible. 

(4) The possibility of a practicable inoculation against 
the piroplasmosis stands in the reverse order of the suscepti- 
bility. The mule may be safely inoculated with immune 



IMORBin ANATO:\IY 



371 



blood of any of the three respective equities ; the immune 
horse-blood produces the severest reaction, the immune mule- 
blood causes little reaction, and so does the immune donkey- 
blood. 

The period of incubation \s stated by Theiler to be 21 days. 

§ 285. Symptoms. An acute and chronic type are 
recognized. The acute type begins with a high temperature. 
There is jaundice, appearing first in the eyes. Death follows 
rapidh^ often at the time of the maximum temperature. In 
the chronic cases the symptoms are prolonged. 

77;<? duration of the disease is from a few to several days. 

§ 286. Morbid anatomy. The animal is emaciated. 
The blood is said to be thin and watery. The conjunctival 
subcutaneous tissue is of a yellowish color. The muscles are 
of a reddish brown. All of the tissues are anemic. The 
spleen is very large. Theiler has found the spleen to be twice 
the normal size. The lymphatic glands, especially those 
of the spleen, liver and kidneys, are tumefied and often hemorr- 
hagic. The liver is yellowish in color and engorged with 
blood. The bile capillaries are distended. The mucosa of the 
digestive tract is pale, or sprinkled with reddish areas. The 
glands in the thorax are enlarged and infiltrated with a gela- 
tinous substance. Occasionally there are ecchymoses on the 
lungs and heart. The heart muscle, pericardium and valves are 
frequently infiltrated with a gelatinous substance. The blood 
clots are soft. The exuded serum is of a yellowish brown 
color. The parasites are found in all parts. Death usually 
follows an acute attack. 

§ 287. Differential diagnosis. Equine malaria is to be 

differentiated from (i) Brustseuche, (2) Nagana, and (3) 
anthrax. In the last two named diseases the finding of the 
specific organisms will determine the diagnosis. The finding 
o'i Xht piroplasinawiW distinguish it horn Brustseuche. 



372 CANINE MALARIA 

REFERENCES. 

1. BowHiLL. Equine piroplasmosis or "biliary fever."' The 
Jour, of Hygiene, Vol. V (igosj.p. 7. 

2. Dale. Piroplasmosis of the donkey. Jour, of Coinp. Path, 
and Thera., Vol. XVI (1903), p. 312. 

3. GugliELmi. Un caso di malaria del cavallo. Clinica Veteri- 
iiaria, 1899, p. 220. 

4. Laverax. Contributions a I'etude de Piroplasma equi. Comp. 
R. de la Societe de biologie, 1901. 

5. Peters. Malaria of the horse. Nebraska Agric. Exp. Sta- 
tion, Press Bulletin 22. 

6. Pricolo. Beitrag zur Piroplasmose des Pferdes. La Clin. 
Vet., 1906, p. 529. 

7. RiCKMANX. Siidafrikanische Pferdesterbe. Berliner iliie- 
rarztl. Wochenschrift, 1902, S. 4. 

8. TheilER. Die Pferde-malaria. These de Berne. Schiveizer- 
Archiv filr Thierheilkunde, 1901, S. 253. 

9. Theiler. Further notes on Piroplasmosis of the horse, mule 
and donkey. Jour. Comp. Path, and Thera., Vol. XVIII (1905), 
p. 229. 



CANINE MALARIA 

Synonyms. Piroplasmosis of dogs; malignaut malarial 
jaundice; malignant jaundice in the dog. 

§ 288. Characterization. This di.sease is characterized 
by a high temperature, rapid course, jaundice and anemia. 
These are due to the invasion of the blood with Piroplas77ia 
ca?iis. 

§ 289. History. In 1895, Plana and Galli-Valerio 
found the piroplasma in the blood of dogs. In 1899, Hutcheon 
described a malarial fever in dogs that could be transmitted by 
inoculation subcutaneously with the infected material. Koch 
found the disease in Africa, and Celli mentions a modified 
form of the affection in Lombardy. In 1901, Nocard and 
Almy reported several cases of piroplasmosis in dogs presented 
at the clinic of the Alfort \"eterinarv School. Robertson 



ETIOLOGY 373 

described the disease under the name of malignant jaundice 
and pointed out its transmission by the dog tick (^Haemaphy- 
salis leachi). In 1902, Nocard and Motas reported an experi- 
mental study of the specific parasite. More recently Nuttall, 
and Graham-Smith have investigated this affection. 

^ 290. Geographical distribution. This disease has 
been found in several places in Africa, in Italy and in I{urope. 

§ 291. Etiology. The Piroplasma canis is the cause of 
this affection. Like Piroplasma bigernhnun it appears in two 
forms, round and pear-shaped. They nearly always occur in 
the red blood corpuscles. It varies in its morphology. Ac- 
cording to Marchoux Piroplasma canis in France is larger than 
Piroplasma bigeminum and single parasites occur more fre- 
quently. They vary in size from 2 to 4//. At the beginning 
of the disease usually single large round forms appear. It is 
said by Nocard and Motas not to be pathogenic for other 
species of animals. The parasite is said to be transmitted by 
means of certain insects. Lounsbur)' has demonstrated that 
Pulex ser7'a liceps, which is very abundant in certain localities, 
plays a role in its transmission. In Italy Piroplasma canis 
is supposed to be transmitted by Ixodes reduvius. In France 
it is supposed to be conveyed by Dcrmacentor reticulatiis. In 
South xAfrica it is conveyed by Haemaphysalis leachi. The 
parasite appears in the blood in from two to four days after 
artificial infection. 

Graham-Smith did not find the parasites in films from the 
peripheral circulation when stained by Leishman's method 
until several days after infection. The earliest day on which 
they appeared was the sixth day and the latest the thirty- 
sixth day. In most cases they were observed between the 
eighth and twelfth days after infection. In a few cases he 
worked out the percentage of red blood corpuscles that were 
infected. He found that it varied from .3 to 1.4^0- ^"ree 
parasites were seldom encountered in the earlier stages but 
later they became more numerous. The day before death he 
found one free parasite to 23 infected corpuscles, and the day 



374 CANINE MALARIA 

of death the free parasites were still more numerous. He 
found little evidence of phagocytosis in the cases examined. 
Nucleated red corpuscles appeared in films from three dogs 
the day before death, and in three other dogs they appeared 
six days before death. Blood pigment was present in nearlj^ 
all samples of urine. 

The period of incubation 2ii\.Q.x direct inoculation is about 
three days. 

?^ 292. Symptoms. Two distinct forms have been 
described : the acute which is nearly always fatal, and the 
chronic which often terminates in recovery. In the acute 
form the dog is dull, drowsy and refuses food. It may be 
thirsty. The temperature is high (io4°F.) but after two or 
three days it drops to subnormal. Icterus is not constant and 
the hemoglobinuria is not always present. The blood is pale 
and it coagulates slowly. The red corpuscles are reduced to 
2,000,000 per cubic millimeter or below. The polynuclear 
leucocytes are increased in number. Death nearly always 
occurs in from three to six days. 

In the chronic cases the fever remains high for from 36 to 
48 hours, when it returns to normal. The anemia is the most 
constant sytnptom. The mucosae become pale and the appetite 
is poor. The symptoms persist for from three to six weeks. 
Recovery is the rule. 

^ 293. Morbid anatomy. The mucous membranes are 
pale and the subcutaneous tissue and fat more yellow than 
normal. The spleen is 3 or 4 times the normal size. The 
liver is engorged with blood which is heavily charged with 
parasites. The gall bladder is distended with greenish bile. 
The mucosae of the digestive tract are slightly, if at all, 
changed. The kidneys are congested, often sprinkled with 
petechise or ecchymoses. The capsule is easily removed. 
The parasites are found in the blood in the early stages of the 
disease. They are more numerous in the capillaries than in 
the heart blood. 

The lungs are in some cases edematous. In all young 



MORinD ANATOMY 375 

animals one finds edema of the lungs with blood stained muco- 
serous substance in the trachea and bronchioles. The 
lymphatic glands are rarely if ever altered in appearance. 

The central nervous system presents nothing of note, 
except a slight congestion of the meninges. 

The histological study of the lesions shows that the tissue 
changes start from greatly engorged capillaries. In these 
vessels containing masses of blood, a large part of the red cor- 
puscles contains the parasite. 

The histological examination of the organs when hardened 
in Miiller's fluid shows, according to Graham-Smith, the capil- 
laries of the alveoli of the lungs to be dilated and in .some 
instances a proliferation of the lining cells some of which are 
seen lying free in the air cells. In other alveoli the process is 
more advanced and proliferated cells, leucocytes, and in some 
cases red corpuscles are present in them. The lumen of many 
of the bronchioles frequently contains desquamated epithelium, 
leucocytes and mucus. There is no evidence of any increase 
in the connective tissue. No pigmentary or fatty changes were 
observed in the heart or skeletal muscles. The liver showed 
the most marked changes. The central vein of the lobule and 
the capillaries lying between the liver cells were dilated. The 
protoplasm of the liver cells .stains feebly but the nuclei take 
the stain fairly well. The cells are distorted between the 
dilated blood vessels and in many cases almost destroyed, 
especially those in the central zone. The vessels in the inter- 
lobular spaces are dilated but the bile ducts are normal. There 
is no increase of fibrous tissue and the capsule is normal. The 
capillaries contain a large number of red blood corpuscles and 
the proportion of leucocytes is high. The latter are also very 
numerous in the larger vessels. In these vessels about 10% 
of the red corpuscles are infected. The parasites usually appear 
in small groups in the cells. The proportion of leucocytes to 
red corpuscles is about i to 10. In the capillaries from 23 to 
53% of the red corpuscles are infected and in some instances 
the proportion of leucocytes to red corpuscles is as high as r 
to 3. In but one dog did he find fatty changes. The smear 



376 CANINE MALARIA 

preparations showed that gS.g% of all infected corpuscles con- 
tained one to four parasites and the balance more than four 
parasites. Free parasites were found in the proportion of i to 
2}4 infected corpuscles. The spleen pulp contains in most cases 
a large quantity of blood and the vessesl in the trabeculae are 
dilated and contain numerous leucocytes. The proportion of 
infected corpuscles in the pulp is small (3 to 12%) but in the 
small trabecular veins it is high (48%). In the kidney there 
were no changes that were constantly present except dilatation 
of the blood vessels. In some cases about 46% of the red 
corpuscles in the vessels of the glomeruli were infected. 
T/ie duration in fatal cases is from 3 to 6 days. 

§ 294. Differential diagnosis. The positive diagnosis 
is made by finding the parasite in the red blood corpuscles. 

REFERENCES 

1. Graham-Smith. Canine piroplasmosis. Morbid .\natomy. 
Jour, of Hygiene, Vol. V (1905I, p. 250. 

2. HuTCHEON. Malignant malarial fever of the dog. The Veter- 
inary Journal, Vol. XLIX (1899), p. 398. 

3. LouNSBURV. Transmission of malignant jaundice. Agricul 
tiiral Journal, Nov. 21, 1901. 

4. Marchoux. Piroplasma canis chez les chiens du vSenegal. 
Cotnp. R. de la Societe de biologie, 1900, p. 97. 

5. NoCARD ET AI.MV. Une observation de piropiasmose canine. 
Bulletin de la Societe cent, denied. Viler., 1901, p. 192. 

6. NocARD ET MoTAS. Contribution a I'etude de la piropiasmose 
canine. Arm. de f Inst. Pasteur, 1902, p. 257. 

7. Nlittall AND Graham-SmiTh. Canine piroplasmosis. Jour, 
of Hygiene, Vol. V (1905), p. 237. 

8. NuTTAi,!.. Canine piroplasmosis. Jour, of Hygiene, \o\. IV 
(1904), p. 219. 

9. PiANA ET Galli-Valerio. // iHodemo Zooiatro. 1895, p. 165. 
ID. Robertson. Malignant jaundice in the dog. 77/.? four, of 

Comp. Path, and Thera., Vol. XI\' (1901), p. 327. 

11. Webb. Piroplasmosis in Fox-hounds in India. The four of 
Comp. Path, and Thera., Vol. XIX (1906], p. i. 

12. Wetzi.. Ueber die Piropiasmose der Hunde. Zeitschrift fur 
Thiermed., Bd. X, S. 369. 

13. Wright. Canine piroplasmosis (on certain changes in the 
blood), four, of Hygiene, Vol. V (1905), P- 268. 



CHAPTER X. 

DISEASES CAUSED BY PROTOZOA 
GENUS AMEBA. 



§ 295. General discussion of Ameba. The ameba 
belong to the class Sarcodina. They include the simpler 
forms of the protozoa. The genus ameba is provided with 
lobar or pointed pseudopodia. A few of these have become 
parasitic. So far as seems to be known, these parasites, with 
possibly a few exceptions, do not produce noxious products 
like bacterial toxines or ptomaines, but whatever damage they 
may cause is due to the mechanical disturbances set up by 
their presence and multiplication. The genus ameba has 
very few pathogenic species. The best known of them is 
Avieba coli, the supposed cause of a form of dysentery in man. 
In animals but few species have been found to stand in a 
causal relation to a morbid process. The term ''amebiasis" 
has been introduced by Musgrave and Clegg to denote an in- 
fection with ameba. 



INFECTIOUS ENTRRO-HEPATITIS IN TURKEYS. 
Synonym. Blackhead. 

§ 296, Characterization. This disease of turkeys is 
characterized by thickening of areas or of the entire walls of 
the ceca and areas of tissue degeneration and necrosis in the 
liver. 

J^ 297. History. In the fall of 1893, Prof. Samuel 
Cushman of the Rhode Island State Experiment Station sent 
a few specimens of the affected organs of turkeys which had 
died of "blackhead" to the Bureau of Animal Industry, where 



378 ENTERO-HEPATITIS IN TURKEYS 

they were carefully examined by Dr. Theobald Smith. In the 
summer of 1894, Smith made a careful study of this disease at 
the Rhode Island Experiment Station. He found that it was 
caused by one of the protozoa {A^neba meleagridis. Smith). 
He published a full description of the disease which, in accord- 
ance with the lesions, he designated Infectious entero-hcpatitis . 

In 1895, the disease was further investigated respecting 
the mode of transmission of the infecting protozoa. The 
results showed that it could be transmitted directly from dis- 
eased to healthy turkeys without the intervention of an inter- 
mediate host. These results were published in 1896. The 
place and the time of the first appearance of this disease are 
not clearly stated, but it seems that New England was the first 
to suffer from it. 

Recently, Chester of the Delaware Agricultural Experi- 
ment Station has shown that a very similar disease attacks 
chickens. 

§ 298. Geographical distribution. The available data 
bearing upon the geographical distribution of this disease in- 
dicate that it is widely distributed. The New England states, 
particularly Rhode Island and certain districts in the Middle 
and Western states, are affected. It has not yet been reported 
from the Southern states. For want of statistics the amount 
of loss to the poultry industry occasioned by this disease can 
not be accurately estimated, but the fact that it has caused 
many farmers and poultry men in New England to discontinue 
the raising of turkeys shows that it is of much economic im- 
portance. It is stated in the report of the Rhode Island Ex- 
periment Station for 1894 that "the eradication of this disease 
would be worth hundreds of thousands of dollars to the east- 
ern farmers alone." These heavy losses in the East, together 
with the accumulating evidence that the entire northern third 
of this country is sprinkled with infected districts from which 
the disease is spreading, indicate that this malady is of more 
than ordinary significance to those engaged in the turkey 
industry. 



KTIOLOCiY 



379 



>^ 299. Etiology. In 1895, Smith described a micro- 
organism belonging to the protozoa which lie found to be 
associated directlj' with the disease process. He designated 
it Amicba rneleagridis. In those cases in which the disease was 
recent, or at its height, the parasites were very numerous in 
the affected tissues, while in those in which the disease pro- 
cess was far advanced and associated with degenerative or 
regenerative changes, the parasites were found with difficulty. 
Curtice finds that the chicken is a host for the causative para- 
sites, and together with the adult turkeys spreads them broad- 
cast through the droppings. He has shown that the ameba 
are not transmitted through the eggs. The young turkeys 
become infected soon after being exposed to contaminated 
surroundings. The young are much more susceptible than 
the older turkeys. 

The most fre- 
quent appearance pre- 
sented by the para- 
sites is that of round 
homogeneous bodies 
with a sharply de- 
fined, si n g 1 e - CO n - 
toured outline. With- 
in these bodies and 
situated somewhat 
eccentrically is a 
group of very minute 
granules, probably 
representing a nuclear 
structure. They vary 
somewhat in size, 
measuring from 8 to 
10 /< in diameter in 
some cases, from 12 to 14// in others. In the fresh ti.ssues 
they are distinctly larger than the parasites within the tissues 
which have undergone the hardening process. The latter are 
from 6 to 10 // in diameter. The difference may be due to 




■scji"--^" 



5^ 



Fig 98. Ameba rneleagridis. (/) Isolated 
organisms, (i-) single parasites, (j 1 groups of 
the parasite (a) of the ameba in the mucous 
Diembrane of a turkey'' s cecum {Smith). 



38o EXTERO-HEPATITIS IN TURKEYS 

shrinkage, on the one hand, and on the other to a sliglit flat- 
tening of the bodies by pressure in the fresh preparations. 
These peculiar homogeneous bodies were found, as a rule, free 
in the crushed preparations, although occasionally giant cells 
were detected which contained a number of them. The cell 
nuclei of the giant cells are not visible in the fresh condition. 
Numerous coarse granules, less frequently fat globules, are 
embedded in its protoplasm. 

Smith believed from the results of his investigations that 
the parasite lived in the interstices and lymph spaces of the 
tissue, but not within cells. This seems certainly true of the 
cecum. The liver cells become necrotic or else disappear so 
rapidly that it is impossible to determine just where the para- 
sites begin to multiply. They do not live within the blood 
vessels, as they are not found within them excepting perhaps 
in a thrombosed vessel. They must, therefore, occupy the 
place of the liver cells. It is probable that they begin to 
multiply in the connective tissue adjoining the blood vessel 
and simply crowed out the liver cells, leaving the connective 
tissue stroma of the lobules in whose meshes they are found. 

Their presence within giant cells is seen in almo.st every 
infected organ subjected to examination. In teased prepara- 
tions the fresh tissues they are frequenth- found with remnants 
of the inclosing cells still attached. This intracellular condi- 
tion is, however, a purely passive one so far as the parasite is 
concerned. 

The microparasites within the tissue of the host seem to 
tend toward destruction. Both the death of the tissue itself 
and the repair seem to lead to the disappearance of the para- 
sites. In most cases there may be seen in the same section a 
partial dissolution of some of the bodies, while others are still 
in good preservation. Evidently their life within the tissues 
is not very long. 

A discharge of the microparasites which escape destruc- 
tion probably takes place from the walls of the ceca, when 
these break down into the contents with which they are carried 
outward. A similar discharge may take place from the liver 



ETIOLOGY 381 

through the bile ducts into the intestine. Another way of 
dissemination is in the death of the diseased turkey and the 
dissolution of its body, whereby the organisms are set free. 

The occurrence of amebre in intestinal affections of man 
was noticed by Losch in 1875. Since that time it has been the 
subject of many investigations. 

The points of analogy between the avian and the human 
disease are that in both there is an affection of the intestine 
(large intestine in man, ceca in turkeys) associated with liver 
disease due to amebae. 

The intestinal wall in amebic dysentery is greatly thick- 
ened, owing to an edematous condition. It is also thickened 
in circumscribed areas and contains cavities filled with gela- 
tinous-looking pus. The aniebae vary much in size and con- 
tain vacuoles. They are found in variable numbers in the 
bottom of the ulcers and in the discharges. The large num- 
bers of amebse found in the intestinal contents led Councilman 
and Lafleur to infer an active multiplication therein. The 
presence of the parasites within the submucosa is described by 
these authors in one case only. 

In the turkey, the parasites are always present in the 
connective tissue spaces of the mucous and submucous mem- 
brane. Their presence in the contents of the cecum is highly 
probable. 

It differs from the Ameba dysenteri<c in being quite uni- 
form in appearance, varying but .slightly in size (from 6 to 
io/< in diameter) and in being free from vacuoles. Move- 
ments characterized as ameboid have not yet been demon- 
strated. 

The liver affection in man appears usually as an abscess. 
In turkeys it appears as a variable number of foci in which 
the microparasites may be present in great abundance. The 
difference in the nature of the lesions must be largely attri- 
buted to the different reaction of the tissues of birds toward 
injuries. 

§ 300. Symptoms. Diarrhea is the symptom which 
sooner or later may be expected to appear. It probably occu- 



382 ENTERO-HEPATITIS IN TURKEYS 

pies the most prominent place among the objective manifesta- 
tions. The disease of the ceca is presumably responsible for 
this. Diarrhea occurs with at least one other disease of the 
ceca and with the presence of tapeworms. Emaciation is pro- 
nounced in very chronic cases but it is not constantly present. 
As it may accompany other wasting diseases, it can not be de- 
pended upon as an indication of this affection. As the disease 
progresses the turkeys become less active, lag behind their 
flock or do not go out with it. Later the comb, wattles and 
even the skin of the head become dark colored, hence the 
popular name "blackhead."" 

§ 301. Morbid anatomy. Turkeys are attacked quite 
young. Smith found a turkey about three weeks old in which 
the disease had already made considerable progress. It seems, 
moreover, as if the disease is contracted only by the young, 
because in the examination of turkeys of different ages the 
oldest show lesions of the longest standing ; that is, such as 
had undergone the most extensive transformation. In general 
it may be said that the age of the turkey corresponds with the 
age of the disease process. The most serious and extensive 
destruction of tissue occurs in the turkeys in the fall. In raid- 
summer the disease is making most progress and the micro- 
parasites are present in greater numbers. It is probable that 
the delicate tissues of the 3'oung are best adapted for the tem- 
porary habitat and rapid multiplication of this parasite. * 

The primary seat of the disease is the ceca. From these 
the liver is secondarily invaded. Other organs have not been 
found to be attacked. 

The lesions of the ceca are in substance a thickening of 
the wall, followed in most cases by a destruction of the 
epithelium and deeper portions of the mucous membrane. 
This destruction results in the outpouring of a coagulable 
fluid into the tube. The thickening of the wall may vary 
considerably in extent from case to case. 

*Iii this regard it simply follows the rule observed by large numbers 
of parasites whose most destructive action is visited upon the young. 



.MOKHin ANATOMY 



383 



It may be uniform over the greater portion of the tube or 
it may be limited to circumscribed patches. The commonest 
seat of these lesions is near the blind end of the tube where it 
evidently starts and whence it spreads to other portions. Not 
infrequently only one cecum is dis- 
eased, the other remaining normal. 

The affection of the cecum is due 
primaril}^ to the multiplication of the 
microorganism which may take place 
chiefly either in the mucous mem- 
brane, or iu the submucous tissue; it 
may, though rarely; extend into the 
muscular coat. The thickening of 
the wall is the result of several 
processes— the multiplication of the 
parasites, the increase of the normal 
tissue elements and later on the ac- 
cumulation of masses of small cells 
and some giant cells. 

In the early stages of the inva- 
sion, the adenoid tissue between the 
tubules and in the submucosa becomes 
greatly increased, owing to the pres- 
ence of large numbers of micro- para- 
sites of round or slightly oval outline 
and from 6 to lo/i in diameter which 
stimulates the proliferation of the tis- 
sue cells. Numerous mitoses have 
been seen in this stage. The parasites 
seem to occupy the meshes of the 
adenoid tissue either singly or in 
groups or nests. In these meshes 
they are soon inclosed in cells acting 
as phagocytes, so that the appearance 

of an intracellular habitat of the parasites is suggested. 

The presence of the parasites in this reticulum probably 

stimulates also the accumulation of lymph cells within the 




Fig. 99. Ceca of a turkey; 
[a) and {h) are diseased 
areas, {c) a section of the 
thick en ed wall. 



384 



ENTERO-HEPATITIS IX TURKEYvS 



spaces, by virtue of which the mucous membrane is thickened. 
In this early stage of invasion the epithehum, both of the 
tubules and of the surface, remains 
unaffected. The parasites do not 
invade the epithelium at any time. 
As the disease progresses there 
is a continued increase in cellular 
elements of the mucous and sub- 
mucous coats and a gradual inva- 
sion of the muscular coat. Here 
the bundles of fibers of the circular 
coat are thrust apart by masses of 
cells, so that this coat also becomes 
greatly thickened. The inflamma- 
tion finally extends to the serous 
covering, where the blood vessels 
become greatly dilated and give the 
cecum a congested appearance. In 
cases of ordinary severity the wall 
of the cecum which is not more 
than 0.2 to 0.5 mm. thick normalh' 
becomes 2 to 3 mm. thick. 

With the progress of the dis- 
ease the mucous membrane may be 
shed and a coagulable fluid poured 
out into the cecum. In some cases 
it appears in isolated masses, which 
adhere to certain spots of the mu- 
cous membrane. In others, this 
exudate fills the entire tube with a 
yellowish-white mass, built up in 
concentric layers consisting of a 
mixture of blood corpuscles, fibrin 
and small round cells in variable 
proportion. 

In the further progress of the local disease it is not im- 
probable that bacteria are also concerned. The exudate con- 




FiG. 100 Diseased cecum, 

shoziiing thickness of zvall 

and ulcerated tnncosa. 



MORBID AXATOMV 



38; 



tains immense numbers of them and the denuded mucosa fur- 
nishes a favorable place of entr>-. It is otherwise difficult to 
explain the continued increase in tliickness of the walls of the 
cecum after the mucous membrane has been shed. This con- 
tinued increase in thickness is due to an extensive infiltration 
of small round cells and the presence of some giant cells. 
Parasites in this advanced stage are scarce and usually recog- 
nizable only as vacuole-like bodies within the giant cells. 

The thickening of the wall is associated in some cases 
with an extension of 
the inflammation to 
the contiguous wall of 
the intestine, which 
becomes firml}^ at- 
tached to the cecum. 
Yellowish exudates 
are sometimes found 
outside of the diseased 
cecum on its serous 
covering and they 
bind it inextricably 
to the other cecum or 
to the intestine or at- 
tach it to the abdom- 
inal wall. In these 
stages, the micropara- 
site is not found. It seems to have done its work by destroy- 
ing the mucous membrane and to have left the field for 
miscellaneous bacteria. 

Other portions of the digestive tract are not affected. 
The secondary lesions are found in the liver, although in some 
cases they do not appear. The organ itself is enlarged to 
probably twice the normal size. Over the surface are distrib- 
uted roundish, discolored spots, distinctly demarcated from 
the surrounding tissue. These may be distributed uniformly 
over the whole surface of the liver or they may be limited in 
number to a few. They vary from 3 to 15 mm. in diameter. 




Fig. ioi. Liver slu 



diseased foci. 



386 



ENTERO-HEPATITIS IN TURKEYS 



Several types of these spots appear corresponding to different 
conditions of the diseased tissue. We have in the early, most 
active disease process sharply defined circular areas of a lemon 
yellow, or a neutral gray or of an ochre yellow color. The 
spot is not homogeneous in structure, but made up of a deli- 
cate network of gi^yish yellow, dead tissue. 

In another class of spots there is a mottled brownish color 
which contrasts only slightly with the surrounding liver tissue 
by its darker color. It may contain a central yellow nucleus 
of dead tissue and a narrow outer border of the same character, 
or the border may be a dark brownish circular line. The 
entire spot has an indistinct appearance and is flattened or 

even slightly depressed 
below the surface. In 
some cases they are 
uniformly whitish and 
shade off somewhat 
gradually into the sur- 
rounding tissue. In 
sections of the affected 
organ it will be found 
that the surface spots 
represent masses of 
liver tissue in the same 
condition, the spots be- 
ing simply the places 
where these diseased 
foci intersect the sur- 
face. Some are found 
deeply imbedded in the 
liver tissue, and therefore not visible on the surface. The 
lesion of the liver is thus represented by few or many foci of 
disease having in general a spherical form and appearing on 
the surface of the organ as round spots. Occasionally the 
lesions become more extensive and the death of large portions 
of liver tissue follows. 

The changes in the liver are most easily explained by 



r^' 


- ■' - 




1 








'. ^ ''^: 
^^" 


^' 



Fig. I02. A drait'iiig of a beginning ne- 
crotic mass, (a) Giant cells, {€) free nuclei, 
and [b) disintegrated necrotic tissue. 



MORI5ID ANATOMY 387 

assuming that the niicroparasites are convej-ed by the blood 
directh' from the diseased ceca into the liver and there de- 
posited in different places, where they begin to multiply and 
spread in all directions. In this way they form the spherical 
foci of disease which appear as circles on the surface of the 
liver. This theory is borne out by the results of the micro- 
scopic examination. 

In sections of hardened tissue from the liver in which the 
disease has but recenth^ begun, the affected regions are invaded 
b}^ large numbers of protozoa which occupy a kind of reticu- 
lum formed probably from the connective tissue stroma. The 
liver cells have partially or wholly disappeared from these foci. 
The border of the necrotic tissue is surrounded bj' a zone of 
giant cells. The parasites occupy the meshes of the tissue 
either singly or in groups. The reticulum is provided with a 
small number of nuclei, some of which are closely applied to 
and curved partly around the parasite. The blood vessels are 
usually much dilated and filled with red corpuscles. 

The yellow masses observed with the naked eye in the 
surface spots are shown to be patches of an amorphous sub- 
stance which take nuclear stains very feebly, the aniline colors 
not at all. This may be described as a coarse network in the 
meshes of which small cells, and very rarely parasites, are 
seen. This substance is assumed to be the result of coagula- 
tion necrosis of the liver cells by which they have lost their 
nuclei and have become fused into a formless mass. It is 
probable that the plugging of blood vessels in the liver by 
parasites carried from the cecum is the cause of the necrosis, 
since such plugs or thrombi are not uncommon in sections of 
the diseased areas. 

With the appearance of the niicroparasites regenerative 
changes begin at once which complicate the process. We 
have at the outset an active multiplication of the niicropara- 
sites which take the place of the original liver tissue and a 
process of coagulation necrosis going on at the same time. 
Soon multinucleated (giant) cells appear. Not infrequently 
they are grouped around what appears to be a plugged 



388 ENTERO-HEPATITIS IX TURKEYS 

vessel or else they occupy the lumen of the vessel itself. 

In still older cases the diseased areas are found more or 
less filled with small round cells which may have passed into 
the dead regions from the blood vessels. In all cases the 
latter are more or less enlarged and they seem to encroach 
upon the liver tissue, thus filling in part the void produced by 
the cell death and giving the surface of the liver a brownish, 
mottled appearance wherever the disease spots are. The 
proce.sses of advancing disease and necrosis or death of tissue 
on the one hand and of repair on the other seem to go on side 
by side, now one, now the other, predominating. 

The results of the investigations thus far made indicate 
that the disease may follow several courses. 

1. After a certain period of disease, regenerative pro- 
cesses begin which tend toward a permanent recover5\ 

2. The disease may proceed so rapidly from the very 
start that the affected turkeys die early in life. 

3. The disease may come to a standstill but the amount 
of dead tissue in the ceca and liver maj' be so great as to favor 
the entrance of bacteria which are directly responsible for the 
death of the bird late in the summer or fall. 

The description of the lesions of a turkey dead of this 
disease is appended. It is quoted from Smith's report. 

" Turkey No. 14. — About 5 months old. Taken from a flock August 
8 because of lack of strength to keep up with the rest when driven. 
Indications of diarrhoea. Placed in a coop, where it died during the 
night. Examined next morning. 

"Slight odor of decomposition. A few small warts on skin of neck. 
The various organs were found normal, with the following exceptions : 

"Mucosa of duodenum almost blackish, from intense injection and 
pigmentation of villi. 

"Both caeca diseased. The left is slightly distended. On serous 
aspect two yellowish spots, with markedly injected borders, correspond- 
ing to thickenings of the walls near the blind end of tube. The mucous 
surface of one is smooth ; to the other an exudate is attached. Besides 
the thickening of these spots, the free half of this caecum is somewhat 
thickened uniformly. 

"The right caecum is very much distended over two-thirds of its 
length. From the serous surface local thickenings are recognizable. 



DIIFERENTIAL DIAGNOSIS 389 

which have a yellowish, mottled appearance. The small intestine is 
firmly attached to one of these. The disease has, however, not invaded 
the wall of the latter. The border of these spots is intensely hypenemic. 
When the caecum is slit open its width is three to four times that of the 
undisturbed tube, and the thickness of the wall varies from one-eighth 
to one-half of an inch, being not less than one-eighth of an inch over 
three-fourths of the entire length. When the brownish feces were 
washed away the increased local thickenings were found covered with 
firm exudates, usually attached in but one spot. 

"Sections were examined of that portion of the caecal walls which 
was very much thickened, and to which the contiguous small intestine 
was inseparably attached by the new growth. 

"The mucosa of the caecal portion had sloughed away, while that of 
the embedded small intestine was intact. The neoplastic tissue between 
caecum and intestine was fully i cm. (two-fifths inch) thick. Inas- 
much as the infiltration probably followed the narrow^ mesentery 
between caecum and intestine the original boundary lines of the caecal 
■wall are no longer recognizable. The muscular coat of the caecum may 
be traced for only a short distance into the neoplasm, when it appears. 
Microparasites were not seen distinctly in the diseased tissue. 

"The liver is very much enlarged, and dotted everywhere with 
roundish spots of varying appearance. The majority are from 5 to 12 
mm. in diameter, round or slightly oval. The center of each is usually 
occupied by a group of yellowish dots and the circle is bounded by a 
narrow yellowish ring. The space of the circle is mottled brownish. 
Among these spots there are also circles of a completely yellowish color. 
On the convex surface of the left lobe there is a very firm, ring-like, 
yellowish mass, cutting like firm cheese. 

"In crushed preparations of fresh liver tissue from within the brown- 
ish circles many giant cells are seen. They consist of a meshwork of 
protoplasm of a rather coarsely granular character inclosing spheres 
which appear homogeneous. The giant cells are up to 30 /< in diameter. 

"Sections of liver tissue hardened in alcohol and in Foa's solution 
were also examined. The foci of disease contain necrotic areas in 
which are numerous giant cells each inclosing a number of micro-para- 
sites. In some portions there is much cell infiltration in the interlobu- 
lar tissue around the portal vessels. Among the cells the protozoa are 
recognizable." 

i^ 302. Differential diagnosis. This disease is to be 
dilTerentiated from certain local affections of the cecum not 
especially uncommon in turkeys. Ztirn {Deu/sc/ie Zeit. /. 
T/iiermed, Bd. A' (1883), p. 189) has described a cecal disease 
in water fowls and turkeys and von Ratz has described a 



390 ENTERO-HEPATITIS IN TURKEYS 

cecal disease in turkeys in which the Hver lesions seem to be 
absent. The lesions in the liver and the presence of the 
microparasite, as previously described, are sufficient to 
differentiate this disease. 

§ 303. Prevention. The present knowledge of this 
disease .shows that the parasite is transmitted directly from 
diseased to healthy turkeys. This suggests that the first pre- 
caution is to avoid the entrance of diseased or seemingly 
healthy turkeys from a diseased flock into a healthy one. 
The discovery of Chester indicates that a like precaution must 
be taken with reference to fowls. If the disease exists the 
best, although mo.st radical, method as suggested by Smith is 
the total destruction of the affected flock, thorough disinfec- 
tion of the roosts and droppings under the same, and the intro- 
duction of healthy turkeys. 

RKFEREXCES 

1. Chester. Report of the bacteriologist of the Del. College 
Agric. Kxp. Station, 1899-1900. (C. reports disease in chickens). 

2. Curtice. Notes on experiments with blackhead of turkeys. 
Circular No. i ig. Bureau oj Animal Industry, 1907. 

3. CuSHMAN. Nature of blackhead in turkey. Report R. Island 
Agric. Exp. Station, 1894, p. 199. 

4. MooRE. The direct transmission of infectious entero-hepatitis 
in turkeys. Circular No. 5, Bureau of Animal Industry, 1896. 

5. MuSGRAVE AND Clegg. Amebas : Their Cultivation and Etio- 
logic Significance. Bulletin No. 18. Bureau of Cover7iinent Labora- 
tories, Manila, 1904. 

6. Smith. Infectious entero-hepatitis in turkeys. Bulletin No. 
S, U. S. Bureau of Animal Industry, 1895. 



chapti<:r XI. 

DISEASES CAUSED BY PROTOZOA 
GENUS TRYPANOSOMA. 



§304. Classification of Trypanosoma. The Trypan- 
osoma belong to the protozoa, but their species diagnosis is 
not satisfactorily determined. A number of classifications of 
these organisms have been proposed. The one suggested by 
Salmon and Stiles is appended. 

Protozoa, class Mastioophora, subclass Flagellata, order 
Monadida, family Trypanosomidae, genus Trypanosoma Gruby. 

According to Stiles the family contains at present two 
genera, which are distinguished as follows : 

1. One flagellum present, extending from the centrosome along 

the undulating membrane and becoming free at the anterior 
extremity Trypanosoma 

2. Two flagella, one extending anteriorly, the other pos- 

teriorly Try paiio plasma 

Generic diagnosis of Trypanosoma. " Body fusiform, presenting a 
lateral, longitudinal, undulating membrane, the thickened border of 
which terminates posteriorly, in the posterior half of the body in a 
' centrosome,' and is prolonged anteriorly in a free major flagellum; 
nucleus generally anterior; there is a tendency to agglomeration by 
the posterior extremity ; divisions longitudinal and unequal. Parasitic 
in the blood of vertebrates." 

In order that a somewhat definite idea of the structure of 
these organisms may be obtained the specific characters of Tr. 
Lewisi are quoted. 

Trypanosoma : " 8 to 10 // long, 2 to 3 // broad, 24 to 34 n long by 
1.44 broad (Laveran and Mesuil. 1901) ; a very refringent granule (near 
centrosome) in place of which a clear vacuole is seen in stained prepara- 
tions. Animalcules exceedingly minute, alternate and vermicular 
under normal conditions, but highly polymorphic and capable of assum- 
ing a variety of contours ; flagellum single, terminal, two or three times 
the length of the extended body. No contraclible vesicle ... as 
yet detected. Habitat, blood of the rat and hamster." 



392 



TRYPANOSOMA 



§ 305. General morphology of trypanosoma, Try- 
panosoma of all species are in general very similar. The mor- 
phology is said to vary greatly in the same species and to a 
greater extent in different species. In general the trypanosoma 
may be said to measure from i to 5 /i in thickness and from 15 
to 45 /< in length, including flagellum. They all show very 

active eel-like movements 
and some motility. The 
nature and extent of the 
motility varies. The fact 
as stated, that variations 
are occasionally found in 
one species, often, indeed, 
in a single preparation, 
which are nearly as great as 
those observed between dif- 
ferent species, renders the 
specific determination dififi- 
cult. The flagellum at the 
anterior end of the parasite 
varies gre.atly in length. It 
is actively motile, pointed 
and continuous, with the 
thickened margin of the 
undulating membrane end- 
ing at or near the centre- 
some. The undulating 
membrane extends along 
the border of the organism 
from near the ceutrosome in the posterior portion to the anterior 
end of the organism, from whence it continues as the free 
flagellum. Its breadth and folds vary considerably. 

The nucleus is usualh' situated in the anterior half of the 
parasite and varies both in size and shape. It is generally 
oval or round, and assumes other contours with the different 
stages of division. The centrosomeas a rule is in the posterior 
and more blunt end, and it appears to have an intimate associ- 




FiG. 103. Trypan- 
osoma Briicei : c, 
centrosome ; f, 
flagellum ; m, un- 
dulating mem- 
brane; n, nucleus. 
X about 2,000. 
{After Laveran 
and Mesnil). 



Fig. 104. Trypan- 
oplasma Borrelli : 
ccentrosome ; fa, 
anterior flagel- 
lu in ; fp ,posterio r 
flag ell u ni; m ,un- 
dulating mem,- 
hrane; n,nucleus; 
X about 1,800. 
{After Laveran 
and Mesnil). 



MULTI PLICATION 



393 



ation with the llaoelhun and undulating membrane. Its loca- 
tion has been used as a diagnostic point in determining species. 
The protoplasm is homogeneous or granular, depending 
upon the age of the parasite, its environment and, perhaps to 
a certain degree, upon the species. Few or many fine or 
coarser granules may be found scattered throughout the 

protoplasm. 

Multiplication. Voges gives three forms of multiplication, 
namely, longitudinal, transverse fission, and segmentation. 




r & 9 ^o n 

Fig 105. 2, Trypanosoma Lewisi completely developed ; n '^^f'^*^J^^ 

ZroLe Jindulatin.rnembrane f,M^^^^^^^^ 

in process of division. 7— other forms of '''''^''tf ''"^"f.^- 

LeLi, //, flagella not stau,ed. X al^out .,000 durm.te,s ^ntte, 

Laveran and Mesnil). 

He did not observe conjugation. The chromatin divides into 

frotn 3 to 10 segments, which assume irregular shapes and loca- 

Uons some of which areoften found well np ,n the flagellum. 



394 TRYPANOSOMA 

The nucleus usually divides into equal parts, but may break 
into several segments. After the nuclear division the proto- 
plasm may assume various irregular forms. The young nuclei 
arrange themselves in groups, and the parasite twists and 
splits by longitudinal or more often by transverse fission 
(Fig. 104). The new forms resulting from the division soon 
assume the regular shape. Plimmer and Bradford consider 
longitudinal and transverse division the more frequent modes 
of reproduction. They observed conjugation, which con- 
sisted in the fusion of the micronuclei, followed by an amoeboid 
stage and division by segmentation. The order of division 
appears to be (i) centrosome, (2) flagellum, and (3) nucleus 
and protoplasm. Other forms of reproduction have been 
described by Martini, Laveran and Mesnil and others. Invo- 
lution forms have been observed by a number of workers. 
Rodet and Vallet state that Tr. Brucci multiply principally in 
the blood and lymph. There is a difference of opinion con- 
cerning the agglutination of Trypanosoma. Musgrave and 
Clegg state as a result of their researches that the so-called 
phenomenon of agglutination is of no value from a diagnostic 
point of view, and it is too uncertain, if it is a reaction, to 
serve as an index of immunity or susceptibility. 

§ 306. Distribution in the body. It is the opinion of 
most students of the Trypanosoma, that in the infected animal 
they are found in all of the body juices, and are not present at 
the same time in great numbers in one part, with but few in 
another. Animals having many parasites in the blood when 
killed show them also in the organs ; and if they are not 
demonstrable in a microscopic examination of tlie one they will 
not appear in the other. The blood of animals suffering from 
the disease is always infectious by animal inoculation, 
although the parasites may not be found microscopically at the 
time. Martini, however, regards the spleen, lymphatics, bone 
marrow, and to a less extent, the liver and kidneys, as the 
places for the destruction of Trypanosoma. It has been found 
that Trypanosoma injected into the peritoneal cavity multipl>^ 
considerably before they enter the blood. 



HISTORY 395 

Disappearance after death. Trypanosoma disappear very 
suddenly after the death of the host. Within two hours signs 
of degeneration begin ; the parasites shrink, assume irregular 
shapes and then disappear. Motile forms are rarely found 
after two hours. 

Distribution in nature. Trypanosoma are not known to 
exist in nature outside of the bodies of living animals. They 
have been found in the blood of a large number of species. 
Now has found them m the blood of many birds. 1 hey 
have been kept alive in blood or salt .solution for a few hours. 
Novy has succeeded in cultivating them, /. e.. getting them to 
multiply on an artificial culture medium. 

R .07 Historical sketch. There is a voluminous 
Hterature on the trypanosoma from which the following brief 
summary was taken. In 1841, Valentin discovered hematozoa 
in trout ^Salmo fario) and in 1842, Glugge found them in the 
blood of frogs. In 1843, Gruby observed a flagellate infusorium 
in frogs which he named Tr. sanguinis. Gruby has generally 
been credited with the discovery of these forms. From 1843 
to 1879 the organisms were found by many observers, not only 
in frogs but in birds as well. 

In 1870-80 Lewis described trypanosoma found in rats in 
India. Liter he states that they are identical with Tr. Evansr 
In 1880 G. Evans discovered trypanosoma in the blood 
of horses suffering with surra, the well known disease of 
India He proved their causal relation to the affection. In 
X885 Steele confirmed Evans' work, and named the parasite 
Spirocheta Evansi. 

The work of Evans and Steele was followed by many 
interesting discoveries of trypanosoma especially in fish and in 

Rouget described Trypanosonm found in the 



man. 



In i: 



in I5QD, iVUUgcL v.^^- .. 

blood of a horse suffering from dourine. W asilewskj . nd 
Senn in ,899, confirmed Rougefs work and deternnned the 
pyogenic acUon of this parasite for the horse. I.averan and 
Mesnil proposed the name Tr. ,ougM for the parasrte of 



396 



TRYPANOSOMA 



dourine. Doflein (Jul.v, 1901) named it Tr. equipeydum, 
which term was adopted b}- Salmon and Stiles. 

In 1901, according to Voges, Elmassian first differentiated 
the Trypanosoma of Mai de Caderas in South America. Voges 
described it the following year, demonstrated its pathogenic 
action, and named it Tr. eqiiimuu . 

In 1902, Bruce and Laveran independently published 
articles inwhich thev credit Theiler with the discovery of a 




Fig. 106. A map shozcing the geographical distribution of 
Trypanosoma disease. 

new Trypanosoma of cattle in South Africa. They each 
proposed the name Tr. TheiUri. 

In 1901, Smith and Kinyoun described a parasite which 
had been observed by Jobling in the blood of a sick horse 
in Manila. Later in the year Smith described it as Tr. 
Evansi. 



§ 308. Trypanosomiasis. Salmon and Stiles have in- 
troduced the term Trypanosomiasis to describe an infection 



TRYPANOSOMIASIS 397 

With parasites belonging to the flagellate family Trypanoso- 
midac The term is analogous to Teniads and Cocc^d^os^s. 
There are a number of different trypanosomiases now recog- 
nized, being caused by different species of Trypanosoma. 
Among these the following may be mentioned : 

1 Surra A disease of equines, camels, elephants and 
certain other animals in India, attributed to Trypanosoma 

Evansi. 

2 Nagana, nvgana or Tsetse JJy disease of Africa. Af- 
fecting cattle, horses, mules, asses, antelopes, camels and 
certain other animals. It is attributed to Trypanosoma Brueei. 

. Do^crine or maladie du eoit of Algiers, France and 
Spain ■ It attacks the horse and the ass in particular, but may 
be transmitted to certain other animals. It is attributed to 
Trypanosoma equiperdnm . 

'4 ^a/«^.m«'.m. of South America. It affects horses 
assesTcattle, hogs and certain other animals. It is attributed 
to Trypanosoma eqitinum. 

. Rat trypanosomiasis attributed to Trypanosoma Uwis, 
By some authors this parasite is alleged to be identical w.th 
the horse surra organism, but it is quite certain that rats may 
Itbo, a distinct s-pecies. Until the results of f-ther mvest,- 
gations are recorded it is deemed best to consider these as d,s- 
Sct infections. Mttsgrave and Clegg include that proof 
sufficient to establish the individuality of the Trypan soma 
cans ng trypanosomiasis in domestic animals has not 5^t been 
advanced These authors consider the trypanosonra found .n 
domesticated animals in the Philippine Islands as Tr. E.ansi 
It is important to note the observation of Musgrave and 
Cle..- that "in all the .forms of trypanosonnas.s the infection 
see^s.o involve particularly the genitalia, the skin, and the 
organs of special sense. The skin symptoms consis of ough- 
e Jng of the hair, which also falls out in places : a thickening 
of the epidermis, often with exfoliation, and in some stages ol 
the disease, various skin eruptions. There may be simple 
ervthema, and more rarely they may assume the severer forms. 



398 TRYPANOSOMA 

as urticaria, or in extreme cases a distinct localized ulceration 
may occur. The scrotum and penis in the male and the vulva 
in the female are often swollen, and ulcerations of the penis or 
vulva are frequent symptoms especially in dourine.'' 

The geographical distribution of the trypanosomiases is 
shown in Fig. io6. 

The following table of trypanosoma compiled by Smedley 
gives the distribution, means of dissemination and the patho- 
genesis of the various species. 

REFEREXCES. 

1. DuTTox AXD Todd. First report of the Trypanosomiasis Ex- 
pedition to Setieganibia (1902). Thomson yai(S,afid Jofiiison Labora- 
tories Report, \o\. V. 

2. LAVERA>r AXD Mesxil. Recherches morphologiques et ex- 
perimentales sur le Trypanosomi des rats (Tr. Lewisi, Kent). Ann. 
de V Inst. Pasteur Vol. XV I 1901), p. 673. 

3. Laverax et Mesxil. Trypanosonies et Trypanosomiases. 
Paris. 1904. 

4. NovY, McNeal and Hase. The Cultivation of Tr. Brucei. 
The Jour, of hi fectious Diseases, Vol. r (1904), p. i. 

5. Petrie. Observations relating to the structure and geographi- 
cal distribution of certain trypanosomes. Jour, of Hygiene, Vol. V 
(1905), p. 191. 

6. RoDET ET VAtLET. Contribution a I'etude des Trypanoso- 
miases. Airh. de Med. Exper., Vol. XVIII (1906), p. 450. 

7. Smedley. The Cultivation of Trypanosomata. The Jour, of 
Hygiene, Vol. V {1905), p. 24. 

8. Thiroux. Recherches morphologiques et experimentales sur 
Trypanosoma Paddae. Ann. de P Inst. Fasteur, Vol. XIX (1905), p. 65, 



TRYPANOSOMATA 



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400 SURRA 

SURRA 

Synonyms. Relapsing fever of equines; pernicious ane- 
mia of horses. 

§ 309. Characterization. Surra is an infectious dis- 
ease of solipeds and camels caused by a flagellate protozoan. It 
is determined by a continuous fever with alternate paroxysms 
and intermissions, with a general or localized eruption of the 
skin, petechiae of the mucosae and more or less subcutaneous 
edema. There is rapid emaciation and great weakness. It is 
usually fatal. It attacks horses, asses, mules, cattle, goats, 
dogs, and rats. It can be inoculated into other animals such 
as rabbits, guinea pigs and mice. From an economic point of 
view it is reported to be essentially a disease of horses. 

In India cattle are said to be infected with the trypan- 
osoma of surra but they are not appreciably affected by them. 
It is reported that horses become infected by insects that have 
first bitten such cattle. 

sj 310. History. This disease appears to have been 
known for many years to the natives of the low lands on both 
sides of the Indus on the northwest frontier of India. Haig 
appears to have observed it in Persia in 1876. In 1880, Evans 
found several cases of it in the Dera Ismael Khan county. He 
was the first to describe it and attribute its cause to an animal 
parasite which he discovered in the blood. In 1885, Steel met 
with a disease among mules in Burma which he regarded as 
identical with Evans' surra, and which he believed to be re- 
lapsing fever. In 1888 there was an outbreak among the 
Bombay Tramway Company's horses. Since then surra has 
become epizootic in Bombay; Lingard reports that thousands 
of ponies, horses, camels and asses died from it during the 
rains of 1893 and 1894. Its ravages in the Punjab and North- 
west Provinces during 1895 are reported to be appalling. 

§ 311. Geographical distribution. It is a disease of 
Asia and Africa. It is reported that " the distribution of this 
malady seems to be entirely influenced by the physical aspect 



ETIOLOGY 401 

of this country; being far more prevalent in those parts where 
floods and inundations occur than in the higher and dryer 
portions" (Pease). If the identity of surra with tsetse fly 
disease proves to be true, which is still questioned, it has a 
wide distribution in Central Africa. 

Surra does not exist in the United States, but because of 
its prevalence and long standing in the Philippines it is liable 
to be introd-uced into this country. For this reason its nature 
.should be understood by American veterinarians. 

j^ 312. Etiology. There is little or no doubt that surra 
is due to the presence in the blood of a flagellated infusorian, 
Tn 'pa n oso m a Ei -a n s i . 

" A motile trypanosoma 20 to 30// in length to i to 2 // in breadth, 
somewhat blunt at the posterior end and gradually tapering at the 
anterior end. The undulating membrane is well defined, beginning at 
or near a small body (centrosome) in the posterior portion of the para- 
site and extending forward as a free flagellum. It is provided with a 
nucleus and agranular protoplasm." 

This organism is invariably found during the paroxysms 
of the disease in the blood of animals which have acquired 
surra either naturally or experimentally. Although blood 
containing these infusoria readily communicates the disease to 
susceptible animals it entirely loses its virulence when it is 
filtered through porcelain, so as to free it from the parasite. 
The disease can be transmitted to healthy, susceptible animals 
even of different species with the unfiltered blood of a diseased 
animal. The microscope reveals the infusoria in vast numbers 
moving with great activity in the blood. When this acute 
stage has passed the organisms disappear, the temperature 
falls, the severity of the symptoms abates, and there is an 
intermission, during which, at the beginning of the attack, the 
patient may appear in good health. Although the blood dur- 
ing an intermission may appear under the microscope to be 
ab.solutely free from the parasites, its inoculation into suscep- 
tible animals will, as a rule, produce the di.sease. The blood 
of surra affected horses loses its power of transmitting the dis- 
ease by inoculation in about eighteen hours after death. 



402 SURRA 

Under the microscope, these parasites are detected in a 
drop of blood by an irregularly intermittent and characteristic 
qnivering of some of the red blood corpuscles, which become 
much altered in form. The leucocytes remain unchanged in 
appearance. After a further and careful examination of this 
slightly quivering blood a minute thread-like organism with 
eel-like movements emerges from the mass of corpuscles. It 
may be seen apparently tugging with all its might at a red 
corpuscle endeavoring to detach it from its rouleau. The 
question of the manner in which these parasites interfere with 
the health of the affected animal has not yet been settled. 
When they are outside the animal body and in a dry state, 
they are killed or rendered inert by prolonged atmospheric 
action. 

The period of incubation seems to be liable to great varia- 
tion. It may be put from six to eight days after inoculation 
or ingestion of blood taken from an animal suffering from 
surra. It appears from Lingard's investigation that the 
period of latency may be prolonged to thirteen days, if the 
blood used for inoculation has been taken from a dead animal. 
When the parasites have been given in water, by the mouth, 
symptoms of surra may not appear for even seventy-five days. 
We have no exact data for determining the time required for 
the disease to manifest itself under natural conditions from 
drinking surra contaminated water. 

i^ 313. Means of transmission. The contagium of 
surra is fixed and can be conveyed only by inoculation or 
ingestion. Stagnant water and grass growing on recently 
inundated land are said to form favorable resting places for 
this organism. 

Lingard considers the ingestion of stagnant water and of 
grass from land subject to inundations a source of infection. 
Salmon and Stiles do not think this method of infection is 
sufficiently proven to look upon it seriously. Liugard stands 
almost alone in the belief that infection can take place through 
healthy mucosae. 

The most coumion demonstrated natural methods of 



SYMPTOMS 403 

transferring the virus from infected to non-infected animals is 
by means of insects, especially the biting fiies. Of the flies, 
the tsetse-fly {G/ossina mors/fa?is) is reported to be the most 
important. Musgrave and Clegg conclude concerning the role 
played by flies in transmitting this disease that " it has thus 
far been conclusively shown that the tsetse-fly {G/ossma 
morsifa?is), at least one other variety of (r/ossmi, Stomoxys 
calcib'ans, Miisca brava if), Taon, and at least one variety of 
Tabani transmit the virus. All other biting insects have 
been looked upon with suspicion, but absolute proof of trans- 
mission by them has not been furnished." The theory as to 
the method of transferring the parasite is that it is purely 
mechanical, although some have thought the Trypanosoma 
passed through one phase of its life cycle in the fly. 

The spread of the disease from one locality to another is 
caused by the introduction of animals carr3'ing the parasite. 

^ 314. Symptoms. The symptoms as given by Lingard 
are as follows: "The chief symptoms are the occasional 
appearance of an urticarial eruption, generalized or localized, 
closely following the first rise of temperature, but w-hich may 
make its appearance at any time during the course of the 
disease ; then the presence of petechiae on the mucous mem- 
branes, chiefly that covering the membrana nictitans, lachry- 
mation and the exudation of a semi-gelatinous material into 
the subcutaneous and other connective tissues. There is rapid 
wasting and great weakness, although in the majority of cases 
the appetite remains good throughout, no matter how high 
the fever. There is extreme pallor of the visible mucous 
membranes, and this is followed at a later period by yellow- 
ness. From first to la.st there is progressive anemia ; the 
blood at first presents a normal character, but after a varying 
period of time it undergoes marked changes. The white cor- 
puscles are increased in number and the red corpuscles usually 
cease to form normal rouleaux, lose their individuality and run 
together forming irregular masses. They are at first dark, 
but gradually, as the disease advances, almost entirely lose 
their coloring matter and become pale." 



404 SURRA 

The respective duration of the paroxysms and intermis- 
sions is very irregular. Lingard puts it down as from one to 
six days. He states that in a few experimental horses the 
paroxysms lasted from eighteen to twenty-two days. 

77/^ flf?^ra//^;z of the disease is, according to Gunn, about 
fifty-two days. In the Philippine Islands the duration in 
horses is from fourteen days to three months. The prognosis 
is always unfavorable, the mortality in most species of animals 
being 100 per cent. In cattle a variable percentage recover. 

^ 315. Morbid anatomy. As a rule there is great 
emaciation, enlargement of the liver and spleen, petechiae on 
various internal organs. A yellow or amber-colored jelly-like 
exudation occurs in the connective tissue of the throat, chest 
and abdomen, about the muscles and other tissues, and espec- 
ially around the base of the heart. The lungs often show 
signs of inflammation. The mucous membranes and other 
tissues are frequently tinged yellow by the coloring matter of 
the bile. 

It has been stated that the hide is often removed with 
difficulty. In the areas corresponding to the edema dur- 
ing life are found yellowish-tinged, gelatinous infiltrations. 
The serous membranes, especially the peritoneum and pleura, 
often show flakes of plastic, fibrous material. These are es- 
pecially numerous over the liver. All of the organs have a 
dry, pale appearance. There are numerous sub-serous hemor- 
rhages, particularly on the right side of the heart and over the 
lower portion of the lungs. The lymphatics are in general 
somewhat enlarged, often markedly so. The heart muscle 
shows parenchymatous changes, in degree depending some- 
what on the duration of the disease. 

In some of the lower animals the scrotum and even the 
testicles in the male and the vulva in the female are greatly 
swollen, and in the male rabbit the tension may be so great as 
to rupture the scrotum. Small preputial or labial ulcers are 
not uncommon. 

Steel noticed ulceration of the stomach in about two-thirds 



MORBID ANATO-AIV 405 

of his cases among mules in Burma. In India this ulceration 
has not been observed among horses as a sequence of surra. 
In the Philippines changes in the intestine due to anemia with 
occasional ulcers are reported. 

The clinical aspect of surra is esseutialh' one of progres- 
sive anemia, accompanied b}- parox3-sms and intermissions, 
during both of which there is a natural decrease in the number 
of the red blood corpuscles and in the amount of hemoglobin 
in the blood, with consequent anemia of the visible mucous 
membranes. 

The importance of this disease renders it desirable to 
reprint "A preliminary note on a parasitic disease of horses," 
by Capt. Allen M. Smith and Dr. J. J. Kinyoun, from the 
Army Pathological Laboratory, Manila, October 17, 1901, as 
it gives a good idea of the appearance of the disease. The 
accompanying photograph showing trypanosoma w'as taken by 
Smith and Kinyoun at that time. 

"On October 15, 1901, information was given by J. W. Jobbing, 
Assistant Bacteriologist of the Board of Health of Manila, that an epi- 
demic sickness of an undetermined nature was now^ prevailing in this 
city, and also that he had just taken a specimen of blood from a sick 
animal which on examination revealed the presence of a parasite, 
whether this was accidental or was the causative agent of the disease in 
question, he was unable to sa^-. On investigation and inquiry it was 
learned from the Veterinarian in charge of the corral of the Quarter- 
master's Department, and from the City Veterinarian, that there was 
now. and had been, a fatal epidemic among the horses in Manila, the 
Quarter-master's Department having lost over 200 within the i)ast four 
months. 

" One of the corrals was visited by us on the 15th inst. , where we 
were shown, by the \'eterinarians in charge, 20 horses and mules, ill 
with an undetermined disease. These animals presented the several 
stages of the malady, some were quite recently attacked, while others 
had been ill for over tw'o months. 

"The symptoms first noticed are : impairment of appetite, constipa- 
tion, fever and thirst. These are followed within a few days by a rapid 
and progressive emaciation. 

" The temperature for the first few days ranges from 104"^ to 107^ F., 
the pulse is full and strong. This may be termed the acute stage. Then 
begins an asthenic state, which may terminate fatally within a variable 



406 SURRA 

period, or by a slow convalescence. During this stage usually within 
lo days after the onset, there appears a commencing oedema above the 
belly, involving the soft parts, coincident with this, or soon after, the 
cedema extends to the feet and legs. The pulse becomes rapid, weak 



-0^ ^Ifc^^^. 






• 



#- 



Fig. 107. Photograph of blood of horse coiilaining Tiypanosoma. 
Taken by Smith and k'iiiyoiiii. 

and dichrotic, the respiration increased, shallow and jerky, the gait 
staggering. Emaciation is rapid and extreme. 

" The disease has a tendency to relapse, this may occur at any time, 
even after convalescence appears to have been fully established. The 
relapses are invariabh- fatal. 

"The mortality in this epidemic has been about 75 per cent for 
American horses and mules, and 100 per cent for native ponies. 

" The gross pathology shows serous effusions into the pleurte, peri- 
cardium, and sometimes the peritoneum. There is also a serous exudate 
into the cellular tissue of the legs and abdomen. The organs are pale, 
but otherwise normal in appearance. 

" At the time of our inspection, five acute cases were examined, the 
duration of the attack being from six days to two weeks. All these 
animals presented the several clinical appearances as above described. 

"Blood specimens were taken from the jugular vein of each and 
examined microscopicall)-, shortly afterwards. In 4 of these a parasite 



M OK HID ANATOKV 407 

was demonstrable. The other was negative, but a specimen taken the 
followiug day showed the presence of this same parasite. 

" On the day following, specimens were obtained from 12 others, all 
chronic cases, with the result of finding this same parasite in the blood 
of four. In three there were very few, whilst in the fourth they were 
present in great numbers, as many as 20 could be seen in one microscope 
field. The animal from which the specimen was taken had suffered a 
relapse 

" It would appear that the parasite may disappear from the peri- 
pheral circulation, or exists there in such few numbers that it is not 
easilj' demonstrable, after the acute stage has passed. It would re(|uire 
repeated blood examination to decide this point. 

" Description of the parasite. The parasite resembles a whiplike 
worm, having much the appearance of the Trichocephalus Dispar, its 
length is from 10 to 14 mikrons, and is from i to 1.2 mikrons in diameter 
through its body, the neck is nearly ', its length, tapering gradually to 
a point representing the mouth (?). It has a limiting membrane, which 
is well defined, the contour is in most cases symmetrical but in some 
the body line is (juite irregular. The larger part of the parasite (body) 
contains granular material and clear spaces, which latter vary in size 
and number; they are ijregularly distributed, and may encroach on the 
wall so as to cause irregular outline. The granular material does not 
extend to the neck. 

" The parasite is activel}- motile, having both a vermicular (con- 
tractile ) and spiral movement. It moves forward in a very peculiar 
manner, the long whiplike process is thrust forward by a spirillar 
motion, followed by a contraction of the body. 

" We have not so far been able to determine its intimate structure, 
further than the limiting membrane, and the protoplasmic substance of 
the body. 

" Two sizes of the parasite have been seen in all the specimens ex- 
amined, the larger appears to be more numerous, and contains consider- 
ably more granular material than the smaller, and usually two or more 
vacuoles. Whether these two sizes represent male and female, has not 
been determined. We are inclined to believe from our observations, 
that they do not represent the male and female, because we have ob- 
served in more than half the fresh specimens, the joining of a large and 
small parasite in such a way as to appear to be something more than 
accidental. 

"The pathological changes caused by this parasite is a rapid de- 
struction of the red blood cells, causing an acute anamia. The changes 
occur in the blood coincident to the invasion of the parasite. In one 
horse which had been ill seven davs, the red blood cells numbered 



408 SURRA 

3,500,900, the white 14,500. In another, ill six weeks, the red blood 
cells were 3,200,000, and the white were 13,900. The blood of a healthy 
horse, taken as a comparison, gave red blood cells 6,900,000, white 
9,Soo. There is also a slight diminution in the amount of httmoglobin, 
about 85 per cent. 

" After convalescence has been fully established, no parasite can be 
found, the blood gradually assumes its normal constitution. 

"The parasite is not confined to the blood, as it can be demonstrated 
in the serous effusions. 

" It is quite easy to detect, all that is necessary is to make a micro- 
scopical examination of fresh bJood films, a }, in. objective will suffice. 
Dried films, fixed and stained with any of the nuclear dyes. 

" The organism appears to be a strict parasite. It lives but a short 
time after removal from the body, the longest time which it has been 
kept alive in blood serum was not more than ten hours. 

"The parasite has many of the properities in common with the 
filaria, and resembles more nearly that of filaria perstans. only it is 
smaller, and its movements dissimilar. Yet on the other hand, the 
clinical history of animals infested by it, the changes occurring in the 
blood, the lesions observed in post-mortem, point very strongly towards 
its classification with the spirochx-te. 

" The mode of transmission has not yet been studied. It does not 
appear to be highly contagious, as it does not appear to spread from one 
to another, even under the most favorable circumstances. 

" It more nearly resembles malaria in this respect. It is more than 
probable that its extra corporeal state is different, or another supposition 
equally tenable, is that its intermediate host is some insect, such as the 
fly or mcsquilo." 

§ 316. Differential diagnosis. Surra is to be differen- 
tiated from anthrax and the other trypanosoma diseases. A 
history of the case or outbreak together with the chronic 
course and intermittent temperature in surra will usually 
suffice to determine the nature of the disease. A positive 
diagnosis can easily be made in the horse, in a majority of 
cases, by a microscopic examination of the blood. The try- 
panosoma are readily observed, and usually they are in suffi- 
cient numbers to be quickly seen. In a suspicious case, where 
the organisms are not found, the examination should be 
repeated daily or small animals inoculated with the blood. For 
this inject about i c.c. of the blood into the abdominal cavitv 



PRKVKNTION 



409 



of a dog. In a few days the trypanosoma will be found in 
the usual way if the disease is surra. Although this requires 
some time the importance of a positive diagnosis demands that 
it should be done. 

Surra may be complicated with broncho-pneumonia, Rin- 
derpest and tuberculosis (especially in cattle), foot and 
mouth disease, pseudo-actinomycosis, neoplasms and septi- 
cemias as yet little understood. 

If no history or symptoms are known, the diagnosis can 
be made post-mortem from the bacteriological examination of 
the tissues or blood, as Bacf. aiifhracisxi^ readily found in cases 
of anthrax. 

^ 317. Prevention. The importation of animals from 
infected countries should be prohibited. If the disease gains 
entrance, the infected animals should be destroyed. In fram- 
ing regulations for quarantine particular attention should be 
paid to the wild animals and to circus animals. 

lyingard found that arsenic has a decided effect in dimin- 
ishing the number of surra organisms in the blood of affected 
animals. Thus far serum therapy is not successful. 

From the latest results, it is very clear that infected 
animals must be destroyed and the healthy ones protected 
from the bites of insects. 

REFERENCES. 

1. BtTKKE. vSurra or progressive pernicious ana-mia. /W. Jour. 
London. Vol. XXV, 1887. 

2. Durham. Tsetse disease. Veterinarian. \o\. LXXMiSgS). 

3. Dl'RRANT. a trypanosoma fonnd in blood of cattle in India. 
Jour. Comp. Path, and 'I'heia. \'o\. X\'II {1904), p. 209. 

4. EvAXS. Report on surra disease in the Dera Ismail Khan Dis- 
trict. 18S0. Military Department. 

5. Evans. On a horse disease in India known as " surra," proba- 
bly due to a Hiumatozoon. I'et. Jour. Loiidoii. \"ol. XIII (1881), 
July, Aug., Sept., Nov. 

6. H.ASSAi.i.. Bibliography of surra and allied trypanosomatic 



41° DOURINE 

diseases. Bulletin No. 42, U. S. Bureau of Animal Industry. 1892, 
p. 132. 

7. Kanthack, Durham and Blandford. On nagana or tsetse 
fly disease. Report made to the tsetse fly committee of the Royal so- 
city, etc. Proc. Royal Soc. London, \'ol. LXIV, p. 100. 

8. LixOtARD. Report on horse surra. 1893. (Bombay.) 

9. LiNGARD. Report on "surra" in equines, bovines, buffaloes 
and canines, etc. Rec. de rued. vet. Par. S. Vol. X'lII, p. 377. 

10. MuSGRAVE AND Ci,KGG. Trypanosoma and Trypanosomiasis, 
with special reference to surra in the Philippine Islands. No. 5. I!u- 
reau 0/ Government Laboratories, Manila, 1903. 

11. Ml'SGRAve AND Clfgg. Report of the Superintendent of Goi- 
ernment Laboratories in the Philippine Islands, 1903. 

12. NocARD. Sur les rapports qui existent entre la dourine et le 
surra ou le nagana. Camp. rend. Soc. de Biol. Vol. LIII (1901). 

13. Ranking. A preliminary note on the nature and pathology of 
the disease known as " .surra '' affecting horses and mules in India. Vet. 
Jour. London, Vol. XXXII (1891 ). 

14- Salmon and vStiles. Emergency report on surra. Bulletin 
No. 42, L'. S. Bureau 0/ Animal Industry, 1892. 

15. Schilling. Bericht iiber die Surra-Krankheit der Pfenle, 
Centralblattf. Bakteriologie u. Parasit. Bd. XXX \\^2), p. 545, 

16. Smith and Kinvoun. A pliminary note on a parasitic disease 
of horses. Army Pathological Laboratory, Manila, Oct. 17, 1901. 

17. Steel. On relapsing fever of equines. Vet. Jour. London. 
Vol. XXII ( 18S6). 

18. Steel. Report upon an obscure and fatal disease among 
transport mules in British Burma. 1885. 

19. Stiles. Trypanosoma in a new role. Am. Med. Vol. Ill 
(1902). 



DOURINE 



Sy?ionyiiis. \'enereal disease of solipeds; equine syphilLs; 
chancerou.s epizootic; breeding paralysi.s; epizootic paraplegia: 
maladie du coit. 

§ 318. Characterization. A contagious affection of 
solipeds, transmitted by copulation and attended by specific 



HISTORY 411 

lesions of the generative organs and nervous system, such as 
local venereal swellings, chancerous ulcers and cicatrices, de- 
mentia and paralysis. 

The disease is essentially an equine one, although the fol- 
lowing species are susceptible to experimental inoculation, 
namely: dogs, rabbits, rats, mice and asses. While the horse 
shows the greatest susceptibility, the ass is comparatively 
resistant to the infection. 

>:^ 319. History. Dourine seems to have first been 
recognized in Algeria. It was first clearly described in 1796 
by Amnion who found it in the royal stud at Trakchnen in 
Northern Prussia. We have later, 1801 and 1807, descrip- 
tions of the disease in the same locality. It was found in 
Bomberg in 1817 to 1820, in Austria and Bohemia in 1821-8, 
in Syria in 182 1, in Switzerland in 1830, in France in 1830-32, 
in Siberia in 1833-40, in Italy in 1836, in Russia in 1843, in 
Poland in 1830-40, in Algiers in 1847-55. In Syria and Asia 
generally it is reported to appear perennially. 

It is not known to have invaded Belgium, Scandinavia, 
England, South America or Australia. All indications point 
to Asia and Northern Africa as the home of the disease where 
it still appears perennially. 

It was found in De Witt County, 111., in 1882. The first 
animal showing the disease was a brown stallion that had been 
imported from France. In this locality it spread to a consid- 
earble number of breeding mares and stallions. The di.sease 
was very largely stamped out of that region by a rigid quar- 
antine of diseased and exposed animals. Some exposed ani- 
mals had. however, left the district, and it is not surprising 
that isolated centers of infection are occasionally found. 

i^ 320. Etiology. ThanhofTer found in the blood, vagi- 
nal mucus, testicle, semen, spinal fluid and roots of the dorsal 
and lumbar nerves, bacteria, especially streptococci and less 
constantly bacilli, to which he attributed the cause. More 
recently Schneider and Buffard have apparently demonstrated 
that one of the Trypanosoma is the specific pathogenic agent. 



412 



Rouget in 1896, described a trypanosoma found in the 
blood of a horse suffering from dourine, and for over two years 
continued the study of this organism in susceptible animals. 
Wasilewsky and Senn confirmed Rouget 's work, and deter- 
mined the pathogenic action of this trypajiosoma for the horse, 
passing it through other animals and back to the horse, repro- 
ducing the disease. Laveran and Mesnil (igoi) proposed the 





Fig. 108. Tr. eqiiiperdmii. 1 , i/i the blood 0/ a mouse four days after 
inoculation, _->, same blood eight days after inoculation {after Rouget). 



name Tr. roitgetii for the parasite of dourine. Doflein named 
it Tr. equiperdiim , which is the name used by Salmon and 
Stiles. 

In its morphology and evolutionary forms, the trypano- 
soma of dourine has not been shown to differ from that of 
surra. The granule form, the spherical, the club shaped or 
pyriform bodies, the fusiform with more or less stellate group- 
ings seem to be generic characteristics. Baldrey states that it 
is smaller than the Trypanosoma of Surra. The specific dis- 
tinction is found in the pathogenesis as shown by the two 
diseases (surra and dourine). 

In the active stages, the parasite is usually found abund- 
antly in edematous fluid, the blood, semen, milk, vaginal 
secretions and the erosions of the vaginal mucosa and penis. 
During intermissions, however, and in the absence of local 
lesions, the parasites are not found in the blood on micro- 
scopic examination, yet the inoculation of the blood into 



KTIOLOCiY 4 ' 3 

a dog will usually produce the disease. The parasite disap- 
pears from the blood and tissues very rapidly after death, 
so that, to prove successful, inoculations should be made 
from an infected individual before or immediately after death. 
Thev are not affected after forty-eight hours. 

Schneider and Buffard, Nocard and others found the try- 
panosoma in the blood and exudates of horses, asses and dogs 
Lffering from dourine. They failed to find it in the same 
localities in animals of the same 
species which were free from 
dourine. The infected blood 
preserved for 24 hours in sealed 
glass tubes, and then inoculated 
into dogs produced character- 
istic symptoms and lesions with 
many trypanosoma in the blood. 
Inoculation into two other dogs, 
with the same material, but at 

the end of 48 hours, produced a ^^^^ ^^^ jy^osoma o/dou- 
slight transient hyperemia only, ^,.^^^, -^^ ^j^^, process of division 
without local lesions or propaga- Rafter Ugnicres). 

tion of the parasite in the blood. • 

The blood from the same animal inoculated after filteen da^s 
eave negative results. 

Baldrey found Romanowsky's and Wright's modifications 
of Leishman-s method the best methods for staining the try- 
panosoma ; the latter is very useful and handy, as no mixing 
of solutions is necessary and no fixing required. 
The following is Romanowskf s Stain : 

STOCK SOLUTION NO. I. 

„, _ I part 
Hochsfs Medicinal Methylene Blue 0.5 parts 

Sodium Carbonate pure ' ^^^ p^^^^ 

Distilled water 

Place this solution in an incubator at 37° C. for two or three da, 
when a purple color will be noticed at the edges of the ^^^ 
depends m>on the formation of a new red color-methylene red-vUnch 
crbinedUheosin forms the active principle of the stain and has a 




414 DOUR INK 

particular affinity for chromatin. Unless this polychroniatophylic 
change takes place the solution is useless. 

STOCK SOLfTION NO. 2. 

Eosin I part 

Water 1000 parts 

For staining, the stock solutions are separately diluted with water, 
5 parts of stock solution to 100 parts of water. 

In order to obtain a smear, prick the center of the plaque and take 
a drop of blood on a slide, which should be chemically clean, having 
been taken from an alcohol bottle and dried with a clean piece of art 
muslin. Then, either in the ordinary way with a piece of cigarette 
paper, make a thin even smear over the slide, or, as an easier and 
equally efficient method, take a perfectly clean flat large-sized needle 
and place it edgeways on the drop, when the capillary attraction of the 
needle will cause the blood to stream right across the slide ; then 
evenly and gently draw the needle down the length of the slide, and a 
very even smear may be obtained. (Juickly dry the smear in the air by 
waving rapidly about, which prevents the red corpuscles from crenat- 
ing ; the slide can then be kept indefiniteh' or used at once. The 
advantages of using a slide instead of a cover-glass are that 3-ou get a 
much larger field on which to work, it is much more easily manipulated 
and it can be kept without any mounting. Place the film in absolute 
alcohol or alcohol and ether, for fifteen minutes to half an hour, to 
fix. This coagulates the albumen and makes a permanent film in which 
the corpuscles and organisms are retained Remove from the alcohol, 
wash in water, and then apply the stain. This is made by mixing equal 
parts of the above two solutions, freshly prepared, in a small glass 
measure or porcelain dish. It is important that the admixture should 
be as fresh as possible. Apply the stain to the whole of the film and let 
it remain for seven to ten minntes ; wash in water and dry in the air, 
no heat being applied. The red corpuscles may have a bluish tinge, 
which may be removed by further washing. If the blood platelets 
appear bluish the film requires further staining ; they shoiild appear as 
ruby-red granular bodies. By continuous application of water the stain 
may be washed out, but the film maj- always be stained over again. 

By this stain the protoplasm of the trypauosome is stained blue, the 
nuclear chromatin a carmine violet, and the flagellum and centrosome a 
brilliant red. The red corpuscles will be a pinkish colour, and the vari- 
ous forms of leucocytes will be well differentiated. In examining the 
smear, time may be saved by looking along the edge of the film, as it is 
here that the parasites will be most numerous if they are present, as 
they, being like the leucocytes of less density than the rest of the blood, 
tend to run to the periphery when the smear is made. 

A film made in this way requires no cover- glass, but if the cedar oil 



SYISIPTOMS 



415 



is left on it tends to withdraw the color ; lio\\ever, if it be carefully 
blotted and wiped off with a soft ra.y after use the film may be kept 
indefinitely. 

§ 321. Symptoms. The first local changes in the geni- 
tal organs begin after a period of incubation, according to 
Maresch, of from eight days to two months. The first symp- 
tom in the stalHon consists in the swelling of the glans penis. 
Reddish spots, vesicles and ulcers may occur on the outer sur- 
face of the organ. The meatus urinarius is reddened and 
swollen and exhibits a raucous discharge. The animal has a 
continuous desire to micturate and frequently manifests sexual 
excitement. The swelling also spreads from the penis to the 
sheath and scrotum in which case the testicles become in- 
flamed. Finally, the inguinal glands and lymph vessels 
become involved. These local affections may, as the disease 
advances, almost entirely disappear. In some cases the ex- 
ternal changes are absent, as the mucous membrane of the 
urethra is first affected, the only visible sj'mptoms being 
strangury and a mucous discharge from the urethra. 

In mares, the disease begins with a dough}' or tense swell- 
ing of the pudenda, which frequently spreads to the udder and 
inner surface of the thighs. The mucous membrane of the 
vagina is red in spots and swollen, sometimes thickened by 
gelatinous elevations and covered with a turbid and orange 
colored secretion. Sometimes nodules, vesicles and ulcers are 
observed on the mucous membrane. They are, however, fre- 
quently absent. In mares, the local manifestations are often 
insignificant. The mucous membrane in the neighborhood of 
the clitoris is more congested than at other points and the cli- 
toris itself is swollen and erect. It is devoid of pigment and 
unnaturally dry. Williams states that this depigmentation is 
" peculiar and characteristic." The spots of discoloration are 
not caused by previous ulcers. At the same time affected 
mares show excessive sexual excitement. They frequently 
suffer from strangur}- and after considerable straining urine is 
discharged in small jets. In his report on the Illinois out- 
break, Williams states that in mares, " The open vulva and 



41 6 DOURIXE 

enlarged, protruding, unnaturally dry clitoris, especially in 
young and otherwise healthy mares is quite pathognomonic." 

Instead of urine small quantities of sticky, discolored 
mucus are discharged. The animals incessantly shake their 
tails and open and close the vagina in rapid succession, show- 
ing the clitoris as mares do in season. The discharge often 
exerts a corrosive action on the tail and legs. In severe cases 
the neighboring lymph glands become inflamed and swollen as 
well as the udder, on which abscesses may appear. The 
swelling may even extend to the hypogastrium. 

The general symptoms develop only after weeks or even 
months; their appearance is often delayed until the local 
symptoms have disappeared. At first the animals are de- 
pressed and weak, they frequently continue to lift up their 
hind feet, alternately, so as to try to avoid putting weight 
upon them, knuckle on their fetlock joints and lose control 
over the movements of their hind legs while walking. The 
temperature is not so high as in other forms of Trypanosma 
infection. 

It is reported that stallions especially suffer from an 
urticaria in the form of sharply defined, round, flat eminences 
which may be raised the breadth of a finger above the surface 
and which may vary in size from two to four centimeters or 
more in diameter. These eminences are caused by a serous 
infiltration of the papillary layer of the skin in the neighbor- 
hood of a small artery and are evidently of a vaso-neurotic 
character. They often appear and disappear very rapidly and 
may shift their position. Usually they persist for several 
weeks during which time they become moderately hard and 
then slowly disappear. Their favorite sites are the croup, 
neck, shoulders, chest and abdomen. 

I,ater in the course of the disease, a progressive paralysis 
of the hind quarters combines with excessive emaciation. The 
animal has a staggering gait and often gives way on the pas- 
terns and at the knees, can raise itself from the ground only 
with difficulty, and sometimes falls down unexpectedly. The 
affected stallion is unable to cover, as he can neither mount a 



SYMPTOMS 417 

mare nor get an erection. Some patients exhibit permanent 
treml)lings over the whole body or local paralysis as for in- 
stance, that of the lips, ears and eyelids. Hyperesthesia of the 
skin is observed particularly in stallions and with it is exten- 
sive pruritis, so that the animal continually rubs itself, bites 
the affected parts and thus produces extensive sores on the 
skin. The patient becomes extremely emaciated especially in 
the hind quarters so that the outlines of the pelvic bones and 
ribs become very prominent. The skin becomes dry, the hair 
is ruffled and loses its gloss. Some animals manifest pain when 
the lumbar region is pressed. The senses become more and 
more blunted and the eyes a.ssume a staring and expressionless 
appearance. As the end approaches the patient persistently 
maintains a recumbent po.sition and finally dies from the effect 
of secondary lesions such as hypostatic inflammation of the 
lungs, septicemia or perhaps general cachexia. Sometimes in 
the final stage the patient suffers from nasal catarrh with 
swelling of the submaxillary glands and conjunctivitis. Severe 
internal inflammation of the eyes has been observed. The 
appetite continues longer than any of the other normal 
functions. 

Baldrey has divided the symptoms into three different 
stages, as suggested by Nocard. These stages are distinct, 
and may, if the case is carefully watched, be recognized com- 
paratively easily. They are : — 

Primary. In which occur the local manifestations of dis- 
charge and urethral irritation, and ulceration of the penis and 

sheath. 

Secoyidary. In which the exanthematous eruptions appear 

in the skin — the .so-called ' ' plaques ' ' . 

Tertiary. Characterized by the formation of lesions in 

the central nervous .sy.stem, and by nervous di.sturbance with 

ultimate paraplegia. 

It was probably on account of these three periods that the 

older writers confounded the di.sease with syphilis, and it is 

also possible that the ulcerations and chronic enlargements of 



4l8 DOURINE 

the sheath and penis gave rise to the idea that it was a form 
of localized glanders. 

The duration of the disease is stated b}- Williams to extend 
from three months to as many years. The prognosis is 
unfavorable. 

§ 322. Morbid anatomy. In the early stages. there are 
phlegmonous or edematous swellings of the sheath, scrotum, 
penis and inguinal glands and a yellowish liquid effusion into 
the scrotal cavity. The skin covering the parts may show a 
papular or vesicular eruption or if this has passed a mottling 
with white spots shows where these lesions have been. Later, 
the inguinal glands shrink and become firm, owing to the 
development of fibroid tissue. The testicles, which are either 
swollen or shrunken, contain foci of suppuration or caseation. 
The connective tissue of the epididymis and the cord is the seat 
of a gelatinous exudate. The walls of the scrotum may be 
greatly thickened and be the seat of abscesses or of caseous 
degenerations. In advanced cases the testicles are usually 
abnormally small, even if the scrotal mass is enormously dis- 
tended. The sheath and penis may be the seat of more or less 
numerous ulcers and swellings. Contraction and contortions 
of the penis are not uncommon. It may, how^ever, retain its 
normal dimensions. The walls of the lymphatics in the 
inguinal region may be the seat of hyperplasia ; the thickening 
causes them to stand out like cords as in glanders. In the 
advanced stages the muscles, especially those of the hind 
limbs, become pale and atrophied. The nerve centers under- 
go profound changes which have been studied by Thanhoffer. 
The pia mater in the affected part ot the spinal cord is the 
seat of active congestion and thickening. The central canal 
of the cord is dilated more at one point than another, contains 
more than the normal amount of liquid and the neuroglia 
around it is thickened and fibrous. The substances of the 
cord, both white and gray, show congestion, blood staining, 
and points of softening and of hyperplasia of the neuroglia. 
The nerve cells are modified in various ways, some being 
granular, some discolored by fine granular pigment, some hav- 



MORHID ANATOMY 4I9 

ing enlarged and multiple nuclei and some show vacuoles. 
The nerve filaments often show a granular degeneration 
extending from the nerve cell to the axis cylinder. The latter 
is liable to be varicosed or enormously enlarged. In the 
affected portion of the cord, leucocytes are numerous and there 
is often hyperplasia. The neuroglia tends to increase, and 
apart from the foci of softening tends to give a special firmness 
to the substance. The subarachnoid and subdural fluid is 
increased and there, may be at the roots of the spinal nerves, 
especially in the dorsal and lumbar regions, a gelatinoid exu- 
date investing the nerve, distending the connective tissue 
beneath the neurilemma and even occupying the interval 
between the nerve filaments. Sometimes large corpuscular 
bodies are found between the nerve fibers. 

Weber and Nocard state that sections show cachexia and 
hemorrhagic softening of the spinal marrow. The parasites 
found in these areas and in the serous effusions resemble those 
of surra and nagana. 

The cerebral meninges are congested and opaque. Foci 
of softening are by no means uncommon and the cerebral 
ventricles contain an abnormal quantity of fluid. 

The bony tissue generall}^ has lost its consistency and the 
medullary matter may be unduly reddened. The large joints 
contain an excess of synovia of a somewhat pinkish color. 
The ligaments of the hip joint are often congested, thickened 
and softened. The articular cartilages may even show areas 
of blood staining. 

The intestines are usually nearl}' empty, soft, pale and 
flaccid. Ruthe has in one case observed rounded ulcers on 
the mucosa. 

The mesentery is thickened with an infiltration and it has 
a yellowish discoloration and the mesenteric glands are usually 
enlarged, softened and friable, though .sometimes firm and 
contracted. The lymph glands adjoining the generative 
organs are often swollen, pigmented and studded with foci of 
ca.seation, varying in size from that of a pea upward. The 
liver is softened, hyperemic or fatt}-. The spleen is small. 



420 DOURINE 

The kidneys are usually large, pale and blackened. The 
thoracic organs may show little change, though hypostatic 
congestions and foci of caseation or suppuration may be 
present. The blood is light colored and forms a loose, pale 
clot. There is a diminution in the number of red blood cells 
and a relatively large increase in the number of leucocytes. 

In the mare, in addition to the lesions in the internal 
organs and blood, the following may be noted in connection 
with the generative system. Phlegmons or edematous swell- 
ings, or ulcers on the lips of the vulva and on the vulvar and 
vaginal mucosae. The parts become variously distorted. A 
crop of pu.stules or vesicles which run into ulcers may appear 
on the urethral orifice, the vulva and adjacent skin. The 
mammary glands are sometimes inflamed, edematous and 
tender, with suppurative or necrotic foci. The adjacent 
lymph glands are enlarged by infiltration or contracted by 
sclerosis. 

In the dog the symptoms and the lesions resemble those 
in the horse. 

>^ 323. Differential diagnosis. Dourine is to be dif- 
ferentiated from the other forms of Trypanosoma disease, and 
also from " Benign venereal disease." 

Dourine is characterized throughout by its intermittence. 
As each fresh crop of parasites appears in their cycle of exist- 
ence, there is an exacerbation of symptoms, but, in contra- 
distinction to the malarial hematozoon of man and the 
piroplasma of cattle, there is no marked rise of temperature 
and a correspondingly low fall. 

Williams describes a benign venereal disease of mares all 
of which had been bred to an imported French draft horse. 
He states that " the margins of the vulva retain their natural 
color in this disease, except at the seat of eruptions, when the 
color quickly returns. The vulva remains naturally closed, 
and does not gape, -as in maladie du co'it. The clitoris retains 
its natural color, size and appearance." The duration of this 
affection is stated to be from two to six weeks, but may persist 



PREVENTION 42 1 

for a longer time if neglected. The cause is not known. He 
reports that when it becomes established it is highly conta- 
gions. It appears to be spread by copulation. 

>j 324. Prevention. The prevention of this disease 
seems to rest in the isolation of all affected animals. It is 
important, therefore, that its diagnosis be made at the earliest 
possible moment. As it is not spread except by copulation, it 
is a comparatively easy disease to control if taken in time. 

Prophylaxis. — In Austria where the disease has ex- 
isted for a long time, the following rules are observed" 
Baldrey states that they sum up the necessary preventive 
measures. It is understood that they apph'^ to a country in 
which the disease is prevalent : — 

"(i) Even when there is nothing to lead to the suppo- 
sition that the disease exists, everj- mare about to be put to 
the horse shall be carefully inspected, and refusal made to old 
and weakly mares, or to those which have a discharge from 
the vulva, or have that organ enlarged or swollen, or which 
do not present the ordinary manifestations of oestrum. It is 
also suggested that an edematous swelling, no matter where 
situated, should negative covering. 

"(2) The stallion's penis to be carefully and frequently 
examined, and on no account is the animal to be used if there 
is the slightest lesion upon it. He is to be kept secluded until 
all doubt as to the nature of the lesion has passed away. 

"(3) Give every information possible to breeders as to 
character, etc., of the disease. 

"(4) Immediate information is to be given in all cases of 
stallions in the least suspected, and the necessary steps taken. 

"(5 ) To prevent extension, the sale of all mares in the 
affected areas to be stopped during the prevalence of the 
disease. 

"(6) If the malady has spread in a district, all breeding 
stallions to be stopped employment, whether Government or 
private property. Those already diseased to be sequestrated 



422 DOURINE 

under police supervision, whether private or Government 
property. 

"(7) Affected animals to be separated from healthy, to 
have their own attendants, and no interchange of clothing, 
utensils, etc., to take place. Those deemed curable to be 
treated, those incurable to be destroyed. 

"(8) All horses attacked to be castrated, as well as those 
which, notwithstanding their apparent good health, have 
transmitted it to mares they have served, and also those which 
have been put to infected mares. 

"(9) Mares that have been in the least affected and 
apparently cured not to be covered the following year, or until 
certified by a veterinary surgeon as cured. It is even better 
to exclude all such mares entirely, and brand them as having 
had the disease." 

REFERENCES. 

1. Baldrev. Dourine. Jour. Coiiip. Path, and T/wra., Vol. 
XVIII (1905), p. I. 

2. Buffard and Schneider. Prophylaxie de la douriue et 
expose de faits nouveaux interessant cette maladie. Jour, de Med. I'et. 
et de Zoolch, 1901. 

3. Faville. Extirpation of maladie dii co'it. Annual Report, 
Bureau oj Animal Industry, 1895-6, p. 13 and 62. 

4. MoHLER. Cultivation of Trypanosoma Equiperdum. Pro- 
ceedings Am. Vet. Med. Asso., 1905, p. 363. 

5. Rouf.ET. Contribution a 1' etude du trypanosome des mammi- 
feres. Amer. de V Inst. Pasteur, \o\. X ( 1896), p. 716. 

6. Thanhoffer. tjber Ziichilahme. Wien. 18S8. 

7. WiLi^iAMS. Maladie-du-Coit, or equine syphilis. Annual 
Report of the Board of Live Stock Commissioners, for the State of 
Illinois Fiscal Year ending Oct. 31, 1887. (A full report of the disease 
and its eradication in Illinois.) 

8. Williams. Benign venereal disease — equine chancroid. Ibid. 
p. 84. 

9. Wilson-Barker. Maladie du coit in Nebraska. Vet. four. 
Lond., Vol. XXXV (1892). Vol. XXXVI, (1893). 



ETIOLOGY 423 

MAL DE CADKRAS 

§ 325. Characterization. Mai de caderas (disease of 
the rump) is a disease essentially of the horse kind, charac- 
terized by an intermittent fever, a progressive paralysis of the 
posterior parts, rapid emaciation and death. It is a "wet 
weather" disease, as it is reported to almost entirely disappear 
in the dry season. Horses, mules and asses are said to suffer 
from it. Horses are said never to recover. 

§ 326. History. Rebourgeon studied this disease in 
1889. He made a bacteriological investigation into its cause 
without success. Leclerc described it clinically in 1899. He 
believed that he had found its pathogenic bacterium. In 
1 90 1, Elmassian showed that this disease was caused by one 
of the trypanosoma. Voges and Lignieres confirmed his 
discovery. 

§ 327. Geographical Distribution. Mai de caderas i.= 
a disease of tropical South America. 

§ 328. Etiology. Elmassian differentiated the try- 
panosoma of this affection in 1901. Voges pointed out its 
pathogenic action and named it Tr. equinuvi. In length it is 
3 or 4 times the diameter of the red blood corpuscles. Its 
width is one-third to one-half the diameter of a red blood cell. 

The anterior end is provided with a flagellum about as 
long as the body of the parasite. It extends backward about 
two-thirds the length of the body as a somewhat thickened 
margin of a distinct undulating membrane. The posterior end 
of the parasite is about one-third the length of the flagellum. 
It is contracted and somewhat beak shaped. 

Its motion resembles that of an eel, but its actual motility 
is not great, the whole body taking part in an excessively 
active wriggling motion with the flagellum and beak ends 
moving in opposite directions. The nucleus is toward the 
anterior end, a very small centrosome near the posterior end, 
and there is a granular protoplasm. 

It is found in the blood of horses, mules, asses, hogs and 



424 MAL DE CADERAS 

water hogs suffering from mal de caderas. It is transmissible 
to white and gray rats and mice, rabbits, dogs, goats, sheep, 
chickens, turkeys, ducks and certain monkej^s found in South 
America. Cattle are said to be immune. 

The parasites are most numerous in the circulating blood 
during the rise of temperature. Upon its reaching 40-41° C 
they gradually disappear, but reappear with the next rise of 
temperature. 

^329. Mode of infection. Unlike dourine, the virus of 
mal de caderas is not transmitted by copulation. It has been 
proven that the virus is disseminated and animals are infected 
with it by means of certain insects. Stomoxys calcitrayis has 
been incriminated and several other insects are under 
suspicion. 

4J 330, Symptoms. The first symptom is an elevation 
of temperature which rises slowly, but suddenly falls to nor- 
mal. Emaciation is rapid. The urine is dark colored and 
usually contains albumin, and perhaps blood. The blood 
changes so that it gives the picture on microscopic examina- 
tion of pernicious anemia. There is an increase in the lym- 
phocytes and in the eosinophiles. The most obvious symptom 
is said to be a symmetrical or asymmetrical paresis of the hind 
legs. Defecation and urination are difficult (coinciding with 
paralysis of the sphincters). The paralysis gradually extends 
to other parts of the body. Edema is often present. The 
appetite remains good until near the end when there is 
extreme thirst. 

The ditratioti of the disease is variable. Some animals 
die after a month, others live for a year or longer. Stiles 
states that it lasts from two to five months in horses and from 
six to twelve months in mules and asses. 

?^ 331. Morbid anatomy. The muscles are pale and 
atrophied in the posterior part of the body. The intermuscu- 
lar tissue is infiltrated with a gelatinous serous-like substance. 
Hemorrhagic foci appear in the muscles of the rump. 



DIFFERENTIAL DIAGNOSIS 425 

The spleen and limphatic glands are enlarged. The liver 
is enlarged and congested. The heart muscle is soft and 
flabby. The lungs often contain ecchymoses and subpleural 
emphysematous areas. There is a serofibrinous exudate in the 
body cavities, especially in the pericardial sac and pleural 
spaces. There are conflicting statements concerning the mor- 
bid anatomy and it is difficult to select those that are not con- 
tradicted. The pathological histology and the lesions in the 
nervous system do not appear to have been described. 

i^ 332. Differential diagnosis. This affection is to be 
differentiated from the other forms of trypanosoma infections. 
There seems to be no other specific disease with which it 
would be confused. The diagnosis is made from the intermit- 
tent fever, emaciation, progressive paresis, anemia, and the 
finding of a parasite. The inoculation of experimental ani- 
mals (mice or dogs) with the blood is of value when the 
parasite is not found on microscopic examination in the blood 
of the horse. 

REFERENCES. 

1. Elmassian. Mai de Caderas. Analcs de la Univcrsidad 
National .Isniicioii, Vol. V (1901). 

2. I^ECLERC. El mal de Caderas. Buenos Ayres, 1899. 

3. LiGNiiiRES. Contribucion al estudio de la trypanisomiasis de 
los Equideos Sud Americanos. Buletin de agricultiira y yanaderia 
{Republic Argentina) 1902, p. 843. 

4. RebourgEON. Note sur le mal de Cadera. Recueil de mid. 
vHi'r. 1889, p. 85. 

5. SivORi AND LECLER. Le Surra Americain ou mal de Caderas. 
Anales del ministerio de agricultura, 1902. Centralbl. fiir allg. Path. 
1902, S. 963. 

6. VOGES. Uas mal de Caderas. Zeitschrifl f. Hygiene, Bd. 
XXXIX (1902), p. 323. 

vSee also literature 011 other trypanosoma. 



426 NAGANA 

NAGANA 

Synonym. Tsetse-fly disease. 

§ 333- Characterization. Nagaua is a disease charac- 
terized by anemia and rapid emaciation caused by one of the 
trypanosoma. It attacks horses, mules, zebras, cattle, and 
sheep. A number of the smaller animals are susceptible. It 
is known to all dialects as the tsetse- fly disease. 

§ 334. Geographical distribution. This disease is 
found in central and southern parts of Africa. There seems 
to be some doubt about its identity with the disease of a simi- 
lar nature in the Transvaal. 

§ 335- History. Livingston pointed out the existence 
of this disease in Central Africa. In 1886, Bruce studied it in 
the Zulu Land. He found constantly in the blood of the sick 
animals a trypanosoma similar to that found in surra. It has 
been carefully studied by Kanthack, Durham and Blandford, 
Koel, Plimmer and Bradford, Theiler, Schilling, Laveian and 
Mesnil. 

§ 336. Etiology. This affection is caused by Trypa- 
nosoma Brucei. It is from 28 to 33 /< in length with the flagel- 
lum and about i /< in width. It is closely related to Tr. 
equiperdiun. Some investigators have been unable to satisfac- 
torily differentiate the two species, while others recognize them 
as distinct. 

The trypanosoma are transmitted from the diseased to the 
healthy animals by means of the tsetse-fly {^Glosshia )norsihi7is), 
which exists in certain parts of Africa. It appears that this is 
the only species of insect responsible for the transmission of 
the virus. The affection is extended into uninfected areas by 
the introduction of diseased animals. 

The pe7iod of incubation, m 2ir\.\^c\a.\\Y ■prod.nctd cases, is 
reported to be about 4 days in the horse. 

§ 337- Symptoms. The first indication of the disease 
is a rise in temperature which lasts for 3 or 4 days, when it 



MORBID ANATOMY 42? 

suddenly drops. After this time the temperature oscillates 
between 35° and 41 ° C. Emaciation is rapid, the hair becomes 
rouo-h and mav fall out. There is a tendency to diarrhea. 
There is edema of the abdominal walls. In cattle the symp- 
toms are not usually so acute as in the horse. 

The duration of the disease is said to vary from a week to 
six months or more. The appetite remains good until near the 
end. According to Bruce recovery is rare. 

^ 338 Morbid anatomy. There appear to be no dis- 
tinctive anatomical changes for this affection. The tissues 
generally are reported to be anemic and infiltrated with a ser- 
ous exudate. If the edematous portions are incised a clear 
amber or citron colored fluid escapes. The spleen may be en- 
larged but the color and consistency are normal. The liver 
and kidneys are said to be slightly affected. 

S 339 Differential diagnosis. The diagnosis is made 
clinically from the progressive anemia and edema, coincident 
with a good appetite. The finding of the parasite in the blood 
is positive evidence. This disease is to be differentiated from 
the other affections caused by trypanosoma. 

REFERENCES 
I. BRrcE. Preliminary report on the tsetse-fly disease or nagaua. 

in Zululand. Durham, 1895. ^ 

2 K^NTH^CK. DURHAM AND Blandford. On nagana or tsetse- 
fly iJ^ Proceedings of the Royal Society, Vol. LVIV (X898) , P-xoo. 

, L^VERAN ANr> MESNiL. Recherches morphologiques et exper- 
i^neniales snr le trypanosome dn nagana ou maladie de la mouche 
tsetse, -inn. de F lust. Pasteur, 1902, p. i. 

4 PUMMER AND BR..DFORD. A preliminary note on the mor- 
phology and distribution of the organism found in the tsetse-fly disease. 
The Veterinarian, Vol. LXXII ( 1899), p. 64S. 

5. TheilER. Die Tsetse-Krankheit. Schz.cizer-Archiv n<r Thter- 

heill:., 1901. S. 97. 

^ 340 Differentiation of surra, dourine, mal de 
caderas and nagana. The divergence of opinion concern- 



428 TRYPANO.SO:\IIASES 

ing the nature of these affections and the specific identity of 
the exciting cause, render a dififerentiation or unification of 
these most interesting diseases exceedingly difficult. Very 
few investigators have had the opportunity of studying all of 
them in their natural environment. The conclusion of Mus- 
grave and Clegg in their recent report is worthy of considera- 
tion. They say: "In summing up the whole matter it 
appears to us, when we take into consideration the work done 
by others and add our own results, that we are justified in 
believing surra, nagana, mal de caderas, and probably dourine, 
the same disease, and that all are caused by Tr. Evansii." 

Koch, who worked with surra and nagana, considered 
the parasites and the resulting infections identical. Many 
others have formed similar conclusions. Other investigators 
such as Voges, Laveran and Mesnil and others maintain that 
certain differences exist. The evidence is convincing that 
dourine and mal de caderas are different in some respects from 
the other two. Voges' reasons for this are : 

1. "Dourine and mal de caderas can not be transmitted 
to cattle. 

2. "In regions where mal de caderas exists cattle do not 
die of surra. 

3. "We Jiave no reason to believe that trypanosoma 
show the same irregularities of virulence as bacteria, so that 
the different forms of the disease may be said to be produced 
by different degrees of virulence in the same trypanosoma. 
On the contrary, during our four years of experimentations, 
the latter have .shown a constant virulence." 

4. The fourth reason which he considers decisive is 
based on the morphological differences in the parasites. 

Voges concludes by saying, "I think these four proofs are 
entirely sufficient to establish for all time the difference be- 
tween surra and dourine as well as between surra and )nal de 
caderas. ' ' I^averan and Mesnil give extensive consideration to 
the differences between surra and nagana. A summary of 
their considerations is appended. 



DIFFERENTIATION 429 

1. "The same animals are susceptible to both diseases — 
the horse, ass, mule, goat, sheep, cow, camel, dog, cat, 
monkey (long-tailed macayo), rabbit, guinea-pig, and rat. 

2. "In the horse the course of the disease is the same, 
whether surra or nagana. The animal dies at the same time, 
in 30 days on the average. In inoculation cases the period of 
incubation is the same, and the same symptoms and lesions 
supervene. 

3. "The other equides, the goat, sheep and dog, die of 
the two diseases in the same length of time and with similar 
.S3'mptoms and lesions. 

4. "Rabbits, guinea-pigs and rats succumb to the infec- 
tion in a like manner. 

5. "Cows rarely survive naga)ia, and they rarely die 
from surra. They become emaciated with surra but recover 
in health and a subsequent inoculation does no harm. This is 
a marked difference between them but it may be explained 
when further experiments are made." 

Laveran and Alesnil believe that the paralysis of the pos- 
terior extremities, a marked symptom in mal de cad eras, is less 
marked in surra and nagana, although they believe the three 
affections verj' closely related. Dourine differs from the other 
three in two distinct points : ( i ) The morphology of the para- 
site is different. {2) In dourine contagion by coition seems 
to be the only natural mode of infection. 

Much additional investigation will be necessary before 
the question of either the identity or the non-identity of these 
affections can be positively determined. As these diseases 
are not liable to become of great economic importance in this 
country, further discussion of the voluminous literature seems 
unnecessarv. 



CHAPTER XII. 

INFECTIOUS DISEASES FOR WHICH THE SPECIFIC 
CAUSE IS NOT DETERMINED. 



§ 341. General consideration. It was not until a 
comparatively recent date that the nature of the infectious 
diseases began to be understood. The}' were, however, differ- 
entiated in so far as that could be done by clinical evidence 
alone. With the work of Pasteur, overthrowing the "spon- 
taneous generation" theory; the introduction of the aniline 
dyes by Weigert in 1877 i the discovery of solid culture media 
by Koch in 1881 ; together with the finding of the specific 
causes of anthrax, Asiatic cholera, tuberculosis and other dis- 
eases, there naturally came new methods for the study of the 
etiology of these affections. By the use of newer methods 
and better instruments of precision and the closer study of. 
these afifections the cause of one after another of the infectious 
diseases was revealed until the etiology of a large number of 
them has been made known. These have already been grouped 
and studied. There are remaining still a number of well 
recognized diseases for which a specific cause has not been 
found. The methods for the investigation of the cause of dis- 
ease that have been effective in case of other diseases have 
failed here. Until other procedures are devised, the specific 
causes of these affections will undoubtedly remain undeter- 
mined. Their study, however, has revealed much concerning 
their nature, so that measures for their prevention have been 
found that are quite as effective as they are with those of 
known etiology. 

RINDERPEST. 

Syno7iy7ns. Contagious typhus ; steppe murrain ; cattle 
plague. 



HISTORY 431 

§ 342. Characterization. Rinderpest is the most fatal 
disease affecting cattle. It is a specific eruptive fever, occur- 
ring both sporadically and in epizootics. It is characterized by 
a more or less typhoid condition, with lesions largely located 
in the mucosa of the digestive tract and skin, and by the in- 
fectious nature of all the tissues, secreta and excreta. It is a 
disease peculiar to cattle, although other ruminants are sus- 
ceptible to it. 

^ 343. History. Rinderpest seems to have been brought 
to western Europe by the importation of cattle from central 
Asia as early as the fourth century. It is supposed that it 
had long existed on the steppes of central Asia and eastern 
Europe The first great epizootic of which there seems to be 
records occurred about 1709 and spread over nearly all of the 
countries of Europe. It is reported that 1,500,000 cattle died 
from its effects during the years from 1711 to 1714- Ramaz- 
zini seems to have been the first (1711) to accurately describe 
the symptoms and lesions. 

It was in connection with this disease that the first veteri- 
nary police regulations were instituted, and it is stated that 
because of the ravages of this affection Veterinary Colleges 
were first established with government aid. In the latter half 
of the eighteenth century, rinderpest was prevalent in nearly 
all of the countries of Europe. During the years from 1740 
to 1750 it was estimated that three million cattle died. The 
importance of this disease is shown in the fact that m Italy 
alone during the year 1792 from three to four million cattle 
died from its effects. In the years 1844 and 1845, Russia is 
said to have lost a million of cattle from this disease alone. 
Nearly all the countries of Europe have from time to time lost 
heavily from it. It is stated, however, that England and Ger- 
many have practically freed themselves from it. Preventive 
inoculation against this disease was introduced into England 
by Dodson as early as 1744 and later by Courtivon into France. 
§ 344 Geographical distribution. Rinderpest is a 
well-known cattle plague in Russia and the steppes of central 



432 RINDERPEST . 

Asia. It has extended from time to time from its home in 
Russia and Asia to nearlj^ every countr}- in Continental 
Europe and Asia. More recently it has occurred in southern 
Africa. In 1882/'^ it appears to have been introduced into the 
Philippines. It has not been introduced into the United States 
or other American countries. At present, it is not known to 
exist in England, although in the past she has suffered many 
destructive epizootics. 

s^ 345. Etiology. The specific etiological factor of rin- 
derpest is not known. vSeveral investigators have isolated and 
studied various species of bacteria from the tissues of animals 
dead from this disease. Semmer of Dorpat has always found 
the same organism in the lesions. His results do not appear 
to have been verified. There seems to be no doubt in the 
minds of those who have worked on this disease that it is 
caused by a specific microorganism, most likely a species of 
bacteria. Koch makes the following statement concerning the 
etiology of rinderpest in the second report of his investigations 
in South Africa in 1897 : " All efforts to find by means of the 
microscope, as well as through cultivation, a specific micro- 
organism in the blood have as yet been fruitless. I also did 
not succeed in finding any specific microorganism amongst the 
microbes which the mucus from the nose, the secretions from 
mucous membranes, and the contents of the intestines natur- 
ally contain in large numbers." Jobling reports that o.i cc. 
of blood taken from a sick animal and injected under the skin 
of a healthy one will produce the disease. 

NicoU and Adil-Bey found that the virus would usually 
pass through the porous Berkfeld cylinders, but not through 
the denser form or the Chamberland tube. 

The virus may be transmitted from the sick to the healthy 
individuals in a variety of ways, both direct and indirect. It is 
said to be present in the various excreta of the diseased animal, 
such as the discharge from the nose, the saliva, the urine and 



*No authoritative evidence of its occurrence there prior to that 
time has been found. 



SYMPTOMS 433 

the feces. It retains its vitality outside of the body in a moist 
state for months, even a year or more, according to some au- 
thorities. Hence, feces and the fodder and bedding soiled by 
the discharges may convey the disease. When dried, how- 
ever, its vitality is said to be lost in a few days. Persons may 
carry the virus on their shoes, clothing and farm implements. 
Even small animals such as cats and rats, which frequent 
barns and stables, have been looked upon as carriers of the 
infection. The hides of animals dead of the disease may trans- 
mit the infection. The virus is destroyed, according to Hutch- 
eon, by complete desiccation. Kraiewsky found that the virus 
was destroyed in hides soaked in corrosive sublimate i-iooo 
for 24 hours, or in 2.4 per cent carbolic acid for the same time. 
It is also claimed that animals after having pas.sed through 
one attack of the disease are able to resist successfully future 
attacks. Inoculation with the virus is said to produce immun- 
ity, but the process of inoculation itself is followed by death in 
many cases. The disease is reported to have developed after 
feeding hay a year after it has lain in an infected stable. It is 
destroyed at a temperature of 131° F. but in animal ti-ssues it 
is said by some to resist putrefaction. Hutcheon, however, 
states that putrefaction appears to destroy it. 

The period of mciibation is stated to be from three to ten 
days. In animals inoculated with virulent blood it is from 
sixty to ninety- six hours. 

§ 346. Symptoms. The symptoms of rinderpest are 
those of a severe, acute, infectious disease. At first the tem- 
perature rises to 105 to 106° F. and remains near that point 
with but slight variations until other symptoms develop. The 
pulse is small, beating from 160 to 120 per minute. There is 
great debility, decrease in the yield of milk and loss of 
appetite ; rumination becomes disturbed and the animal may 
have slight attacks of shivering. 

After these preliminary symptoms there are well marked 
rigors, respiration becomes accelerated and the visible mucous 
membranes assume a scarlet color. There is entire loss of 



434 RINDERPEST 

appetite, arrest of the function of rumination, thirst, consti- 
pation with the feces dry and covered with mucus. Some- 
times there is slight colic. Later there is a discharge which 
is first serous and subsequently sero-raucous from the eyes, 
nose and vagina. The saliva flows from the mouth. The 
feces gradually become thinner until violent diarrhea accom- 
panied by colic sets in. The evacuations become fetid, viscid 
and sometimes mixed with blood. The animal becomes rapidly 
emaciated, staggers when w^alking, is very sensitive to pressure 
on the loins and lies down a great deal. In exceptional cases 
the patient manifests nervous symptoms. Others exhibit vio- 
lent dyspnea and symptoms of severe inflammation of the lungs. 

As the disease advances characteristic changes are to be 
seen in the mucous membranes. Red patches which may be 
flat or in the form of wheals and which quickly become cov- 
ered with a grayish white, loose crust appear on the mucous 
membrane of the lips, tongue, cheeks, gums, nostrils and 
vagina. The uppermost epithelial layer consequently becomes 
opaque and yellowish gray spots develop on it. Less frequently 
crusts are formed from the tumors bj- their caseous disintegra- 
tion. The crusts on being shed leave dark red hollow places, 
the so-called erosion ulcers, which readily bleed. In slight 
cases of the disease there may be no crusts or erosions. It is 
stated that sometimes an eruption in the form of very minute 
pimples and pustules occurs on the abdomen, inner surface of 
the thighs, perineum and udder. In these cases it may be con- 
fused with that of variola. Pregnant animals frequently abort. 

In sheep and goats the disease is milder, and its infec- 
tiousness is said to be less than in cattle, although the symp- 
toms are essentially the same. Sheep are reported to suffer 
frequently from pneumonic affections when attacked by 
rinderpest. 

§ 347. Morbid anatomy. Authors differ somewhat on 
the lesions characteristic of this disease. Walley has pointed 
out the fact that none of the morbid changes are constant and 
consequently they vary with the stages of the epizootic, the 



MOKBII) AXATO>rV 435 

condition of the animal and the treatment. There is always 
emaciation, the muscular tissue is dark and the capillary con- 
gestion is marked. All the tissues of the body may be the 
seat of effusions, exudations and blood extravasations. If 
symptoms referable to the nervous system have occurred, 
brain lesions will be found at post-mortem. 

The muscle of the heart is pale and relaxed. Blood extra- 
vasations beneath the endocardium are not rare. The kidneys 
are usually the seat of congestion or ecchymoses either beneath 
the capsule or in their structure. There are also parenchyma- 
tous changes. The liver is congested, often giving a mottled 
appearance. It is often bile stained. There are more or less 
parenchymatous changes in the liver cells. The lymphatic 
glands are usually enlarged and the mesenteric glands are 
often hyperemic or even hemorrhagic. 

The structures most often affected are the mucous mem- 
branes of the digestive, respiratory and genito- urinary tracts 
and the skin. 

Nodules and pustules are sometimes found on the skin, 
especially of the udder. The mucous membrane of the mouth 
and pharynx is congested in spots, swollen and exhibits 
rounded, yellowish gray, caseous plates or deposits. The 
removal of plates discloses ulcerous and highly congested 
depressions in the mucous membrane, the so-called erosion 
ulcers. These changes are best marked on the inner surface 
of the lips, lower surface of the tongue, buccal mucous mem- 
brane and gums of the inferior maxilla. 

In the first three stomachs the mucous membrane is usu- 
ally normal or slightly congested in spots, and the epithelium 
is so loose that it can be easily detached. The contents of the 
rumen and reticulum are soft and those of the omasum are 
often dried, rarely they are fluid. Generally the abomasum 
is empty and contains only a small quantity of tough, muco- 
purulent, yellow or sanious material. Its mucous membrane 
is highly congested, especially in the neighborhood of the 
pyloric orifice. The congestion is partly diffuse, partly in 
spots, in the form of points or streaks. Its color may be 



436 RINDERPEST 

purple or reddish-brown with a tinge of slate-gray. The 
epithelium exfoliates. On the mucous membrane may be 
found small, brownish-yellow, caseous deposits, in the form of 
plates, which become detached in shreds, leaving indented, 
highly reddened areas which are studded with petechiae. The 
glands (peptic and mucous) of the stomach are .swollen and 
show considerable cellular hypertrophy. Like changes are 
present in the small intestine, where there is a good deal of 
swelling and congestion of the mucous membrane with isolated 
scab-like caseous deposits and erosions. In very severe cases 
these deposits form tube-like casts of the intestinal canal. At 
the same time there may be considerable infiltration of the soli- 
tary glands and of Peyer's patches, which become enlarged. 
Jobling states that he never saw them ulcerated. 

In the large intestine the inflammatory changes are much 
less pronounced. They are greatest in the cecum. 

The nasal mucous membrane is of a dark red color and 
covered with grayish-yellow, soft scabs. After they are re- 
moved, the true tissue of the mucous membrane lies bare. 
Similar changes are found in the larynx and trachea, where 
the deposited masses are frequently purulent and of a creamy 
consistence. The lungs are sometimes hyperemic, sometimes 
edematous, hepatised or emphysematous. Pneumothorax and 
subcutaneous emphysema may be present. 

The duration of the disease is usually from 2 to lo days, 
the average period is about 6 days. The prognosis is not 
favorable. The mortality ranges from 60 to 90 per cent. 

§ 348. Differential diagnosis. It is very difficult to 
diagnose rinderpest from the first cases that occur, especially if 
there is no history of infection. The diagnosis is based upon 
the symptoms, morbid anatomy, progress of the epizootic and 
the history. The most characteristic diagnostic symptoms are 
the rise in temperature (which often occurs some days before 
other symptoms), formation of red spots and a yellow coating 
on the visible mucous membranes and later the development 
of erosion ulcers. A mucous discharge from the mouth, nares, 
eyes and vagina with symptoms of severe intestinal disturb- 



PRKVENTION' 



437 



ances and excessive emaciation are of differential value. 
Rinderpest is to be differentiated from " foot and mouth 
disease," and malignant catarrh if complicated with emph\- 
sema of the lungs. Anthrax, Texas fever, and other affections 
such as contagious pleuropneumonia and enteritis may be mis- 
taken for it. The differentiation may be made from the specific 
nature of eacii disease. 

s^ 349. Prevention. In this connection the proclama- 
tion for the prevention of the spread of rinderpest in Cape 
Colony recently issued by the British Government authorities 
is of interest. It is as follows : 

"Disinfection of hides, /loo/s, horns, skins and feathers, i. Hides 
skins, hoofs, horns and feathers will only be allowed south of Orange 
River and will onl}' be accepted for conve3^anGe by rail after being 
thoroughly disinfected in the manner hereafter described at railway 
stations and the authorized crossing places in terms of Regulation 5 
issued under Proclamation No. 387 of 1896, or at each of them as shall 
hereafter be notified. 

2. No hides, skins, horns or hoofs shall be passed by the Supervis- 
ing Officer unless accompanied by a declaration signed V)y the consignor 
(or his agent) that they are from animals that have not died from rinder- 
pest. Any hides, skins, horns or hoofs not accompanied by such declar- 
ation, shall be immediately destroyed by the Supervising Officer at the 
consignor's expense. 

3. Disinfection shall be supervised by the officer appointed by the 
Government for the purpose, but shall be performed by the owners or 
consignors or their agents. 

4. Dried hides, horns or hoofs shall be immersed in a li(|uid disin- 
fectant for at least 30 minutes. 

5. (ireen hides and skins shall be immersed in a liciuid disinfectant 
for a period of at least 15 minutes. 

b. The disinfectant used may be either a two per cent solution of 
carbolic acid or a five per cent solution of Jaye's Disinfectant, Odam's 
Disinfectant or I/.al. 

7. Feathers shall be hung up for three hours in a chamber charged 
with sulphurous acid produced by burning an excess of sulphur in a 
closed chamber. 

8. Hides, skins, horns, hoofs and the packages containing feathers 
when disinfected, shall be marked for the guidance of the railway offi- 
cials, and shall l)e accompanied by a certificate that disinfection has 



438 RINDERPEST 

been efficiently performed, signed bj^ the supervising oi^cer without 
which the railwaj' officials shall refuse to receive the articles. 

9. When disinfection is completed, the articles disinfected shall be 
loaded direct into a previously disinfected railway truck. 

10. Drying, salting or any other subsequent treatment of the hides 
or skins shall be done by the owners or their agents at their own risk." 

"Disinfection 0/ travelers or passengers. 1. Travelers and passen- 
gers shall be disinfected at railway stations and at authorized crossing 
places, in terms of Regulations 7 and 8 issued under Proclamation No. 
587 of 1896, by the police or other persons duly authorized by the Sec- 
retary of Agriculture in the manner hereafter described. 

2. Natives shall strip and enter a bath containing 2 per cent solu- 
tion of carbolic acid; they shall then be provided with a blanket or 
other suitable clothing until the clothes they are wearing have been 
disinfected. 

3. The clothing of all natives, and the blanket?, rugs, karrosses, 
wraps, etc., of all Europeans, whether from disinfected areas or not, 
shall be subjected to sulphurous acid fumes produced by burning an 
excess of sulphur in a closed chamber for at least 15 minutes, pending 
arrival and erection of a proper steam disinfecting apparatus. 

4. Europeans coming from an infected farm or place or who have 
otherwise rendered themselves liable to infection from contact with 
natives or their huts or kraals, shall be disinfected in such a manner as, 
in the discretion of the disinfecting officer, may be deemed necessary 
and their clothing as provided by clause 3. 

5. The disinfectant to be used shall be 

2 per cent solution of carbolic acid or 

5 per cent solution of Jaye's Fluid or 

5 per cent solution of Odam's Disinfectant or 

5 per cent solution of Izal. 

6. Boots of Europeans and natives shall be well dry brushed, and 
then the uppers and soles well wiped with the disinfecting solution by 
means of cloths. 

7. Europeans on coming from an infected farm or place and all 
natives presenting themselves at a railway station, siding, halt or other 
place north of the Orange River, shall, before the station master, clerk, 
guard or other officer permits them to obtain a traveling ticket, hand to 
the station master or booking clerk a certificate signed by the disinfect- 
ing officer in terms of Form A, to the effect that they and their clothes 
have been properly disinfected as well as such articles and things in 
their possession as are intended to be carried by rail, not being articles 
or things actually prohibited to be carried south of the Orange River. 



niMUNIZIXG 



439 



8. Any European not coming from an infected farm or place or 
who has not in any way been liable to infection, shall si.<<n a certificate 
to that effect in terms of Form B, and without such certificate shall be 
deemed as coming from an infected farm or place, or otherwise been 
liable to infection, and shall be subject to all provisions and regulations 
attached to persons coming from infected areas or liable to infection ; 
and if the above certificate contains any false statement, the person 
signing the same will be liable to a penalty not exceeding loo pounds 
or, in default of payment, to imprisonment with or without hard labor, 
for a period not exceeding six months." 

Riudcrpcst 



This is to certify that together with his 

clothes and the articles or things in his possession, authorized to be car- 
ried by rail, have been properly disinfected as required by the Govern- 
ment Regulations, 

Disinfecting Officer. 
Riyiderpest. 
FORM B. 

I of do hereby 

certify- that I have not come from any farm or place infected with rin- 
derpest, and I have not in any way, to the best of my knowledge and 
belief, come in contact with infection. 

(Signed). 

^ 350. Immunizing cattle. Koel found that the 
serum of an aniinal that had suffered from rinderpest and 
recovered possessed immunizing powers. This fact being 
demonstrated, its utility has been availed of in immunizing 
animals for procuring the serum. The method given by 
Jobling and which is u.sed extensively in the Philippines is 
appended. 

The animal first receives an inoculation by the "simulta- 
neous method" of Kolle and Turner. This consists in inject- 
ing under the skin on one side from 15 to 55 cc. of .serum 
from an immune animal and on the other side i cc. of virulent 
blood from a sick animal. If the reaction from this double 
injection is good, i. e., a rise of temperature after the proper 
period, it is given 1000 cc. of virulent blood after the tempera- 



440 RINDERPEST 

ture again drops to normal. This is followed, under the same 
circumstances, by 500 cc. and again 1000 cc. After this the 
animal is bled for serum. They are bled with a trocar and 
canula from the jugular vein. The animals are bled three 
times at intervals of a week, after which they are injected 
again with 1000 cc. of virulent blood. 

In using the serum from 50 to 100 cc. should be injected 
subcutaneously by aseptic methods. 

The advantages of this method of immunizing cattle are : 
(i) It produces no reaction, (2) it does not check the flow of 
milk, (3) it confers immunity almost immediately, (4) if 
the disease has just begun it will modify the attack resulting 
in a milder form, (5) no deaths follow its use, (6) pregnant 
animals do not abort, and (7) the serum can be prepared in 
any quantity and it can be kept for seven or eight months. 

The disadvantages of this method are ( i ) the short period 
of immunity — 2 to 4 months, (2) skill required to obtain the 
serum, (3) occasionally, according to Jobling, very little 
immunit\' is conferred. 

The other methods that have been tried with more or less 
success are : inoculation with attenuated virus ; injection of 
the bile of animals dead of the disease ; injecting the bile 
associated with virulent liquid ; the injection of the serum 
from immune animals. 

REFERENCES. 

1. Danvs/., Brodet Axn Theiler. The / V/. /onrnal. \o\. 
XLVI (1898), p. 298. 

2. EdingTox. Report of investigation. T/ir Veieriiiary Journal, 
Vol. XLVI (189S), p. 64. 

3. G.wigee. The cattle plague. London. 1866. 

4. Holmes. vSome diseases complicating rinderpest among cattle 
in India. Jour. Comp. Path, and Thera., Vol. XVII (1904), p. 317. 

5. JoBUNG. Report of the Director of the Serum Laboratory. 
Fourth annual report oj the Philippine Islands. 1903. Ibid. Bulletin 
No. 7, Bureau of Governtnetit Laboratories. Manila, igo^. 

6. Koch. Report. The Veterinary Journal, \'ol. XLV (1897), 
p. 204. Wso Centralblf. Bakteriol. Bd. XXI (1897), S. 526. 



CONTAGIOUS PLEURO-l'NKUMONIA 44^ 

- KoLiE IND Turner. Uber SchutzimpfmiKen und Heilseruti. 
bei Rinderpest. Zeit. f. Hygiene, Bd. XXIX (.898), S. 309- 

8. Ram.'^/./-INI. Dissertatio de Contagiosa Epidemica, Padua, 1711. 

9. TiRNEK AND K01.LK. Report of investiKations. The Vet. 
lour. Vol. XLV (1897), p. 462. 

10. Wai.t.kv. The four bovine scovirges. London. i.S79- 

1 ■ Wai kkr The prophylactic treatment of rinderpest by means 
of preventive hiocnlations, more especially considered i" regard to the 
conditions prevailing in India. Jour. Con.p. Path, and fhera., \o\. 

XVII (1904), P- 326. 



CONTAGIOUS PLEURO^PNEUMONIA IN CATTLK 

Synonyms. Lung plague ; pleuro-pueumonia zymotica ; 
Peripnenmonie contagieuse : Limgenseuche. 

^351. Characterization. Contagious pleuro-pneu- 
nionia of cattle is a specific epizootic disease which affects 
bovine animals and from which other species are exempt. 
When the disease results from exposure in the usual manner, 
it is characterized by an inflammation of the lungs and pleurae, 
which is generally extensive and which has a tendency to 
invade portions of these organs not primarily affected and to 
cause death of the diseased portion of the lung. 

§ 352 History. The first account of the appearance of 
contagious pleuropneumonia dates from the end of the seven- 
teenth century. It is stated that it was observed in Hesse tor 
the first time in 1693, and that its earliest appearance as an 
epizootic was in 1713 and 1714, when it prevailed chiefly in 
Switzerland and the neighboring countries of W urtemberg, 
Baden and Alsace. There are detailed reports of its occur- 
rence from the year 1743. I" ^773. Haller published an essay 
on this disease, which was raging severely at that time. He 
described the symptoms, anatomical characters and protective 
measures laid down at that time by the sanitary police. In 
17. S the disease appeared in England and in 1765 m France 
From 1790 it spread over the whole of Germany. France and 



442 CONTAGIOUS PLEURO-PNEUMOXIA 

Ital}^ At the commencement of the nineteenth century it 
visited all the countries of Western Europe. 

South Africa was infected b}' a bull brought from Holland 
in 1854, and Australia received the contagion with an English 
cow in 1858. It is also reported as existing in various parts 
of the continent of Asia ; but the time of its first appearance 
and the extent of its distribution are very uncertain. 

Some countries which have only been infected for a short 
time, such as Norway, Sweden and Denmark, have succeeded 
in eradicating the disease without much difficulty by slaugh- 
tering all affected and exposed animals. Other countries long 
infected and in which the contagion was thoroughly estab- 
lished, like Australia, South Africa, Italy, France, Belgium 
and parts of Germany, have labored long, in some cases mak- 
ing no progress and in others being only partially successful. 
Holland was one of the first of the thoroughly infected coun- 
tries to free itself from the contagion. 

The disease has been brought to the United States several 
different times. Probably its first introduction was in a dis- 
eased cow sold in Brooklyn, N. Y., in 1843. It came to New 
Jersey by importing affected animals in 1847. Massachusetts 
was infected in the same way in 1859. Massachusetts eradi- 
cated pleuro-pneumonia during the period from i860 to 1866. 
New York and New Jersey made an attempt to eradicate it in 
1879 but were not successful. Late in 1883 the contagion was 
carried to Ohio, probabl)^ by Jersey cattle purchased in the 
vicinity of Baltimore, Md., to which place it had extended 
previous to 1S68. From the herd then infected it was spread 
by the sale of cattle during 1884 to a limited number of herds 
in Illinois, to one herd in Missouri and two herds in Kentucky. 
By cooperation between the United States Department of 
Agriculture and the authorities of the affected states, it was 
found possible to prevent its further spread and to completely 
eradicate it after a few months. 

In 1886, pleuro-pneumonia was discovered in some of the 
large distillery stables of Chicago and among cows on neigh- 
boring lots. This led to renewed efforts to secure the com- 



KKADICATIOX 443 

plete extirpation of this disease from the country. Congress, 
in 1887 enlar-ed the appropriation available for this purpose 
and gave more extended authority. During the same year the 
disease was stamped out of Chicago and has not since appeared 
in any district west of the Allegheny Mountains. 

The work of eradication was at the same time commenced 
in all of the infected States. Before the end of the year 1889 
Pennsylvania, Delaware, Maryland, the District of Columbia, 
and Virginia had been freed from the disease. More difficul- 
ties however, were encountered in the States of New York 
and New Jersev on account of the larger territory infected and 
the density of the population. The long struggle was crowned 
with success, however, and the last animal in which the dis- 
ease appeared in the State of New York was slaughtered early 
in 1891 and the last one affected in New Jersey met the same 
fate early in the spring of 1892. 

On the 26th dav of September. 1S92, the following procla- 
mation was issued, declaring the United States to be free from 
this disease. 

PROCLAMATION -ERADICATION OF PLEURO-PNEUMONIA. 
U. S. Department OF AcRicri/ruRE, 

OFFICK OF THE SKCRHTARV. 
To ALL WHOM IT MAY CONCl'RX : 

Notice is herebv given that the quarantines heretofore existing in 
the counties of Kings and Queens, State of New York, and the counties 
of Essex and Hudson, State of New Jersey, for the suppression ot con- 
tagious pleuro-pneumonia among cattle, are this day removed 

The removal of the aforesaid quarantines completes the dissolving 
of all quarantines established by this Department in the se^-eral sections 
of the United States for the suppression of the above-named disease. 

No case of this disease has occurred in the state ot Illinois since 
December 29, 1887, a period of more than four years and eight months. 
No case has occurred in the state of Pennsylvania since September 
2Q 1888, a period of four years within a few days. 

No case has occurred in the state of Maryland since September iS, 

1889, a period of three years. 



444 CONTAGIOUS PLEURO-PNEUMONIA 

No case has occurred in the state of New York since April 30, 1891, 
a period of more than one year aiid four months. 

No case has occurred in the state of New Jersey since March 25, 
1892, a period of six months, and no case has occurred in any other 
portion of the United States within the past five years. 

I do therefore hereby official!}- declare that the United States is free 
from the disease known as contagious pleuro-pneumonia. 

J. M. RUSK, Scctr/ary. 

Done at the City of Washington, D. C, this 26tli day of September, 
A.D., 1892. 

The time required for its eradication was only about five 
years and the total expenditure was but a little in excess of 
$1,500,000. 

§ 353- Etiology. The specific cause of contagious 
pleuro-pneumonia has not been fully demonstrated. The 
infection may be introduced either by diseased cattle, or, less 
commonly, by bearers such as cattle dealers, attendants, uten- 
sils, fodder, dogs, etc. The sheds in cattle markets are very 
dangerous centers for the dissemination of the disease. All 
cattle are not equally susceptible. It is generally supposed 
that about one animal in four is immune. The virus is spread 
principally by the respired air. Infected cattle are reported to 
be able to transmit it even during the period of incubation, 
before the symptoms are apparent. The disease is particularly 
infectious when it is at its height and the animal remains 
capable of transmitting the disease for eight or ten weeks or 
even longer after the infection, especially when necrotic foci 
remain in the lungs. Walley estimates the duration of infec- 
tiousness in cases of encapsulated necrotic foci to be as long as 
fifteen months. It is said, but the evidence is not given, that 
the virus may be conveyed by the respired air for as great a 
distance as forty yards or more. In exceptional cases, the 
contagium is transmitted from the pregnant cow to the fetus. 

Pols and Noleu, in 1886, at Amsterdam, found micrococci 
alway present in the exuded matter of the lungs. These mi- 
crococci were about 0.9// in diameter and occurred either iso- 
lated or in chains up to six in number. In the unstained 



SYMPTOMS 445 



preparation, the cocci were surrounded by a distinct envelope 
which could be stained only with great difficulty and which 
was absent from cultivated micrococci. 

Arloing believed that he had found the existing cause of 
the disease hi various bacilli, especially in one which he calls 
Pneiivio-bacillns liqiie/ade7is bovis, which forms short nonmotile 
rods. Arloing believes that his experiments prove that the 
pneumo-baciUus is the cause of pleuropneumonia. 

In 1898, Nocard and Roux succeeded in obtaining a very 
feeble growth of an exceedingly minute organism in bouillon 
containing cow or rabbit serum in proportion of one part 
serum to 25 parts bouillon, when cultivated in collodion sacs 
within the abdominal cavity of rabbits. The rabbits which 
received the inoculated capsules become emaciated, and some 
of them died. Those inoculated with uninoculated capsules 
remained well. Rabbits inoculated with the pleuropneumonia 
lungs were not affected. With the cultures obtained in the 
collodian sacs the disease was produced in cattle. The virus 
passed through a Berkefeld filter and Chamberland F cylinder 
but it was held back by a Chamberland filter B. 

§ 354. Symptoms. The symptoms are such as would 
be expected with inflammation of the lungs and pleurae, but 
they varv considerably according to the course which the 
disease runs. If the attack is an acute one, as is frequently 
seen in hot weather, the symptoms appear suddenly. The 
breathing becomes rapid and difficult, the animal grunts or 
moans with each expiration, the shoulders stand out from the 
chest, the head is extended on the neck, the back is arched, 
the temperature ranges from 104 to 107° F., the milk secretion 
is suspended, there is loss of appetite, rumination is stopped, 
the animal may bloat and later be affected with a severe 
diarrhea. Such cases are generally fatal in from seven to 
twenty da vs. 

Very often the attack comes on slowly and the symptoms 
are more obscure. In the mildest ca.ses there is a cough for a 
week or two but no appreciable loss of appetite or elevation of 
temperature. The lungs are but slightly affected and recovery 



446 CONTAGIOUS PLEURA-PNEUMONIA 

soon follows. Such animals may disseminate the virus for a 
long time without being suspected and for that reason are the 
most dangerous of all. 

A more severe type is commonly seen. The cough is fre- 
quently more or less painful, the back somewhat arched and 
the milk secretion diminished. These symptoms increase, the 
appetite is affected, the animal loses flesh, the breathing 
becomes more rapid, the cough more painful, pressure of the 
fingers between the ribs produces evidence of tenderness, the 
hair loses its gloss and stands erect, the skin becomes adher- 
ent, the temperature rises to 103 to 105° F. Animals thus 
affected may continue to grow worse and die in from three to 
eight weeks or they may after a time begin to improve and 
make an apparent recovery. The inflammation of the lung 
does not, as a rule, subside and the organ does not return to 
normal condition as in ordinary pneumonia, but with this dis- 
ease the life of the affected portion of the lung is destroyed, the 
tissue dies and a fibrous wall is formed around it to shut it 
away from the living parts. The tissue, thus encysted, gradu- 
ally softens, becomes disintegrated into a purulent-like sub- 
stance. The recovery, therefore, is only partial. 

By those accustomed to examining the lungs of cattle, 
other and extremely important symptoms may be detected 
during the course of the disease. By auscultation an area of a 
certain extent may be found where the natural breathing 
sound is diminished or entirely lost. This represents the dis- 
eased portion of the lung. In other cases a loud blowing 
sound may be heard, quite different from any sound produced 
when the lung is in a healthy condition. In some cases 
crepitation is heard near the border line of the diseased area 
and friction sounds produced by the roughened pleura may be 
detected. By percussion an area of dullness may be discov- 
ered corresponding to the portion where the respiratory mur- 
mur has disappeared. This loss of respiration detected by 
auscultation and the dullness brought out by percussion are 
the most important evidences of an area of inflamed or con- 
solidated lung. 



MORBID ANATOMY 447 

Seriously afifected animals remain standing if they have 
sufficient strength, but those which lie down are said to always 
lie on the affected side. 

The proportion of animals that become affected after being 
exposed varies according to the virulence of the outbreak, the 
susceptibility of the animals and the length of time during 
which exposure is continued. Sometimes not over 15, 20 or 
30 per cent of the animals exposed will contract the disease, 
while at other times 80 or 90 per cent may be infected. The 
proportion of cases in which the disease proves fatal also varies 
greatly, it may not exceed 10 per cent and it may reach 50 
per cent. In general it may be said that about 40 per cent of 
the exposed animals will contract the disease and about one- 
half of these cases will prove fatal. 

§ 355. Morbid anatomy. Anatomically, contagious 
pleuro-pneumonia is characterized by a progressive interstitial 
pneumonia with secondary hepatization of the lungs and exu- 
dative pleuritis. Usually only one lung, the left as a rule, is 
affected. The anatomical changes vary according to the dura- 
tion of the disease. 

The otherwise healthy lung shows, in the initial stage, 
small, circumscribed, inflammatory centers from the size of a 
hazelnut to that of a walnut. The interlobular tissue in it 
is hyperemic, permeated by single hemorrhages and infiltrated 
with serum. The reddened lobules of the lungs are surrounded 
by bright margins, which are i to 2 ram. broad and which 
are filled with a serous or lymphatic fluid. When the deposits 
are superficial, the plurtc become opaque and covered with 
slight clots. 

At the height of the disease there is a lobular pneumonia 
with pleuritis which is usually spread over the greater part of 
one lobe of the lung. The lung is considerably enlarged, of 
firm consistency, very heavy (weighing up to one hundred 
pounds), sinks in water and does not crackle when cut. Its 
section appears marbled, in consequence of the interstitial con- 
nective tissue having become thickened into broad lines which 



448 CONTAGIOUS PLEURO-PNEUMONIA 

var}' in color from orange to dirtv white and which surround 
the dark colored lobules of the lung. The larger lobules 
have a thickness of from .2 to 5 cm. ; and the smaller ones of 
from .25 to .50 cm. The color of the enclosed lobules of the 
lungs depends on the duration of the process and varies from 
brown-red to dirt}' yellow. The recently infected lobules have 
a blood-red, reddish-brown or dark brown color (stage of red 
hepatization). The color of the older ones varies from orange 
to yellow (yellow hepatization) and that of a still older date is 
gray (gray hepatization). The central foci, because they are 
the oldest, are usually in a stage of yellow or gray hepatization. 
Some of the enclosed lobules of the lungs are normal or only 
compressed, while others are merely hyperemic. If we closely 
examine the bright interstitial lines, we find that they consist 
at first of an edematous infiltration, which later on becomes 
plastofibrinous, gelatinous, indurated and finally tends to the 
formation of adventitious connective tissue. The lymph-spaces 
in the lines are dilated like lacunae and filled with a serous or 
fibrinous fluid. In robust animals, the exudate in the alveoli 
is firm ; but is of a more serous character in animals of a weak 
constitution. In the former case, a section made through the 
lung will be found to be granular. Besides these changes, the 
other 13'mph vessels of the lungs are dilated, their walls are in- 
filtrated wfth cells and their lumen is in a state of thrombosis. 
The blood vessels frequently show thrombi and small hemor- 
rhagic infarcts. The contents of the finer bronchi are often 
infiltrated with numerous white corpuscles. The bronchial 
glands and frequently the mediastinal glands are inflamed and 
swollen. 

The pleurae are covered with soft, membranous, fibrinous 
masses, which are sometimes lumpy or crumbled and which- 
can easily be detached. These deposits have a reticular sur- 
face and may attain a thickness of 2 cm. If we remove them, 
we shall find the pleural vessels highly injected with ecchy- 
moses, and the surface of the pleurae in a rough and uneven 
condition. In the thoracic cavity we generally find, in vary- 
ing quantity, an inodorous fluid exudate, which may be clear 



MORBID ANATOMY 449 



in 
rou 



or opaque and which contains flakey or lumpy masses. Simi- 
lar fibrinous masses often lie on the outer surface of the peri- 
cardium. 

After the disease has existed for some time, the affected 
parts of the lungs undergo induration, cicatrization, caseation, 
calcification, necrosis or suppuration. At first the inter.stitial 
infiltration becomes dense, solid and dry and changes into 
firm connective tissue which makes a crunching noise while 
it is being cut with the knife. In other places we have fatty 
degeneration, caseation, calcification or suppuration, in which 
the enclosed lobules of the lungs, in consequence of the exist- 
g suppuration, become gangrenous, and form sequestra sur- 
ounded by sequestral cavities which have smooth walls. The 
dead portions of the lungs may remain unchanged in these 
cavities for a long time. Frequently they become softened to 
the consistency of a greasy, yeast like paste. Sometimes, when 
they are comparatively small, they become absorbed, and a 
scar is formed. The hepatized lobules of the lungs rarely re- 
gain their normal condition after the absorption of the exudate. 
More frequently they atrophy or collapse, undergo atelectasis, 
calcification or softening, become necrotic or suppurating or 
form cavities. On the pleurae we find thick and wart-hke 
hypertrophies of connective tissue, which frequently cause 
the lungs to adhere to the sides of the chest. 

The changes in the lungs and pleurae are the most im- 
portant general changes in cases of pleuro-pneumonia. It is 
stated that we may sometimes meet with an interstitial fibrin- 
ous exudate in the liver with atrophy of the liver cells ; sero- 
fibrinous effusions into the articulations, tendon sheaths, sub- 
cutis, dewlap and brisket ; intestinal catarrh ; areolation ot 
Peyer's patches and ulcers on the gastro-intestinal mucous 

membrane. 

The views of pathologists differ as to the nature ot the 
earliest changes in contagious pleuro-pneumonia and it is not 
within the scope of this work to present imperfectly developed 
or controverted theories. Without entering into a discussion ot 
the various views, it is clear that there is an inflammatory 



450 CONTAGIOUS PLEURO-PNEUMONIA 

condition of the connective tissue between the lobules, result- 
ing in the exudation of coagulable lymph. This inflammation 
is equally marked around the blood vessels and air tubes. It 
leads to inflammatory changes in the inner wall of the veins 
and these cause a deposition of thrombi or plugs in the vessels, 
which prevent the return of the blood. The blood pumped 
into the lung tissue leaves the meshwork of capillaries around 
the air vesicles, enters the latter and produces the firm hepa- 
tized condition so characteristic of this disease. It will be 
easily understood how the different shades of color from dark 
red to grayish or yellowish red are produced if we bear in 
mind that the veins in different parts of the lung ti.ssue are 
plugged at different times and that the affected regions are in 
different stages of the disease. 

One of the most conspicuous features in a microscopical 
section from a lung affected with acute contagious pleuro- 
pneumonia is the presence of intensely stained foci and lines^ 
These lines, to which Welch seems to have been the first to 
call attention, are visible to the naked eye and when viewed 
with a hand lens suggest by their peculiar curves the contour 
lines of a map. They are situated at the margin of and 
within the inflamed connective tissue which surrounds the 
large vessels and separates the lobules from one another. A 
closer examination ot these lines indicates that they coincide 
with the boundaries of the lobules and of the individual lymph 
spaces of the interlobular tissue. Under a high power of the 
microscope they are resolved into dense masses of leucocytes in 
various stages of degeneration. These dense bands are pre- 
sumabl}'' attracted to the connective tissue boundary of the 
lobules and to the walls of lymph spaces within the connective 
tissue by the unknown cause of the 'inflammation, presumably 
the cause of the disease itself. The space between the lines is 
filled with fibrin, in which very few leucocytes are found. 

§ 356. Differential diagnosis. It is extremely difficult 
to form an exact diagnosis of the disease during its develop- 
ment, because the symptoms which are present are few in 



DIFPERKNTIAL DIAGNOSIS 451 

number and b}- no means characteristic. The slight fever and 
cough are the only symptoms of diagnostic importance in the 
prodromal stage. In the second or acute stage a positive 
diagnosis i)it7-a vitam can be made only when cases of pleuro- 
pneumonia have previously occurred or when several occur 
simultaneously. As a rule, a correct diagnosis can only be 
made by a post-mortem examination. The following diseases 
are to be differentiated from it : — 

1. Non-infedioits iujlammation of the lu7igs. This may 
be distinguished clinically, as a rule, by its more acute and 
more typical course and by its sporadic and sudden appearance 
and, anatomically, by the fact that the parts which have under- 
gone hepatization are practically all of the same age and that 
the interstitial lung tissue and pleurae are but slightly involved. 
Nocard states that in exceptional cases pleuro-pneuraonia may 
run a very acute course and show hepatization of equal ages. 

2. Tuberculosis. The disease cannot be positively distin- 
guished clinically from pleuro-pneumonia. Tuberculin may be 
used as a diagnostic agent, although it is not at all certain 
that animals which have suffered for some time from pleuro- 
pneumonia do not react to tuberculin. After all, an anatomi- 
cal examination is the only real test. Tuberculosis and con- 
tagious pleuro-pneumonia have occasionall}^ appeared simul- 
taneously in the animal. See description of lesions in tuber- 
culosis. 

3. Traumatic pneumonia or pneumonia due to foreign 
bodies may exhibit the same symptoms as pleuro-pneumonia. 
Evidence, during life, of changes in the heart caused by trau- 
matic carditis will be conclusive in making the differentiation. 

4. Broncho or i7iie7'stitial pneumonia. In making a diag- 
nosis between contagious pleuro-pneumonia, based on the lung 
lesions alone, it should always be borne in mind that the entire 
lung should be subjected to examination. Attention should 
be given to signs indicating injury to the chest wall, to the 
possible presence of foreign bodies and to severe inflammation 
of the air passages which may result from the aspiration of 



452 CONTAGIOUS , PLEURO-PNEUMONIA 

irritant or corrosive fluids. Where these agents may be 
excluded special attention should be paid to the condition of 
the pleura and to the distribution of the disease, careful notes 
being made of the lobes involved. Next in order come the 
peculiar perivascular and interlobular thickening and the 
thrombosis of the veins. Care should be taken not to con- 
found mere clots with adhesive thrombi. In acute pleuro- 
pneumonia, after death, the arteries are usually distended 
with clots. The different features of the hepatized and 
edematous portions of the lung ti.ssue should be carefully 
noted. Lastly, the peculiar exudation and infiltration in the 
connective and fatty tissue of the dorsal mediastinum and of 
the embedded glands should not be overlooked. With the 
microscope the peculiar dense cell masses of the diseased con- 
nective tissue should be looked for and the nature of necrotic 
tissue determined in case microscopical appearances are no 
longer reliable owing to hardening processes. 

Finally it should be borne in mind that the lesions of 
broncho-pneumonia and the interlobular changes which may 
follow it may coexist with contagious pleuro-pneumonia, and 
that both kinds of lesions may be encountered in the same 
lungs. Hence, great caution must be exercised in expressing 
an opinion when only a. small portion of the lungs 'are pre- " 
sented for examination, because only that portion which is 
affected with broncho-pneumonia may have been submitted. 

§ 357. Preventive inoculation and eradication. ' In 
Europe inoculation has been practiced for a long time as the 
principal means for combating pleuro-pneumonia. As early 
as the beginning of the last century it was proposed in Ger- 
many by Hausmann and others. Its employment was greatly 
increased by the investigations which were made in 1850 by 
Wilhelms in Holland and which were published in 1852. 
Since that time these inoculations have been practiced in 
nearly every country. The literature on the subject is very 
copious. 

The advocates of inoculation, among whom we may 



PREVENTION 453 

mention Haubner, Bouley, Schiitz and others, start from the 
well known fact that one attack of pleuro-pneumonia success- 
fully passed through confers immunity for the remainder of 
the animal's life. By inoculation, a local, specific, inflamma- 
tory process which is analogous to that in the lungs, is pro- 
duced and is followed by subsequent immunity of the whole 
body. Haubner calculates that the mortality from the inocu- 
lation is from I to 2 per cent and that the tips of the tails are 
lost in from 5 to lo per cent of the cases. In Holland, among 
59,180 cattle inoculated in 1878 and 1879, the mortality 
amounted to only 0.66 per cent. 

The opponents of inoculation, among whom we may men- 
tion Rolof, Ziindel, Kitt, M'Fadyean and others, assert that 
up to the present no positive case of immunity has been proved 
to have been obtained from inoculation. They also point to 
the fact that even the advocates for inoculation are unable to 
give the exact duration of the immunity and consequently 
make several inoculations. Dujardin-Beaumetz finds that the 
inoculation in the tail with a bouillon culture of the organism 
gives a local swelling. It confers immunity quite as well as 
the injection of the serous fluid. Already he reports its use 
in 675 cattle, of which 14 died as a result of the inoculation. 
The best procedure seems to be the stamping out of the dis- 
ease by means of thorough disinfection or destruction by fire 
of all infected sheds and barns. The success of this method 
is illustrated by the eradication of the disease from the I nited 
States. 

RKFERKNCES 

I. DUJARDIN-BEAUMETZ. Le microbe cle la peripneumonie et la 
culture. Thesis. Paris, 1900. 

2 NOCARD ET Roux. Le microbe de la peripneumonie. Recueil 
de Med VHerinaire, March 24, 1898, p. 212. i Trans, m the Veterinary 
Journal, London, Vol. XLVII (1898), p. 147- Ann. dc V Inst. Pasteur, 
Vol. XII (1898), p. 240.) 

3. Salmon. Annual Reports 0/ th^ Bureau 0/ Animal Industry, 
I 884-1892. 

4. SMITH. Annual Report of the Bureau of Animal Industry, 

1895-6, p. 143- 



454 FOOT AND MOUTH DISEASE 

5. Walley. The four bovine scourges. 1879. 

6. WllvHELMS. Memoire sur la peripneumonie epizootique du 
betail, 1852. 



FOOT AND MOUTH DISEASE 

Synonyms. Eczema epizootica ; epizootic aphtha ; vesi- 
cular aphtha ; vesicular epizootic ; aphthous fever ; murrain ; 
cocotte ; MaiU-iind Klaue7iscnche. 

§ 358. Characterization. Foot and mouth disease is 
a highly infectious disease of animals. It is determined by 
the eruption of vesicles in the mouth, around the coronet of 
the foot, on the udder and between the toes. It is said to be 
more common among cattle, but swine are quite susceptible ; 
sheep, goats, horses, dogs, cats and fowls are said sometimes 
to be attacked. The human species is also susceptible. Peo- 
ple may be infected by drinking the unboiled milk of animals 
suffering from the disease. The mortality is not high. 

§ 359- History. Foot and mouth disease was quite 
accurately described in the eighteenth century. \'ery destruc- 
tive outbreaks are reported in 1809 and in the early part of the 
nineteenth century it was the source of much loss in southern 
Europe. In 1883, Great Britain lost heavily from its ravages. 
In 1892, Prussia is reported to have had 8,000,000 cattle 
affected. It was during the years 1890 and 1893 that the last 
severe epizootic appeared in Germany. 

§360. Geographical distribution. This disease seems 
to be very largely restricted to Europe, although it has been 
introduced into almost every cattle raising country. In 1870, 
it was brought to the United States from Canada. At that 
time it spread into New York and New England. It appears 
that this disease was mild and its spread was quickly and 
easily checked. This according to Law was accomplished so 
easily because the cattle were in winter quarters. In 1880, a 
few infected animals were brought to the United States, but 
the disease did not extend bevond the animals introduced. In 



ETIOLOGY 455 

1884, there was a small epizootic at Portland caused by 
imported cattle. 

The most serious outbreak in the United States was in 
1Q02. The first herds affected were at Chelsea, Mass., in the 
vicinity of the docks, to which place the infection was probably 
carried from shipping. It is not known exactly how the infec- 
tion was introduced, but it is highly probable that it came 
through some one of the many possible channels other than 
infected imported cattle. In this outbreak, the disease ap- 
peared in Massachusetts, New Hampshire, Vermont and 
Rhode Island. A total of 4.712 cattle were affected. The 
comparative freedom of the United States from this disease is 
attributed to the enforcement of rigid quarantine measures. 

§ 361. Etiology. The specific cause of foot and mouth 
disease has not been clearly demonstrated. It has been shown, 
however, that it is caused by a specific infection and that 
every outbreak starts from some previous case or cases. The 
virus is contained in the eruptions and given off from the 
mouth and feet, causing its wide distribution. Loeflfler and 
Frosch have shown that the cause— presumably a germ of 
some form-would pass through a Berkefeld filter. Uater 
Loeffler showed that it did not pass through the finer kitasato 
filter Animals may be infected directly by coming in con- 
tact with the disease, or indirectly by being exposed to the 
virus in stables, cars or other places recently occupied by 
infected animals. It is stated that the virus is destroyed in a 
short time by drying, but some writers maintain that it wiU 
persist for several months. Penberthy states that under ordi- 
nary circumstances the virus does not retain its effectiveness 
lono- Animals that have passed through the disease may 
carry the virus for several months. The infected matter may 
be carried on the clothing or hands of human beings and thus 
be transmitted to animals or men. Milk is often the carrier of 

the virus. 

The period o/mcHbatwn\ss\mn,iron\ 2^ io -2 hours in 

inoculated cases. It may be longer than this. 



456 FOOT AND MOUTH DISEASE 

^ 362. Symptoms. The symptoms of foot and mouth 
disease vary greatly in different epizootics, sometimes they are 
quite mild and at others very severe. The first evidence of 
the disease is a rise of temperature which in cattle rarely 
exceeds 104° F. The mucous membrane of the mouth becomes 
reddened, the appetite is diminished, and rumination ceases. 
The mouth is usually kept closed and the quantity of saliva is 
increased. A smacking sound is not infrequently made by the 
animal. These symptoms are chiefly due to the pain accom- 
panying the disease in the mouth. After two or three days 
the eruption appears. This consists of small yellowish-white 
vesicles or blisters, varying in size from a hemp seed to a pea, 
on the gums and inner surface of the lips, the inside of the 
cheeks, the border and the under surface of the tongue. Thej' 
may become half an inch or more in diameter. In some cases 
the back of the tongue may be the seat of large blisters. 

These vesicles burst soon after their appearance, some- 
times on the first day. More rarely they may persist for two 
or three days. After they have ruptured the grayish-white 
membrane forming the blister may remain for a day or more 
or disappear speedily and leave deeply reddened areas or ero- 
sions which are very painful. These exposed areas may soon 
become covered again with the normal epithelium or they may 
be converted into ulcers. In this stage the saliva forms in 
large quantities and hangs in strings from the mouth. In 
eight to fourteen days the disease may have entireh' disap- 
peared. 

In addition to the changes in the mouth, one or more feet 
may become diseased. The skin around the coronet and in 
the cleft between the toes becomes hot and tender and may 
swell. Blisters appear as in the mouth, but they are speedily 
ruptured and the inflamed, exposed areas are covered with a 
viscid exudate. 

The udder, more particularly the teats, may be the seat of 
lesions. Some authorities regard the udder di.sease merely as 
the result of infection during milking. The vesicles are 
broken by the hands of the milker and the teats become cover- 



MORBID ANATOMY 457 

€d with reddened areas deprived of the superficial layer of the 
skin and are very tender. The healing, however, goes on 
quite rapidly. The milk is said to be somewhat changed in 
appearance and unfit for making butter or cheese. These are 
the main symptoms accompanying the uncomplicated cases of 
foot and mouth disease. In all such cases recovery is usually 
rapid and complete. In certain other cases, however, compli- 
cations arise which are not only injurious but may be fatal. 
Thus the mouth lesions may be accompanied by nasal catarrh 
or pneumonia. The feet may become very much swollen and 
the inflammation and suppuration extend to the tendons and 
bones, resulting in the loss of the hoof. Such cases are usual- 
ly fatal. Asa result of the general affection young calves may 
succumb to a secondary inflammation of the stomach and 
bowels and older animals ma\- abort or suffer from inflamma- 
tion of the udder. 

The duration of the disease \\\ uncomplicated cases varies 
from 10 to 20 days. When complications occur either with 
the regular course or as sequelae the duration becomes indefi- 
nite. The mortality varies with the severity of the attacks, 
the age and condition of the animals and the treatment. 
Ordinarily the mortality is not high, excepting in very young 
animals. 

v^ 363. Morbid anatomy. The tissue changes found at 
post-mortem vary to a marked degree. There are in certain 
cases hyperemia and edema, catarrh of the nares and mucosa 
of the lungs and dilatation of the heart. There may be fatty 
degeneration and hemorrhagic infarcts in the heart muscle. 
In other cases there is severe gastro- enteritis with intestinal 
hemorrhage. In the stomachs of cattle oval reddish areas 
which ultimately form ulcers appear. These often become 
confluent. The involved portion of the mucous membrane 
becomes thickened. The areas of necrotic tissue in which the 
ulcers appear become surrounded by a reddish line of demar- 
cation which, in the healing process, forms a cicatrix. The 
lesions on the mucous membrane rarely extend deeper than 



45^ FOOT AND MOUTH DISEASE 

the mucosa. Ulcers of a nature similar to those found in the 
stomach occur in the intestines. On the feet inflammations 
may follow the simple vesicles about the coronet. These may 
extend deep into the tissues, pass under the hoof and cause it 
to slough off, extend into the bone producing necrosis or 
permanent arthritis. It is stated by some authorities that in 
the mild non- fatal cases the obvious lesions are so slight that 
frequently they escape notice. In sheep and swine the lesions 
are more frequently restricted to the feet. 

The period of dicratkni oi \h& d\SQ2ise \3ix\es from 9 to 14 
days. The immunity resulting from a natural course of the 
disease is placed by Penberthy as being brief, probably not to 
exceed six months. 

S 364. Differential diagnosis. Foot and mouth dis- 
ease must be differentiated from (i) various forms of stoma- 
titis caused by different fungi and often referred to as sporadic 
aphthae, (2) from stomatitis due to drugs and injuries, (3) 
from actinomycosis of the tongue and (4) from variola. It 
must also be differentiated from simple cellulitis, often of 
streptococcic origin, in the subcutaneous tissue about the 
coronet and from the sloughing of the hoof resulting from the 
extension of the inflammatory process, and from eczemas due 
to dietary causes. The means of differentiating these must be 
found largely in the history of the cases and in the study of 
the nature of the lesions themselves. 

§ 365. Prevention, Preventive inoculations do not 
seem to have given satisfactory results. The isolating of the 
diseased animals and the placing of the well ones in non-in- 
fected fields and stables tend very largely to the checking of 
the spread of the disease. The milk of the diseased animal 
should be sterilized before it is used. 

In England the slaughter of infected animals has fre- 
quently been resorted to in recent years to stamp out the dis- 
ease. In the recent outbreak in the United States, the prompt 
destruction of all infected and exposed animals proved to be 
very satisfactory. The failure in the past to control the dis- 



ClIAKACTKRIZATION 459 

ease in Europe bv quarantine and disinfection necessitated the 
radical measure of slaughter of infected and exposed animals 
in order to eliminate the disease from our country. 

Loeffier has recently produced artificial immunity against 
this infection by a method which promises to be successful for 
practical immunization. 

REFKRRNCKS. 

1 Coi'K Foot and mouth disease. Re.poU, 7th International 
Congress of Vet. Surgeons. Iladcn Baden, Vol. I (1899), P- '84. 

2 LOEFFLER UND Frosch. Berichte der Komniission x.ur Erfor- 
schung der Maul uud Klaueuseuche bei dem Institut fUr Infektious 
Krankheiten in Berlin. Cent, f BaM. Bd. XXIII (.898), S. 37i- 

3. LOEFFLER. Ibid, Bd. XXIV (1898), S. 569- 

4 LOEFFLER. Ein neuer Verfahren der Schut/.impfung gegen 
Maul und Klauenseushe. Munch. Med. II 'oc/iensc/ir., 1906. S. 1036. 

5. PENBERTHV. Foot and mouth disease. Jour. Comf. Path, 
and T/iera., Vol. XVI ( 1901), p. 16. 

b P..-TERS Foot and mouth disease. Second Semi-annual 
Report of the Chief of the Cattle Bureau. Mass. State Board of Agric. 

1903. P- 321- , ,, C /I A/ ^Z- 

7 SALMON- Foot and mouth disease. Year hook U. S. Dcpt. oj 
Agric. "1902. p. 643. Ibni. Annual Report Bureau of Animal 
Industry, 1902, p. 391. 

8. W.\LLEY. The four bovine scourges. 1879- P- ^i- 



RABIES 

Synonyms. Hydrophobia ; canine madness ; lyssa; Rage ; 
Tolhvnt ; Wutkrankheit. 

§ 366. Characterization. Rabies is an acute infectious 
disease transmitted from animal to animal or from animal to 
man bv the bite of the rabid individual or by direct inocula- 
tion It is not known to be contracted or tran.smitted in any 
other manner. It is characterized by a long and variable 
period of incubation, followed by symptoms referable to the 
nervous svstem, lasting from one to ten days and ending in 



460 RABIES 

paralysis and death, without recognizable gross anatomical 
changes. 

The dog is the animal most commonly affected, although 
all of the canine and feline races seem to suffer from rabies 
more than other species. All warm blooded animals appear to 
be susceptible. It is a serious disease in man, cattle, sheep, 
horses and swine. An explanation for its greater frequency 
among dogs is found in their tendency to bite. A very large 
percentage, in fact nearly all, of the cases in man and in the 
domesticated animals are caused by inoculation from the bites 
of rabid dogs. 

§ 367. History, Rabies was described by Aristotle in 
the fourth century B. C. Rewrote. "Dogs suffer from mad- 
ness that puts them in a state of fury, and all the animals that 
they bite, when in this condition, become also attacked by 
rabies." Cornelius Celsius, who lived in the first part of the 
Christian era, seems to have been the first to refer to human 
rabies and to employ the term "hydrophobia." 

The transmission of the disease by wolves to man was 
recorded in 159 1. In 1803, and for a number of years follow- 
ing, it was epizootic among foxes in Southern Germany and 
Switzerland. 

During the latter part of the eighteenth and the beginning 
of the nineteenth century the disease extended over Europe 
and about this time it appeared in America. The first out- 
break in this country was reported from Boston in 176S. In 
1770 and 1 77 1 it was observed in dogs and foxes in the vicinity 
of Boston ; in the year 1779 it appeared in Philadelphia and 
in the state of Maryland ; in 1785 it was prevalent throughout 
the Northern States and soon after it spread to the Southern 
States. During the last century it has caused heavy losses 
among farm animals throughout E^urope and America. 

It has called forth careful study from many of the ablest 
men in the medical professions. Among them may be men- 
tioned John Hunter in England, Viborg in Copenhagen, Wal- 
dinger in Vienna, Hertwig in Germany and Pasteur in France. 



GEOC.RU'HICAI. DISTRIHUTION 46 1 

Without detracting in the least from the great work of other 
investigators, we may say that to Pasteur and his co-laborers, 
Nocard'and Roux, we owe much of the knowledge ot the 
nature of rabies which we possess at the present time. 

ii 368. Geographical distribution. Rabies is known 
to exist in almost every country on the globe. Australia is 
the largest area which is said to be absolutely free from it. 
This exemption is the gratifying result of a rigid quarantine 
enforced against dogs imported on that island. Rabies is very 
common in France, Belgium and Russia. In the latter 
country it is perhaps more often seen in wolves than in any 
other part of the world. In Holland, Denmark and Sweden it 
is very rare. In England, it has from time to time been wide- 
spread, but at present it is practically eradicated. Salmon 
has found that rabies exists in nearly every part of the United 

States. 

Inquiries which the writer has made during the last tew 
years, by verifying current newspaper reports of rabies, show 
that the larger number of cases come from certain districts in 
which the disease seems to have become established. Newly 
infected districts are constantly springing up, due presumably 
to the introduction in some manner of an infected dog. 

The prevalence of the disease cannot be accurately deter- 
mined, as there are no reliable statistics concerning it. 
Ravenel has reported that the State Live Stock Sanitary Board 
of Pennsvlvania has investigated 82 cases of rabies since 1897. 
Of these there were 58 dogs, 4 horses, 17 cows, i cat and 2 
human beings. During i90o-'o4 the New York State Veteri- 
nary College investigated 64 cases of rabies, of which 47 
were in dogs, 11 in cattle, 2 in horses, i in sheep, i in swine, 
and 2 in men. In 1907 a much larger number of cases were 
presented for diagnosis. Salmon states that in the District of 
Columbia from 1893 to August 1900 rabies has been positively 
diagnosed in animals in 91 cases. These consisted ot 80 dogs, 
5 cows, 2 horses, 2 foxes and 2 cats. In addition to these the 
records of the health department of the District of Columbia 
show that since 1874 there have been seven deaths from rabies 



462 RABIES 

in the human species. These illustrations from the experi- 
ences of a few laboratories could be duplicated from the records 
of many others. 

In Europe the disease seems to be more prevalent. In 
1898 the official reports show 1,202 cases of rabies in animals 
(most]}' dogs) in German}-. In 1899, 2,374 rabid animals 
were reported from France and 444 cases from Belgium. 



Fig. 1 10. A draiL'ing from a section of a rabid brain, s/ioiuttig large 
nerve cells containing Negri bodies, {a) Nerve cell, {b) nucleus of 
nerve cell, [c) Negri bodies. Much enlarged. 

§ 369. Etiology. Although rabies has long been recog- 
nized as a specific disease, its primary etiological factor has but 
recently been discovered by Negri in the brain and spinal cord 
of the affected animal. In certain instances the presence of 
the virus has been reported in the salivary glands, pancreas 
and milk. It has not been found in the blood. 

In 1903, Negri, of the University of Pavia, described 
small bodies or cell inclusions, since called Negri bodies, which 
he found in the Purkingie cells of the cerebellum and in the 



ETIOLOGY 4^13 

large ganglion cells of the Amnions horn. Negri believed 
these bodies to be the etiological factor of the disease and clas- 
sified them among the protozoa. 

He believes the bodies are specific microorganisms which 
are characteristic of the disease, found only in animals affected 
with rabies. They appear early in the course of the disease. 
They occur in larger numbers and are of greater size as the 
disease progresses. They are most numerous and largest at 
the time of death. Smears or sections are stained in saturated 
alcoholic solution of eosin for from 10 to 30 minutes after which 
they are counter-stained in alkaline methylene blue. No 
special technique is necessary to demonstrate these bodies. 
Their constant appearance in cases of rabies forms a basis for a 
positive opinion and diagnosis and they are affected very little 
by beginning decomposition of the surrounding nervous tissue. 

Williams and Lowden state concerning the channels of 
infection that "in whatever way the virus enters the body, so 
far as we know, there is no development of the organism, or 
none, to any appreciable extent, until it reaches the central 
nervous system, and not until after a certain amount of deve- 
lopment there does it infect the peripheral organs. Before the 
disease was well studied it was thought that the salivary glands 
were the chief site of the infection. But it has been shown 
that these glands are not always infective, and when they are, 
not until comparatively late in the disease and that when the 
virus is inoculated into tUem, the animal .seldom comes down 
with the disease and probably never if the centripetal nerves 
are cut (Bertarelli). This means that the parasite does not 
grow in the salivary glands, that it is only carried there inci- 
dentally by its spread from the central nervous system along 
the nerve branches. That the organisms escape into the blood 
and are carried in this way in small numbers is shown by the 
fact that the blood in large quantities has been found infective 
(Marie). Principally by the nerve channels, secondarily by 
the blood and lymph channels, the organisms are carried in 
small numbers to all parts of the body. With other investiga- 
tors, we have found the suprarenal cepsules infective." Their 



464 RABIES 

conclusion relative to the nature and diagnostic value of the 
Negri bodies are as follows : 

1. The smear method of examining the Negri bodies is 
superior to any other method so far published for the follow- 
ing reasons : (a) It is simpler, shorter and less expensive ; (b) 
The Negri bodies appear much more distinct and characteristic. 
For this reason and the preceding one, its value in diagnostic 
work is great ; (c) The minute structure of the Negri bodies 
can be demonstrated more clearly ; (d) Characteristic staining 
reactions are brought out. 

2. The Negri bodies are shown by the smears as well as 
by the section are specific to hj'drophobia. 

3. Numerous "bodies" are found in fixed virus. 

4. "Bodies" are found before the beginning of visible 
symptoms — i. e., on the fourth day in fixed virus, on the 
seventh day in street virus, and evidence is given that the}' 
may be found early enough to account for the appearance of 
infectivity in the host tissues. 

5. Forms similar in structure and staining qualities to 
the others, but just within the limits of visible structure at 
(1,500 diam. magnification) have be seen. Such tiny forms, 
considering the evidence they give of plasticity, might be able 
to pass the coarser Berkefeld filters. 

6. The Negri bodies are organisms belonging to the class 
Protozoa. The reasons for this conclusion are : (a) They 
have a definite, characteristic morphology ; (b) This morpho- 
logy is constantly cyclic, i. e., certain forms always predomi- 
nate in certain stages of the disease, and a definite series of 
forms indicating growth and multiplication can be demon- 
strated ; (c) The structure and staining qualities as shown 
especially by the smear method of examination resembles that 
of certain known Protozoa, notably of those belonging to the 
sub-order Microsporidia. 

7. The proof that the "Negri bodies" are living organ- 
isms is sufficient proof that they are the cause of hydrophobia ; 
a single variety of living organisms found in such large num- 



ETIOLOGY 465 

bers in every case of a disease, and only in that disease, 
appearing at the time the host tissue becomes infective in 
regions that are infective, and increasing in these infective, 
areas with the course of the disease, can be no other, accord- 
ing to our present views, than the cause of that disease. 

The Negri bodies or cell inclusions vary in shape. The 
most common forms are round or oval. The round bodies are 
from .5 to 231.1 in diameter, while the oblong ones vary from 
.5 to 15// to 5 to 2J/1. The round or oval forms are by far the 
most common. Irregular forms are occasionally seen. In 
preparations stained with eosin and methylene blue they ap- 
pear as bright red bodies containing one or two nuclear-like 
structures which are surrounded by a number of other small 
circular, regular bodies. They are said to preserve their form 
even when the brain tissue has undergone marked degenera- 
tive changes, after prolonged immersion in glycerin and after 
several days' drying. A number of workers report finding 
them quite uniformly. Schuder does not consider them as 
the cause, largely because his virus passed through a filter that 
retained the cholera spirillum. 

Remlinger and Riffat-Bey found that the virus would 
pass through a Berkefeld filter "V," but its passage was not 
constant, as rabbits inoculated with the filtrate did not all die 
of rabies. The filter which he used held back the organism 
of chicken cholera, which was used as a check on the filter. 
Remlinger more recently stated that the virus will pass through 
the more porous Berkefeld filter only. The firmer Berkefeld 
and Chamberland filters keep the virus back. 

Babes states that the Negri bodies are not always present. 
He seems to consider them as a result of the local reaction of 
the cells to the cause of the disease. 

i^ 370. Method of invasion. When introduced into an 
animal either experimentally or by the bite of a rabid dog, the 
virus remains for a time without producing either local or 
general symptoms. The period of incubation varies withm 
quite wide limits. The virus penetrates the nervous system 
bv following the nerve trunks from the site of infection to the 



466 RABIES 

spinal cord, then through the spiual cord to the brain. This 
has been proven by inoculating an animal in one of the legs 
with virulent material. After a suitable time, but before the 
symptoms of rabies appear, the virus will be found, on killing 
the animal, in the nerves of the limb, and even in the part of 
the spinal cord into which the nerve enters, while the upper 
part of the cord and the brain are still uninfected. This ex- 
plains the fact why the earliest symptoms, both in man and 
animals, such as itching, tingling, numbness and other nerv- 
ous sensations, often appear in the part of the body which re- 
ceived the virus. In the case of a bite about the face and 
head the route along the nerve to the central nervous system 
is much shorter. While the nerves seem to form the main 
route by which the virus travels, the circulation may at times 
assist, especially in small animals. Inoculation into the large 
nerve of the leg is almost as certain to produce the disease, as 
inoculation directly into the sub-dural space, while injection 
beneath the skin of the leg is not so sure. Nicholl finds that 
the virus passes from the point of infection to the brain ex- 
clusively through the nerves. He also finds that it is rapidly 
destroyed in the blood. 

Resistance of the virus. The action of the virus is de- 
stroyed b}' drying and by the action of light. In dry air, pro- 
tected from light and putrefaction, the virulence of the spinal 
cord of rabbits is destroyed in fourteen to fifteen days. When 
spread in thin layers it is entirely destroyed by drying in from 
four to five days. Sunlight destroys it in about forty hours. 
The loss of virulence by drying is gradual but quite regular, 
which fact was taken advantage of by Pasteur in the prepara- 
tion of his vaccine. The virus may be preserved in neutral 
glycerin at ordinary temperature for a long time. Roux found 
that after four weeks in glycerin at 30° C. , the virus in a rabid 
brain had the same power as when perfectly fresh. The writer 
has found that rabbits inoculated with rabid brains that had 
been kept in glycerin from three to four weeks did not develop 
the di.sease as quickly as those that were inoculated with the 
freshly removed brain. 



PERIOD OF INCUBATION 467 

It is quite resistant to putrefaction. Galtier found the 
virus active in the central nervous system of rabbits that had 
been buried for twenty-three days, of sheep buried thirty-one 
days and of dogs buried forty-four days. Other observers have 
found it still active in animals buried for twenty-four days. 

It is destroyed completely by a temperature oif 50° C. in 
one hour or 60° C. in one-half hour. It is uninjured by ex- 
posure to extreme cold, resisting the prolonged application of 
a temperature from 10 to 20° C. below zero. 

Its activity is destroyed in one hour by a five per cent, 
solution of carbolic acid, or by a i to 1,000 solution of corro- 
sive sublimate. Water saturated with iodine destroys it in 
ten minutes. 

§ 371. Period of incubation. The period of incuba- 
tion is quite variable, depending on the site of the wound, 
whicli is almost always a bite, the amount of virus introduced 
and its virulence. In general it may be said for all animals 
that the period of incubation seldom exceeds sixty days, al- 
though in man and in some larger animals, it sometimes, 
though very rarely, reaches one year. A few cases of a longer 
period have been reported. The average period as given by 
Ravenel is as follows : 

In man, 40 days. 

In dogs, 21 to 40 days. 

In horses, 28 to 56 days. 

In cats, 14 to 28 days. 

In pigs, 14 to 21 days. 

In goats and sheep, 21 to 28 days. 

In birds, 14 to 40 days. 

In rabbits inoculated subdurally with the brain from rabid 
animals, the writer has found the period of incubation to vary 
from 12 to 62 days and the duration of the disease to range 
from a few hours to three days. Westbrook reports a period 
of incubation in rabbits to extend in one case over a hundred 
days. In the disease as it is naturally contracted from the 
bites of rabid animals, the period of incubation varies with 



468 RABIES 

reference to the location and extent of the bites. If the indi- 
vidual is bitten about the head the period of incubation is 
much shorter than if the injuries are on the extremities. 

In the dog, the period of incubation in 144 cases was 
clearly determined by Peuch. His table with the addition of 
percentages is appended. 

PERIOD OF INCUBATION OF RABIES IN THE DOG. 



Number of days of 
incubation. 


Number of 

cases. 

3 


Per cent. 




5 to 


10 


2.0S 




10 to 


15 


8 


5-55 




15 to 


20 


13 


9-03 




20 to 


25 


25 


17.36 




25 to 


30 


13 


903 




30 to 


35 


25 


17-36 




35 to 


40 


6 


4.17 




40 to 


45 


II 


7-64 




45 to 


50 


9 


6.25 




50 to 


55 


4 


2.78 




55 to 


60 


2 


1-39 




60 to 


65 


7 


4.86 




65 to 


70 


I 


.69 




70 to 


75 


5 


3-47 




Soto 


90 




4.86 




100 to 


120 


4 


2.78 




365— 


tal 




.69 




Toi 


144 



The somewhat popular opinion that most of the cases of 
rabies occur in the summer, especially in "dog days," is not 
founded upon facts. Rabid dogs are nearly if not quite as 
numerous in winter and early spring as in summer. Salmon 
has collected 14,066 cases of rabies in dogs with the months 
in which the disease occurred. The results are exceedingly 
interesting as the appended table shows. 



SYMPTOMS 469 

CASES OF RAHIKS IN DOGS, BV MONTHS. 

^ , ~ -^ ' V. >> = >■ M a ^ ^ s i "S 
Source 5,,^ g ^ ?. ^ — . ^tcloSS Q H 

^^......89.55.53 .84 ;8, -9 ;57 X47 ;33 -IjoS Jg ;6,. 

IsgS :::::: 139 M8- I8.^^_)85_i77_^-^^3_|54_i78i 
Total .___ ^ ^ 960 7^^ M^ 1467 1435 1294 1 145 965 933 ii37 14066 

§ 372 Symptoms. Rabies is generally divided into 
two forms, furious and dumb. In the first the animal is irri- 
table, aggressive and bites nearly every object which comes m 
its way • in the second the muscles of its jaws are paralyzed 
almost from the beginning and being unable to bite the ani- 
mal remains more quiet and tranquil. Essentially the two 
forms of the disease are the same, but probably owing to the 
parts of the brain attacked or the acuteness of the attack or 
both paralysis appears much sooner in the dumb form than in 
the other. The saliva from a case of dumb rabies is just as 
dangerous and virulent as that from a case of furious rabies. 
Dogs affected with dumb rabies are less dangerous simply be- 
cause thev are unable to bite and thus to infect others. 

Dumb rabies and furious rabies do not always represent 
two distinct tvpes of disease. The typical cases belong to the 
two extremes'of symptoms and there are always graduations 
between them. In fact, almost every case of furious rabies 
sooner or later changes to the dumb form, that is, the final 
stage of the disease is almost invariably paralytic In the 
typical development of the dumb form, the paralysis occurs on 
the first day of the disease. It may not appear, however, 
until the second or third or even a day later. 

A-ain a dog does not necessarily bite everything about it 
even iflt has rabiesand its jaws are not paralyzed. It may be 
combative and furious all of the time or only part of the tune. 



470 RABIES 

or not at all. There is perhaps no other disease in which the 
symptoms may vary more than in rabies of the dog. 

Furious rabies. The symptoms appear very gradually. 
The animal's habits and behavior are changed. It may be 
more restless or affectionate than usual, seeking to be near its 
master or mistress, fawning, licking the hand or face and 
apparently seeking sympathy and assistance. Such caresses 
are, however, extremely dangerous, for the animal's tongue, 
moist with virulent saliva, coming in contact with a part 
where the skin is thin, abraded or wounded, may fatally infect 
the person to whom it is endeavoring to demonstrate its affec- 
tion. The reported cases in which rabies have developed from 
such inoculations are quite numerous. 

In most cases dogs first become dull, gloomy, morose, 
seeking solitude and isolation in out-of-the-way places or retir- 
ing under pieces of furniture. But in their retirement they 
cannot rest, they are uneasy and agitated, they lie down and 
assume the attitude of repose, but in a few minutes they are 
up walking about "seeking rest, but finding none."" Occa- 
sionally this restlessness may disappear for a time and the 
animal becomes lively and affectionate ; oftener it sinks into a 
sullen gloominess from which even its master's voice rouses it 
but temporarily. At this period dogs may have aberrations of 
the senses which cause hallucinations and lead them to think 
they are being annoyed by something or that some animal or 
person is endeavoring to injure them. They crouch ready to 
spring upon the enemy ; they rush forward and snap at the 
air ; they throw themselves, howling and furious, against the 
wall as though they heard sounds beyond it. 

While at first the affected dog may not be disposed to bite, 
it becomes more dangerous as its hallucinations and delirium 
increase. 

The disturbance of the sensations leads to chills and itch- 
ing. If the place where the bite occurred is acces.sible, the 
dog licks the scar and later may bite and tear the tissues. In 
this case it bites into its own flesh with apparent pleasure and 
satisfaction. Food is taken at first if it is something that can 



SYMPTOMS 471 

be swallowed without mastication, otherwise it is soon drop- 
ped. Difficulty in swallowing is an early symptom. Mad 
dogs have no fear or dread of water, they continue to drink 
until paralysis prevents them from swallowing. 

When the furious symptoms appear, the dog may leave 
his home and start upon a long chase with no apparent object 
in view other than to be traveling. He trots at a rapid pace, 
eyes haggard and tail depressed. He is indifferent to the sur- 
roundings. He often flies at and bites persons whom he 
meets, but usually he does not search for them or even notice 
them if they remain quiet. Dogs in this condition may travel 
many miles and finally drop from exhaustion and die. Often 
after an absence of a day or two they return to their homes, 
exhausted and emaciated, presenting a most forlorn and mis- 
erable appearance. Those who have pitj' for such an animal 
and try to make it clean and comfortable are in great danger 
of being bitten, as the di.sease has advanced to a point where 
the delirium or insanity is most marked and where a treacher- 
ous bite is most common. 

If the animal, instead of being allowed to escape, is kept 
confined, the paroxysms of fury are seen to occur intermit- 
tentl)' or, in the absence of provocation, the}' may be entirely 
wanting. If excited it howls, rushes upon objects that are 
thrust toward it or throws itself against the bars of its cage 
and bites with great fury. 

As death approaches the animal becomes exhausted and 
is .scarcely able to stand. The eyes are dull and sunken and 
the expression is that of pain and despair. Paralysis appears 
in the jaws or in the posterior extremities and extends rapidly 
to other parts of the body. The animal, being unable to 
stand, lies extended upon its side, the respiration becoming 
more and more difficult. There are spasmodic contractions of 
certain groups of mu.scles, complete prostration and finally 
death. 

The usual course of the disease is four or five days. It 
may be as short as two or as long as ten days. 

Dumb rabies. When this form of the disease is typical, it 



472 RABIES 

comes on with restlessness, depression, a teudencj^ to lick 
objects and paralysis of the muscles which close the jaws. As 
a consequence of the paralysis, the lower jaw drops, the 
animal is unable to close the mouth, the tongue hangs out and 
an abundance of saliva escapes. The mucous membrane of 
the mouth becomes dry, discolored and covered with dust. 
The animal remains quiet, it does not respond to calls and 
appears to understand its helplessness. Bouley states that the 
animal cannot bite and does not desire to bite. When dumb 
rabies follows the furious form, the desire and tendency to bite 
may be retained even after the jaw is paralyzed. 

The course of the disease is short, death usually occurring 
in from two to four days. 

§ 373. Morbid anatomy. One of the striking charac- 
teristics of rabies is the absence of constant, recognizable 
lesions. The mucosa of the pharynx and larynx are con- 
gested. The spleen is sometimes enlarged and dark colored. 
In dogs the stomach often contains a variety of foreign matter 
such as earth, stones, pieces of iron, bits of leather, wood, etc. 
Axe reports finding such foreign substances present in 90 per 
cent, of 200 cases he examined. Galtier reports such findings 
in from 50 to 70 per cent. In experimental animals and cattle 
the writer has rarely found them. It seems to be true that 
the obvious lesions are not constant and it is probable that 
the pronounced changes occasionall}^ found in a single organ 
are accidental or secondary rather than primarily related to 
the disease. The lesions in the brain and spinal cord are 
likewise variable. In some cases there is a marked hyperemia, 
while in others the brain appears to be normal. 

Certain investigators, however, have found histological 
changes which to their minds have been pathognomonic of the 
disease. The close simulation of the nervous lesions to those 
due to other diseases, and the possibility of greater or less 
post-mortem changes will foster an element of doubt in the 
minds of the majority of working histologists. This doubt in- 
stead of diminishing shows a tendencv to grow when a review 



MORIUD ANATOMY 473 

is taken of the conflicting results and opinions held by those 
who have already inv^estigated this field. It also appears that 
some portions of the nervous system may exhibit lesions of a 
pronounced character, other portions very slightly, and still 
others none at all, thus presenting additional difficulties. 

One of the most common lesions that has been observed is 
of an inflammatory character, the congested blood \essels fre- 
quently showing diapedesis and, according to some, a perivas- 
cular exudation of a granular or a hyaline substance. Hypere- 
mia and lymph-stasis, although of not so much significance 
when taken by themselves, have been taken into consideration 
along with other changes. The blood vessels quite as much 
or even more than the nerve structures have been noted as 
the focus of some of the most marked changes, among which 
are the proliferation of the epithelial cells and of the connect- 
ive tissue elements of the outer coat, with the infiltration of 
lymphoid cells. Such lesions may be nodular primarily, but 
later become diffuse. The inflammatory process may progress 
to such an extent as to obliterate certain vessels. 

Pathological miliary centers have been noted not only in 
the axial portions of the nervous system, but in the gray 
matter as well. These centers were formed by lymph cells 
which accumulate notably around the blood vessels T perivas- 
cular) and the nerve cells (pericellular) as well. The lesions, 
when present, are observed most frequently in the motor 
centers of the oblongata and spinal cord. 

The following observations were made by Babes, in 1887 : 

1. "In animals dead from street rabies there are found 
usually a hyperccmia and an acute generalized oedema of the 
cerebral meninges, acute hemorrhages localized around certain 
vessels, as well as inflammatory lesions. On microscope exam- 
inations we find an increase of the plasma cells, augmentation 
of the reticular substance, fibrinous in character, between the 
several layers of the meninges. 

2. " The epithelium of the cerebrospinal central canal 
has proliferated. In the gray matter which surrounds the 



474 RABIES 

canal, and especially in that of the floor, hemorrhages, some- 
times symmetrical, are often found. Microscopically, we often 
find an obliteration or thrombosis of a vessel by a reticulated, 
hyaline, pigmented material or by leucocytes or hyaline glob- 
ules, and sometimes a hyaline degeneration or even inflamma- 
tion of the vascular tunic. The extravasated blood also con- 
tains much of the hyaline material. The hemorrhages are 
often limited by the lymphatic sheath of the vessels. At the 
same time the epithelium of the ventricles and central canal 
may be partially lost. This last is occasionally filled with 
blood or plugs, either granular or hyaline in character. 

3. " With the naked eye small centers of degeneration 
may sometimes be noted in the gray matter, but often they 
may be sought for in vain. 

4. " The most constant lesions are microscopic in char- 
ter ; they are found more especially in the gray matter sur- 
rounding the cerebrospinal canal and in the motor centers of 
the medulla and spinal cord. These lesions consist at first in 
hypersemia and accumulations of embryonic cells around the 
small vessels, perithelial or migratory in origin, often showing 
indirect division ; finally there are also found lesions of nerve 
cells. 

5. " The lesions of the nervous elements of the parts in- 
dicated is quite characteristic ; it consists of signs of prolifera- 
tion, namely, in the presence of several small cells in place of 
one large one, or in a uniform degeneration and often in the 
appearance of vacuoles with a reduction in size or disappear- 
ance of the nucleus, pr again, its chromatic network disap- 
pears. These cells frequently contain pigment. Round uni- 
nuclear, more rarely multinuclear, elements of a lymphatic 
origin often invade the protoplasm even of the cell and fill out 
the dilated pericellular lymphatic spaces by a multiplication ot 
small nuclei. 

6. "The lesion of medullary substance is less pro- 
nounced, it consists chiefly of an edema of the medullary 
sheath of the nerve fibers. 



MORBID ANATOMY 475 

7. "In certain plasma cells, in the interior of and around 
vessels, sometimes in leucocytes, in lymphatic spaces, in the 
altered parts of certain nerve cells, and in the dilated sheath 
of nerve fibers may be seen round or ameboid granules about 
I A' in diameter, pigmented or stainable by aniline dyes, and 
which in part seem to possess the power of movement. " 

More recently Babes has noted, besides the lesions above 
mentioned, that the alteration of the nerve cells is usually 
accompanied by a modification of their protoplasmic network 
and concludes that "Whilst admitting that the lesions of rabies 
are not absolutely characteristic, and that it may be that in a 
case of diffuse, very acute myelitis similar lesions may be 
found, it is necessary all the same to state, that neither in 
writing nor in my personal experience have I ever met with a 
similar case, so that at present we may consider the lesion ot 
rabies as characteristic. In other infectious diseases there 
have also been found histological lesions characteristic as a 
whole, although composed of elements not absolutely specific.'* 
Golgi draws attention to the following morbid changes in 
rabies : 

(i) Changes in the structure of the nucleus, all the vari- 
ous phases of karyokinesis may be simulated, yet no true 
nuclear division may take place. (2) Changes in the body of 
the cells, such as vacuole formation, bladder-like transforma- 
tion of the cells. Changes may also be recognized by methods 
directed to the study of the outer form of the cell. Here 
varicose appearances of the cell processes may be seen. 
Granular fatty changes may also be present. An important 
change lies in the displacement of the nucleus. The periphery 
of the cell becomes homogeneous. CUanular fatty changes 
are also seen in the neuroglia cells. (3) Changes in the inter- 
vertebral ganglia. The author would look upon these ana- 
tomico pathological changes found by him as characteristic, 
while here not only the sum total of the changes, but also 
their order of occurrence and mutual interdependence are taken 
into consideration. 

The morbid process is parenchymatous encephalo-myel- 



476 RABIES 

itis, of which the exact exciting cause is as yet unknown. The 
changes are thus grouped: (i) appearance of nuclear chro- 
matin, peculiar cell division (neuroglia cells and vascular 
endothelium), nuclear movements also in nerve cells, diffuse 
vascular distension and leucocyte infiltration, revealing a con- 
dition of irritation ; (2) swelling, vacuolation, changes of 
form, granular appearance of nerve cells and neuroglia ; and 
(3) more advanced changes in the nerve elements. The 
changes in the first group may be seen as early as five days 
after inoculation. 

In a more recent article by Germano and Capobianco * 
attention is called to the fact that the destruction of some of 
the nerve cells in rabid animals is not accepted by everybod)^ 
but that in their researches they have been able to confirm the 
statements made by Golgi, that instances of the complete dis- 
appearance of nerve cells have been observed, while other cells 
show fatty degeneration, and partial destruction of the irentirety 
represent intermediate stages between the normal cell and its 
total disappearance. The alteration of the nucleus ma)^ pre- 
cede or follow that of the cell body. 

The nerve fibers, either in the white or gray matter, 
undergo a certain amount of change. In a longitudinal sec- 
tion of the myel, especially through the ventro-lateral columns, 
there are noted marked changes in the axis cylinders. In 
some cases they appear uniformly swollen for their whole 
length, while in others there are varicose enlargements. In 
the swollen portions there were frequently observed small 
vacuoles which interrupted the continuity of the axis cylinder. 

During the year 1900, the discovery of changes distinctive 
of rabies was announced by Van Gehucten and Nelis. These 
changes are found in the peripheral ganglia of the cerebro 
spinal and sympathetic systems and are especially marked in 
the plexiform ganglion of the pneumogastric nerve and the 
gasserian ganglion. Normally these ganglia are composed of 
a supporting tissue holding in its meshes the nerve cells, each 
one of which is enclosed in a capsule, made up of a single 
layer of endothelial cells. The action of the rabic virus seems 



DIFFERENTIAL DIAGNOSIS 



477 



to exercise its effect on these cells particularly, bringing about 
an abundant multiplication of the cells forming this capsule, 
leading finally to the complete destruction of the normal gang- 
lion cell and leaving in its place a collection of round cells. 
Ordinarily a considerable number of ganglion cells will be 
found which have undergone only a slight change, but under 
certain conditions the process is so widespread that all the 
ganglia cells are destroyed. The intensity of these changes 
varies in different animals ; they are perhaps most pronounced 
in the dog, less marked in man and still less in the rabbit. 

Much of the practical value of these findings consists in 
their making it possible to make a sure and quick diagnosis. 
It is possible to complete the examination within .six hours 
after the death of the animal, and under ordinary circum- 
stances a positive opinion can be given in from 24 to 36 hours. 
It is important that the animal should be allowed to die, and 
not be killed prematurely, as where the disease is not permitted 
to run its full course ending in death, the changes may be 
absent or only slightl}'^ developed. 

^ 374. Differential diagnosis. From the often obscure 
manner of infection, the long period of incubation, the varia- 
ble symptoms and the absence of gross morbid changes char- 
acteristic of the disease, it is easy to mistake rabies for various 
other nervous disorders and vice versa, unless a definite method 
of diagnosis can be availed of. 

Diaonosis by aiiimal inoculation. The method which the 
experience of pathologists has shown to be the best, is the sub- 
dural inoculation of rabbits or guinea-pigs with a suspension 
of the brain or spinal cord of the suspected animal. The sub- 
dural inoculation with the brain tissue of rabid animals was 
first demonstrated by Pasteur to be more reliable and more 
rapid in its results than the subcutaneous injections. The 
procedure is simple. The brain of the suspected animal is 
removed with aseptic precautions as soon as possible after 
death. A small piece of the brain or spinal cord is placed in a 
sterile mortar and thoroughly ground with a few cubic centi- 



478 RABIES 

meters of sterile water or bouillon. This forms the suspension 
to be injected. 

The hands of the operator and all instruments are care- 
fully disinfected. The rabbit is etherized, the hair clipped 
from the head between the eyes and ears, and the skin 
thoroughly washed and disinfected. A longitudinal incision 
is then made, the skin and subcutaneous tissue held back by 
means of a speculum, a crucial incision is made in the perios- 
teum on one side of the median line, to avoid hemorrhage from 
the longitudinal sinus, and the four parts of the periosteum 
reflected or pushed back. By the aid of a trephine a small 
button of bone is easily removed leaving the dura mater 
exposed. With a hypodermic syringe a drop or more of the 
rabid brain suspension is injected beneath the dura, the perios- 
teum is replaced, the skin carefully sutured and disinfected 
and the rabbit returned to its cage. As soon as the influence 
of the anesthetic* has passed off the rabbit shows no appear- 
ance of discomfort. If the operation is performed in the fore- 
noon the animal partakes of its evening meal with the usual 
relish. The inoculation wound heals rapidly, and the rabbit 
exhibits every appearance of being in perfect health until the 
beginning of the specific symptoms, which occur ordinarily in 
from fifteen to thirty days after the inoculation. Occasionally 
the symptoms appear earlier than fifteen days and in some 
cases the rabbits are not attacked for from one to three months. 

The symptoms following the inoculation are quite uni- 
form. There is, however, a marked difference in the length of 
time the rabbits live after the initial manifestation ot the dis- 
ease. The fact should be clearly stated that rabbits do not 
ordinarily become furious. In some instances they are some- 
what nervous for a day or two preceding the paralysis. There 
appears to be marked hyperesthesia. Usually the first indica- 
tion of the disease it a partial parah^sis of one or both hind 
limbs. This gradually advances until the rabbit is completely 

*Ether should be used in preference to chloroform for rabbits, as 
the latter frequently causes death, while the former can be administered 
with comparative safety. 



DIFFERENTIAL DIAGNOSIS 479 

prostrated, the only evidence of life being a slight respiratory 
movement. The head occupies different positions. In some it 
is drawn backward as in tetanus ; in others it is drawn down 
with the nose near the fore legs ; and in still others it is 
extended as if the animal were .sleeping. The period of this 
complete paralysis varies from a few hours to a few days, but 
ordinarily it does not exceed twenty-four hours. Although 
these animals are unable to move voluntarily, there is a reflex 
action of the limbs until a very short time before death. 

During the period of incubation the temperature of the 
rabbit is normal. As the time approaches for the first symp- 
toms to appear there is an elevation of temperature of from i 
to 2 degrees, which continues for a variable length of time, 
but rarely longer than two days. This is followed by a grad- 
ual or usually a more rapid drop to the subnormal, which con- 
tinues to the end. 

The differential diagnosis in experimental animals is not 
difficult. Rabbits inoculated with several varieties of patho- 
genic bacteria frequently exhibit symptoms of paralysis for a 
brief period preceding death. In cases of injury to the brain 
or spinal cord there may be paralysis, which in the absence of 
the history of the case might be taken for that of rabies. In 
these cases, however, the symptoms appear very soon after 
inoculation. This is especially true when the paralysis is due 
to mechanical injury of the brain or to irritation of septic sub- 
stances. In the case of the pathogenic bacteria if paralysis 
occurs at all it is almost invariably preceded by marked disa- 
bility. This method of diagnosing rabies requires that the 
inoculated animals remain apparently well for a considerable 
length of time after the sul)dural inoculation and before the 
paralytic symptoms appear. 

The lesions found on the post-mortem examination are 
also of much assistance in making a diagnosis. If the animal 
died from .septicemia or brain injury there will be lesions 
almost invariably recognizable in the brain or viscera. In the 
case of septicemia a bacteriological examination will reveal the 
presence of microorganisms. If the death was caused by 



48o 



:^^ 



..O- 

4*^- 









vi/% 






Fig. III. Section of a normal 
plexiform ganglion ; {a) and 
{b) ganglion cells, {c) intercel- 
lular substance. 



rabies the inoculation wound in the head should be healed 
perfectly, there should be no abscess and the menings should 
be free from exudates and the brain should appear perfectly 
normal, except that in rare cases 
there may be a slight injection 
of the blood vessels. The viscera 
are ordinarily normal in appear- 
ance, with possibly the exception 
of the liver, which we have 
frequently found to be deeply 
reddened and the gastric mucosa, 
which not infrequently shows 
dark patches, indications of dis- 
integrated hemorrhagic areas. A 
bacteriological examination fails 
to reveal the presence of micro- 
organisms in either the tissues 
or blood. Another important 
point which has been noticed 
is an intense rigor mortis fol- 
lowing death from rabies. Kin- 
youn states that this was a 
constant feature of this disease 
in all of the produced cases 
which have come under his ob- 
servation. Wesbrook did not 
observe this condition. 

Animals other than rabbits 
have been used and a number of 
of other methods of inoculation 
have been proposed. 

Diagnosis by histological cx- 
The rapid diagnosis by means 
of the histological changes pointed out by VanGehuchten 
and Nelis has been very successful in the experience of 
a number of workers. Ravenel was the first to publish 
upon this method in this country. He used it very 



'V 









^, 



Fig. 112. Section oj plevi- 
fortn ganglion from a case of 
rabies ; {a) ganglion cell, (b) 
cells infiltrating the ganglion 
cell and space. 

aminatioii of the gatiglia. 



DIFKHRKNTIAL DIAGNOSIS 4^1 

successfully in the Laboratory of the Pennsylvania State Live 
Stock Sanitary Board. He reported its use in 52 cases. We 
have used this method with success. 

We have found the plexiform ganglion, which is situated 
just outside of the cranial cavity near the foramen lacerum 
basis cranii, on the pneumogastric nerve, the most convenient 
and the most desirable for study. The removal of this gang- 
lion is comparatively easy and simple. 

There are two ways by which this ganglion can be easily found : 

1. Take up the pneumogastric nerve and trace it anteriorly to the 
point where it enters the cranium. Near this point a slight enlarge- 
ment, the ganglion of the trunk of the vagus, will be found. 

2. Cut through the skin from the mandibular symphysis posteri- 
orly along the neck and reflect it back. An incision is then made 
through the mylohyoid muscle near the inner face of the mandible 
posteriorly past the digastric muscle and superiorly until the lingual 
nerve going to the tongue is exposed. Trace this posteriorly until the 
point where it enters the cranium together with the vagus is reached. 
In this way it is easy to locate the vagus nerve and the plexiform gang- 
lion. We have found either one of these methods or a combination of 
the two very convenient, and with a knowledge of the location of 
these parts there is no reason why the ganglion should not be removed 
quickly and easily. 

After the ganglion is removed there are a variety of methods which 
may be used in fixation and staining. The following we have found to 
be very satisfactory. As soon as the ganglion is removed it is placed in 
Flemming's fluid or in a standard aqueous solution of mercuric chloride 
for a few hours, washed in water, carried through the alcohols and sec- 
tioned by the paraffin method. With this method of fixation it is 
almost imperative that the sections be stained with iron or Dela- 
field's hematoxylin, of which we have found the latter the most 
convenient. Alcohol, either 95 per cent, or absolute, may be used as a 
fixer, in which case other staining methods may be used. However, 
the fixation by this method is not as good, but it admits of a trifle more 
haste. 

Normally this ganglion is composed of a fibrous capsule from which 
a supporting fibrous tissue extends into the interior, holding in its 
meshes the nerve cells, each of which is enclosed in an endothelial cap- 
sule. The changes characteristic of rabies consist in the atrophy, the 
invasion and the destruction of the ganglion cell as a result of new 
formed cells, evidently from the endothelial capsule. These cells appear 



482 RABIES 

first between the nerve cell and its capsule. These changes are quite 
uniform through the entire ganglion and in advanced cases of the dis- 
ease nearly all of the nerve cells are often times destroyed. 

Robineaux examined 37 cases that died of rabies with positive re- 
sults. In animals killed during the course of the disease the results 
varied. In 40 such cases, he found the lesions in 11 and they were 
absent in 29. The rapidity with which ganglionic changes appear seems 
to vary greatly in different individuals. 

The fact must be kept in mind that this is a method for rapid diag- 
nosis in case the animal dies and not a means for an early diagnosis. 

Diagnosis from the presentee of Negri bodies. The presence 
or absence of Negri's bodies is used as a means of diagnosis in 
most if not all laboratories. These bodies, which are often 
quite large, are readily brought out by proper staining. These 
bodies, whether the cause or specific degenerations, appear to 
be of much value in making a rapid diagnosis. Unlike the 
ganglion changes they appear early in the course of the dis- 
ease, and consequently they are of value in making an early 
diagnosis when the animal is killed soon after the appearance 
of the first symptoms. Thus far these bodies, or those easily 
mistaken for them, have not been found in the brains of ani- 
mals dying from other diseases except one report of their 
possible presence in a case of tetanus. 

Bohne uses for diagnosis of rabies a piece 'j-rU mm. 
thick from the Ammons horn which after 30-40 minutes of 
fixing and hardening in aceton for 60-75 minutes he puts it in 
paraffin. In this way it is possible for them by the aid of a 
short staining after the Mann method to get stained sections 
in the course of three hours. 

In his 170 investigations (157 dogs, 6 cows, 4 people. 3 
cats) he found the later discoveries of Negri and Volpino con- 
firmed according to the presence of the Negri bodies and their 
finer structure. 

Besides he investigated 50 dogs attacked with other dis- 
eases without finding Negri bodies or similar forms. He 
therefore holds the Negri bodies as specific for rabies and the 
diagnosis as assured by a positive find. Their parasitic nature 
seems to him for the present still doubtful. 



PREVENTION 483 

§ 375. Prevention and treatment. The prevention 
of rabies infection resolves itself into two procedures, (i) 
The destruction of all ownerless and vagrant dogs, and (2) the 
muzzling of all dogs that appear upon the streets or in public 
places. In thus preventing the propagation of the virus, as 
shown by the results obtained in German}- and Great Britain, 
the disease will be practically exterminated. 

There is no treatment for rabies except the preventive 
inoculation known as the Pasteur treatment by which an im- 
munity is produced by the subcutaneous injection of the virus 
of rabies in an attenuated form, beginning with the mildest 
virus and going gradually up to one which possesses nearly or 
full virulence. The attenuation of the virus is brought about 
by drying at a fixed temperature and the action of the atmos- 
phere. Depending upon the length of time the virus is ex- 
posed to the influences, we can obtain any degree of virulence 
desired, the loss of virulence under fixed conditions being 
quite uniform. 

The disease as seen in dogs infected naturally was called 
by Pasteur "street rabies" and the virus of such animals is 
known as the " virus of street rabies." Such virus will as a 
rule produce the disease in rabbits by intra-cranial inoculation 
in from three to four weeks. By inoculating rabbits in series 
one from the other, a reduction of the period of incubation is 
obtained. After about 100 passages rabbits will die with cer- 
tainty and great regularity on the sixth or seventh day after 
inoculation. Beyond this point no increase of virulence has 
been obtained. This is the fixed virus of Pasteur. 

The simultaneous method which consists in the injection 
simultaneously of a strong virus and the serum of an immune 
animal is now being used with reported success in the Pasteur 
Institute of Paris. 

RKFERKNCKS 

1. Babks. Sur certains caracteres des lesions histoloijiques de la 
rage. Ann. dc I' Insiitui Pasteur, Vol. \'I (1892), p. 299. 

2. B.\BKS. Untersuchungen iiber die Negrischen Korper und ilire 



484 RABIES 

Beziehung zu dem Virus der Wutkrankheit. Zeitschr. f. HygienCy 
Bd. LVI (1907), S 435- 

3. BOHNE. Beitrag zur diagnostischen Vervverthbarkeit der Negri- 
scheii Korperchen. Zeitschr. f. Hygiene, Bd. LII, S. 87. 

4. Cabot. Report on experimental work on the dilution method 
of immunization from rabies. Jour. Experimental Med., Vol. IV 
(1899), p 181. 

5. Dulles. Disorders mistaken for hydrophobia. Trans, of the 
Med. Sac. of the State of Penn., 1884. 

6. Fleming. Rabies and hydrophobia. 

7. FROTHINGH.A.M. The rapid diagnosis of rabies. Jour. Med. 
Research. 

8. Keirle. a report on the autopsies on four recent cases of 
rabies and a bacteriological examination of a rabid dog, together with 
the recent laboratorj' experiments. Maryland Med. Jour., Vol. 
XXXVIII (1897). 

9. Law. Rabies. A System of Practical Medicine by American 
Authors, Vol. Ill (1898). 

10. MacClure. Rabies-hydrophobia. Supplement to the Annual 
Report of the Michigan Board of Health, 1894. 

11. MoHLER. Pathological report on a case of rabies in a woman. 
Annual Report, U. S. Bureau of Animal Industry, 1903, p. 54- 

12. Moore and Fish. A report on rabies in Washington, D. C. 
Annual Report, U. S. Bureau of Animal Industry, 1895-6. 

13. Moore and Way. A rapid method for the diagnosis of 
Rabies. American Veterinary Reviezv, Oct., 1904. 

14. Negri. Beitrag zum Studium der Aetiologie der ToUwuth. 
Zeit. f Hygiene, Bd. XLIII (1903), S. 507. 

15. Poor. Recent studies in the diagnosis of rabies. Medical 
Record, Apr. 15, 1905. 

16. Public Health Commission, District of Columbia. 
Rabies. But. 25, U. S. Bureau of Animal Industry, 1900. 

17. Ravenel and McCarthy. The rapid diagnosi.-; of rabies. 
Univ. of Penn. Med. Magazine, January , 1901. 

18. Ravenel. Rabies. Bui. 79, Dept. of Agr., State of Penn., 
1901. 

19 RemlingER. Le passage du virus rabique a travers les filtres. 
Ann. de I' Inst. Pasteur, Vol. XVII (1903), p. 834. 

20. Remlinger ET RiffaT-Bev. Sur la permeabilite de la bougie 
Berkefeld au virus rabique. C. R. Soc. de Biol., Vol. LV. (1903) p. 974- 



DIIMITHHRIA IN KOWI.S 



485 



SCHUDHR. Der Negrische Erreger der Tolhvuth. Deul. Med. 



21. Salmon. Rabies, its cause, frequency and treatment. Year 
nook, Dcpt. of Agriculture, Washington, D. C. 1900. 

22. Salmon. Rabies in the District of Columbia. Circular No. 
JO, U. S. Bureau of Animal Industry, 1900. 

23. SirzOR. Hydrophobia. An account of M. I'asteurs system. 
1887. 

24. 
Wochenschrift, 1903, No. 39, S. 700. 

25 VanGehuchtenandNelis Diagnostic histologique de la 
rage. Annates de Med. Vet., Vol. XLIX ( 1900). p. 234. 

26. WAV. The Negri bodies and the diagnosis of rabies. Amer. 
Vet. Review, Vol. XXIX (1905^. P- 937- 

27 WKSBROOK AND WiLSON. Preliminary report on the labora- 
torydiagnosis in twenty cases of suspected rabies. Trans. Am. Pubhc 
Health Assn., 1S9S. 

28. Williams and Lowde. The etiology and diagnosis of hydro- 
phobia. Jour, of Infectious Diseases, Vol. 3, 1905, P- 452- 



DIPHTHERIA IX FOWLS. 

Synouxms. Roup--, pip; canker; swelled head. 

§ 376. Characterization. Diphtheria of birds is an in- 
fectious disease the lesions of which first appear on the mucous 
membrane of the nasal passages, the eyes, the mouth, the 
pharvnx and larvnx, and which may extend to the trachea, 
bronchi, the air sacs, the intestines and possibly to other 
abdominal organs. The disease is determined by a grayish- 
yellow fibrinous exudate which forms upon the mucous surface 
of one or more of the parts mentioned. The exudate may be 
so abundant as to obstruct the air passages. In some out- 
breaks, it is very acute, progres.ses with great rapidity and de- 
stroys most of the birds attacked. 

'Fowls (genns Callus) and pigeons (genus Columba ) are 
most commonly attacked and they are the only ones considered 

*The origin of this term is somewhat obscure, but it is supposed to 
be a corruption of croup, and its application explained on account of a 
peculiar hoarseness accompanying the respiration of the aftected birds. 



486 DIPHTHERIA IN FOWLS 

in this discussion. Avian diphtheria is reported, however, to 
attack turkeys, ducks, pea-fowls, pigeons and pheasants. It 
is presumed that wild birds may be affected. 

Avian diphtheria is quite distinct from human diphtheria. 
There are cases on record, however, which indicate that the 
diphtheria of fowls may be communicated to children and 
cause a serious and even fatal sore throat. On the other hand, 
it is asserted that diphtheria of children is sometimes com- 
municated to fowls and that the virus may be thus preserved 
for a considerable time and again be transmitted to children. 
Concerning this point additional investigations are needed. 

§ 377. History. The history of this disease is some- 
what obscure. It is evident from the literature, that fowls 
have always been subject to various affections of the head but 
the first investigation of this class of maladies seems to have 
been made by Loeffler-'^ in 1884. Since that time Klemmeri", 
Babes and Puscarin +, Eberlin ||, Loir and Ducloux*, and 
others have studied diseases known as diphtheria in pigeons, 
fowls and other birds. The disease was investigated by the 
Bureau of Animal Industry in 1893-4. It has more recently 
been studied in California by Ward, in New York by Mack, 
and at Guelph, Ontario, by Harrison and Streit. 

§ 378. Etiology. In 1884, Loeffler discovered a bac- 
terium which he believed to be the specific cause of diphtheria 
in fowls and with which he could produce the disease. It 
differed from the diphtheria bacterium in man. Loir and 
Ducloux isolated a still different organism. The writer found 
in the exudates of the earlier stages of the disease a bacterium 
belonging to the septicemia hemorrhagica group. It was 
rapidly fatal to rabbits but the diphtheritic lesions could not be 
produced by inoculation in fowls. In the examinations of the 



*Mitt. aus dem Kaiserlichen Gesundheitsamte. Bd. II ( 1884), S. 214. 
tBerliner theirarzt. Wochenschrift. 1890, No. ib, S. 138. 
jZeitschrift f. Hygiene. Bd. VIII (1890), S. 374. 
IIMonatshefte f. Thierheilkunde. Bd. V (1894), S. 433- 
lAnn. de I'Inst. Pasteur. Tome VIII (1894), p. 599. 



ETIOLOGY 



4S7 



last three years this organism has not been found in the diph- 
theritic lesions of fowls. King found a bacterium on the con- 
junctiva of a healthy fowl that belongs to this group. Ward 
failed to find it in his study of the disease in California. Har- 
rison and Streit have described an organism, Bacillus cacosmus, 
which they consider specific. Ps. pyocyaiieus has also been 
obtained in pure culture from the exudates. Mack, who has 
made a careful study of this disease, has failed to find anv 




Fig. 113. Fowl shorving eye closed. The conjunctiva is covered uitk 
a tliick exudate ( Ward). 

organism constantly present in the lesions. He also failed to 
produce the disease with />. cacosmus. It is not positive, how- 
ever, that the same di.sease was studied by the different writers. 
Roup is usually introduced into a flock by the exposure 
of the birds to sick ones at shows or by bringing affected fowls 
on the premises. The contagion may be carried by birds 
which have the disease in .so mild a form tliat thev show no 



488 DIPHTHERIA IN FOWLS 

symptoms of it. There is a general belief that the disease ma}- 
be developed by exposure of birds to draughts of air or b}^ 
keeping them in damp, filthy and badly-ventilated houses. 
It is presumable that this belief in its etiology is not well 
founded because of confusion existing concerning the early 
symptoms of acute diphtheria and those of all stages of the 
chronic form, and those of simple colds and catarrhs. Ward 
was unable to produce the disease by exposing fowls to unfa- 
vorable conditions, but when infected fowls were introduced 




Fig. 114. Fo^i'l s/i07tniig- the suborbital sinus distended. T/ie eye is 
partially closed. 

the disease spread rapidly. Dampness and lack of ventilation 
110 doubt favor the maintenance of the virus when introduced. 

The specific cause of the disease known as diphtheria or 
roup in chickens and pigeons, in the opinion of the writer, is 
not known. It is not impossible that a number of organisms 
may share in the production of the lesions of this affection. 

Guerin considers it a general disease caused by a cocco- 
bacillus (resembling the fowl cholera organism). This is not 
unlike the bacterium of septicemia hemorrhagica. He finds 



SVMl'TOM^ 



4«9 



it in the blood and organs. Moore, Mack and Ward have 
failed to find this organism in the tissues. 

^ 379- Symptoms. There is a watery secretion from 
the nostrils and often from the eyes, with general weakness 
and prostration greater than would be expected from snnple 
catarrh The birds sit with the back arched, the head and 
neck drawn out towards the body, the plumage roughened ; 
the respiration is more or less obstructed, rapid and audible, 
the vision is impaired and swallowing is difficult. There is 



"Li' 




Pt 



Fig. 115. /uu'/y sfa.Qrs of diphtheritic necrosis in the throat of a pi-eon. 

frequent shaking of the head, sneezing and expectoration of 
mucous secretions. If the mouth is examined at this early 
period the tongue is found to be pale, while small grayish 
spots shaded with black and slightly projecting above the 
surface, may be seen along the border, the upper surface or at 

the base. 

The following day the condition is aggravated, the tem- 
perature is several degrees above normal, the appetite has dis- 
appeared and there is diarrhea with greenish or yellowish 
evacuations. From the open beak there escapes a thick, 
strino-v grayish mucus. The eyes are unnaturally dilated, 
projecting and possibly partly covered with the thick secretion 
which has accumulated between the lids. The nostrils are 
obstructed by the thickened and dried secretion. W alking is 



490 DIPHTHERIA IN FOWLS 

irregular and difficult. The mucous membrane of the mouth 
and pharynx is congested and shows numerous dark red eleva- 
tions covered with fibrinous exudate. The patches on the 
tongue have increased in size, the}' are gray in color, dried 
along the edges of the tongue but soft and flattened upon its 
upper surface. They are covered with membranous deposits. 
The voice often fails. 

§ 380. Morbid anatomy. The lesions are largely local- 
ized on the mucosa of the head. With tlie exception of ema- 




Pmu. 






■W'lyy 






Fig. 116. A section through a diphtheritic exudate, late in the course of 
the disease, from a pigeou's throat. 

ciation, there are no lesions or evidence of organic disease. 
The cause of death and the extreme emaciation are difficult to 
explain in those cases where the lesions are confined to one 
eye or to the mucosa of the nares, excepting on the supposi- 
tion that some poisonous or toxic substance was absorbed 
from the seat of the disease. In those cases where the lesions 
are in both eyes, or in the mouth and throat, difficulty in find- 
ing or swallowing food affords a rational explanation. 

In some cases the exudate is of a croupous character, in 
others of a diphtheric nature. Three stages or varieties of 
lesions, which represent the types of this disease as en- 



MORBID ANATOMY 491 

countered in this country, may be more definitely defined as 
follows : 

1. An exudate of a serous or muco-purulent character in 
the conjunctiva and nasal cavities. Ordinarily this condition 
cannot be recognized in the mouth. The mucosa in these 
cases is apparently but slightly altered. 

2. The mucosa over a small or larger area is covered 
with a spreading exudate of a grayish or yellowish color. It 
is firmly attached to the mucous membrane and when removed 
leaves a raw, bleeding surface. Sections through this exudate 
and the subjacent tissues show that the epithelial layer is de- 
stroyed and the underlying tissue infiltrated with cells. The 
extent of the infiltration varies in different individuals. 

3. The mucosa is covered with a thick mass of exudate, 
varying in color from a milky white to a lemon yellow or 
brown. It is easily removed, leaving a more or less granular 
and healed surface. This sloughed mass is frequently dried at 
its margins to the adjacent tissue. It emits a strong putrid 
odor, due to decomposition. The drying of the margins pre- 
vents the fowl from expelling the exudate after it becomes 
separated from the underlying tissue. 

The evidence to support the supposition that the three 
forms or types of exudate described are different stages in the 
same morbid process, as gathered from the post-mortem notes 
and bacteriological study of the cases investigated, may be 
summarized as follows : 

(a) Abnormal conditions, representing the intermediate 
and connecting links between the types of lesions, are fre- 
{{uently encountered. 

(/') Although at the time of examination (post-mortem) 
but one form of exudate is usually present in a single fowl, 
there are exceptions, in which two and occasionally the three 
forms are coincident. Thus the eye is covered with a sloughed 
exudate, the posterior nares contains a layer of muco-purulent 
substance and on the mucosa of the mouth are areas of diph- 
theritic exudate. 



,|TY 



) 



492 



DIPHTHERIA IN FOWLS 



In fowls which die, the exudates are for the greater part 
in the advanced stage, although fatal cases occur in which the 
lesions are restricted to an abnormal quantity of a serous or 
muco-purulent, more or less viscid, exudate in the conjunctiva 
or nasal cavities. The best illustration of the diphtheritic 
process is found in fowls killed for ex- 
amination in the second stage of the 
disease. The distribution of the lesions 
shows that the conjunctiva is most fre- 
quently affected. The exudate in the 
nasal cavities is in some cases undoubt- 
edly the result of the coagulation of the 
liquid which has passed during the 
course of the first stage from the con- 
junctiva through the lachrymal duct into 
the nares. In certain cases, however, 
the lesions appear in the nares primarily. 
In some cases the exudate appears in the 
larynx and extends down into the 
trachea. In these cases the fowls are 
liable to die from suffocation. It occa- 
sionally happens that the lesions are 
restricted to the larynx and as the fowls 
die suddenly the cause of death is not 
suspected. Sections of the exudate with 
subjacent tissues from the cornea and the 
mouth, show that there is a cell infiltration into the mucosa 
which destroys the epithelial layer and frequently the sub- 
mucous tissues to a considerable depth. 

The fact should not be overlooked that the disease in the 
eye is usually confined to the conjunctiva and the cornea, the 
posterior portion remaining apparently normal. 

Mack in his work on thirty-three cases found 40 per cent 
had lesions in the conjunctiva ; in 44 per cent the nasal 
mucosa was affected ; in 41 per cent the mouth was invoh^ed 
and in 33 per cent the suborbital sinuses were distended with 
exudates. 




Fig. 117. A drazviuo- 
shoii'ing areas of diph- 
theritic e.vudate in the 
throat of a pigeon. 



MOKHID ANATOMY 493 

From the observations thus far made the provisonal 
theory is entertained that the three forms of the exudate — 
serous or muco-purulent, diphtheritic and sloughed mass- 
represent three stages in the course of the same disease. It is 
easily understood that fowls examined in the first stage would 
be said to be affected with a catarrhal condition of the mucosae 
of the eyes or nares. It is highly probable that in many cases 
the disease never reaches the second stage and if these cases 
alone were examined the diphtheritic condition would not be 

^■iJMik-^:: (X M 






'W^^^:^-'0' 





• -^"^ Fig. 119. A longitudinal sec- 

FiG. 118. Dip/it /untie e.vu- Hon through the larynx and 

date in the larynx of a fowl : trachea of a fowl {same as 118) , 

(a) the grayish-white exudate showing the exudate: («) in the 

projecting from the glottis. larynx and (b) in the trachea. 

suspected. It appears, however, that in the majority of cases 
the disease runs its course and membranes are formed, slough 
and recovery follows. It is furthermore presumable that the 
disease in que.stion appears sometimes in a virulent and de- 
structive form. I am in possession of statements from poultry 
raisers which show that there are occasionally epizootics of a 
disease characterized by exudates in the eyes, nose or mouth. 



494 DIPHTHERIA IN FOWLS 

which run a rapidly fatal course. It appears that it is such 
outbreaks which have been reported in Europe as diphtheria 
and not the low form of chronic inflammation which has been 
studied in this country. 

§ 381. Differential diagnosis. The differential diag- 
nosis of diphtheria in fowls cannot be made until we are pos- 
sessed of a knowledge of its cause. At present all affections 
of the head characterized by the range of lesions admitted by 
the description of the morbid anatomy are accepted as cases of 
diphtheria or roup. Chicken pox is separated by the nodular 
character of the lesions. Manson's eye worm (oxyspirura 
Mansoni) of chickens produces lesions that might be mistaken 
for roup. The finding of this worm would determine the 
diagnosis. 

§ 382. Relation of diphtheria in man to that in fowls. 
A comparison of the bacillus of diphtheria in man (Klebs- 
Loeffler) with those described from diphtheria in fowls shows 
that morphologically and in their pathogenesis for experimen- 
tal animals the organisms are in no way alike. There is also 
a marked difference in the nature of the exudates in fowls and 
in man. The non-identity of these diseases has been clearly 
pointed out by Menard.* Although these maladies are shown 
by several observers to be unlike in their etiology and the 
character of their lesions, the transmission of fowl diphtheria 
to the human species, and vice versa, is affirmed by several 
writers. 

Gerhardt reports 4 cases of diphtheria in Wesselhausen, 
Baden, among 6 workmen who had charge of several thousand 
fowls, many of which died of diphtheria. There were no 
other cases of diphtheria in the neighborhood and the evidence 
was quite conclusive that the disease was contracted from the 
affected fowls. 

Debrie:{: reports briefly the transmission of human diph- 



*Revue d'Hygiene. Tome XII (1890), p. 410. 

t Reviewed in Centralblatt f. Bakteriologie. Bd. XIII (1893), 
S. 730. 



PKKVKNTION 495 

theria to fowls. He is inclined to the view that human diph- 
theria is transniissable to fowls and fowl diphtheria to man. 
Cole* reports a case of supposed transmission of the disease 
from a fowl to a child. 

The diphtheritic disease of fowls reported by Loir and 
Ducloux in Tunis, in 1894. spread to the people of that place, 
resulting in an epidemic of serious proportions. Menard re- 
fers to the fact that men employed to feed young squabs con- 
tracted diphtheria by blowing the masticated food into the 
mouth and crop of squabs suffering with that disease. vSchrev- 
enst reports several cases of diphtheria in children in which 
he traces the source of infection to certain poultry. 

Guerin has pointed out with emphasis that there is no re- 
lation between diphtheria in man and in fowls. 

Although the number of reported cases of the transmission 
of fowl diphtheria to the human species and vice versa is small 
in comparison with the extent of the disease in poultry, the 
evidence that such a transmission is possible is quite sufficient 
to discourage the careless handling of diseased fowls. It is a 
quite common practice, especially in the rural districts, to 
bring the sick chickens into the house for treatment, where 
the children of the household are allowed to fondle them at 
will. It is not improbable that when this disea.se is thorough- 
ly investigated the number of cases of direct infection from 
this source will be found to be much less than it is at present 
supposed. Until such investigations are satisfactorily com- 
pleted the indiscriminate handling of diphtheritic chickens es- 
pecially by children and the exposure of fowls to the infection 
of diphtheria in the human species, whereby they may become 
carriers of the virus, should be strenuously avoided. 

;< 383. Prevention. In order to prevent this disease it 
is evident that many conditions must be strictly complied 
with. The character of the food and the general sanitary cou- 



* Archives of Pediatrics, XI {1894), p. 38 
II Bulletin 
(1894), p. 380- 



II Bulletin de 1' Acad. Royale de M^d. de Helgique. Vol. \III 



496 



DIPHTHERIA IN FOWLS 




6 



Fig. I20. Scciions of the heads of a normal and of a diphtheritic foivl. 



PREVENTION 497 

ditions, including cleanliness, ventilation and the temperature 
of the poultry houses, must be considered. Undoubtedly there 
is much to be learned in connection with the proper sanitary 
care of poultry. In addition to the general sanitary methods, 
the following rules should be observed. 

1. Fowls which have an exudate on any of the mucous 
membranes of the head or which have come from flocks in 
which such a disease exists or has recently existed, .should not 
be placed among healthy poultry. 

2. If the disease appears in one or more fowls of a flock 
they should be immediately separated from the well ones. If 



Fig. I20. Photographs of transections of fowl's head. 
I, 2 and 3. Sections from a normal head. 

4, 5 and 6. Sections from approximately corresponding levels from 
the heads of fowls suffering with diphtheria. 

1. Cross-section of a chicken's head just posterior to the nasal 
openings, a Nasal passage, b turbinated bone, c portion of the wall of 
the false nostril, d sub-orbital sinus, e palate. 

2. Cross-section of a chicken's head midway between the nasal 
openings and the eyes, d Sub-orbital sinus, </' superior portion of the 
sub-orbital sinus, which connects with d posterior to the lachrymal 
duct,/ lachrymal duct opening into the mouth through the cleft palate. 

3. Cross section of a chicken's head on a level with the anterior 
part of the eyes, d Sub-orbital sinus and the duct connecting it with 
the nares. 

4. Cross-section of a chicken's head just posterior to the nasal 
openings, showing the swollen condition of the nasal mucosa in the first 
stage of the disease. The nasal passages are nearly occluded, h Tur- 
binated bone with swollen mucosa, d' sub-orbital sinus containing a 
small amount of exudate. 

5. Cross-section of a chicken's head midway between the nasal 
openings and the eyes, showing extensive exudate in the left sub- 
orbital sinus d and nasal passage extending into the cleft palate ;«. 
The exudate is crowding upon the turbinated bones and nasal septum. 

6. Cross-section of a chicken's head through the eyes, showing 
exudate in the conjunctival sac, inflammatory thickening of the eyelids 
and membrana nictitans, and ulcerated cornea, a' Kyelid, // membrana 
nictitans, i exudate in the conjunctival sac, k ulcerated cornea, /eye. 

All sections are magnified two diameters. 



49^ DIPHTHERIA IX FOWLS 

possible, the source of the infection should be determined and 
removed. 

3. The quite common practice of allowing fowls from 
different flocks to run together during the day should be dis- 
couraged. 

4. Care should be taken to avoid the possibility of bring- 
ing the virus of the disease from affected flocks in the dirt or 
excrement which naturally adheres to the shoes in walking 
through an infected chicken yard. The same care is necessary 
in the interchange of working implements, such as shovels, 
hoes and the like. 

Ward has found that this disease can be prevented by 
keeping infected fowls away. 

It is evident to any careful observer that the fact is too 
often overlooked that fowls, owing to their method of living, 
are more liable to infection than other farm animals. This is 
especially true when they are allowed to run at random, pick- 
ing their living from the garbage pile and barnyards, or secur- 
ing even more unwholesome food. There is little doubt that 
many so called outbreaks of contagious disease among fowls are 
simply enzootics brought about by various infections to which 
they have been exposed. 

The wide distribution, the large niimber of fowls affected 
and the usual chronic course of this disease render it one of 
the few poultry affections for which curative measures promise 
to be of some practical value. The most certain of the known 
methods of treatment is the local application of disinfectants, 
among which a weak solution of carbolic acid appears to be 
the most satisfactory. The dipping of the heads of fowls in a 
solution of I to 2 per cent of permanganate of potash, or a 3 
per cent solution of creolin is reported to be very effective in 
cases where the lesions are external and in the early stages. 
The fact that the lesions are so much exposed renders the dis- 
ease especially favorable for topical applications. When the 
exudates are in the suborbital sinus or in the nares there is 
less opportunity for treatment. 



INFLUENZA 499 

REFEREN'CKS. 

1. GuERiN. Siir la non-identite de la diphtherie humaine et de la 
diphtheric. Recueil de Med. VH., 1903, p. 20. 

2. Gratia et LiEnaux. Contributions a I'ctude bacteriologique 
de la diphterie. Annales de Med. Vet., Vol. XLVII (189S), p. 401. 

3. Harrison and Streit. Roup. Am. Vet. Review, Vol. XXVH 
(1903), p. 26. 

4. Harrison and Streit. Roup : An experimental study. lUil- 
letin 132. Ontario A,q-ric. Coll. and Exp. Farm, 1903. 

5. Holmes. An outbreak of diphtheria associated with a similar 
disease among fowls and a vesicular eruption on the udders of cows. 
Jour. ofComp. Path, and Tliera., Vol. XVII (1904), P- i- 

6. Loeffler. Untersuchungen iiber die Bedeutung der Mikro- 
organisnien fiir die Entstehung der Diphtherie beim Menschen, beim 
Taube und beim Kalbe. Mitthiel. a. d. Kaiserlichen Gesundheitsamte, 
Bd. II (1884), S. 421. 

7. Loir et Ducloix. Contributions a I'etude de la diphterie 
aviare en Tunisie. Ann. de /' Inst. Pasteur, Vol. VIII (1894), p. 559- 

8. Mack. The etiology and morbid anatomy of diphtheria in 
chickens. Am. Vet. Rev., Jan., 1905. 

9. Moore. A preliminary investigation of diphtheria in fowls. 
Bulletin No. 8. U. S. Bureau of Animal Industry, 1895. 

10. Ransom. Manson's eye worm of chickens. Bulletin No. 60. 
U. S. Bureau of Animal Industry, 1904. 

11. Salmon. The diseases of poultry , 1899, p. 216. 

12. Ward. Poultry diseases in California. Proceedings of the 
Amer. Vet. Med. Asso., 1904, p. 164. 



INFLUENZA. 



Synonyms. Epizootic catarrhal fever ; epizootic catarrh ; 
horse distemper ; pink eye : mountain fever ; shipping fever. 

i; 384. Characterization. Influenza is an acute infec- 
tious disease characterized by a rise of temperature and a 
catarrhal condition of one or more of the mucous membranes, 
more especially of the head. One or more of the internal 
organs may become affected. It usually appears in epizootic 
form. It is a disease of honses, although asses and mules are 



500 INFLUENZA 

susceptible and a few cases are reported of its being transmit- 
ted to man and to dogs. It appears sometimes in sporadic 
form and often in epizootics. 

Influenza is a generic term emploj-ed to designate a large 
variety of symptoms. A somewhat careful analysis of its 
manifestations suggests that possibly it includes a number of 
etiologically distinct diseases, i. e. , morbid conditions brought 
about by different causative factors. The term has long been 
employed to designate a considerable variety of equine epizo- 
otics, the independence of which could not be established. 
The disease, as it is seen in the horse, suggests further that 
possibly it is in its beginning a general affection because of 
the early rise of temperature and that later in its course it 
becomes, to a limited extent, localized. At present influenza 
is restricted to groups of symptoms and lesions in the horse 
that are not verj^ unlike those of la grippe in man. Its 
symptoms, lesions and sequelae warrant such a view at least 
for a working hypothesis. As it is not usually fatal, little 
progress seems to be made in acquiring knowledge concerning 
the nature of its morbid anatomy. There is much need for 
careful investigation of this very common malady. 

^ 385. History. According to the writings of Falke, 
influenza was recognized in very early times. There is evi- 
dence that it was known in the fourth and fifth centuries. It 
was described by Low in 1729 in an equine epizootic which 
had spread over Southern Europe. It is also stated that cases 
of its having been transmitted to man had occurred. Gibson 
observed it in 1872 in London and in different districts of 
England. It raged in epizootics in 1760, 1776 and. 1803. The 
disease was widely disseminated during the last century. The 
more important epizootics are reported in the years from 18 13 
to 1815, 1825 to 1827, 1836 to 1840, 1846, 1851, 1853, 1862, 
1870, 1873, 1881 to 1883, and 1890. Anker, who described 
influenza in Switzerland in 1826, laid stress on its contagious 
nature and stated that in his opinion "a volatile infectious 
matter was the cause." 

Influenza spread as an epizootic in 1872 to 1873 over the 



ETIOLOGY 



-1-eater part of the United States where it received the name of 
-pink eve" (French, iTcvre typhoide). It started in Canada 
and extended sonth and west, reaching into British Columbia 
to the north and Mexico at the south. The last great epizo- 
otic raoed in Europe from 1881 to 1883 during which time 11 
is said to have spread over nearly the whole continent. In the 
Prussian army, 3-434 horses became affected in 1890 ; 2,497 m 
1891 ; and 3.645 i" ^^9^- I" Copenhagen, 3,000 horses were 
affected in 1890 and 1891. 

^ 386 Geographical distribution. Influenza seems to 
be known in nearlv if not all of the countries of Europe and 
America In certain sections of the United States it is almost 
a con.stant affection. This is especially true of certain cities, 
owing to the constant introduction of "green" horses. 

§ 387. Etiology. Influenza seems to be produced by a 
specific infection the nature of which has not yet been deter- 
mined A number of bacteria have been described as the 
probable cause but thus far none of them have been found to 
be sufficientlv constant to warrant their acceptance as the 
etiological factor. It spreads rapidly among horses. 1 he 
virus appears to lose its virulence quickly outside of the animal 
body but within the body it seems to be preserved for a long 
time According to the observation of Jensen and Clark, 
stallions which have had the disease may transmit it to the 
mares thev serve for months after apparent recovery. Dieck- 
erhofi- succeeded in transmitting the disea.se to healthy animals 
bv subcutaneous and intravenous injections of the blood of in- 
fected horses, but Friedberger and Arloing failed to do so. 
Horses are most susceptible. Sex, breed, stable management 
and feeding appear to have little or no influence on their 
individual su.sceptibility. 

Infection usually takes place from horse to horse. The 
virus appears to be carried by infected human beings, litter, 
harnesses and thermometers. In many cases one attack con- 
fers immunity but a second infection or a relapse trequent y 
occurs Toward the end of an epizootic the disease is usually 



502 INFLUENZA 

milder in form, probably due to a gradual attenuation of the 
virus. 

The period of incubation varies from two to seven days. 
Siedamgrotzky places it at from four to five days and in rare 
cases from 12 to 24 hours. In some cases symptoms have not 
appeared until from two to five weeks after the latest known 
exposure. 

§ 388. Symptoms. The disease appears suddenly and 
may attain its highest point of intensity within twenty-four 
hours. The organs of circulation, nervous centers, digestive 
and respiratory mucous membranes and conjunctiva are 
especially affected. There is partial or entire loss of appetite 
and depression. The temperature rises suddenly from 3 to 
4° F. or even more. It remains high with but slight variations 
for from three to six days and then falls rather quickly, often 
within twenty-four hours, to the normal. At first the fre- 
quency of the pulse is but little increased in comparison to the 
elevation of the temperature, but later it rises to from 60 to 70 
and in fatal cases from 80 to 100 or more. It generally con- 
tinues high for some time even after the temperature has 
fallen. The fever is characterized by unevenness in distribu- 
tion of the external temperature of the body. The early rise 
of temperature, while the affected horses appear to be healthy, 
is of much diagnostic value. 

Usually the nervous depression coexists with the fever. 
The animal may hold its head down and appear to be coma- 
tosed. Extreme muscular debility is frequently associated 
with this stupor. Tremors may occur, the hind legs ma\^ give 
way while walking and paralysis of the hind quarters appears 
in a few cases. 

The oral mucous membrane is greatly congested, hot, dry 
or covered with mucus. There is sometimes difficulty in 
swallowing. The animal frequently yawns. There is usually 
constipation in the beginning of the disease which may be 
accompanied with colic. The feces are formed into small hard 
balls and are covered with masses of mucus. Later diarrhea 



SYMPTOMS 503 

with considerable teuesinus usually occurs The feces are 
of a thin, pulpy and even fluid consistence and sometimes 
have a fetid odor. At the beginning of the attack the urine 
is alkaline but it becomes acid when the intestinal lesions are 
developed. It rarely contains albumin but desquamated epi- 
thelial cells of the bladder are often present in large quantity. 

A severe affection of the eyes is quite a constant charac- 
teristic symptom of influenza. At first it consists chiefly of a 
catarrhal and later of a phlegmonous conjunctivitis with con- 
siderable swelling of the eyelids, which may be followed by 
keratitis and possibly by an exudative or hemorragic iritis. 
Usually both eyes are affected. The first indications are the 
presence of tears, intolerance of light, intense hyperemia of 
the conjunctiva and contraction of the pupil. The eyelids 
swell, are hot, painful and kept more or less continually 
closed. A gray, muco-purulent secretion accumulates be- 
tween the eyeball and eyelids and the eyeball becomes very 
sensitive to pressure. The cornea, which at the beginning of 
the keratitis has a greasy lustre, first becomes iridescent, but 
later in the course of the disease it may be opaque. It is con- 
siderably injected with blood at its edge ; the iris becomes 
swollen and yellowish in color. Often the.se inflammatory 
changes of the eye disappear in a strikingly short time. 

During the further progress of the disease, swellings 
appear on the extremities, sheath, epigastrium and lower part 
of the chest. It may be concluded that these swellings are 
due to edema caused by passive congestion. Less frequently 
the swellings are of an inflammatory nature. The swelling of 
the extremities causes the gait to be stiff and un wieldly. In- 
flammation of the sheaths of the tendons is sometimes ob.served. 

The respiratory mucosae are congested. At first there is 
a -serous and, later on, a muco-purulent discharge from the 
nose, slight swelling of the submaxillary glands, moderate 
acceleration of respiration and a cough. As a rule the animal 
becomes emaciated during the cour.se of the disease. Pregnant 
mares may abort. 

In certain cases complications may ari.se, such as cardiac 



504 INFLUENZA 

debility, grave cerebal symptoms, severe gastro-intestinal 
inflammation, laminitis and petechial fever, all of which have 
been described as accompanying complications. 

The duratioti of the disease is from six to ten days, although 
severe cases may run for two or three weeks and very mild 
cases may recover in from three to six days. 

The mortality varies at different times and in different 
places. The average appears to be from 0.4 to 4 per cent. 
Dieckerhoff saw a loss of 4 per cent among 1,700 horses; 
Aureggio, one of 3 per cent among 800 horses ; Friedberger, 
one of 9 per cent ; and Siedamgrotzky, one of 10 per cent. It 
is stated that in 1872, in Philadelphia, 7 per cent of 30,000 
infected horses died. 

§389. Morbid anatomy. The principal tissue changes 
of influenza are met with in the organs of digestion. The 
mucous membrane of the pyloric portion of the stomach and of 
the intestines is hyperemic, swollen and sprinkled with slight 
hemorrhages. The submucosa is yellowish in color and infil- 
trated with a gelatinous substance causing the membrane to 
form thick, somewhat translucent, elevations containing a fluid 
which coagulates. Peyer's patches are enlarged, especially 
those in the neighborhood of the ileo-cecal valve. The 
rnucous membrane of the mouth and sometimes that of the 
pharynx show similar changes. 

The mucous membrane of the upper air passages is 
hyperemic and swollen. In rare cases, the mucosa of the 
larynx is inflamed, also the subcutis when inflammatory swell- 
ings appear on the skin. Schiitz found that in the brain and 
spinal cord the arachnoid spaces are filled with a fluid which 
is generally clear, although it may contain leucocytes. He 
reports one case in which the lateral ventricles contained a 
large quantity (20 c. c.) of fluid. The other lesions which 
may be found depend upon the extent or localization of the 
disease. Usually the spleen is slightly enlarged ; .small 
hemorrhages in the intestines, under the serous membranes 
and in the lungs, eyes and brain ; gelatinous infiltration of the 



DIFFERENTIAL DIAflNOSIS 505 

renal connective tissue and mesentery ; swelling of the lymph 
glands ; yellowish serous exudates in the larger cavities of the 
body and imperfect coagulation of the blood. One or all of 
these changes may appear in a single animal. 

§ 390. Differential diagnosis. Influenza must be dif- 
ferentiated from strangles and contagious pneumonia. The 
differentiation between pleuro-pneumonia and influenza is 
difficult only at the beginning, when merely general symp- 
toms, such as fever, loss of appetite and weakness are present. 
It should be mentioned that the two diseases may affect the 
horse simultaneously. When the skin is greatly swollen, 
influenza may resemble petechial fever, from which it can, 
however, very .soon be distinguished by the absence of 
petechiae, by the mildness of its course and its greater conta- 
giousness. In case of strangles, the lesions in the lymphatics 
may serve as distinguishing characters. If abscesses are in 
evidence the finding of the streptococcus of strangles would be 
quite conclusive. It would be positive providing streptococcus 
equi could readily be distinguished from the pyogenic 
streptococci. 

With these diseases, a diagnosis, save in the more typical 
forms, is difficult. Without a definite, recognizable, etiologi- 
cal factor or other exact tests, a positive diagnosis in doubtful 
cases can not be made. 

REFERENCES 

1. LiGNiHRES. The etiology of equine influenza or infectious 
pneumonia. Jour, of Comp. Path, and Thera., Vol. XI (189S), p. 312. 

2. M'Fadve.\n. Influenza of the horse — what is it? Jour, of 
Comp. Path, and Thera., Vol. II (1889), p. 105. 

3. Marsden. Influenza. The Vet. Jour. New series. Vol. II 
(19C0), p. 315. (M. describes three forms, (i) catarrhal fever, (2) 
bilious fever, (3) epizootic cellulitis. ) 

4. Nelsox. Influenza. Bulletin 22. State Ai^ric. Fxper. Sta- 
tion, Washington. 1S96. 



506 DOG DISTE.MPER 

DOG DISTEMPER. 

Synonyms. Dog plague; dog disease; bench show dis- 
ease; typhus fever in the dog; typhoid fever iu the dog. 

§ 391. Characterization, Distemper is an infectious 
disease appearing in sporadic cases or in epizootics. It is 
usually determined by a rise of temperature, loss of appetite 
and lassitude, followed by a catarrh of the conjunctiva, re- 
spiratory passages and digestive tract. Frequently there are 
serious disturbances of the nervous system. It is the most 
important canine disease. It is reported that cats, wolves, 
foxes, jackalls, hyenas and monkeys suffer from it. 

§ 392. History. This disease of dogs was known in 
quite early times. Its history shows that possibly it was in- 
troduced into Southern Europe from Peru, South America, 
about the middle of the eighteenth century. It was regarded 
as being closely allied to a number of diseases of the human 
species such as the plague and typhus. Trasbot believed it 
to be closely allied to, if not identical with, small-pox. 

§ 393. Geographical distribution. Distemper in dogs 
is a widespread disea.se. It is exceedingly common in the 
United States and its ravages extend throughout America and 
seem to be no less in Europe. It is stated that there is no 
country or climate in which the dog is exempt from distemper. 

§ 394. Etiology. The specific cause of distemper has 
not been demonstrated. A large number and variety of bac- 
teria have been thought by different investigators to stand in 
a causal relation to this disease. Schantyr stated, in 1891, 
that canine distemper should be divided into three different 
diseases and that each is produced by a distinct species of bac- 
teria. More recently (1899) Jess has isolated a bacillus from 
the catarrhal secretions, blood, serous exudates and organs. 
He reports having reproduced the disease in dogs with pure 
cultures of this organism. The writer has not been able to 
find this bacillus in the few cases which he has examined, but a 



SVMI'TOM.S 507 

Streptococcus has often appeared in pure cultures from the 
various organs. Carre has shown that the serous discharge 
obtained at the outset of the disease possesses great pathological 
power, and that its virulence was due to the presence of an 
organism suflficiently small to pass through certain filters. 
There is much need for further investigation into the etiology 
of this malady. That it is produced by a specific cause is very 
clearly indicated by the reported results of investigations to 
the effect that dogs inoculated with the nasal discharge of 
affected animals develop the disease. 

i^ 395- Symptoms. The symptoms appear after a period 
of incubation of from four to six, possibly eight days. They 
vary to such a degree that it is impossible to refer to all of the 
manifestations. In some cases the symptoms suggest a gen- 
eral disorder. In others they are referable to certain parts or 
organs such as the mucosa of the digestive and respiratory 
tracts, the brain or integument. As a rule several organs are 
implicated. 

The initial symptoms such as depression, roughened con- 
dition of the coat, lo.ss of appetite and elevation of temperature 
are suggestive of a general disturbance. 

In a large majority of cases, conjunctivitis is the primary 
ocular symptom. Tears flow from the eyes and photophobia 
is present. The mucous membrane of the eyelids becomes 
conjested and a purulent exudate may appear. The exuded 
matter consists of pa.sty mucous or dirty yellowish pus. This 
exudate collects under the lower eyelids, chiefly at the inner 
canthus of the eye and soils the edges of the eyelids, upon 
which it frequently dries and causes the lids to adhere, espec- 
ially during the night. Ulcers form on the cornea in conse- 
quence of the action of the accumulated and decomposing pus 
and the patient wiping and rubbing the eyes with its paws. 
The epithelium of the cornea sometimes suffers more or less 
from shallow flat lesions which give the surface of the cornea a 
rough and uneven appearance. Frequently smaller and deeper 
ulcers form especially toward the center of the cornea. 



508 DOG DISTEMPER 

In Other cases, there is a diffuse, parenchymatous keratitis 
which renders the cornea, to a considerable extent, opaque and 
gives it the appearance of ground glass. These extensive 
opacities sometimes develop in a comparativeh- short time. 
This affection of the cornea, the so-called "distemper of the 
eyes," is frequently the only evidence of distemper with the 
exception of the high temperature. 

There may be vomiting, well marked congestion and dry- 
ness of the oral mucosa. There is usually constipation at 
first, but later a diarrhea in which the feces, as a rule, are 
very fetid, often slimy and frothy. Hemorrhagic intestinal 
catarrh sometimes exists. The urine frequently contains 
albumin and bile pigment, especially when the patient is weak 
or in an advanced stage of the disease. 

The nasal discharge is serous at first, mucous or purulent 
later on. It is followed by sneezing, panting and a nasal pru- 
ritis, which causes the animal to rub its nose with its paws. 
The purulent discharge from both nostrils may be very copious. 
It is sometimes mixed with streaks of blood, and varies in 
color from a dirty yellow to a dirty green. Later, it may be- 
come fetid and even watery. Ulcers may appear on the nasal 
mucosa. 

Laryngeal catarrh usually accompanies the nasal catarrh 
and manifests itself by a cough, which comes on in paroxysms 
and which is at first hoarse and dry, but later moist and 
accompanied by a discharge of phlegm. The cough excites 
vomiting. The catarrh spreads from the larynx to the trachea 
and bronchi. The resulting bronchitis is followed by an in- 
creased rate of breathing and manifests itself b}' a cough and 
hoarse, sharp, vesicular, respiratory murmurs. Frequentlj- 
there is a catarrh of the mucous membrane of the smaller 
bronchi. There may be difficulty in breathing and a feeble 
cough which the patients try to suppress. The cough may be 
excited by percussion of the thoracic walls, by the animals 
getting up and by their being taken out of their kennels. 
Young and weak animals that cannot remove the accumulated 
phlegm from the bronchi by coughing become affected with 



SYMPTOMS 509 

catarrhal pneumonia. The pneumonia can be recognized by 
the elevation of the temperature. 

Distemper often begins, especially in anemic animals, with 
great depression and dullness. Strong animals, however, more 
usually exhibit symptoms of acute hyperemia of the brain, 
such as excitement, restlessness, yelping and even attacks of 
fury, which give way later on to manifestations of cerebral 
pressure. Spasms frequently occur either generally or con- 
fined to particular limbs which swing backward and forward 
as if affected by chorea. The animal may fall down as if suf- 
fering from epilepsy, bark, become unconscious and exhibit 
.spasms of the muscles generally. The sphincters of the anus 
and bladder become relaxed and consequently feces and urine 
are involuntarily passed. There is a gradual return of con- 
sciousness which in a short time is complete and the dog 
manages to get up, although he is very weak. Such an epi- 
leptiform attack may pass directly into long continued coma. 

Paralysis may follow the convulsions or it may come on 
simultaneously with them. It seldom occurs at the beginning 
of the disease. It may be confined to certain groups of muscles, 
as those of a limb, the whole of the hind quarters or even 
the entire body in the form of paresis, especially of the motor 
nerves, combined with excessive muscular weakness. The 
sick dog staggers and his hind quarters sway from side to side 
or he becomes incapable of supporting him.self on his hind 
legs. Frequently he knuckles on all four legs and in severe 
cases is unable to stand. Permanent paresis of the hind quar- 
ters with paralysis of the bladder and rectum is a frequent 
result of distemper. In some cases there may be paralysis of 
the muscles of the tongue. 

A characteristic pustular exanthema is frequently observed 
on the inner surface of the thighs and abdomen and in abor- 
tive cases it may be the only symptom of distemper. It first 
appears in the form of minute red spots, which after twenty- 
four hours develop into miliary nodules that are surrounded by 
a red ring. These nodules change into vesicles and pustules 
which may become as large as a pea or bean. They dry into 



5IO DOG DISTEMPER 

a 5'ellowish brown crust or burst, leaving a raw surface. Heal- 
ing takes place with desquamation of the epidermis after 
about eight days, leaving pigmented, pale reddish areas which 
persist for some time. Generally, there are only a few pus- 
tules present. The exanthema may spread in the form of a 
scabby eczema over the whole body, to the membrane of the 
external auditory meatus and less frequently to the mucous 
membrane of the mouth and eyes. This eruption, contrary to 
that of sarcoptic mange, is accompanied by only slight pruritis. 
Intense catarrh of the prepuce may appear simultaneouslj- 
with the skin eruption. 

The temperature, which is usually very irregular, is 
higher during the initial stage than when local manifestations 
appear. It often falls with remarkable rapidity below normal 
towards the approach of death. If the disease runs a pro- 
tracted course, the patient becomes emaciated and the hair 
loses its lustre, the body exhalations have a very fetid odor, 
the eyes are sunken, the mucous membranes become pale and 
the patient grows weaker, staggers when walking or lies in a 
state of coma. 

In abortive cases recovery may take place in eight or ten 
days, although the disease usually lasts three or four weeks. 
With severe complications, especially those of the nervous 
system, distemper assumes a protracted course and is frequently 
followed by sequelae, such as paralysis or convulsions at 
longer or shorter intervals, which may persist for months and 
even longer. The average mortalitj^ appears to be from 50 to 
60 per cent. 

§ 396, Morbid anatomy. The anatomical changes in 
the respirator}-- system are those of rhinitis, laryngitis, bron- 
chitis and catarrhal pneumonia. The nasal mucous membrane 
is either very pale or greatly congested, swollen and covered 
with a thick, purulent, grayish green or dull reddish inflam- 
matory exudate which is mixed with coagulated blood and 
collects chiefly between the lamellae of the turbinated bones 
and in the frontal sinuses. Hemorrhagic ulcers are some- 



MORHID ANATOMY 5II 

times present. The mucous membrane of the larynx and 
bronchi is hyperemic, swollen, often infiltrated with hemor- 
rhages and covered with pus. Sometimes catarrhal ulcers 
appear. The large bronchial tubes often fail to exhibit 
changes which might have been expected from the symptoms. 
The smaller bronchi are on the other hand frequently filled 
with a dirty gray and even bloody, viscid pus. There are 
areas of congestion on the surface of the lungs, some parts of 
which may contain but little air. There may be areas of col- 
lapse or those abnormally filled with air. The inflammatory 
foci of the lungs are usually consolidated. In very young 
animals there may be a fibrinous exudate which is very soft 
and which readily liquefies. The hepatization frequently 
involves an entire lobe. The hepatized parts are frequently 
studded with small suppurating foci, or are difFu.sely infiltrated 
with pus. The pleura over the affected parts is often inflamed. 
The bronchial glands are swollen or infiltrated with a serous 
fluid or with pus. 

In the digestive system, the mucous membrane of the 
stomach and intestines, especially that of the small intestine, 
is hyperemic and swollen. It may be covered with a tough 
mucus and is often sprinkled with hemorrhages. In other cases 
it is very pale, swollen and easily torn. Frequently the con- 
tents of the intestine are blood stained and the mesenteric 
glands enlarged and edematous. 

The brain is anemic and often there is a .serous effusion 
into the lateral ventricles and subarachnoid spaces. In a few 
cases there are signs of a purely venous, cerebral hyperemia, 
as for instance, great congestion of all the sinuses, venous 
plexuses and vessels of the pia and the appearance on the cut 
surfaces of the brain of numerous blood points which can easily 
be wiped off. Kolesnikoff found microscopically the brain 
substance, especially the walls of the vessels, infiltrated with 
leucocytes. Krajewski noticed dilation of the vessels, cellular 
infiltration of their walls, filling of the perivascular spaces 
with lymphoid cells and migration of lymphoid cells into the 
stroma of the brain and into tlie protoplasm of the ganglionic 



512 DOG DISTEMPER 

cells. The changes in the spinal cord, which are not well 
marked, consist chiefly of anemia and slight edema, especially 
in the lumbar region. Maznlewitsch states that in acute 
paralysis there are changes in the walls of vessels, with an 
exudate along the vessels and in the interstitial tissue of the 
gray matter of the spinal cord. In chronic distemper, there is 
a localized interstitial myelitis with partial atrophy of the 
cord. Hadden found groups of emigrated blood corpuscles in 
it. In severe cases, according to Trasbot, the spinal cord and 
its membranes are often considerably injected with a sero- 
fibrinous exudate in and under the arachnoid and even into 
the substance of the spinal cord. 

Among the other changes which have been described we 
may mention decrease in the total quantity of the blood of the 
body, combined with a certain degree of hydremia. There 
may be fatty degeneration of the liver and kidneys. The 
muscular tissue of the heart is discolored in consequence of 
cloudy swelling and fatty degeneration of the fibers. The 
lymph glands may be edematous. 

^ 397. Differential diagnosis. Distemper is to be dif- 
ferentiated from : 

1. A simple catarrh, such as that of the eyes, nose, 
lungs, stomach or intestines. The differentiation is often diffi- 
cult at first, as distemper frequently manifests itself in a single 
mucous membrane or in one organ. In general the diagnosis 
is obtained from the epizootic nature of the disease, age of 
the patient, high temperature, simultaneous implications of 
several organs and the unfavorable course of the malady. The 
finding of the pustules of dog distemper is of much diagnostic 
value. 

2. Rabies. The symptoms of cerebral irritation which 
occur at the beginning of the disease may give rise to the 
suspicion of rabies. The characteristic aggressive behavior of 
animals suffering from rabies is, however, absent in cases of 
distemper. The further course of the disease soon enables a 
diagnosis to be made. 



PRKVKNTION 513 

3. The eruption of distemper if widely distributed over 
the body may resemble that of mange. The mild character of 
the pruritis, the presence of pustules on the hypogastrium and 
inner surface of the thighs, the rapid spreading of the exan- 
thema over the whole body and the development of other 
symptoms of distemper and those of mange, however, often oc- 
cur simultaneously in the same animal, in which cases certain 
precautions are necessary in making the correct diagnosis. 

4. Epilepsy. The epileptiform attacks in distemper are 
distinguished from true epilepsy, essentially by their being less 
acute. 

5. It must also be differentiated from simple coryza, 
bronchitis, chorea and paralysis. 

Until the specific cause is found and can be availed of in 
making the diagnosis, much doubt will necessarily exist re- 
specting the nature of the disease where many of the symptoms 
and lesions are atypical. It may be found on further investi- 
gation and the discovery of the etiological factors that the 
symptom-complex of distemper may be differentiated into two 
or more distinct affections. 

ij 398. Prevention. The lack of knowledge concerning 

the specific cause has rendered it impossible thus far to close 

all channels of infection, but its spreading can be checked to a 

considerable degree by isolation and the use of disinfectants. 

It has been stated that the inoculation with the virus from 

very mild cases, which produces a mild attack, will immunize 

an animal for several years. This method is as a rule not to 

be recommended. 

rkfkrp;ncks. 

1. C.-VRRK. Sur la "Maladie des chiens." Rtil. de la Soc. Ccutr. 
lie Med VH., Vol. I.IX (1905), p. 335- 

2. Hertwig. Krankheiten der Huiide. 1S81. S. 48. 

3. jKss. Der Bacillus der Hundestaupe (Febris catarrhalis epizo- 
otica Canum.) Cent. f. Bak. u. Parasiteuk., Bd. XXV (1S99), vS. 541. 

4. Laossom. I'eber Geschichte und KontagiositHt der Staupe. 
Dorpat. 1892. 

5. NiCKOi.DS. Dog distemjier. Am. I'ei. Reviezc, 1900. j). 180. 



514 CEREBRO-SPIXAL MENINGITIS 

CEREBRO-SPINAL MENINGITIS IN HORSES. 

SjJionvfus. Staggers ; craz\- disease : forage poisoning ; 
acute epizootic leucoencephalitis. 

^ 399. Characterization. This is a disease that seems 
to be infectious in its nature, exhibiting s\-mptonis referable to 
a disturbance in the central nervous system. It is called 
epizootic cerebro-spinal meningitis because it often attacks a 
number of animals in the same locality. It often occurs in 
sporadic ca.ses. Although the literature contains numerous 
accounts of its seemingly contagious nature, an analysis of the 
facts fails to bring forth conclusive evidence that it is ever 
transmitted directly from one horse to another. In nearly if 
not all outbreaks, the animals affected have been subjected to 
like conditions of life. This disease is, at the present time, 
peculiar in that its cause is not known, that obvious tissue 
changes are usually absent, and that it has a very high 
mortality. 

J^ 400. Etiology. The cause has been attributed to a 
great variety of conditions, such as fermented food, forage 
laden with fungi or toxic moulds, various unsanitary con- 
ditions and possibly other ill-defined agencies. It seems to be 
true that in most outbreaks all of the animals that suffer have 
had at least some one thing in common either in surroundings, 
food or management. The bacteriological and other examina- 
tions which have been made to determine the cause have not 
resulted in finding a specific agent. Micrococci and various 
bacilli have been found associated with the disease. The 
writer has had an opportunity of making a careful examina- 
tion of animals in two outbreaks. In one of them all inocu- 
lated media and histological examinations gave negative 
results, in the other pure cultures of a colon bacillus were ob- 
tained from the brain. No specific organism, therefore, is 
charged with its production. Xo virus has been isolated that 
is capable of producing it. The nature of the affection sug- 
gests a poison rather than a specific virus. 



SYMPTOMS 5'5 

j^ 401. Symptoms. The mildest attacks are manifested 
by paresis or loss of perfect control over the limbs, loss of 
power over the tail, impairment of appetite and some difficulty 
in swallowing, together with areas of hyperemia and reddish- 
brown discoloration of the orbital and nasal mucosae. In 
other cases paralysis of one or more limbs may supervene but 
without marked fever or coma. 

The more severe forms are ushered in by violent tremb- 
ling, or by stupor, apathy and extreme muscular weakness or 
actual paralysis. In such cases the animal may stagger or 
fall. The inability to swallow is often a marked symptom, the 
saliva falling in strings from the lips. Another common 
phenomenon is the rigid contraction of the muscles of the 
neck, back and loins, the parts becoming tender to the touch 
and a more or less prominent opisthotonos setting in. Twitch- 
ing of the muscles of the shoulders and flanks may be noticed. 
Trismus is sometimes seen. The breathing is usually rapid 
and catchy and the temperature ranges from 104° to 106° F. 
The pulse may be accelerated and hard, soft and weak, or al- 
ternating. The eyes are usually violently congested, of a 
brownish or yellowish-red color, and the eyeballs may be 
turned to one side. Paroxysms of delirium may set in when 
the animal will push against the wall or perform any of the 
disorderly movements following meningo-encephalitis. Sooner 
or later coma and paralysis supervene and death occurs in from 
five to forty-eight hours. In the most acute cases the animal 
falls and dies in convulsions. On an average the disease lasts 
from eight to fourteen days. In the more favorable cases, 
improvement may begin on the third or fourth day. One 
attack does not protect the animal against a subsequent one. 

jj 402. Morbid anatomy. Most writers report lesions of 
leptomeningitis, hyperemia of the brain and .spinal cord, with 
extensive effusion into the ventricles and subarachnoid spaces. 
Petechia; and parenchymatous degeneration of the solid organs 
of the body are also mentioned. In the cases examined by 
the writer tiiere has been an absence of lesions in the nervous 



5l6 CEREBRO-SPINAL MENINGITIS 

system and other organs that could be detected by a gross 
examination. In one case the brain, spinal cord, and organs 
were studied histologically with like results. 

MacCallum and Buckley have found in the brains of 
horses dying of this disease areas of softening " in the frontal 
region on each side, anterior to the motor region of the 
cortex." This lesion was practically confined to the white 
matter immediately under the cortex. In the affected areas 
there was "complete destruction of the brain substance, in 
which the anatomical structures are disintegrated and largely 
replaced by a colloid-like material ". The neighboring blood 
vessels were acutely inflamed, with exudation of leucocytes 
and passage of red corpuscles into the peri-vascular lymph 
sheath and adjacent tissue. In a later epizootic they failed to 
find the brain lesion but did detect the vascular changes. 

McCarthy and Ravenel in a study of fifteen animals found 
certain lesions in the upper gastrointestinal tract and in the 
central nervous system. These were'(i) in the intervertebral 
and Gasserian ganglia where a peri-capsular, small round cell 
accumulation was present. The cells were all of the same 
type, the nucleus and protoplasm being about the size of a red 
corpuscle. There was no evidence that these cells were the 
result of proliferation of the original layer of capsular cells. 
(2) Cortical lesion. These consisted of congestion of the 
cerebellar and cerebral cortex. There were also capillary 
hemorrhages. The meninges were normal. ( t,) Changes in 
the choroid plexus. In three cases the choroid plexus was 
changed into a triangular, tumor-like mass, of a yellowish red 
color and of a firm consistency. . The increase in size was 
found to be due to a proliferation of the elastic tissue sur- 
rounding the vessels. (4) Changes in the peripheral nerves. 
There was a distinct degeneration of the nerves supplying the 
larynx and neck. This was present in the nerve up to the 
ganglion, but was not found in the posterior roots. Other 
slight changes were detected. 

These authors conclude that this disease is not a true 
meningitis, but that the evidence goes to show that it is caused 



CORNSTALK DISKASE IN CATTLE 517 

by some poisonous substance contained in the forage. They 
propose the name "forage poisoning" tor "cerebrospinal 
meningitis" and leucoencephalitis suggested by MacCallum 
and Buckley. It is highly probable that up to the present 
time, cases of uncomplicated meningitis and possibly cerebritis 
have been confused with the disease in question. The entire 
subject must await the results of further investigation. 

§ 403. Differential diagnosis. This disease is to be 
differentiated from other forms of cerebral affection and rabies. 
The differentiation can be made from the clinical history of 
the case, and from the character of the lesion in the interver- 
tebral ganglia and if necessary by the results of animal 
inoculation. 

RKFERKNCES. 

1. Favillk. So-called spinal meningitis. Am. Vet. Revieio, 
Vol. XVII, p. 9. 

2. Hickman. Epizoc'itic cerebro-spiual meningitis of horses. 
Tzcoity-tlnrd annual report, Jlureau 0/ Animal Industry, 1906. 

3. Martin. Cerebro-spinal meningitis. Ibid. Vol. XXI, p. 289. 

4. McCallum .and Buckley. Acute epizootic Leucoencephalitis 
in horses. Bulletin No. So, 3Id. Agric, Exp. Station, 1902. 

5. McCarthy and Ravenel. A pathology for forage poisoning, 
or the so-called epizootic cerebro-spinal meningitis of horses. The 
Journal of Medical Research, Vol. X (1903), p. 243. 

6. SiEDAMGRoTZKY AND ScHLEGKL. Kpizootic cerebro-spinal 
meningitis in the horse. Archiv fi'ir zviss. u. prakt. Thicrheilk. Bd. 
XXII. (.lbstract),y(7«;-. Com. Path, and Thera., Vol. IX, p. 233. 



CORNSTALK DISE.\SE IX CATTLE. 

^ 404. Characterization. The name "cornstalk disease" 
has been given to a somewhat mysterious affection from which 
cattle sometimes suffer while feeding in cornstalk fields late in 
the fall and early winter. The meaning generally accepted 
and intended to be conveyed by this term is, that an animal or 
a number of animals, usually cattle, have died suddenly after 
feeding in a corn.stalk field from four to ten da\ s. From a 



5l8 CORNSTALK DISEASE IN CATTLE 

pathological point of view, therefore, the term is meaningless, 
but it has served admirably as a general term to designate cer- 
tain fatalities occurring under a given condition, which are 
not easily explained. 

This disease is very insidious, frequently causing the 
death of animals before its presence is suspected. Cattle that 
act perfectly well at night are dead on the following morning. 
Usually all the animals in the herd that die of this affection 
perish in a single night or at the longest within a few days 
after the first death occurs. It is generally believed to be in- 
variably fatal and its symptomatology has not been fully 
determined. 

§ 405. History. This affection of cattle has been known 
to exist for many years. The time and place of its origin, 
however, are not known, but it seems to be peculiar to the 
United States and to have first appeared west of the Alle- 
gheny Mountains. We are told of its occurrence in the Mis- 
sissippi Valley forty or more years ago. It made extensive 
ravages in 1864-65 and again in 1868. PVom an historical 
standpoint, no positive statements can be made concerning it 
prior to 1868, when the first recorded investigations into its 
nature and cause were made. After that time the disease 
seems to have escaped the attention of investigators until 1889, 
when Billings, of the Agricultural Experiment Station of 
Nebraska, published the results of his investigations. 

In 1868, Gamgee was employed by the United States 
Department of Agriculture to investigate this disease. The 
"smut theory" of its etiology appears to have been the pre- 
vailing one at that time and consequently Gamgee's report 
deals almost exclusiveh* with the effect of improperly prepared 
food, smuts and the like. Corn smut was unusually abundant 
in 1868 and he carried out experiments to test its etiological 
value with the conclusion ' ' that smut is not a very active 
poison in combination with wholesome food.'' 

In 1889, Billings described the cornstalk disease as an 
"acute extraorganismal septicemia, due to micro-organisms 



HISTOKV 519 

belonging to the class of ovoid-belted germs, to which vari£ty 
of disease also belongs the swine plague, southern cattle 
plague. Wildescuche, hog cholera, and yellow fever in man. " 
BVom the organs of cattle dead from the disease he reported to 
have invariably isolated a bacillus which he affirms to be its 
cause. He identified the bacillus which he found in the 
animal tissues with the one described by Burrill as the cause 
of a disease in cornstalks. In 1893, Dr. Theobald Smith iden- 
tified the bacillus described by Professor Burrill as Bacillus 
cloaca-. 

Billings also found pneumonia to l)e one of the lesions 
characteristic of this affection and in a subsequent bulletin he 
places great importance upon this lesion, although he adds 
very few additional observations to sustain the claim. 

In 1890, a few animals from a shipload of American cattle 
landed at La \'illette, France, died of pneumonia. They were 
examined very carefully by Nocard and other French veterin- 
arians. From the diseased lung Nocard obtained a micro- 
organism which corresponded very closely to the description of 
the bacillus of the corn.stalk disease of cattle described by 
Billings in America. The publication of this fact gave rise to 
a temporary supposition that this American cornstalk disease 
might be a menace to the cattle of Europe and consequently 
initial steps were taken to require American cattle to be (quar- 
antined against it. The fact was subsequently determined 
that the bacillus isolated by Nocard belonged to the septicemia 
hemorrhagica group of bacteria which is usually found to be 
associated with a form of bovine pneumonia occasionally met 
with in America, but not known to be contagious, and the 
matter was dropped. 

A single experiment was made at Champaign. Ill , in 
1889. in which the etiological importance of corn smut was 
tested with negative results. A bacteriological examination 
of the organs from an animal that died in a cornstalk field, 
supposedly of this disease, was made with negative results by 
Professor Burrill in 1889. 

In 1892, Moore investigated this disease and his report 



520 CORNSTALK DISEASE IN CATTLE 

furnishes the information here given concerning the symptoms 
and morbid anatomy of this affection. 

§ 406. Geographical distribution. Geographically, 
this affection is restricted very largely to those sections of the 
United States where the farmers harvest their corn by picking 
the ears from the standing stalks, after which cattle are turned 
into the cornstalk fields. At present, therefore, it is limited 
in its distribution to the middle and northern portions of the 
Mississippi Valley. It is believed that there are exceptions to 
this and that infrequently cattle die from its effects in the 
eastern part of the country. 

vj 407. Etiology. The definite cause of this disease has 
not been determined. It has been shown, however, that the 
former theories respecting salt, water and the bacillus of the 
Burrill disease of cornstalks are not substantiated. The 
hypothesis that the cause rests in the cornstalks themselves 
seems to be the most tenable. It is well known that cattle 
rarely if ever die from eating cornstalks in moderate quanti- 
ties. However, the results of such investigations as have been 
made point as the cause to an intoxication from an excessive 
quantity of one or more elements existing in the cornstalks 
themselves. 

§ 408. Symptoms. The insidious nature and rapid 
course of the disease usually result in the death of the animal 
before its presence is detected. In a few instances, however, 
the sick animals have been observed very carefully by their 
owners, from whom all of our knowledge of the symptoms is 
obtained. One owner found a steer lying down and unable to 
rise. His head was extended, resting on the ground and 
moving continually from side to side ; this was kept up for 
several hours, when he died. In the second place a steer was 
found to remain behind the other animals when they were 
driven to water about 11 A. M. At 3 p. m. he was found in a 
dying condition. 

Another man reported that he found his animals apparently 
well at 5 A. M. At 7 A. M. a heifer was found resting squarely 



MORHID ANATOMY 521 

on her knees, the head extended and resting npon the ground. 
She was frothing at the mouth and groaning as if in great 
distress. She died in about two hours. 

Another report states that the sick animals were dull, 
exhibited great weakness and walked with a peculiar jerky 
movement of the hind legs. The animals trembled as if suffer- 
ing from a chill. In a short time they fell down and appeared 
to be in great distress, heads moving continually backward 
and forward. A fourth owner observed a sick animal tremb- 
ling violently for al)0ut two hours before it died. 

j^ 409. Morbid anatomy. In twelve animals which 
died in cornstalk fields and were examined, post-mortem 
changes were more or less advanced in the greater number. 
A few were examined soon after death. The structural changes 
in the organs were slight. This confirms the statement of 
many veterinarians that the organs of the cattle dying of corn- 
stalk disease are normal in appearance. 

The only gross pathological changes observed were those 
of a hemorrhagic nature. The hemorrhages were mostly con- 
fined to the serous membranes and especially those of the 
heart. Ecchymoses were more or less numerous, however, 
beneath the pleura and under the capsule of the liver and of 
the spleen. The mucosa of the intestinal tract showed areas 
in which the capillaries were deeply injected. Occasionally 
there were hemorrhages. In one case there were pronounced 
hemorrhagic areas in the heart muscle, aorta and pleura. In 
most cases the liver was pale in color and the acini presented 
deep reddish centers with pale peripheries. The inner and 
middle zones of the lobules were more densely congested than 
the peripheral ones. A layer several lobules in thickness 
immediately beneath the capsule was usually more engorged 
with blood than the deeper portions of the organ. In the 
more densely injected areas not only the blood spaces were 
filled, but the liver cells were separated from each other by 
a space of variable width containing blood corpuscles. In 
some cases there were slight changes in the appearance of the 
cellular protoplasm. 



522 CORNSTALK DISEASE IN CATTLE 

In all of the animals examined, the hemorrhages were of 
recent origin and the blood normal in its microscopic appear- 
ance. There were no discolored areas indicative of old ecchy- 
moses. The distribution and general character of the hemor- 
rhages, which are the most conspicuous microscopic lesions 
observed, are ver}^ similar to those described in certain cases of 
vegetable poisoning, more particularh- that of fern root. 

Although certain symptoms described by the owners were 
referable to the nervous system, lesions were not discovered in 
the brain or spinal cord excepting in one case in which there 
was considerable hemorrhage beneath the pia mater. 

In one animal certain of the lymphatic glands exhibited 
more or less blood extravasation, particularly in the interlob- 
ular tissue. 

<^ 410. Differential diagnosis. This disease is to be 
differentiated from sudden deaths from accidental causes, 
deaths directly due to engorgement, or to the consumption of 
too much corn, as occasionally happens during the first days 
that the cattle are in the stalk field. The diagnosis of the 
cornstalk disease must, for the present, depend upon the hem- 
orrhagic lesions and the period of feeding upon the stalks. 
Mayo has pointed out the fact that occasionally cattle die from 
eating cornstalks excessively rich in nitrate of potash. It is 
not impossible that the hemorrhagic lesions are those of .septi- 
cemia hemorrhagica. The only argument against this view is 
the negative results of the bacteriological examinations that 
have been made. 

Of the specific infectious diseases which might be confused 
with the affection, acute anthrax, symptomatic anthrax and 
septicemia hemorrhagica should be mentioned. Each of these 
affections can be determined by its specific nature as pointed 
out under the description of each of these affections. 

REFERENCES. 

I. BiLtiNGS. The cornstalk disease in cattle. Bulletins Xo. 7, S, 
9 and 10. Neb. Aoric. Ex per. Station, 1886-S8. 



INFKCTIOUS AHOKTION 523 

2 BiiiiNGS. The corn fodder disease in cattle and other farm 
animals, with especial relation to contagious pleuro-pneumoma m 
American beeves in England. BuUelins No. 22 and 2:,. C mv. of Nch. 
Agric. Expcr. Station, 1S92. 

7 i)K ScHWKiNiTZ Chemical examination of cornstalks presum- 
ably the cause of cornstalk disease in cattle. Bulletin No. w, U. S. 
Bureau of Animal Industry, 189b. 

4. Gamgek. Diseases of cattle in the United States. U.S. Pe- 
partmeint of Agriculture, 1869. 

5. Mavo. Cattle poisoning by nitrate of potash. Bulletin No. 49. 
Kansas A^rir. l-lxper. Station, 1895. 

6. Mavo. Cornstalk diseases in cattle. Ibid, 1896. 

7 MooRK An investigation into the nature, cause and means of 
preventing the cornstalk disease (Toxemia Maidis) of cattle. Bnllettn 
No. 10, U. S. Bureau of Animal Industry, 1896. 



INFECTIOUS ABORTION. 

^ 411. Characterization. The disease or condition 
known as infectious abortion consists in the expulsion of the 
immature fetus, usually before it has sufficiently developed to 
live after birth, by a large proportion of pregnant animals that 
are kept together. Usually the abortion occurs m cattle be- 
tween the fifth and eighth month of gestation. The disease 
as described bv European writers is characterized by certain 
morbid changes in the uterine mucosa and fetal membranes. 
American observers have not described these changes. In 
cattle it usually affects the young cows. After two or three 
consecutive abortions cows, as a rule, become immune to it. 
Cows suffer most from this condition, although mares, ewes, 
and other species are occasionally reported to be affected. 

In Xorwav infectious abortion is scheduled under the so- 
called "milder contagious diseases." Tlie ow