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Oskar Doty 


THE CLINICAL. PATHOLOGY OF THE BLOOD 
OF DOMESTICATED ANIMALS 


THE MACMILLAN COMPANY 


NEW YORK «+ BOSTON + CHICAGO - DALLAS 
ATLANTA + SAN FRANCISCO 


MACMILLAN & CO., LimitepD 


LONDON + BOMBAY - CALCUTTA 
MELBOURNE 


THE MACMILLAN CO. OF CANADA, Lt. 
TORONTO 


@ 


THE CLINICAL PATHOLOGY 
OF THE BLOOD 


OF 


DOMESTICATED ANIMALS 


BY 
SAMUEL HOWARD BURNETT, A.-B., M.S. D. V. M. 


PROFESSOR IN COMPARATIVE PATHOLOGY, NEW YORK STATE VETERINARY 
COLLEGE, CORNELL UNIVERSITY, ITHACA, N. Y 


SECOND EDITION REVISED AND ENLARGED 


WITH FOUR COLORED PLATES AND 


TWENTY-THREE FIGURES 
q 
353 ; 28. 
3 


23. 


Nem ¥York 
THE MACMILLAN COMPANY 
1917 


All rights reserved 


Copyriant, 1908, 

By SAMUEL HOWARD BURNETT. 
Copyrigut, 1917, 

By THE MACMILLAN COMPANY. 


Set up andelectrotyped. Published October, 1917. 


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bay 


B81 
Bene 


Norwood jfress: 
Berwick & Smith Co., Norwood, Mass., U.S.A. 


Cu 


JAMES LAW 
A PIONEER AND LEADER 
IN VETERINARY EDUCATION IN AMERICA 
THIS WORK IS AFFECTIONATELY 
DEDICATED BY ONE OF HIS PUPILS 


PREFACE TO THE SECOND EDITION 


The purpose of this book is to furnish a text-book of hematology 
for the use of students and practitioners of veterinary medicine. 
It is also intended to render easily accessible for investigators 
data concerning the blood of the kinds of experimental animals 
commonly used. 

Compared with the investigations made on the blood of man, 
but little has been done on the blood of domesticated animals. 
Some work, however, has been done. The results obtained are 
of more value than their mere amount would indicate because 
we have learned from the studies made that similar pathological 
processes produce changes in the blood similar to those produced 
by such processes in man. So the rich results obtained from man 
are made available to the veterinary practitioner. 

Free use has been made in preparing this book of the standard 
works on the blood of man. Those of Ewing, Cabot, Da Costa, 
v. Limbeck, Naegeli and Grawitz were used most freely. Refer- 
ences will be found in the text to the source from which material 
has been taken. A list of references is given at the end of each 
chapter for the use of advanced students. 

In the first edition what was reported by different investigators 
as normal was given without indicating which of these the author 
considered more reliable. Undergraduate students and most 
practitioners can hardly be expected to know what to consider 
as normal when they find considerable variation. In this edition 
what is considered to be the normal for each species is stated. 
Tables summarizing the results obtained by the different investi- 
gations are also given. 

praca, N.Y. 

Feb., 1917. 
S. H. BURNETT. 


TABLE OF CONTENTS 


PAGE 

PE SCERCHMS METS TE AUET ONS 2 cys 4 1S Sihicrs ui Yoven 2 trate a nnkas Gey take meen Leola aes Xill 
__ DEESIDE 1 i pe ecg olas ie ee OR a oh A XV 

CHAPTER I 
METHODS OF EXAMINATION 
Re SaRTTAVITRH EUS OOEL ce em in, acct ee Caetano heen). 2 eth ahs Se AOE 1 
Smiiinescne Ted COrPUSELES. f=. Jackie awk ala Shece hh her dso ate waade wake ene 2 
MntrprrbiH AUN GUCUEOEV LES a 65) fois dogo costo nae mw hoe ele ns cee 8 
Ono ihe, DGGE PHALESi io. +e 2 lates es hae seed genesis ob cs lRatees 9 
Estimation of the amount of hemoglobin. ........................4.. 11 
SPER CINE: a CIOL OMIEN SCAIC 58: 02h 4p estcnAaty ohana Ss ooh Ce 11 
ower s hemoplobinometer: 2°48 Sachs oe lowe tee cet oe 12 
Danes shemoglobimometer.c Ao c..6 sen oo ee eee all) 
Mleisehl-Miescher hemometer .:2). s.4...¢ 043.0) oe he nee os ns ere ee 15 
Peo icminex Anni AIO 10 bats = Cae cy baa LS oc MR late 16 
Reis ite Freak COMEMMOMS f-0s Soa sto kd ae ike Wert kesh eke oa ee 16 
in-itxed!and(stamed preparations: =. 20.000 oe. ne Se. oe cen soe 17 
Ditterentialcountime of leucocytes! mw... vhs ss oe ee eee Zyl 
sles tHlonsel Gores. may scam yes) hey her, Wi eed emer ctl 22 
Test for fat. SR eR lon PE aA RIE peter Oe EE ALAS RA ere 23 
The total volume a blood aad Its OXV ECM CAPACliy> 7i. Mares soe: 23 
The relative volume of corpuscles and of plasma..................... 24 
SUIS ICGLNE PCAVIN eee se 27s, 5. he, ots ae pe es one SG 4 ace ae ie 25 
ESE DRETTE AGLERE TG C7 FAG SR ks nce de a eT Ee 25 
hestiton specitmmagelutinins or precipitins=., 5. -.... a8 o40.225.5508 26 
nacteniolopical- examination of blood: 2.2. <5...) ....06= asemren ot os Soe 26 
RELCRCNGCR era eee Pr ie a heen ee MY crue Ey UIA cy. oi ole Dil 
Partial list of text-books on hematology...) ) 2... 20. 50 ess oe elon 27 
CHAPTER II 
MORPHOLOGY OF THE FORMED ELEMENTS 

REM EP EOI SG LES cn tir arent NO am eg ee hn aha Lees so Sone « Ge SRI 29 
TGC CO CNL CS tale te We ee te aN, EER RI A: 3 Tans DSN cae as 8 Aur, ee Meet ah es 30 
Degenerative epee INBIGUCOCYLES a. ewes ae a eae Ree ee ee 35 
LD TIS UOA ae Mes gk gee 2 en oe eee ge 36 
TUDTOMDOCY LEB ew ae te. ect Ne AMS ea aa aso Stan tah reccbots lsemare es 36 
“BLOGS GMS ci Ree Re a rite ae, gn re ea 37 
aE RE CMs eye WIR 2 sd Gea ol hs apes hemes 2 Ree oomins AY OMe 38 


x TABLE OF CONTENTS 


CHAPTER III 


NORMAL BLOOD OF THE SEVERAL DOMESTICATED ANIMALS PAGE 
TLOVSPS woo. ecihis 0 ok cia Baye, bce iat ioe Ana Een eit eb eee ere 40 
Go) ee eee i ey MP Paired Gel etl haat ee tities 0 42 
POPE ID seagate 622g oi, <n e a sNews eee ev et ro ee oat ee ene ae 44 
0: nS PEPER Es rte eb mbls Se) eS mee d b 45 
PIE Sass. os se Ries a Bre oad 0 usleniains et OREN g @ tae Rl tine rm Pct nie reasecente cet eae 45 
(6) Nn ee ea Rear tnpeny Yeu itor een A ee OL eee ee OS 2 hs mT 47 
SWINGS nk Soc foe Gatla lb oblige ike 3 SOREN AT e eta reTae Ce Ent OPE ts ee na 49 
(15) 6) | i rma ie mpi vis yates ECan Ares cian dl, Soa o 50 
OPT ae 6) | a Pere abl mene) vos cereale Ci: tty Nee! 52 
Wamestic Ow]... : ss. cos Wiis 2 Races tee one ie tens aie eee a ae ee 53 
RRGLETeD GOB: bas Foci ere eyes ee Ste geass ee ere ees ence cra ee 55 

CHAPTER IV 
VARIATIONS IN RED CORPUSCLES AND HEMOGLOBIN 
Blood from different portions of the vascular system................-. 60 
Rolyéy.thenaigis.( 255) os WG vss ol Aveta ie oe eee eae ae ee 61 
ag eae et ee eRe ies Mid citar Leo nes cise rahcks Ja) < 62 
Of Sn nn a Mean tenors bare e Cee ene PocrmamS Oo Ayo tic Nasi 2 62 
Preenancy andparturition/is: 1. e sae aales ee eee eee 63 
High altitudes. fo. ..i4 « «lane ¢ Soceis aes falamels Oa re stein keys era e 64 
I 00 ae ee ern eenet Minn te Sls ey yy cpa SA a AOD elo ho 64 
Iya: err AS ane tenet OMA MAA SO SCAU GAS SS 68 
CHAPTER V 
INFLUENCES AFFECTING THE LEUCOCYTES 

TeuiCoeytOsis: Sass eae vw en Cec ope Ces cae eae oh ee ee 70 
Digestion: ac..a™ < ..-8 2s ss halon ee peeey: de Ones Gis geen 70 
Pregnancy atid parturition. 5.0 3. 3. ons tee elaine eee ol ge ral 
Tn“the new: born: :./.:.°><teies. oo ms cee fas beet te meh agli ure ee 72 
Violent exercise, cold baths and massage........................-... 73 
Inflammatory leucocytosis. <<). crt «Soke ene eee ae 73 
Experimental leucocytosis; ¢ cd. <nq0es ot ore te aie oe 75 
Post hemorrhagic lewcocytosis;...;.. 5 .\ca; sx ose ce ens oe 78 
Ante mortem leucocy tons .:.\25. dssfe\. wie aco gage io beter alae orca chan omen 79 
TiymphocytOsis. «is 3/5 5.0c0'2 <2 bin cto uh mere so ie ae ot eee a ee 80 
Bosinophilia... =... os oc ccs ble TA ok sheer: Grebe teat tee So Rte eee ee 80 
Basophilay.- so ccc 2 ss ob wie bo Bla he ea tae ISDE ae Np ete eo 82 
Occurrence of myelocy tes: . 2 olay -euerre reas le ates tds nee eter 82 
Leucopeniian « .... 26. seks bee 30 ak) Weta Bika lh © tate eee enreaeiee eeeas 82 


References... <5 c= ss 0s dis bitin Vehoca delay Se are oe One ete en OUI PI en 83 


TABLE OF CONTENTS xi 


CHAPTER VI 

SPECIAL DISEASES OF THE BLOOD PAGE 

FRSDINIGIOUS ATA CIAL ge at ayes SS esis tes He ais Latter de hiss cerns CURIE eee 85 
He Girl eGyea yo, ee Re eign Sot ol Se tie Sn) a ee ee he eh EA 87 
Mirxedacellediecins cis ects eon eo ae nee eRe ceriche eens eta O87 

IDS via ay a) TENCE Siete aoe RANI SiS Pano ace ae Wier eS ae Geen eee . 89 
OCCU CE Veet fia ae ee eer ees en eh anes Oa ye a 91 
AISOTI OL SUE ETN Se eels sean ee aE ee ST Pec nO. es mania deena « De cbenavag 92 
Relation of pseudoleukemia to leukemia and sarcoma................. 93 
FRG RENGM CESEe bag Hatem Bet ie Ce Fos: Wen tee Bavtals 5 Mk ayn Se ae 94 


CHAPTER VII 


GENERAL AND INFECTIOUS DISEASES 


ET eLGONSIC CHALLONG ys © oS tree ehsrese ol clothe crane oie srcle witches al aay Pee 95 
BITeTC HE CULOLMGV. CTE Ayn eas yee cher sco aor Neate eck oh hehe ROPE ea Oe 95 
Simplen(don-s pectic infections, see. ac cts Gta eee esse om eis oe ee 96 
TRUBS CES a 1k Bo ee eared his Ane a aOR roe DUS: EG ERR ys Fe 99 


CHAPTER VIII 


SPECIFIC INFECTIOUS DISEASES DUE TO BACTERIA AND FUNGI 


NSU VEH Gish sh dat SA TIS See a eee SP Eccl Rema 100 
Sroupouspponeumoniay IM MOVSeS’s vi acts. asf isioe deo teat ese sep 101 
TUR OSHS cg SG ER a ee Oe Aa 6 rE RIAU INES oo SO eee MES est 7 Aey Mi hee 102 
Mow! cholera. : =... 2.0... oN ee RY eek gE Da Mer steed Nt 103 
[ERO XA TE] 0) OCG Os Ree eR on A ee a ey eee) an OS RPE RB or ws 2 104 
ANTI CREB Si oe REO Cane Gace OCICS ROR RC ERT ES” SCRE aE Ci CR A> Peer Atroe 105 
(GHITT GIRS. 6 thos UR Ay RE tee oS ae TL gee re es pene ee eer a 108 
SRE CNIS EV! As Gh ots oh ge Nee cco cpa oe cacti eis ale kh deme alee ene 111 
TRECISTORTDS eyes c allbcckt eee nC en” oc Sah ant i Regie ROE ee rene Rene NE re 2 112 
PNG HINMOLTY COSISMEE SAP aA oy Sista, oye ceees ohm ico buctagtlests 6 ois SEA EE See eae i 113 
ESO GTA OILY GOSS ces eacens aie, a9 ccuks says siekotay ucla estan oenaln srneiabe lsat seeteermeeye Nee ee, wale 
VERDES MUOHSUITATIS ae eters) ote fa aes oe Sia oe theyre arorele aioe Meteo isc me a alee 114 
[NXE ESREVINOSEIA. 5 G3 Cg RG Cho CICERO a CIS ACRE oo, OR ae ote acee aeRO peacteens rat & 114 
CHAPTER IX 
INFECTIOUS DISEASES DUE TO PROTOZOA 
SS DNL SITS Oe pales lle 2 aN es Nr ar ea Pear Shy ey ae o 2 116 
pet COME Ea RM UE SG to tM ied 0. 3 ete wuts ecco ea as AMES arte 117 
“TPES EISS TNH SS OI en ORS eG EOC Ne REED ORT Ue es een ae 118 
RIF EGP ADTOGISIS: 35): su2 2s 2 26 tC ieralthe «we Rae DA HeS weceancin Geae wisn aa aes 123 
Re RRR SURES PASHILOBIS Sp: 0 55) = (2°. s Wi SSR ne Bolt ee hacer aes thane ns tlre 129 
EULESS UTAG (a Sa SS a Oe CPE ee eR 131 
1Bir] OGTR Aaa NIE a Saeco aver hese ROM Oo pee ae OOO Sees lencene citaa ai aetna 131 


xii TABLE OF CONTENTS 


PAGE 
Hast coast f6ver. dic ©. <Sece eh oo ee de een sade RT ae 132 
Piroplasmosis ‘in. cattle in. Transcaucasia.” << 24.2. fneiene ss as eee ees 133 
Trypanosomatosias ..(... 30... 65 sane eee bees Hee ee le cece aan 133 
S109 0: ee anne sR Deere ee owe ert ae Nr A ee ie he eS. 5 < 135 
DN CT 0 eo eee aU tree Arp osha no ciewo.s OE bc on & 137 
OUTING fof) o Feae ooh 3 kc ONS oR en Te ee 138 
Mal de. caderag oo Seles si. 4 Fee Se ee ee 139 
Gambian horse: sickness: :\ <5. doth cere Oe ee Oe ee 142 
Trypanosoma thelleri. ¢ :.3.¢ Se ieee eae Ae ae ee 143 
RRefETeNCS's:fsa.w. eas oe ee eee eee 144 

CHAPTER X 
DISEASES WHOSE CAUSE HAS NOT BEEN DEFINITELY DETERMINED 
Dog distemper s.. = mtcer secrets eres Sere cee ae 148 
Rinderpest S65 els ccs ccs cteress « etal oe ates oe Te a 148 
Hop: cholerai: 2. 5h. xa jo ss cosas tcc ee orate eee ee 150 
Higuineinfectinusanemiar 55 san. ee ce reo Ht RO eee 150 
UH eumMatisnns « j)soc0s ener ea Os eee noha a eee ea ee 152 
References. 6 2 42.6:0 505-5 tgs wucioelis ne epee Mens 1. Cheetos BRO e Ee one eee 153 
CHAPTER XI 
DISEASES DUE TO ANIMAL PARASITES 

YC hg Gl) er ee ON SEE Bid uSpousoud onc 155 
Rel Minthiasis'e scr oe acco dosh ones OB oie ee Oe EE eee eae 153 
Sclerostomatosis in horses... us) oc) nc woos Cee ee eee 157 
TriGhinOSi8 iS 8.c6% s5t ew vaso bie Aa eee as okie SE Oe Sy 
Hilariasisin Cogs s. « :...- 5s dchcer neers Seine euch ere one ea ee 158 
"POMIASIS 2s S05 ccc eats is es Oe Oe re 159 
WMCINATISSIS:: 825 eis See sk ae ead ooo ate, extn Dd 159 
Oxyuris, Strongylus'and Ascaris. 3.) ..0:22ece 8. ee ee Si a 159 
1 Ac) (3) 2) 13 rr ere ne. OEE as it GIS Sia > nicih ay on wo ~ 160 


|G 000 (=>. de ee ne eine E ener t Me Ae hee Sa Se oa a neo 161 


LIST OF ILLUSTRATIONS 


PAGE 
meawn rs. Normal blood of animals. 2.2 .....5. «ied see. cde ede oom oi: 29 
eenepul sem eOLpHSGles., 54 bof 2s wee oa seed Lie ig Sain ha ee 30 
Piers Til. Blood of the domestie fowls: onc... nce cece cae oe ede 32 
Puate IV. Lymphatic and mixed celled leukemia.................... 88 

FIGURES IN THE TEXT 

hic ienuhewkthomayhematocytometer)... 425 0... 206s acne eee 4 
Biass2—55 ulmesiot countins chambers: «1.2. ..2..ss.e8ss-e eee ook 4 
Bie G er balla wist aehemoplobin Seale, es.) 24's. ac\e occa ea ooh ore mlee eae 11 
Haws. Gowers hemorlobinometer. 3) 25 .c6c 605 sees eeee ceca. ck ee 12 
easton Hare's hemoglobinometers.... 24 60:6. oles coe os oho 14 
Fic. 9. Fleischl-Miescher hemometer.....................-.+-2-8- 15 
reel spreading film on glass SUG... 2. ne eile ce ce ba cts eee 17 
RirGasiieelood-ofcaseof anthrax, COW 2... acta oss aes ao oes nee 106 
Ree EES ANES A IPCI! 2 52 ok, on ee Som Astatte ok Saltese eee 119 
Petes caret Eset CR Ioe CANIS "se 42 02 na, S Meals vce RRA ate wt By ores Bae TE 124 
Peer l rren ES APICAL EHUEEANIS He e.5--,)-. « o.0!-sic's) co ptitan hn Satie o tee wet ene 132 
RiGee mmeh eilertanparvarsd serv Aeore k.. tee so AIO one ie eee 133 
Hee GO eelry PASGSOMaGVANSIS. ore che c.chti etree a aoe le mach eee ee 136 
Geel peelryp an Osoniss DEUCE! cer gaes fl: 5 aeons oan oc eck crs tetera 137 
re) Ubry panosoma Cquiperdunm: 2252). Ger snc Sef ltwrnies os dee o nae f 139 
re. 19. Trypanosoma equiperdum, mice: .5....:.....00-5+600ee res 140 
Bec 2 OR iry paAnOsOma CQUINUMA ts qee - hohe ina ae ee ee aioe ee 141 
Dre 22 ny peOSONIA, GHMOT POM: <.). {p62 ci, sisal ogc oss «a eR 143 
areca Wey AMOR Oin GHETELE ie 6a, vals alec tc oa aan eee eee 143 
MiG. 2s. sBilsriy mutts in blood; dog: .)\.. eaves 2s yds se esse seer 158 


1 
ha, 


— = | 


—— 


A an 


Cee eae 


INTRODUCTION 


The blood may be considered as a tissue composed of a cellular 
part and an intercellular substance. The cellular part comprises 
the colored and white corpuscles and the plates while the inter- 
cellular substance consists of the fluid portion. The blood is a 
peculiar tissue in that it is in intimate relation with practically 
all the other tissues of the body, bringing substances to them and 
carrying away other substances. Thus the blood is affected by all 
the tissues. One might expect that the blood would give a good 
deal of information as to the state of the activities of the tissues; 
but at the present time comparatively little use is made of the 
chemical substances contained in the plasma. In the first place 
they are present in very small quantities, as an excess is prevented 
by prompt elimination; and in the second place many of these 
substances have very complicated structures. In fact the chem- 
ical make-up of the blood is but little known. Ina clinical examina- 
tion main reliance is placed on physical and histological rather 
than chemical methods. 

The value of an examination of the blood varies in different 
conditions. In general it may afford sufficient information to 
make a diagnosis in a few diseases, such as leukemia, Texas fever, 
surra, anthrax and filariasis. It gives more or less valuable as- 
sistance in a very large number of conditions, as secondary anemia, 
sepsis, suppurative processes, intestinal helminthiasis and hemorr- 
hagic diseases. Finding that the blood is normal is often a great 
help, as it enables one to differentiate from the diseases in which 
the blood is not normal. Hodgkin’s disease is diagnosed by a 
blood examination, yet the blood is normal in the early stages, 
this serving to distingiush it from leukemia, which produces 
marked changes in the blood but has otherwise similar symptoms. 
Besides its value in diagnosis, the blood frequently gives most im- 
portant indications as to prognosis and treatment and is of value 
in examinations for soundness. For example, in pneumonia there 
is ordinarily an increase in the number of leucocytes. If instead 


XV 


xvi INTRODUCTION 


of there being an increase the number is below the normal it is a 
bad sign. During the course of this disease the reappearance of 
the eosinophiles is a favorable sign, indicating that the crisis is 
passed. In an anemia in which the hemoglobin is much lessened 
while the number of red corpuscles remains nearly normal, the 
indications for a prompt improvement under the administration 
of iron are good; while but little improvement is to be expected 
when the amount of hemoglobin in each corpuscle is normal and 
practically no improvement when the hemoglobin index is above 
normal, iron being practically contraindicated in the more severe 
cases when the blood shows very large red corpuscles each having 
an increased amount of hemoglobin. In examinations for sound- 
ness the blood offers valuable aid, as has been pointed out by 
Moore. When an examination reveals that the blood is not nor- 
mal a close search for the cause is indicated. The presence of 
disease, unsuspected it may be by the ordinary means of examina- 
tion, may be shown by the blood. Though the fact that an animal’s 
blood is normal is not indicative that the animal is sound, it is 
an added safeguard, and on the other hand an animal having an 
abnormal condition of the blood cannot be certified as being 
sound. 

In interpreting the results of an examination of the blood it 
must be kept in mind that this is but one symptom. A diagnosis 
should be made after duly considering all of the symptoms avail- 
able. The blood is not supposed to supplant other means of ex- 
amination, but is to be used with them. In fact it will have a 
strong tendency to sharpen one’s powers of observation for other 
symptoms. 


THE CLINICAL PATHOLOGY OF THE BLOOD 
OF DOMESTICATED ANIMALS 


THE CLINICAL PATHOLOGY OF THE BLOOD 
OF DOMESTICATED ANIMALS 


CHAPTER I 


METHODS OF EXAMINATION 


Ordinarily a clinical examination of the blood consists of count- 
ing the red and white corpuscles, obtaining the amount of hemo- 
globin, and making a histological examination of stained speci- 
mens. Occasionally other information is desired, as the total 
volume of blood and its oxygen capacity, the relative volume of 
corpuscles and of plasma, the number of blood plates, the specific 
gravity, the time of coagulation, the presence of specific agglutinat- 
ing or precipitating substances, and the presence of parasites. 

Procuring the blood. Blood may be procured from any part 
of the body where the circulation is normal. Inflamed or edema- 
tous areas are especially to be avoided. A cold or bloodless part 
is unsuitable. If a cold part is warmed, sufficient time should be 
given to allow the circulation to become normal before procuring 
blood for examination. In the horse and cow the under side of 
the tail where free from hair, slightly to one side of the median 
line to avoid the middle coccygeal artery, is a convenient site, or 
if preferred, the rump or the side of the neck may be chosen; in 
smaller animals the lobe of the ear will be found suitable; in the 
domestic fowl the comb and in the pigeon the under surface of the 
wing are easily accessible and convenient. 

Preparation of the site. The part from which blood is to be 
obtained should be washed with water, in the larger animals 
where the incision is to be made with a fleam, disinfected, and 
then dried with alcohol. Vigorous rubbing of the part should be 
avoided as it produces a transient local change in the blood. In 
case the neck, or other part in the horse or cow having long hair, 
is selected the hair may be parted and the skin, exposed in the 

1 


2 METHODS OF EXAMINATION 


parting, washed as indicated. It is not ordinarily necessary to 
shave the site. 

Puncture. In the larger animals it is advisable to use a fleam 
or a scalpel for making the puncture as a blood lancet does not 
yield sufficient blood. In the smaller animals a blood lancet or 
straight surgeon’s needle is preferable. Whatever instrument is 
used should be sharp. A dull needle or fleam causes more pain 
and affords less blood than one that is sharp. In the domestic 
fowl blood may be readily and easily secured by snipping off the 
tip of one of the points of the comb. 

Securing the blood. Before making the puncture whatever 
apparatus or material is to be used should be ready and within 
reach so that there may be no unnecessary delay in securing the 
blood for examination. Slides for making smear preparations, 
the hemoglobinometer and the pipette for making the dilution 
should be clean and within reach. The bottle of diluting fluid 
should be unstoppered. A towel or clean cloth should be at hand. 
After the puncture is made the first three or four drops of blood 
should be wiped off. Then freshly exuded blood should be secured 
for examination, for counting the red corpuscles and leucocytes, 
for obtaining the hemoglobin value, for making smears for his- 
tological examination or for other kinds of examination. The 
more rapidly blood is secured for these several processes the 
better. Blood quickly changes when exposed to the air. Clotted 
blood is wholly unsuitable and even before it clots blood undergoes 
certain changes, some of which simulate changes found in patho- 
logical conditions. Blood should be obtained as nearly as possible 
in the condition in which it is in the blood vessels. After sufficient 
blood has been secured the edges of the wound in the larger ani- 
mals should be held together for a few seconds until they adhere. 
On the following day it will require careful search to find the 
wound. 


COUNTING THE RED CORPUSCLES 


The red corpuscles are so numerous in the blood that it is neces- 
sary to dilute it considerably to be able to count them. The 
diluting fluid must be of such a nature that it will prevent coagula- 
tion, will not change the corpuscles and should be of such a specific 
gravity that the corpuscles will settle, not too rapidly or it will be 


COUNTING THE RED CORPUSCLES 3 


difficult to get an even distribution of them in the counting cham- 
ber, nor too slowly or one will have to wait too long for them to 
settle. Toisson’s fluid combines these qualities perhaps the best 
of the diluting fluids in use. It has an added advantage in that it 
stains the leucocytes, rendering it possible to count them in the 
same preparation with the red corpuscles. Toisson’s fluid should 
be filtered before using as fungus will grow in it producing spores 
which may be confusing in making a leucocyte count. Hayem’s 
fluid is also a suitable diluting fluid. 

Under some conditions Toisson’s fluid is not the best that may 
be used. Jones has called attention to the counts being lower 
with Toisson’s fluid than with Hayem’s in certain cases of severe 
anemia. He found that Toisson’s fluid gave lower counts in cases 
of pernicious anemia in man and in experimental cases of anemia 
in rabbits produced by bleeding or by phenylhydrazin. It would 
be better to use Hayem’s fluid in cases of severe anemia. It is 
not certain that the formula for Toisson’s fluid is the best for the 
several species of animals. 


Formule: 
Torsson’s FLuip 
SATE UMPC 8.08 2s heh S-okh eiciaes Soe ISG A oe Sets 8 grams 
psesemoumrenchilnnlelese = -7.>-\. Se 2 csetus des Ps Fo. So re ee hoe 1 gm 
G lyon Me minal sates see sate in A Seas Bene ahh pas 30 ce. 
DISEMIECIWALEKC ee ae Re einai at De ee. ie LOO ce. 
Niethwertolet-s lr. nr meme sts eel Nei) vena oe .025 gm. 
Hayem’s Fiuip 
Wercurierchlorid Gm aps se eerie eke ee eee hee oe eas Oe 0.5 gm. 
SENT 1 J TAPE Bn oops nn Ae Pee ha ea ae Re ong Tomei 5 gm. 
SodiurmmchlOnid cece ge ore oe ka. se a ear pene ero» Lona: 
Dishilledswatermme cee es Aes ee ie sisi Gees ve eae a 200 ce. 


While several methods of counting the corpuscles have been 
used, Thoma’s hematocytometer, which is a combination of the 
older instruments of Malassez, Hayem and Gower, has come to 
be used as the most reliable. 

The instrument consists of a counting chamber with an ac- 
curately polished plano-parallel cover glass and a diluting and 
mixing pipette. The counting chamber is a thick glass slide on 
which is cemented a square plate having a circular piece cut out 
of the center. In this circular space is fastened a small circular 


t METHODS OF EXAMINATION 


—— 
a7 . - 
pS aFiara) Rih e ei sh Baadlsand edd ST) eet mg oo re eco ta 


INA 
B 


Fig. 1. The Thoma hematocytometer. 


dise which is thinner than the surrounding plate. The distance 
from the top of the disc to the under surface of a cover glass placed 
on the plate is exactly 0.1 millimeter. The upper surface of the 
disc is ruled as shown in Fig. 2. The central square is ruled with 


1 


lines ;45 mm. apart giving 400 squares each containing zy5 Sq. mm. 


HH 


Fie. 5. Turck. 


Rulings of Counting Chambers. 


COUNTING THE RED CORPUSCLES 5 


The Zappert-Ewing ruling, the one to use preferably, has besides 
this central 400 squares additional lines as shown in Fig. 4 giving 
a ruled space of nine sq. mm. With each instrument are thick 
and thin cover glasses with plane ground surfaces. The thick 
covers give more accurate results. The mixing pipette is a cap- 
illary tube divided into ten equal divisions and terminated by a 
bulb of 100 times the capacity of the tube. Thus when blood is 
drawn to the mark 1 on the tube and diluting fluid is drawn to 
the mark 101 a dilution of 1:100 is obtained. The bulb contains 
a glass bead to facilitate mixing the blood and diluting fluid. 
Attached to the pipette is a flexible rubber tube having a mouth- 
piece. The pipettes are made in a long and a short form. The 
longer form is preferable as the shorter form is constricted at the 
point rendering it liable to become clogged and making it very 
difficult to clean should it become clogged. 

Method of using. The bottle of diluting fluid should be 
within reach and should be unstoppered. In using, the point of 
the pipette is immersed into a freshly exuded drop of blood. With 
gentle suction blood is drawn up to one of the divisions on the tube, 
the pipette is withdrawn and the blood on the outside of the tube 
quickly wiped off. As quickly as possible it is placed in the dilut- 
ing fluid with the point well below the surface and the diluting 
fluid drawn in filling the pipette exactly to the mark 101. The 
blood and diluting fluid are then thoroughly mixed by shaking 
and rotating the pipette: Care must be taken to draw in fresh 
blood, the slightest clotting will necessitate cleaning the pipette 
and repeating the operation. Care must also be taken not to 
draw in air with the blood or with the diluting fluid. If any air 
should be drawn in it is well to at once draw in diluting fluid to 
prevent the blood clotting in the pipette as it is difficult to remove 
clotted blood. With the blood thoroughly mixed with the diluting 
fluid it is not necessary to make the count at once. If the pipette 
is kept in a horizontal position it may be carried some distance. 
It is better to make the count as soon as possible, though the 
blood will keep for several hours unchanged in the diluting fluid. 

Filling the counting chamber. When ready to fill the count- 
ing chamber, the pipette should be shaken and rotated to get an 
even distribution of the corpuscles. One minute will usually be 
found sufficient for this. The diluting fluid in the long arm of the 


6 METHODS OF EXAMINATION 


pipette is then expelled by compressing the rubber tube and twist- 
ing it. 

One should never blow in the tube as that would be apt to cause 
saliva to mix with the diluted blood. After a few drops have been 
expelled a medium sized drop, obtained by simply compressing 
the rubber tube, is placed on the center of the counting chamber 
and the cover glass adjusted. In placing the cover glass care must 
be taken to avoid including air bubbles. If one side of the cover 
is placed in position and the other gradually lowered there will be 
no danger of including air bubbles. The cover glass should be 
placed as quickly as possible. A delay will result in an uneven 
distribution of the red corpuscles, the surface of the drop before 
being covered being rounded the corpuscles fall on the ruled dise 
from unequal thicknesses of fluid. The drop should be large 
enough to fill or very nearly fill the central dise without running 
into the trench or between the cover glass and the plate. The 
proper size of the drop must be learned by experience. With a 
little practice one can get the proper sized drop at the first trial. 
If the cover glass fits closely a play of colors (Newton’s rings) will 
be seen between the cover glass and the plate. If they are not 
seen it is because the cover glass is not in place. The layer of 
blood is consequently more than 0.1 mm. in thickness. Gentle 
pressure on the corners of the cover glass may facilitate the ap- 
pearance of the colors, but they must remain after the pressure is 
removed. The counting chamber and cover glass should be cleaned 
and another drop adjusted if the fluid runs into the trench or be- 
tween the cover glass and the plate, if the disc is not well filled with 
fluid, if air bubbles are included, if the interference colors (New- 
ton’s rings) are not seen, or if the blood is found to be unevenly 
distributed. Time is saved by brushing off dust or lint from both 
counting chamber and cover glass with a small camel’s hair brush 
before filling the counting chamber. 

Counting. The counting chamber should be kept level after 
the drop of blood is placed in it. The count is made on a micro- 
scope with a level stage. It is convenient to use a x 4 (2 inch) 
ocular and a five mm. (4 in.) objective or a special four mm. (% in.) 
objective with a long working distance, N. A. 66. After the 
counting chamber is placed on the stage one must wait until the 
corpuscles have settled on the lines. Count the corpuscles in one 


COUNTING THE RED CORPUSCLES t 


hundred squares. It is well to count blocks of 25 squares in each 
corner of the ruled space. Clean the counting chamber and cover 
glass, place another drop and count the corpuscles in another 
100 squares. The pipette should be shaken for a minute and a 
few drops expelled before placing the second drop in the counting 
chamber. If the two counts do not agree closely count another 
100 squares in another drop. 

Computation. Divide the number of corpuscles counted by 
the number of squares counted, divide this by the dilution and 
multiply this quotient by 4000 as each square represents z555 
of a cubic millimeter of blood. The result will be the number of 
corpuscles per cubic millimeter. 


N O. Corpuscles counted x dilution x 4000 _ No. of corpuscles per 


y No. of squares ith 
For example suppose 1321 corpuscles were counted in 200 squares 
with blood. diluted .5:100. The computation would be: 


1321 x 1000 x 4000 
200 x 5 


= 5284000 


The blood examined has 5,284,000 red corpuscles per cmm. 

Limit of error. Using such a high dilution and such a small 
quantity of blood the error is at best rather high. Thoma and 
Lyon obtained an error of five per cent. in counting 200 corpuscles, 
two per cent. with 1250 corpuscles and one-half per cent. with 
20,000 corpuscles. A variation of 100,000 corpuscles is not or- 
dinarily important. This is close enough for clinical purposes. 

Cleaning the apparatus. It is important to clean the ap- 
paratus as soon as the counts are made. If blood dries in the 
pipette it may take several hours to remove, while if cleaned 
promptly, it requires only two or three minutes. The counting 
chamber is to be cleaned with pure water only. As the plate and 
disc are cemented to the slide by Canada balsam, alcohol or any- 
thing that will act on balsam must not be used. The cover glass 
may be cleaned with water, then with alcohol. For drying the 
counting chamber and cover glass about the best thing is a linen 
handkerchief that is practically worn out. A new one is too harsh. 
Japanese lens paper may be used but it is not so convenient as 
soft linen. Anything more harsh than lens paper or old soft linen 
should not be used. The pipette should be cleaned, after expelling 


cal 


8 METHODS OF EXAMINATION 


the remaining diluted blood, with pure water, drawing in water 
and expelling it several times, then with alcohol, then with ether, 
finally forcing air through until it is thoroughly dry. When the 
pipette is dry the glass bead will roll about freely in the bulb with- 
out adhering to any part. An aspirating bulb will be found time 
saving in cleaning the pipette. To draw fluid into the pipette the 
rubber tube may be attached or the aspirating bulb may be com- 
pressed and the thumb placed over the valve. Care must be 
taken not to allow the aspirator to become moistened during 
cleaning as the last step is to force dry air through the pipette. 
Even when care is taken to clean the pipette well it will be found 
necessary at more or less long intervals to fill with strong nitric 
acid and let it act for several minutes. All trace of the acid must 
be removed by drawing water through the pipette several times, 
following the water with alcohol, ether and dry air as ordinarily. 


COUNTING THE LEUCOCTYES 


If the counting chamber with the Zappert-Ewing ruling is used 
the leucocytes may be counted in the same preparation as the 
red corpuscles. The leucocytes in the entire ruled space, nine 
sq. mm., are counted. The leucocytes are readily distinguished 
as they have a bluish tinge in contrast to the straw color of the — 
red corpuscles. A dilution of 1:100 is more accurate when the 
leucocytes are to be counted. Repeat the count with a second 
drop as with the red corpuscles. : 

Computation. As with the red corpuscles divide the number 
of leucocytes counted by the volume of blood counted (.9 emm.), 
and this by the dilution. The count should be repeated with a 
second drop. The formula for leucocytes counted with a dilution 
of 1:100 is: 

No. of leucocytes counted x 10 x 100 
ae eas, ——_—— = No. of leucocytes per'emm. 

When the counting chamber having only the central square 
millimeter ruled is used, a pipette giving a dilution of 1:10 should 
be used. As it costs more to get the two pipettes and is less con- 
venient to use it is recommended to get the counting chamber 
with the Zappert-Ewing ruling. 

With the special pipette for leucocytes it is necessary to have 


COUNTING THE BLOOD PLATES 9 


a larger drop of blood than for the red corpuscles. As the fluid 
will run out of this larger pipette it is necessary to keep it as nearly 
horizontal as possible. Acetic acid one per cent. (glacial one-third 
per cent.) is preferable as the diluting fluid. With this fluid the 
red corpuscles are made transparent, the nuclei of the leucocytes 
standing out in bold relief. With a dilution of one part of blood 
to ten of the acetic acid it is necessary to mix the blood and dilut- 
ing fluid quickly; otherwise the leucocytes will be found in clumps, 
making an accurate count impossible. The method of adjusting 
the drop in the counting chamber is the same as for counting red 
corpuscles. The leucocytes in the entire ruled area of the Thoma’s 
counting chamber, 400 squares, should be counted. In computing 
the results multiply the number of leucocytes counted by 10, 
since- the 400 squares represents .1 emm. of diluted blood, and 
multiply this product by 10, if the dilution was 1:10, to give the 
number in undiluted blood. 


COUNTING THE BLOOD PLATES 


The blood plates show a marked tendency to undergo dissolu- 
tion soon after the blood is taken from the blood vessels and to 
adhere to each other and to foreign substances. Special precau- 
tions must be taken in enumerating them. Several methods have 
been used, three of which are given in detail. 

Pratt’s method. Pratt used the following diluting fluid, 
which keeps indefinitely unless moulds or bacteria develop: 


Sodium metaphosphate (Merck)..................00-- 2 grams 
“S PEICTST OE DUT Ts a a ee a A a Pee SP 0.9 gm. 
stile d wy aber s esas ca stat of cks sala en a ayer oo 100 ce. 


The number of erythrocytes is determined in the usual manner 
with the Thoma hematocytometer. A few cubic centimeters of 
the diluting fluid are placed in a watch glass. All the glassware 
used must be perfectly clean. Blood is obtained from a puncture 
free enough to allow the blood to flow freely. A sterilized platinum 
loop, as used in bacteriological work, with a diameter of about 
three mm. is filled with diluting fluid and the center of the loop 
brought in contact with a fresh drop of blood. There should be 
three or more parts of fluid to one of blood. A portion of the 
mixture is at once placed on a slide and covered with a cover glass. 


10 METHODS OF EXAMINATION 


The diluted blood should spread so that the erythrocytes are well 
separated. It is not necessary to mix the blood and diluting fluid 
by long stirring. Two preparations should always be made. If 
the count varies much in the two, other preparations should be 
made. Examination is made with an oil immersion objective. 
A square diaphragm in the ocular, easily made of stiff paper, 
facilitates counting. Both the blood plates and erythrocytes are 
counted in fields taken at random in different parts of the specimen 
until 250 to 500 erythrocytes have been seen. This will give the 
ratio of plates to erythrocytes. The number per emm. is obtained 
by multiplying the number of erythrocytes per emm. by this ratio. 

Kemp and Calhoun’s method.— Kemp and Calhoun used the 
following diluting and fixing fluid: 


Pormialin: (AOS eee esto oehe ORs Corer tel eater an ee Tee OE 10 ce. 
Sodium, chioride (1%, sq: soln.) s 2257 osc ee ae ee ee 150 ce. 


(Color with methyl green or methyl violet if desired). 


In this method the blood comes in contact with the fixing fluid 
before touching anything else. The site of puncture is carefully 
cleaned and dried. Puncture is made, the first drop wiped off and 
diluting fluid placed on the site of puncture so that the next drop 
as it emerges flows into the diluting fluid. Mix thoroughly for a 
few seconds with a clean glass rod then transfer a large drop with 
the glass rod to the Thoma counting chamber and cover with a 
thin cover glass. If the corpuscles are fairly evenly distributed, 
let the chamber rest quietly for about five minutes. Count the 
red corpuscles and blood plates in about six frames of 16 squares 
each. This usually gives about 100 blood plates. With a small 
number of blood plates or with not so even a distribution more 
than six frames should be counted. The number per cmm. is 
obtained by multiplying the number of erythrocytes, obtained in 
the usual manner, by the ratio of blood plates to erythrocytes. 

Wright and Kinnicutt’s Method.— The diluting fluid is com- 
posed of two parts of an aqueous solution of “‘brilliant cresyl blue ” 
(1:300) and three parts of an aqueous solution of potassium eyanid 
(1:1400). These two solutions must be kept in separate bottles 
and mixed and filtered immediately before using. 

The blood is diluted 1:100. The process should be done as 
rapidly as possible. Count in the ordinary counting chamber, 
using a high power dry objective. The authors used the thin 


ESTIMATION OF HEMOGLOBIN 11 


cover glass of Zeiss with the central excavation. After the count- 
ing chamber is filled, it is let stand 10-15 minutes to let the plate- 
lets settle. The red corpuscles are decolorized and appear as 
“‘shadows.”’ The nuclei of leucocytes are stained dark blue. The 
platelets appear as sharply outlined round or oval or elongated 
lilac colored bodies. 

After the blood and diluting fluid are mixed precipitate does 
not form. The count may be made after some hours if necessary. 

The cresyl blue solution is stable but should be kept on ice to 
prevent the growth of mould. The cyanid solution should be 
made up at least every ten days. 


ESTIMATION OF HEMOGLOBIN 


There are several instruments for obtaining the amount of 
hemoglobin, the more important of which are Tallqvist’s, Gower’s, 
Dare’s and Fleischl-Miescher’s. 

Tallqvist’s hemoglobin scale. This apparatus consists of 
fifty leaflets of absorbent paper 
bound in a booklet with a scale 
of ten standard tints correspond- 
ing to the color of blood stains 
having a hemoglobin value of 10, 
20, 30, 40 to 100. In making the 
test a small piece of the absorb- 
ent paper is touched to a drop of 
blood which is allowed to soak in 
gradually. As soon as the blood 
has lost its humid gloss and be- 
fore drying has taken place the 
stain is placed against a white 
background and compared with 
the tints of the standard scale. 
The tints should be compared by 
daylight. This is one of the most 
convenient of the hemoglobinom- 
eters. The.booklet is of a size 
convenient to be carried in the pocket, requires only a few seconds 
to make a test and has no pipettes or other parts to be cleaned. 


Fia. 6. Tallqvist’s hemoglobin scale. 


12 METHODS OF EXAMINATION 


The error in use does not amount to more than ten per cent. 
This instrument is sufficiently accurate for ordinary clinical work. 

Gower’s hemoglobinometer. This instrument consists of two 
sealed glass tubes containing glycerin tinted with picrocarmine 
to represent the tint of a one per cent. solution of normal blood. 
One of these tubes, marked with a white dot, is for use by daylight 
and the other, marked by a black dot, for use by candle light. 
Besides these tubes there is a tube of similar size graduated into 
140 parts, each of which contains 20 cmm., a capillary pipette 
marked at 20 cmm. and a block for holding the tubes when making 
the comparison. 

Method of using. The blood is drawn into the pipette to 
the mark 20 cmm., the outside wiped off and the contents expelled 
into the diluting tube, 
which should contain a lit- 
tle distilled water. The 
inside of the pipette is 
rinsed out by alternately 
drawing in and expelling 
water from the tube. 
While expelling blood or 
water from the pipette the 
point of the pipette should 
be raised slightly above the 
surface of the water in the 
tube to avoid blowing bub- 
bles. Rinsing the pipette 
also serves to mix the 
blood with the water. 
After rinsing the pipette, 
water is added gradually 
to the diluted blood in the tube until it is of the same tint as the 
standard tube. The blood and water should be mixed by closing 
the tube with the thumb and inverting it several times. Do not 
shake the tube and produce bubbles in it as bubbles will render it 
difficult to read the amount. Comparison is made by placing 
both the standard tube and the diluted blood in the block and 
viewing them by reflected light. It is better to hold a paper or 
other white background behind the tubes and let the light fall 


Fic. 7. Gower’s hemoglobinometer. 


ESTIMATION OF HEMOGLOBIN 13 


over the shoulder while making the comparison. When they 
are of the same tint the hemoglobin value is read from the dilut- 
ing tube, reading at the middle of the meniscus. As the readings 
on the lower part of the scale are not accurate, it is advisable to 
use two pipettes of blood for low percentages, dividing the result 
obtained by two. 

Gower’s hemoglobinometer is used extensively, though not 
so extensively as a few years ago. A decided disadvantage is 
that the tint of the standard solution is not permanent, becoming 
darker after a time. It does not give the hemoglobin value closer 
than about five per cent. The instrument is not enough more 
accurate than Tallqvist’s to make it advisable to use. 

There are modifications of Gower’s hemoglobinometer in which 
the standard solution of picrocarmine is replaced by modified 
hemoglobin, permanent solutions it is claimed. This is an ad- 
vantage in that the same things are compared since the blood is 
modified in the same manner as the standard solution. As the 
same substances are compared any kind of light may be used. 

In Haldane’s modification the standard tube contains CO 
hemoglobin. The sample of blood is treated, before making the 
comparison, with illuminating gas. Some of the blood may easily 
be lost, bubbles form and illuminating gas is not always available 
clinically. 

In Sahli’s modification the standard solution is hemoglobin in 
glycerin. The blood to be tested is treated with a one-tenth normal 
HC! solution. Sahli’s standard solution is claimed to be perma- 
nent; but on standing for some time the hemoglobin sometimes 
settles and cannot be made a uniform solution again. 

Dare’s hemoglobinometer.—The instrument consists essen- 
tially of a capillary pipette and a standard color scale representing 
the hemoglobin values from 10-120. The pipette is composed of 
two glass plates, one transparent and the other white which has a 
depression of measured depth ground in one end so that when the 
plates are clamped in the holder the depression forms a capillary 
chamber which fills automatically when either of the three sides 
is touched to a drop of blood. The standard color scale consists 
of two prismatic glass plates tinted to give the color of undiluted 
blood by candle light and arranged in the form of a semicircle, 
the outer part of which increases in depth of color. The percent- 


14 METHODS OF EXAMINATION 


age scale is etched into the edge of a corresponding semicircle of 
glass and is placed directly opposite the standard scale. These 
semicircular plates are fastened to a white disc and are protected 
by a circular rubber case. The standard is rotated by a milled 
head placed on the upper 
part of the case. The speci- 
men of blood is compared 
with the standard scale 
through two small holes 
horizontally placed and 
Zz viewed through a camera 
tube, the eyes of the oper- 
ator being protected from 
the light by a shield. Light 
is afforded by a candle at- 
tached to the instrument. 
Method of using. The in- 
strument is prepared for use 
by screwing the camera tube 
into place and rotating the 
shield so that the two holes 
through which the blood and 
standard scale are viewed 
are uncovered. The candle in its holder is then placed in 
position. The candle wick should be straight or the candle 
rotated so that it will illuminate both apertures equally. The 
pipette is removed from the instrument. It should be scrupulously 
clean and dry. The pipette is filled by touching it, plain glass 
uppermost, to a drop of blood. As soon as it is filled it is placed 
in position. It is not necessary to wipe blood from the edges of 
the pipette, none should however be on the surface of either of the 
plates. The instrument is held horizontally and should be pointed 
toward a dark surface. Comparison is made by rotating the milled 
head, making rather quick turns. When the tint of the standard 
scale is made to exactly match that of the blood the hemoglobin 
value is read from the edge of the instrument, the reading being 
the one indicated by the beveled edge of the opening. 
Dare’s instrument gives the amount of hemoglobin with greater 
accuracy than Tallqvist’s or Gower’s. It has given in my ex- 


Fig. 8. Dare’s hemoglobinometer. ° 


ESTIMATION OF HEMOGLOBIN 15 


uum a 


+ £2 i 
Hi eed |) 
| 

| 

| 


“al 


i 
= Tn f] 


ee Se CC 


Fic. 9. Fleischl-Miescher hemometer. 


perience practically the same readings as the more expensive instru- 
ment of Fleischl-Miescher and is much easier to manipulate and 
to clean. One hundred per cent. in Dare’s hemoglobinometer 
represents a mixture of 13.77 grams of hemoglobin diluted with 
100 ec. of serum. 

Fleischl-Miescher hemometer.—This instrument consists of 
a stand having a stage with a circular opening in which a metallic 
mixing cell fits. Beneath the stage a standard colored glass wedge 
with a graduated scale works by means of a rack and pinion. A 
graduated pipette marked +, ; and 5 serves to dilute the blood, 
1:200, 1:300 or 1:400. The mixing cell has a glass bottom. A 
metal partition which projects slightly above the surface divides 
the cell into two vertical halves, one for diluted blood, the other 
for water. A grooved glass disc covers the mixing cell and this is 
in turn covered by a metal cap having a rectangular opening which 
serves to cut off from view all but a narrow strip of the colored 
wedge. 

Method of using. The blood is procured with the usual pre- 


16 METHODS OF EXAMINATION 


cautions and is drawn into the pipette to the mark +, 4 or 4. 


Diluting fluid, a filtered one per cent. solution of sodium ear- 
bonate, is drawn up to the mark as in the hematocytometer. It 
is well shaken, and the diluting fluid expelled from the long arm 
of the pipette. Then one compartment of the mixing cell is filled 
with the diluted blood, the other compartment filled with water, 
the glass dise slid into place and the metal cap adjusted. The 
cell is placed in position on the stage so that the part containing 
water is over the colored wedge. Comparison should be made 
by the light of a candle or petroleum lamp placed at some distance 
from the hemometer. A better result will be obtained in match- 
ing the blood and scale by moving the scale by short quick move- 
ments. 

A table accompanies each instrument in which is given the 
number of grams of hemoglobin corresponding to the reading 
obtained with that instrument. The Fleischl-Miescher hemom- 
eter is one of the most accurate of those used for obtaining the 
amount of hemoglobin. The feature of being able to get the 
number of grams of hemoglobin is a very desirable one and should 
be given in all hemoglobinometers. It is more reasonable to learn 
the amount of Hb, given in grams per 100 ee. of blood, than the 
percentage of a supposed normal, which is fixed at different values 
in different makes of hemoglobinometers. 


HISTOLOGICAL EXAMINATION 


For histological examination blood is examined fresh and in 
fixed and stained preparations. Fresh preparations are made 
by touching the center of a thoroughly clean cover glass to the 
top of a freshly exuded drop of blood then dropping the cover 
gently on a clean slide. If a proper sized drop is obtained the 
blood will spread between the cover and slide in a thin layer. The 
cover glass should not be pressed down as pressure may rupture 
or distort the red corpuscles. If it is desired to keep the specimen 
longer than a few minutes the edges of the cover glass should he 
sealed with liquid paraffin or castor oil. 

For fixed and stained preparations the blood should be spread 
in a thin smear. The method of making smears on glass slides 
will be found a simple and convenient one. The slides should be 


HISTOLOGICAL EXAMINATION 17 


thoroughly clean. Unused slides may be cleaned in strong soap 
or “gold dust” solution, well rinsed in water, then placed in al- 
cohol from which they are wiped and polished. Slides with ground 
edges are preferred. The edge of a slide is touched to the top of a 
fresh drop of blood then 
applied to another slide 
at an angle of about 
forty degrees (Fig. 10). 
As soon as the blood has 
spread along the line of 
contact of the two slides, 
the smearer is drawn Fig. 10. Spreading film on glass slide. 
along with very gentle 

pressure slowly leaving a thin smear of blocd on the other slide. 
The smear should cover one-half or two-thirds of the slide. <A little 
practice will enable one to make good smears at each attempt. 
The smears may be kept for some time without altering their 
staining properties if they are kept dry. After several weeks, 
however, not so good results can be obtained from certain of the 
more delicate stains, Jenner’s, Wright’s and Hasting’s. 

Fixation and staining. Jenner’s stain is one of the most rapid 
and easy to manipulate of the many methods in use and stains 
each of the several kinds of granules in the leucocytes. It is rec- 
ommended for ordinary examinations. The staining fluid is a 
five-tenths per cent. solution of the dye (Gruebler’s) in pure methyl 
alcohol (Merck’s). This acts as both fixing and staining fluid. 
The smear, previously unfixed, simply dried in the air, is flooded 
with the staining fluid which is allowed to act two or three minutes, 
when it is washed in distilled water until the better spread portions 
have a pinkish tint, which usually requires about ten seconds. 
The water should then be shaken and blown vigorously from the 
specimen which is then dried rapidly in the air. As soon as it is 
thoroughly dry it. may be examined using a two mm. (,/,; in.) oil 
immersion objective. It is not necessary to place a cover glass 
on the specimen as the index of refraction of homogenous oil is 
the same as that of glass. If a dry objective should be used a 
cover glass would be necessary; but as high a magnification as 
that given by a two mm. (,/; in.) objective is needed. The stained 
films keep as well without being covered as when mounted in 


18 METHODS OF EXAMINATION 


balsam. Immersion oil may be removed from the film by dropping 
on chloroform or xylene. 

With Jenner’s stain the red corpuscles should have a pinkish 
or terra cotta tint; nuclei blue; the fine granules of polymor- 
phonuclears pinkish; eosinophile granules, deeply stained pinkish; 
basophile granules, deeply stained dark violet. Bacteria are well 
stained, blue. 

Wright’s stain. The staining fluid may be obtained ready 
for use from dealers in microscopic supplies or the dye may be 
purchased in dry form and made up as needed. The staining fluid 
is a solution in pure methyl alcohol of eosinate of polychrome 
methylene blue, 0.1 gm. to 60 ec. The unfixed film, which has 
dried in the air, is covered with the stain which is allowed to act 
one minute. Then the same number of drops of distilled water 
are added drop by drop. This is allowed to act two or three min- 
utes longer when the specimen is washed with distilled water until 
the better spread portions have a pinkish or orange tint. A few 
seconds will usually suffice, but it may take one to three minutes. 
The excess of water is shaken and blown vigorously from the 
specimen which is then dried in the air. When it is dry examine 
with the two mm. (,' in.) oil immersion objective. 

Wright’s stain is an excellent one, staining the several kinds of 
granules well. The red corpuscles should have a pinkish or terra 
cotta tint; nuclei blue; the fine granules of polymorphonuclears 
pinkish; eosinophile granules reddish; basophile granules a deep 
royal purple. This stain also stains bacteria well. Wright’s is pref- 
erable to Jenner’s stain for staining the protozoa found in the blood. 

Hasting’s stain. The fluid, a solution of eosinate of poly- 
chrome methylene blue in pure methyl alcohol, may be obtained 
ready for use from dealers in microscopic supplies. The air dried 
film, previously unfixed, is covered with the staining fluid which 
is allowed to act one minute, then is diluted by adding a few drops 
of distilled water until a greenish metallic scum begins to form on 
the surface of the film. Let the diluted staining fluid act for five 
minutes longer. Then wash in distilled water for two or three 
seconds and dry immediately by blotting. This is an excellent 
stain for blood, staining the various kinds of granules. The effect 
is practically the same as is produced by Wright’s stain. Hasting’s 
stain is especially good for staining the parasitic protozoa. 


HISTOLOGICAL EXAMINATION 19 


Eosin and methylene blue. The films must be fixed before 
applying the staining solutions. Fixation may be secured by heat- 
ing over the flame of a Bunsen burner or alcohol lamp, passing the 
slide film side up through the flame until it is decidedly too hot 
for the hand to bear then keeping it at this temperature for about 
two minutes; or by heating in an oven ata heat of 110-120° C. for 
5-10 minutes. Ether and absolute alcohol equal parts or absolute 
alcohol alone is a satisfactory fixing agent. Ten to thirty minutes 
are sufficient, though a somewhat longer time will not harm the 
specimen. After the film is fixed it is covered with a saturated 
alcoholic solution of eosin (Gruebler, alc. sol.) which is allowed to 
act about 10 seconds. Then wash in water. The washing should 
be rapid enough to give the red corpuscles a pinkish tint. With 
slow washing they will be too deeply stained. As soon as the 
eosin is washed off cover the film with a saturated aqueous solution 
of methylene blue and Ict it act for one minute, then wash hastily 
in distilled water. Shake off the water and dry quickly in the air. 

This stain is a good one though the fine granules of the poly- 
morphonuclears are not stained. Jenner’s, Wright’s or Hasting’s 
stains are preferable. With eosin and methylene blue the red 
corpuscles are pinkish, nuclei blue, eosinophile granules pink, 
basophile granules deep blue. The fine granules of polymor- 
phonuclears are unstained unless the specimen is much over stained 
with eosin. The cell bodies of polymorphonuclears take a faint 
pinkish tint. 

Giemsa’s stain. The stain may be obtained already pre- 
pared. It is made according to the following formula:— 


ANAate LO EGYOSINT eh ee aes CP EG a Ru ates ger perce gar Ri eM OEE ce 3 gms 
PAVZANORLILE 2 aes RAT ee NONE NCES cet teen Rote. MIT ead as oie enchenerae Re 0.8 gm 

Gly cermin (Mierckd Camber ernie haee ] stare erate ee citer ertes 250 gms. 
Meth yIcAlcohols (ahi baumisl)Pecrr sis acerca. orice eee 250 gms. 


The blood film is dried in the air and fixed in absolute alcohol for 
15 minutes or methyl alcohol for 2-3 minutes. Remove the al- 
cohol with blotting paper, cover the preparation at once with the 
freshly diluted staining fluid and let it act 10-15 minutes. The 
staining fluid is diluted by adding one drop of the stain to 1 ce. 
of distilled water in a small graduate and shaking gently. After 
the diluted stain has acted 10-15 minutes wash the preparation 
in a stream of distilled water. Remove the excess of water with 


20 _ METHODS OF EXAMINATION 


blotting paper and dry in the air. A more intense staining is 
secured if 1% potassium carbonate solution is added in the propor- 
tion of 1 or 2 drops to 10 ce. of distilled water before the stain is 
mixed with it. 

Giemsa’s stain is excellent for protozoa, but is not so good for 
the blood corpuscles. 

Pappenheim’s modification of May-Giemsa’s method. Two 
staining mixtures. are needed each of which may be purchased 
ready prepared. They are May-Griinwald’s eosin—methylene 
blue disssolved in methyl alcohol and Giemsa’s stain (new formula). 
The Giemsa’s stain must be diluted just before use in the propor- 
tion of 15 drops of the stain to 10 ce. of distilled water. 

The air dried film is covered with the May-Griinwald stain 
which is allowed to act for 3 minutes. An equal number of drops 
of distilled water is then added to the stain and allowed to act one 
minute. The fluid is then poured off and, without washing, the 
freshly prepared Giemsa solution added. This is allowed to act 
for 15 minutes when the preparation is thoroughly washed, then 
dried, not over a flame. Pappenheim regards this method as su- 
perior to any other now in use and states that it is the only one 
he now uses. 

_ Graham’s alphanaphthol-pyronin method. The smear is al- 

“ lowed to dry thoroughly in the air. It is fixed one or two minutes 
in a freshly prepared mixture of nine parts ninety-five per cent. 
alcohol and one part formalin. 

Wash in water and flood with the following alphanaphthol 
solution, which keeps well so far as its staining powers are con- 
cerned. 


Alphanaphthol (Merck’s “ Reerystallized”’ or ‘‘ Reagent”’). . 1 gm. 
Alcohol, 40%. 6355 5 sug. ccs ate anaes doce ere ears ere ote ae 100 ce. 
Hydrogen peroxide; <5... ncmens to perre er ee sia ane .2 ce. 


Allow it to act four or five minutes. Wash and place in a dish 
of running water for about fifteen minutes. 
Stain two minutes with the following solution: 


1 Af 0) 11s PN nS liane Out om .1 gm. 
Amilin : oosisc ce < tins ch nsitee G5 bin leno tevsehe ote eee ee eee epee 4icc: 
Alcohol, 40% «. 63.5 Sased cnc. Scere eee he eee ey ae ane OG) =Gc: 


Dissolve the pyronin in the alcohol and add the anilin. This 
solution keeps well. 


DIFFERENTIAL COUNTING OF LEUCOCYTES 21 


Wash in water. 

Stain one-half to one minute with a five-tenths per cent. aqueous 
solution of methylene blue (Griibler’s BX). 

Wash in water, blot. 

The resulting picture is much like that afforded by the Ro- 
manowsky stains excepting that the granules of leucocytes and 
myelocytes are much more prominent. The granules of polymor- 
phonuclears, eosinophiles and myelocytes are purplish red, those of 
mast cells a deep purple. Red corpuscles are greenish yellow to 
pink, platelets blue, nuclei of all cells blue and cytoplasm light 
blue. The best results are obtained with freshly made smears as 
the reacting substance begins to disappear after ten days to two 
weeks. 


DIFFERENTIAL COUNTING OF LiSUCOCYTES 


In making a differential count ordinarily at least 500 leucocytes 
should be examined; for critical work twice that number should 
be counted. For recording the results it will be found convenient 
to rule a sheet of paper as follows, giving a column in which to 
record each variety of leucocyte and a blank space for recording 
myelocytes, degenerated leucocytes, abnormal red corpuscles, et 
cetera: 


22 METHODS OF EXAMINATION 


After bringing the specimen into focus, using the 2 mm. objec- 
tive and the x 4 ocular, and before beginning to make the count, 
it is well to examine a few leucocytes to see how the stain has taken 
in this specimen. After beginning the count determine the variety 
to which each leucocyte belongs and record it in the appropriate 
column. In making the count move the slide so the field of view 
travels across the width of the film moving back and forth until 
the entire film or the desired number of leucocytes has been ex- 
amined. With a mechanical stage one need move to the right or 
left on reaching the edge of the film only the width of the field of 
view, which is easily determined by noting a corpuscle at the ex- 
treme edge of the field and then moving the slide so that this 
corpuscle just disappears on the opposite side of the field; but 
without a mechanical stage one must allow some space to avoid 
the danger of running into the track previously examined and 
counting some leucocytes twice. When a sufficient number of 
leucocytes has been examined the percentage of each variety is 
determined by dividing the number of each variety by the total 
number counted. For example, suppose a specimen of horse’s 
blood was examined and was found to have 119 lymphocytes, 
26 large mononuclears, 338 polymorphs, 16 eosins and 1 mast 
cell. The total number examined was 500, then 55% = 23.8% 
lymphocytes, =~, = 5.2% large mononuclears, = Brae 
polymorphs, s¢5 = 3.2% eosins, s55 = 0.2% mast cells. It is 
well to add the percentages to see if they make 100 or nearly that. 
It is not necessary to give the percentage for more than one decimal 
place. 


TEST FOR GLYCOGEN 


In making a test for glycogen in the blood, smears are made 
in the usual manner and are allowed to dry in the air. A drop of 
the following solution is placed on the film which is then covered 
with a cover glass. 


Todine cdf ia ie ott orte tierce eae dh eer erccetenl sue = Tere eerie 1 gram 

Potassiumi1odides 757 ti cea tes eo ee 3 gms 

Distilled waten:s, yack cle ae Eee ee ee ee tee 100 ee. 

Add powdered gum arabic, about 50 gms., sufficient to produce a syrupy 
fluid. 


Examine with a two mm. oil immersion objective after four 


TEST FOR FAT 23 


or five minutes. The glycogen appears as reddish brown granules 
in the cell bodies of the polymorphonuclear leucocytes, rarely of 
basophiles and myelocytes or as a diffuse reddish brown coloration 
of the cell bodies and as small or larger masses similarly tinted 
outside the corpuscles. A small amount of extra cellular glycogen 
may be found in normal blood. 


TEST FOR FAT 


The presence of fat may be proven by fixing a smear for 24 
hours in one per cent. osmic acid. The specimen may be counter- 
stained with eosin. A control smear should be fixed 24 hours in 
alcohol and ether, then in one per cent. osmic acid for 24 hours. 
A control specimen in which the fat is dissolved by ether is needed, 
since osmic acid will blacken other substances than fat. Fat may 
be detected with greater certainty by staining with Scharlach R 
or Sudan III. Films spread on slides are fixed at once, before 
drying takes place, in formaldehyde vapor for five or ten minutes 
and are then stained in a saturated alcoholic solution of Scharlach 
R or Sudan III for 15 or 20 minutes, preferably in a tightly stop- 
pered bottle. Wash in water, mount in glycerin and examine with 
two mm. oil immersion objective. 


THE TOTAL VOLUME OF BLOOD AND ITS OXYGEN CAPACITY 


The importance of knowing the total quantity and oxygen 
capacity of the blood is evident. Haldane and Smith have de- 
vised a method for determining these. A small and carefully 
measured quantity of carbon monoxide is administered and then 
the percentage to which the hemoglobin has become saturated is 
determined by the carmine method. This gives data to deter- 
mine the total volume of CO (or oxygen) capable of being taken 
up by the blood. At the same time the volume of CO (or of oxy- 
gen) capable of being taken up by 100 grams of blood is deter- 
mined by comparing its color with that of an equal volume of ox 
blood whose oxygen capacity has been determined. This will 
give data to determine the total quantity of blood. Haldane and 
Smith found that the total amount of blood in man is about 4.9% 
of the body weight and varied in 14 healthy persons between 3.34 
and 6.27%. The total oxygen capacity they found to be 0.85% 


24 METHODS OF EXAMINATION 


of the body weight in kilograms and varied between 0.57 and 
0.95%. Douglas found that the same method can be readily ap- 
plied to animals. He found the volume of blood in male rabbits 
to be 4.85% of the body weight in grams, varying in seven cases 
between 6.09 and 4.2% and in female rabbits 5.82% of the body 
weight, varying in four cases between 6.28 and 3.71%. The 
oxygen capacity per 100 grams body weight he found to be 0.706 
ec. in the buck, varying between 0.968 and 0.577 cec., and 0.739 ec. 
in doe rabbits, varying between 0.825 and 0.596 ce. 


THE RELATIVE VOLUME OF CORPUSCLES AND OF PLASMA 


The hematocrit as modified by Daland consists of a horizontal 
armature carrying two capillary tubes to be placed on the shaft 
of a centrifuge in place of the armature carrying the urine tubes. 
The capillary tubes of the hematocrit are each graduated in 100 
degrees and are held in place by springs. One of the tubes is filled 
with water and placed in the armature, the other tube is filled 
with blood by touching one end to a large drop of blood and hold- 
ing the tube horizontally or the other end somewhat depressed. 
It is at once placed in the armature with the zero end outward. 
The tubes are revolved at a speed of 8000-10,000 per minute for 
three minutes, by which time the column of red corpuscles will be 
found unchangeable. The volume of red corpuscles is read easily, 
the tubes having a lens front. If the blood cannot be centrifuged 
at once it must be diluted. Daland used a 2.5% aq. soln. of potas- 
sium dichromate, mixing the blood with an equal volume of dilut- 
ing fluid. This is done, using the red pipette, by drawing blood 
to the mark 1, then a small air bubble, then an equal volume of 
diluting fluid, then another small air bubble and so on until three 
or four tube lengths are obtained. The blood and diluting fluid 
should be mixed at once by gentle shaking, care being taken not 
to produce air bubbles. Both capillary tubes are to be filled with 
the diluted blood and centrifuged as with fresh blood. The result 
must be multiplied by two. This method seems to be sufficiently 
accurate for determining the relative volume of corpuscles and 
plasma, excepting in cases of leukemia or extreme leucocytosis, 
when enough leucocytes are entangled with the red corpuscles to 
make the result unreliable. 


SPECIFIC GRAVITY 25 


SPECIFIC GRAVITY 


Hammerschlag’s method is the most simple for obtaining the 
specific gravity of the blood. A urinometer is partly filled with a 
mixture of benzene (CsH,) and chloroform having a specific gravity 
of about 1060. With the pipette a drop or two of blood, obtained 
with the usual precautions, is placed in the fluid. Care must be 
taken not to expel air with the blood. It is better to have more 
than one drop present as a drop may stick to the bottom of the 
vessel. By adding benzene or chloroform the specific gravity of 
the fluid may be made the same as that of the drops of blood, that 
is the blood will neither sink nor rise in the fluid. The gravity of 
the fluid is at once taken in the same manner as for urine. 


TIME OF COAGULATION 


Wright has devised a simple instrument for measuring the time 
it takes the blood to coagulate. The instrument consists of a 
reservolr containing a rack holding a thermometer and twelve 
calibrated glass tubes. The tubes are placed in the reservoir, 
which contains water at a desired temperature (18.5 or 37° C) and 
allowed to remain until they become of the same temperature. 
Then they are dried, five ec. of blood drawn into each, and re- 
placed in the reservoir. At varying intervals the tubes are ex- 
amined by attempting to blow out the blood. When the blood 
cannot be expelled, coagulation may be considered as complete. 

There are several other methods of obtaining the time of co- 
agulation. In Hinman and Sladen’s modification of Mailian’s 
method glass slides are used. Any glass surface will do. The 
puncture is made in the usual manner. The first drop is wiped 
off and time counted from the appearance of the second drop. The 
under surface of a slide is touched lightly to the drop of blood in 
two or three places. Coagulation is considered complete when 
tilting the slide produces no change in the slope of the drop of 
blood. The drops at different examinations should be of about 
the same size, 3, 4,5 or 6 mm. in diameter. Coagulation takes a 
longer time with larger drops, longer with 6 mm. than with 3 mm. 
drops. 

Bogg’s modification of the Brodie-Russell method is a slide 


26 METHODS OF EXAMINATION 


method. The instrument consists of an inverted truncated glass 
cone in an air chamber which is pierced at one side by a fine metal 
tube adjusted to throw a fine stream of air at a tangent to the 
edge of the hanging drop of blood. The drop of blood is placed 
on the end of the truncated cone. Before coagulation has taken 
place a very light draft of air sets the corpuscles in the drop of 
blood in motion. When coagulation has occurred motion is not 
produced. The process is watched under a low power of the 
microscope. 

Comparison of the time of coagulation may be made only in 
cases where the same method and technic have been used. A 
description of the several methods of obtaining the time of coagula- 
tion with a discussion of each will be found in Hinman and Sladen’s 


paper. 


TEST FOR SPECIFIC AGGLUTININS OR PRECIPITINS 


The presence of specific agglutinating or precipitating sub- 
stances is important for the diagnosis of certain infectious dis- 
eases, as glanders. The blood should be drawn under aseptic 
precautions. It is convenient to obtain the blood (10-20 ce. is suf- 
ficient) from the jugular vein by means of a sterile syringe. The 
bottle and cork in which the blood is placed should be thoroughly 
sterilized. The technic of making the test is essentially bacterio- 
logical and will be found in special papers on the subject (see Moore, 
Taylor and Giltner). 


BACTERIOLOGICAL EXAMINATION OF THE BLOOD 


The blood is obtained under strictly aseptic precautions. Five 
to twenty cubic centimeters are usually desired. The blood may 
be obtained from the jugular vein or other blood vessel. A hypo- 
dermic syringe will be found the most convenient instrument for 
obtaining the blood. The bottle and cork in which the blood is 
placed must be carefully sterilized, preferably by long boiling. 
If sterilized by chemicals the chemicals must be completely re- 
moved by rinsing several times with sterile water. The methods 
of examining blood for bacteria will be found in works on bac- 
teriology. 


REFERENCES 27 


REFERENCES 


1. Douauas, C. G. A method for the determination of the volume of blood 
in animals. Journ. of Physiol., xxxii, 1906, p. 493. 

2. Exrutcu, P. Farbenanalytische Untersuchungen zur Histologie und 
Klinik des Blutes. Berlin, 1891. 

3. FusseELL AND Marcexuus. The value of various forms of hemoglo- 
binometers to the general practitioner. Journ. Am. Med. Assn., 45, 1905, 769. 

4. GraHam, G. 8. The oxidizing ferment of the myelocyte series of cells 
and its demonstration by an alphanaphthol-pyronin method. Journ. Med. 
Res., xxxv, 1916, 231. 

5. HALDANE AND SmitH. The mass and oxygen capacity of the blood in 
man. Journ. of Physiol., xxv, 1900, p. 331. 

6. Hastinas, T. W. A method for preparing a permanent Nocht’s stain. 
Journ. of Exper. Med., vii, 1905, p. 265. 

7. HINMAN AND SLADEN. Measurements of the coagulation time of the 
blood, and its application. Bul. Johns Hopk. Hosp., xviii, 1907, 207. 

8. JenNER, L. A new preparation for rapidly fixing and staining blood. 
Lancet, 1899, I, p. 370. 

9. Jonns, C. P. A source of fallacy in counting red cells. Brit. Med. Journ., 
1910, 1351. 

10. Kemp, CaLHouN AND Harris. The blood plates, their enumeration in 
physiology and pathology. Journ. Am. Med. Assn., xlvi, 1906, pp. 1023 
and 1091. 

11. Moorr, V. A. Principles of Microbiology. 1912, The Macmillan 
Company, New York. 

12. Moorr, Taytor AND GILTNER. The agglutination method for the 
diagnosis of glanders. Proceed. Am. Vet. Med. Assn., 1906, p. 194, also Am. 
Vet. Rev., Oct., 1906. 

13. PaPppENHEIM, A. Clinical examination of the blood and its technique. 
Translated and adapted by R. Donaldson. 1914, Wm. Wood and Co., New 
York. 

14. Pratt, J. H. A critical study of the various methods employed for 
enumerating the blood platelets. Journ. Am. Med. Assn., xlv, 1905, p. 1999. 

15. Wess, GILBERT AND Havens. Blood platelets and tuberculosis. Trans. 
Natl. Assn. for Study and Prevent. of Tuberc., 10, 1914, 180. 

16. Wricut, A. E. On a simple procedure for making for oneself coagu- 
lation tubes of standard calibre, ete. Lancet, 1902, II, p. 15. 

17. Wricut, J. H. A rapid method for the differential staining of blood 
films and malarial parasites. Jowrn. Med. Research, vii, 1902, p. 138. 

18. WRIGHT AND Kinnicutr. A new method of counting the blood platelets 
for clinical purposes. Journ. Am. Med. Assn., lvi, 1911, 1457. 


TEXT-BOOKS ON HEMATOLOGY 


Casot, R. C. Clinical examination of the blood. 5th edn., 1904, Wm. 
Wood and Co., New York. 

Couzes, A.C. The diseases of the blood. 3d edn., 1905, J. and A. Churchill, 
London. 


28 METHODS OF EXAMINATION 


DaCosta, J. C. Clinical hematology. 2d edn., 1905, P. Blakiston’s Sons 
and Co., Philadelphia. 

een AND Lazarus, trans. by Myers. The histology of the blood. 
1900. Cambridge Univ. Press. 

Ewrna, James. Clinical pathology of the blood. 2d edn., 1903, Lea Bros. 
and Co., Philadelphia. 

Grawitz, E. Klinische Pathologie des Blutes. 3te Aufl., 1906, Georg 
Thieme, Leipzig. 

Haye, Gro. Du sang et de ses alterations anatomiques. 1889, G. Masson, 
Paris. 

von Limpeck, R. R. The clinical pathology of the blood. Trans. by 
Latham, 1901, New Sydenham Society, Vol. CX VII. 

Narceut, O. Blutkrankheiten und Blutdiagnostik. Erst. Heft, 1906, 
Veit und Comp., Leipzig. 

Parrenneim, A. Clinical examination of the blood and its technique. 
Translated and adapted by R. Donaldson. 1914. Wm. Wood and Co., 
New York. 


a if : = - 7 
| MRS Be As eee 
ca © : - > 
: per 


PLATE I 


NORMAL BLOOD OF ANIMALS 


CHAPTER i 
MORPHOLOGY OF THE 


BED CORPUS Gao eters ete, : : 


is In the circulating bicwd th 
‘man, horse, cow, shew, », clteg. APAIT 


2 Lewis) and presunatiy im ether & : e. 
“_ - eamels. DDE toner isl eroaog ,bookd hua na , | ‘ 


a * Poisson’ 9 fuig is ota aot herd ‘aaitag booid fuse saloarigtos hast q 
; - ~ physiological oa Yeo (staly bodld baa sefsecpon bat + ie 
; solution of soda Inca pie ‘iete ody VT es pohtiq book gar 
*hen canneine nm tha front “artiste atin 0 yoetol Jodgondqrayd rh bon: = 
ie Ted eo i, pitiate 8 stair A, woo ehwedqaryh : . 
Be ask pose x ait ia soning euloalova gorwords ae bende aah} 
oe ote ities aonb. serord Agslounonont axe 
Te Bie he COPA ies Fost ods ‘esloutloltoat bgutd 
Varese ln differen! conc lata creates peas syred™ 
tively large. The mistee'seanebsziquwscing wolsumonos syd OL © oe 
ia abfegbe pinecone Resiemiaeni ereaeRe ab, naiwods rgelnynocum,syiial IL 
~33 “Sapall het aite vic i nue es: aidghn getodl_givclspandgaaryloT ot 2 
’ 5 4h a erent HOS 1b abpunianigronny lod ef 
a enlating blood im the yo ‘it a'adyin to teslopaontionrrlod +1 a 
> puscles are elliptical auclenterlanges'sennst wos" slisdgontioot 21 
wy i puscles varies vath the dither waheninalaaaal aton jslidqenieedl (Of 3 
is for each a ill Le Loupe a -Ciptag Sdn an slulgonieott «if 


pter TH fu li x aint eo ,bomsigim olidqenwed .21 “ 
“fide easel, orton disa Jag. Li 
me! © stain, the chferenne between. tf Cais ran | wo bs se ‘be 

PP) colored periphers! pari beiteg cess se pe | 
ae eonditions marked changes in the sizé deive and staring proper ad 


rer : die Rare + ‘ 


al ties are BOmetimes shown, Tnstend of being about the e Bixe, 
a varia ion. TRAY per rin ade di aumiia. Itiste he noted ie 
os that pie] the SCANS ther. a t pins: ; Heaieramte carnation aS 


me 
e 


Pe ae be ' ry 


‘> ‘ . 
sie, Weuy pervall: sorpransdee aba coped! the otros 


« called sasepneytin, poslinnitne poe hail ees ; 4 hae. ae _* meat of 
Bo a of the average ape cain! Se Sas Kemaics od eae 
“various shapes tray fe, fas, ees» Satie sake Yo +H a 
te Thee are’ called pedhlories aot the chtu@tiins & Bummer sa pve ay 


Wes 


ODNAA Pwd = 


. Red corpuscles and blood plates, horse, Jenner’s stain. 

. Red corpuscles and blood plate, cat, Wright’s stain. 

. Blood plates, cat, Wright’s stain. 

. Lymphocyte, horse, Wright’s stain. 

. Lymphocyte, cow, Wright’s stain. 

. Lymphocyte showing nucleolus, guinea pig, Wright’s stain. 
. Large mononuclear, horse, Jenner’s stain. 


. Large mononuclear, cow, Jenner’s stain. 

. Large mononuclear, guinea pig, Jenner’s stain. 
. Large mononuclear showing degeneration, guinea pig, Jenner’s stain. 
. Polymorphonuclears, horse, Wright’s stain. 

. Polymorphonuclear, cow, Jenner’s stain. 

. Polymorphonuclear, cat, Wright’s stain. 

. Eosinophile, cow, Jenner’s stain. 

. Eosinophile, horse, Jenner’s stain. 

. Eosinophile, cat, Wright’s stain. 

. Eosinophile ruptured, cat, Wright’s stain. 

. Mast cell, horse, Jenner’s stain. 

. Mast cell, cow, Jenner’s stain. 


PLATE I 


Normal blood, camera lucida drawings. x 1200 


Large mononuclear, cow, Jenner’s stain. 


CHAPTER II 
MORPHOLOGY OF THE FORMED ELEMENTS 


RED CORPUSCLES (ERYTHROCYTES) 


In the circulating blood these elements have a cup shape in 
man, horse, cow, sheep, dog, cat, rabbit, guinea pig (Weidenreich, 
Lewis) and presumably in other domesticated mammals excepting 
camels. This shape may be seen in the counting chamber when 
Toisson’s fluid is used as a diluent, or when blood is examined in 
physiological salt solution; but better when examined in a 2.5 to 5% 
solution of sodium metaphosphate freshly prepared. Ordinarily 
when examined in the fresh condition or in dried preparations 
the red corpuscles appear as bi-concave discs of a pale straw color, 
the color being deeper in the peripheral part of the disc and nearly 
absent in the central part. The size of this central clear area 
varies in different conditions. In cases of anemia it may be rela- 
tively large. The red corpuscles in mammals are not nucleated 
as a rule in the circulation except during the intra-uterine period. 
Small numbers of nucleated red cells may be found in the cir- 
culating blood in the young. In the domestic fowl the red cor- 
puscles are elliptical nucleated cells. The size of the red cor- 
puscles varies with the different species of animal. The averages 
for each animal will be found in the tabulated summaries in Chap- 
ter III. In stained preparations the red corpuscles take the acid 
stain, the difference between the central clear area and the deeper 
colored peripheral part being clearly shown. In _ pathological 
conditions marked changes in the size, shape and staining proper- 
ties are sometimes shown. Instead of being about the same size, 
marked variation may appear in cases of anemia. It is to be noted 
that in the young there is normally a considerable variation in 
size. Very small corpuscles, about one-half the average size are 
called microcytes. Corpuscles one-half larger to twice the diameter 
of the average are called megalocytes. In anemia corpuscles of 
various shapes may be found, the most usual being pear shaped. 
These are called poikilocytes and the condition is known as poi- 

29 


30 MORPHOLOGY OF THE FORMED ELEMENTS 


kilocytosis. Nucleated red cells (erythroblasts) occur in certain 
abnormal conditions, as in severe cases of anemia and after con- 
siderable hemorrhage. In the very young nucleated red cells 
may be normally found, they may be numerous in the dog and 
cat. A few nucleated red cells have been found by Sherrington 
and by Traum in adult dogs and by Sherrington in adult cats. 
Nucleated red cells of the average size are called normoblasts, 
those considerably smaller than the average are microblasts, those 
considerably larger than the average are megaloblasts. Under 
certain conditions one meets with red corpuscles that take the 
stain irregularly. They may take the basophile stain in small 
puncte, the corpuscle presenting a coarsely stippled appearance, 
which is called punctate basophilia. Sometimes corpuscles appear 
darker, taking some of the basophile stain diffusely. This condi- 
tion is known as polychromasia or polychromatophilia. Punctate 
basophilia and polychromasia have been observed in the circulat- 
ing blood of young animals that were apparently in perfect health. 
In adults it is not usual to find these changes present except in 
cases where there is a rapid formation of red corpuscles, as after 
severe hemorrhage. Walker regards the red corpuscles that take 
a basophile tint as being younger forms than those having a greater 
amount of hemoglobin. 


LEUCOCYTES 


In fresh blood the leucocytes are distinguished by being color- 
less, somewhat refractive bodies of a spherical or irregular form. 
Some have a rounded nucleus and hyaline or refractive cell bodies. 
These ordinarily show but little if any ameboid movement. Others 
have irregularly shaped nuclei and granular cell bodies. The 
granules in some are minute, showing as dark points; in others 
the granules are larger, appearing as refractive bodies having a 
greenish tint. The cells with granules possess active ameboid 
movement. The several varieties are best distinguished in stained 
preparations. 


NORMAL VARIETIES OF LEUCOCYTES 


Five normal varieties are found in the circulating blood of the 
domesticated animals and are differentiated in stained prepara- 
tions by the following characters. 


PLATE II 


Red corpuscles, camera lucida drawings. «x 1200 

. Polychromasia, guinea pig. e 
. Punctate basophilia, guinea pig. 
. Erythroblast, puppy. 
. Erythroblast, puppy. 
. Erythroblast, dog. 
. Erythroblast, dog. 
. Megaloblasts, one showing punctate basophilia, homo. 
. Poikilocytosis and polychromasia, homo. 

. Pernicious anemia, homo, showing megalocytes, microcytes, poikilocytes, 
77 scuedablsati and punctata basophilia, Jenner’s stain. 


CONOR WNH 


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NORMAL VARIETIES OF LEUCOCYTES 31 


Variety I. Lymphocytes. This variety includes cells usually 
about the size or smaller than the average red corpuscle. Each 
has a relatively large nucleus that occupies nearly all of the cell. 
The nucleus is usually round but may be incurved or show a deep 
notch or sinus at one side. The cell body usually shows as a nar- 
row rim about the nucleus. Both nucleus and cell body are coarsely 
reticular. With careful staining a nucleolus may be seen. The 
cell body has a strong affinity for basic stains, often staining a 
deeper blue with Jenner’s stain than the nucleus. With Wright’s 
stain the cell body has a greenish blue while the nucleus has a dark 
violet tint. Cells falling in this group have practically the same 
appearance in the several domesticated animals. 

Variety II. Large mononuclears (hyaline cells, Kanthack and 
Hardy; large monocytes, Pappenheim). Cells belonging to this 
variety are larger than those of Var. I, usually about twice the 
diameter of the average red corpuscle. The nucleus usually oc- 
cupies only about one-half of the cell and is situated at one side 
of the center. Its shape is oval or curved (kidney or horse-shoe 
shaped). Both nucleus and cell body are finely reticular and stain 
less deeply than do those of lymphocytes. The cell body is faintly 
basophile. These cells have much the same appearance in the 
several species of the domesticated animals. In the guinea pig, 
however, a large number of cells of this variety contain within the 
cell body one or more rounded bodies that are in some cases ap- 
parently clear vacuoles and in other cases appear as homogenous 
or occasionally reticular bodies (see Plate I, Fig. 11) of a purplish 
tint with Wright’s or Jenner’s stains. They vary from about one 
micron in diameter to a body occupying nearly one-half the cell. 
The true nature of these bodies is not certainly known. Kurloff, 
who first described them, regarded them as vacuoles containing a 
secretory product. That they are products of secretion or de- 
generation has been followed, at least passively, by the majority 
of those who have written on the subject (Burnett, ’04, Staubli, ’06, 
Howard, ’07, and Canavan, 712). By some, however (Ledingham, 
’06), the bodies are regarded as possibly organisms, parasitic in 
nature. 

In the majority of instances there is no difficulty in distinguish- 
ing the cells belonging to Var. I and Var. II, but a certain number 
of intermediate forms do occur. In fact one can find all stages 


32 MORPHOLOGY OF THE FORMED ELEMENTS 


between typical lymphocytes with a small amount of strongly 
basophile, coarsely reticular cytoplasm and typical large mono- 
nuclears with a much larger amount of faintly basophile, finely 
reticular cytoplasm. 

Variety III. Polymorphonuclears (polynuclears, polynuclear 
neutrophiles, polymorphonuclear neutrophiles, finely granular 
oxyphile cells). The nucleus in this variety is several lobed, the 
different lobes being connected by slender portions. Rarely the 
nucleus consists of several separate parts. In shape the nucleus 
is polymorphous; it may be twisted, spirally coiled, S-shaped, 
U-shaped, Z-shaped or elongated. It is usually well stained and 
is coarsely reticular. The cell body contains many fine granules, 
so small that they appear as mere points. These granules show 
a rather weak affinity for acid stains, showing as reddish points 
with Jenner’s or Wright’s stains. The cell body is usually un- 
stained. In size these cells vary from the size to about twice the 
size of red corpuscles. 

In the domestic fowl the cells belonging to this variety differ 
strikingly as to the granules from polymorphonuclears in mam- 
mals. The nucleus varies in shape as in mammals and stains 
similarly. The cell body contains many large granules, spindle 
shaped with tapering ends, rod shaped with rounded ends, club 
shaped or oval, that stain a reddish color with Jenner’s stain or 
eosin and methylene blue and a dark reddish with Wright’s stain. 
The tint with Wright’s stain is darker with a little violet than 
the clear reddish of the eosinophile granules of fowl’s blood. With 
Ehrlich’s triacid stain the polymorphonuclear granules take a 
deep reddish purple. The granules vary in size from one to three 
micra in length by about one micron or less in width. 

This cell has generally been classed as an eosinophile * but it 


*It has had different names, more or less descriptive as,— crystalloid 
eosinophile,”’ “polynuclear leucocyte with eosinophilic rods.” The last name 
is inexcusable. Polymorphonuclear is used as a descriptive term. The word 
polymorphonuclear was coined, I believe, as the specific name of a certain 
kind of leucocyte. At any rate it is now used as a specific term. Polymor- 
phonuclears are not merely leucocytes with polymorphous nuclei. There 
would be little difficulty if teachers would have beginning students use Roman 
numerals or something as little descriptive to designate the several varieties 
of leucocytes until their distinguishing characters are learned. The names 
then would be recognized not as descriptive but as specific terms. That this 


PLATE III 


Domestic fowl, normal blood, Jenner’s stain, from photographs 


. Red cells, young cell in center, x 780. 


2. Red cells and thrombocytes, x 780. 


. Lymphocyte, thrombocyte and red cells, x 640. 


Large mononuclear, x 800. 
Lymphocyte and polymorphonuclear (ruptured), x 640. 


. Polymorphonuclear and red cells, x 640. 
. Eosinophile and red cells, x 640. 

. Mast cell and red cell, x 640. 

. Thrombocyte and red cells, x 1280. 

. Lymphocyte and red cell, x 1280. 

. Large mononuclear and red cell, x 1280. 
. Lymphocyte and polymorphonuclear, x 1280. 
. Polymorphonuclear, x 1560. 

. Eosinophile, x 1560. 

. Mast cell, x 1280. 

. Mast cell (ruptured), x 780. 


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Wieulty if teachers would hate heagnning stadents use Rorean 
onsmbvine at ite descriptive to designate the several “varieties y 
«o)- theit distinguishing chameters are learned. The nama ™ 
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PATHOLOGICAL VARIETIES OF LEUCOCYTES 33 


evidently does not belong to that variety. The domestic fowl has 
an eosinophile leucocyte with round granules, similar to the 
eosinophile found in mammalian blood. As stated above the 
nucleus of the avian polymorph varies much exhibiting the same 
shapes asin mammals. In affinity for stains the granules resemble 
the polymorphs rather than the eosinophiles. The cells have ac- 
tive ameboid movement. In its physiologic properties, this cell 
resembles the polymorphonuclears. This is the cell found in 
abundance in purulent exudates and is the one that reacts in acute 
inflammatory conditions as does the mammalian polymorphonu- 
clear. 

Variety IV. Eosinophiles (coarsely granular oxyphile cells). 
The nucleus is polymorphous, ordinarily being bi- or tri-lobed. 
The lobes are coarsely reticular and usually stain well. The cell 
body contains many coarse, strongly acidophile granules which 
are commonly round in outline though oval, ovate or oblong ones 
are found. In the cat these granules are ordinarily short rod- 
shaped with rounded ends. The granules vary in size in the dif- 
ferent species. In the horse they are very large, generally one to 
one and one-half micra in diameter. These cells are of about the 
size of the polymorphonuclears. 

Variety V. Mast cells (coarsely granular basophile cells, 
Kanthack and Hardy). In this variety the nucleus usually takes 
the stain so faintly that it is difficult to make out its shape. It 
varies in shape from rounded or curved to bi-, tri- or many lobed. 
The cell body contains many strongly basophile rounded or oval 
granules that take a deep violet tint with Jenner’s and a royal 
purple with Wright’s stains. Mast cells are as a rule slightly larger 
than eosinophiles. 


PATHOLOGICAL VARIETIES OF LEUCOCYTES 


Besides the varieties just described which are found in normal 
circulating blood there are other kinds that are sometimes found 
in pathological conditions. In some cases of disease severe enough 


leucocyte is homologous with the mammalian polymorphonuclear was first 
stated in a paper read before the American Association of Pathologists and 
Bacteriologists on May 7th, 1907. It was first published in the first edition 
of this book, March, 1908. 


34 MORPHOLOGY OF THE FORMED ELEMENTS 


to affect the blood forming organs immature forms of leucocytes 
may pass into the blood stream. In certain cases of leukemia not 
only immature but even parent forms of leucocytes may be found 
in the circulating blood. The immature leucocytes occur in the 
circulating blood only in small numbers except in cases of leukemia. 
lt is important to recognize them when they do occur as their 
presence indicates a serious condition, involvement of the blood 
forming organs. It is sometimes difficult to distinguish immature 
cells belonging to the myelocytic from those of the lymphocytic 
series. The granules of the myelocytes usually do not stain well 
with the ordinary blood stains. Graham recommends the use of 
his alphanaphthol-pyronin method, by which myelocytic cells 
are made easier to recognize as the granules are made prominent. 

Myelocytes are cells whose cell bodies contain fine or coarse 
granules like those of polymorphonuclears or eosinophiles. The 
nucleus is rounded or may be indented. According as the granules 
are fine or coarse the cells are known as finely granular myelocytes 
(usually simply myelocytes) or eosinophilic myelocytes. The eo- 
sinophilic myelocyte is found in the circulating blood practically 
only in cases of mixed celled leukemia. 

Metamyelocytes or transitional leucocytes are intermediate 
between myelocytes and polymorphonuclears. The nucleus in- 
stead of being round or oval as in a myelocyte is bent or twisted. 
It differs from a polymorphonuclear in that the nucleus does not 
consist of lobes connected by slender portions or of separate divi- 
sions. 

Metamyelocytes and myelocytes are sometimes found in small 
numbers in the circulating blood in severe cases of infection or 
intoxication. Large numbers of myelocytes and metamyelocytes 
are found in the circulating blood in cases of mixed celled leukemia. 

The leucoblast is a still more primitive type of cell. Its neuclus 
is like that of a myelocyte, but the cell body is feebly basophile 
and is without the granules that distinguish the myelocytes, 
metamyelocytes and polymorphonuclears. Leucoblasts closely 
resemble large lymphocytes. They are found in cases of acute 
mixed celled leukemia. So far as I know leucoblasts have not 
been recognized in the circulating blood of the domesticated 
animals. 

Plasma cells (reizungsformen, Tiirk) are non-granular, mono- 


DEGENERATIVE CHANGES IN LEUCOCYTES 35 


nuclear cells usually somewhat smaller than large mononuclears, 
but are sometimes very large. The round or oval nucleus is rela- 
tively small and is generally excentric. The cell body is strongly 
basophile and frequently contains minute vacuoles, giving the 
cell a honey-comb structure. These cells are apparently de- 
generative forms of mononuclears and are found in the blood in 
various inflammatory conditions. 


DEGENERATIVE CHANGES IN LEUCOCYTES 


It is important in making a histological examination of blood 
to note the degenerative changes in the leucocytes as well as in 
the red corpuscles. Among the more common changes observed 
are those in the nuclei. Sometimes they appear swollen and stain 
less deeply; again the lobes of the nuclei are shrunken and have 
an irregular contour. The nucleus may consist of several separate 
divisions, each of which stains deeply. The nucleus may show 
hydropic degeneration. In severe leucocytosis one often finds 
leucocytes with the cell bodies ruptured, the granules scattered 
and the nucleus pale. Vacuoles may be found in the cell bodies. 
Small or larger, rounded, purplish granules with Wright’s or 
Jenner’s stain may be observed in lymphocytes and in polymorphs 
as well as in large mononuclears, as was mentioned in describing 
the latter variety. In acute leucocytosis a diminished number of 
the granules in polymorphs is often seen. 

Glycogenic degeneration is observed in certain conditions. It 
consists in the presence of glycogen granules in the leucocytes, 
especially the polymorphs. Locke and Cabot have applied the 
term iodophilia to this condition. A certain amount of extra- 
cellular glycogen may be found in normal blood. The reaction 
consists in finding glycogen in leucocytes and in an increased 
amount as extracellular masses. A positive reaction according to 
Locke and Cabot signifies a general toxemia such as might be 
produced by abscess, gangrene, uremia or malaria and has been 
observed in local and general infection with pyogenic organisms, 
in toxemia of bacterial origin, in non-bacterial toxemia, e. g., 
uremia, in disturbances of respiration and in grave anemia both 
primary and secondary. The reaction (Barnicot) does not run 
parallel to leucocytosis other than having a common cause; its 


36 MORPHOLOGY OF THE FORMED ELEMENTS 


continued presence in pneumonia after the crisis is further aid to 
other clinical signs that lead one to suspect delayed resolution or 
other complications; when accumulations of pus are suspected 
the absence of the reaction is of very great negative value. 


BLOOD PLATES 


The blood plates or platelets in mammals are flattened, color- 
less, very finely granular bodies, usually about one-third the di- 
ameter of red corpuscles, that show a marked tendency to collect 
in clumps. They are very vulnerable, changing quickly when 
blood is drawn. On Deetjen’s agar the blood plates show ameboid 
processes. According to Wright, confirmed by Bunting, Ogata and 
others, the blood plates are formed by detached fragments of 
certain giant cells, the megakaryocytes (Howell), of the bone mar- 
row and spleen. There has been a great deal of confusion as to 
the nature of the blood plates because bodies extruded from red 
corpuscles and somewhat similar to the appearance of the blood 
plates may be seen in fresh blood and in films prepared in the 
ordinary manner. The extruded bodies, however, differ from true 
blood plates, as pointed out by Sacerdotti, by being not flattened, 
by being homogenous and by often having a faint hemoglobin 
tint. The blood plates may be studied in freshly drawn blood 
diluted with physiological salt solution (0.9% NaCl solution) or 
preferably 10% sodium metaphosphate solution which prevents 
the clumping of these and avoids the formation of the extruded 
bodies from red corpuscles. In fixed and stained smears the blood 
plates take a bluish tint with eosin and methylene blue; with 
Wright’s stain the central part of the blood plate shows granules 
of a reddish purple tint while the outer portion appears homog- 
enous and has a bluish tint. 

Thrombocytes (spindelzellen, v. Recklinghausen), Pl. III, 
Figs. 2 and9, in the blood of the domestic fowl are elliptical, oblong 
or spindle-shaped cells with an elliptical to broadly oval nucleus. 
In size the cell has nearly the length and about one-half the width 
of the average red cell. The nucleus occupies about one-half the 
length and nearly the entire width of the thrombocyte and is 
usually situated in the central part of the cell. The cell body is 
pale and often contains one or more clear vacuoles and occa- 


BLOOD PLATES 37 


sionally one or more compact, rounded, deeply staining (deep 
purple with Wright’s stain) bodies about the size or somewhat 
larger than a mast cell granule. These bodies are probably a 
result of degeneration. The thrombocytes show a marked tend- 
ency to collect in clumps. In fresh blood and in the less thinly 
spread parts of films, they collect in masses in which it is difficult 
to distinguish the outline of individual cells. This indistinctness 
of cell‘outline and structure shows another property of these cells, 
that is their vulnerability. They change quickly when taken 
from the blood vessels, passing through a characteristic series 
of changes. Both cell body and nucleus become less distinct, the 
cell body losing its structure first. Finally both become structure- 
less, appearing in stained preparations merely as a diffusely stained 
mass, the nucleus being distinguishable by having a slightly 
deeper stain. 

Hayem and Goodall call these cells hematoblasts. Their func- 
tion and properties, however, show them to be similar to the 
blood plates in mammals. As the thrombocytes are nucleated 
they cannot be homologous with blood plates. Wright considers 
them homologous with the megakaryocytes from which the blood 
plates are derived. For his opinion he gives two reasons, first 
that the forerunners of the megakaryocytes are circulating cells, 
as may be seen in embryo guinea pigs, and second that in certain 
Amphibia the thrombocytes regularly lose their cytoplasm by 
a pinching off process similar to that which takes place in the for- 
mation of blood plates. 

Blood dust (hemokonia). These are minute spheroidal or 
spindle-shaped bodies of one-fourth to one micron in diameter 
found in the blood. They were first described by Bizzozero and 
later by Miiller. These bodies are insoluble in acetic acid, alcohol 
and ether and are not blackened by osmic acid. Stokes and Wege- 
farth found them to vary in size in different animals according to 
the size of the granules of leucocytes. They regard them as 
extruded granules of polymorphs and eosinophiles. These 
bodies have not been shown to have any special clinical sig- 
nificance. 


38 MORPHOLOGY OF THE FORMED ELEMENTS 


REFERENCES 


1. Barnicot, J. The iodine reaction in the leucocytes. Journ. of Path. 
and Bacter., xix, 1906, p. 304. 

2. Bizzozero, J. Ueber einen neuen Formbestandtheil des Blutes und 
dessen Rolle bei der Thrombose und der Blutgerinnung. Arch. f. path. Anat., 
xc, 1882, S. 261. 

3. Buntina, C. H. Blood-platelet and megalokaryeyte reactions in the 
rabbit. Journ. Exp. Med., xi, 1909, 541. 

4. Burnett, 8S. H. A study of the blood of normal guinea pigs. Journ. of 
Med. Research, xi, 1904, p. 537. 

5. Canavan, M. M. The blood cell picture in horse serum anaphalaxis 
in the guinea pig: note on Kurloff’s inclusion bodies. Journ. Med. Res., 
xxvii, 1912, 189. 

6. Cutten, E. K. A morphological study of the blood of certain fishes and 
birds, ete. Bul. Johns Hopk. Hosp., xiv, 1903, 352. 

7. DeretseN. Untersuchungen iiber die Blutpliittchen. Arch. f. path. Anat., 
elxiv, 1901, S. 239. 

8. Dexuuyzen, M. C. Ueber das blut der Amphibien, Verhandl. d. anat. 
Gesellsch., 6 ten Versamml., Wien, 1892, 8. 90. 

9. DexHuyzen, M. C: Ueber die Thrombocyten (Blutplittchen). 
Anat. Anz., xix, 1901, 8. 529. 

10. Goopaut, A. The numbers, proportions and characters of the red and 
white blood corpuscles in certain animals. Journ. of Path. and Bacter., xiv, 
1910, 195. 

11. Granam, G.S. The oxidizing ferment of the myelocyte series of cells 
and its demonstration by an alphanaphthol-pyronin method. Journ. Med. 
Res., xxxv, 1916, 231. 

12. Grinsera, C. Beitrige zur vergleichenden Morphologie der Leuk- 
ocyten. Arch. f. path. Anat., elxiii, 1901, 303. 

13. Howarp, C. P. The relation of the eosinophile cells of the blood, peri- 
toneum and tissues to various toxins. Journ. Med. Res., xvii, 1907, 237. 

14. Howrtt, W. H. The life history of the formed elements of the 
blood especially of the red blood corpuscles. Journ. of Morphol., iv, 1890, 
Dol. 

15. KanrHack AND Harpy. The morphology and distribution of the 
wandering cells of Mammalia. Journ. of Physiol., xvii, 1894, p. 81. 

16. Kuruorr.. Cited by Ehrlich und Lazarus, Die Andmie, Nothnagel’s 
Specielle Pathologie und Therapie, viii, 1898, 8. 56. 

17. Lepincuam, J.C. G. On the vacuolated mononuclear cells in the blood 
of the guinea pig. Lancet, i, 1906, 1675. 

18. Lewis, F. T. The shape of mammalian red blood corpuscles. Journ. 
of Med. Research, x, 1904, p. 513. 

19. Locke aNp Caxsor. Iodophilia. Journ. of Med. Research, vii, 1902, 
p. 25. 

20. Masstow, G. Einige Bemerkungen zur Morphologie und Entwicke- 
lung der Blutelemente. Arch. f. mikr. Anat., li, 1897, 61. 


REFERENCES 39 


21. Mtuter, H. F. Ueber einen bisher nicht beachteten Formbestandtheil 
des Blutes. Centralbl, f. allge. Path. u. path. Anat., vii, 1896, S. 529. 

22. OaaTa. Untersuchungen iiber die Herkunft der Blutplittchen. Beitr. 
z. path. Anat., lii, 1912, 192. 

23. PappENHEIM, A. Atlas der menschlichen Blutzellen. 1905-1912. 
Gustav Fischer, Jena. * 

24. PappeNHEIM, A. Uber verschiedene Typen von Lymphozyten und 
Monozyten, zum Teil im scheinbar normalen Blut. Fol. Haemat., xii, 1911, 26. 

25. PappeNHEIM, A. Clinical examination of the blood and its technic. 
Translated and adapted by R. Donaldson, 1914. Wm. Wood and Co., New 
York. 

26. v. RECKLINGHAUSEN. Ueber die Erzeugung von rothen Blutkér- 
perchen. Arch. f. mikr. Anat., ii, 1866, 8. 137. 

27. Sacervorri, C. Erythrocyten und Blutplittchen. Anat. Anz., xvii, 
1900, S. 249. 

28. Srausui, C. Klinische und experimentelle Untersuchungen iiber 
Trichinosis und iiber die Eosinophilie im allgemeinen. Deutsch. Arch. f. klin. 
Med., \xxxv, 1906, 312. 

29. Strokes AND WrEGEFARTH. The presence in the blood of free granules 
derived from leucocytes, ete. Bull. Johns Hopk. Hosp., viii, 1897, p. 246. 

30. Turx. Klinische Untersuchungen iiber das Verhalten des Blutes bei 
akuten Infektionskrankheiten. Wien, 1898. 

31. Waker, E. L. A comparative study of the red corpuscles of Verte- 
brates. Journ. of Med. Research, xiii, 1904, p. 61. 

32. WeipenrercH, F. Studien iiber das Blut. I Form und Bau der rothen 
Blutkérperchen. Arch. f. mikr. Anat., Ixi, 1902, S. 459. 

33. Wricut, J. H. The origin and nature of blood plates. Bost. Med. and 
Surg. Journ., cliv, 1906, p. 643; also Virchow’s Arch., 186, 1906, 55. 

34. Wricut, J. H. The histogenesis of the blood platelets. Journ. of 
Morphol., xxi, 1910, 263. 


CHAPTER III 


NORMAL BLOOD IN THE SEVERAL SPECIES OF THE 
DOMESTICATED ANIMALS 


Different investigators have reported widely varying results of 
the examination of the blood of normal animals. More examina- | 
tions have been made of laboratory animals,—dog, rabbit and 
guinea pig. Consequently what is the normal for these animals is 
better known than for other domesticated animals. More work 
is needed to determine the normal for the majority of the domes- 
ticated animals, especially for the numbers and percentages of the 
several varieties of leucocytes. 

For convenience in reference the normal condition of the blood 
is presented in tabular form for each species—horse, cow, sheep, 
goat, dog, cat, swine, rabbit, guinea pig and domestic fowl with 
references to the investigators who have worked with each species. 


HORSE 


There is considerable normal variation in the number of red 
corpuscles in the horse. The normal number for the stallion is 
from 7 to 10 millions per emm. with an average of 8 to 814 mil- 
lions; for the gelding 51% to 9 millions with an average of 714 to 
8 millions; for the mare 514% to 71% millions with an average of 
614 to 7 millions. Perhaps observations on a large number of 
normal horses will show that the smaller numbers, those below 
6 millions, are not of strictly normal animals. 

The hemoglobin varies fully as much as the red corpuscles. 
Moore, Haring and Cady give the normal as 85 to 100 with an 
average of 94. Wetzl found the normal to be from 62 to 80. 
Sabrazés, Muratet and Durroux give the normal as from 68 to 84. 
More examinations of the hemoglobin of healthy horses are needed. 

Prus gives the number of blood plates as 500,000 per emm. 

The normal number of leucocytes seems to be from 5,000 to 
10,000 with the average about 8,000. Widely varying results are 
reported by different investigators. Wiendieck found differences 

40 


HORSE 4] 


in the leucocytes of stallions, geldings and mares. In the stallion 
he found 8,400 to 11,000 with an average of 9,300 per cmm. In 
the gelding there were from 6,900 to 9,400 with an average of 
8,200 per cmm. In the mare there were from 6,500 to 9,000 with 
an average of 7,900 per emm. Gasse also found differences in 
the leucocytes in stallions, geldings and mares. He found the 
leucocytes in stallions to vary from 8,500 to 9,900, with an average 
of 9,000 per emm., in the gelding 7,800 to 9,300 with an average of 
8,500 and in the mare 5,400 to 8,300 with an average 6,900 per 
emm. Moore, Haring and Cady obtained much lower counts. 
They found from 4,400 to 6,800 leucocytes with an average of 
5,600 per cmm. 


Taste I.—SuMMARY OF EXAMINATIONS OF THE BLoop oF NorMAL HorsES 
BY DIFFERENT INVESTIGATORS 


Red 
Sr ee ey ee a | ates 
per cmm. 
11,000 - a o ae 2 Bidault. 
6.5-9.2 | 7,200—-8,800 | ——— a a Franke. 
9.41 9,000 —_—— -——— ee Gasse. 
8.28 ” 8,500 — —— —_—— Gasse. 
Geo 6,900 ——. — — Gasse. 
en —— 5 Gulliver. 
TA 9,500 —_——- — 5.58 Hayem. 
6.3 —— —_—— yao Malassez. 
7.95 8,500 _——— — - —. Meier. 
7.198 12,000 6.5 eS 5.78 Mikrukow. 
7.9 5,625 94 —- Moore, Haring 
and Cady. 
—_- 7,000 es —. ——_— Nicholas et Cour- 
mont. 
Ue 15,000 — — ee Prus. 
6.75-8.66| 3,720-11,500| 68-84 1,049 4.5-7.8 | Sabrazés, Mura- 
tet et Durroux. 
7.639 4 10,460 ——. —- —- Storch. 
9.395 14,034 oa — Storch. 
bed —- 1,060 5.8 Sussdorf. 
(a! —_—— oe — Trasbot. 
8.45 — oe — — | Wendelstadt und 
Bleibtreu. 
6.16-8 .69 62-80 a a Wetzl. 
5.4-10.3) 6,500-11,000) —-— —— Wiendieck. 


1 Stallions, 2 Geldings, * Mares, 4 Adults, * Colts. 


42 NORMAL BLOOD IN DOMESTICATED ANIMALS 


Wide differences occur in the findings of different investigators 
in the numbers and percentages of the several varieties of leu- 
cocytes. The results obtained by different investigators are given 
in the following tables II and III. 


Tasie IIl.—NumBERS or LevucocyTES AND PERCENTAGES OF THE VARIETIES 
IN THE BLoop or NormMau Horses 


Percentage of Varieties 

Leucocytes 

per cmm. I II III | IV V 

Lymph». Large M.| Polymor.} Eosins Mast Author 


——-— 


11,090 37 57 5 —— | Bidault. 
—— 34-38 60-65 1-2 —— | Cozette. 
= 22.5 ao 67 5 —— | Fischer. 
7,200-8,800 15-35 |2.5-12 | 60-70 |0.8-5. | 0-0.4 | Franke. 
5,400-9,900 |23.7-41.29) 0-3 52-73 |0.5-5.8) 0-0.4 | Gasse. 
8,500 30 Bp 63.5 3 —— | Meier. 
5,625 30 6 59 4 1 Moore, Haring 
and Cady. 
5,400-10,300 35-45 |1.5-3.5} 50-70 |1.5-4 |0.2-0.7| Wiendieck. 
TasLe II]—NUMBERS OF THE VARIETIES OF LEUCOCYTES PER CMM. IN THE 


Bioop or NormMat Horses 


I II IIL IV Vv 
Lympho. Large Polymorphs Eosins Mast Author 
Mon. Cells 


1053-2431 | 137-518 | 2414-4107 | 161-364 | 6-125 | Moore, Haring and 
Cady. 
1687 340 3316 228 51 | M. H.C. Average. 
1600-4300 78-376 | 3208-7964 26-553 | 0-126 | Wiendieck. 
2500-3500 | 150-300 | 4000-5000 | 200-350 | 20-60 | Wiendieck Average. 


COW 


The red corpuscles vary from about five to eight millions. The 
average in this country has been found to be about six millions. 
Wetzl found an average of seven millions (9 cattle). The hemo- 
globin ranges from 45 to 85 with an average of 60 to 65. Hibbard 
and Neal found an average of seven million red corpuscles and 
97 per cent hemoglobin in five yearling heifers. 


COW 43 


Considerable variation in the leucocytes is reported by different 
investigators. The normal seems to be from 5,000 to 10,000. A 
very great variation in the numbers of the several varieties has 
been found by Dimock and Thompson in apparently normal 
cattle. 

Further investigation of the blood of normal cattle is needed, 
especially as to the numbers of the several varieties of leucocytes. 


TaBLe I1V.—SumMMARY OF EXAMINATIONS OF THE BLooD OF NORMAL CATTLE 
BY DIFFERENT INVESTIGATORS 


Red 


See een Sree ee | autos 
per cmm. 
6.2 = — —— ——— | 467.2¢| Bethe: 
Gal 5,486 59.7 ——. eo Dimock and 
Thompson. 
—. —— — 5.95 Gulliver. 
7.03 4 8,950 97 —- Hibbard and 
Neal. 
4.2 —— —- —_—-— 6 Mallassez. 
6.0 9,730 —— — 5-6 Smith and 
Kilbourne. 
5.0 — — ae + Stéltzing. 
Gees 7,841 — — Storch. 
6.6? 9,367 —= —- ——— Storch. 
5.43 8,241 = ——— —-- Storch. 
AVE 11,614 —— — —— Storch. 
8.55 15,739 - oa a Storch. 
7.0 65 —- ——- Wetzl. 


1 Bulls, 2 oxen, * cows, * young cattle, ° calves. 


Dimock and Thompson obtained the following numbers and 
percentages of the several varieties of leucocytes in the blood of 
normal cattle: 


Averages Minimum Maximum 
Lymphocytes....... 2,992 per cmm. 54.2 % 31 % 76 
Large mononuclears 86 1.4 0.2 33° 
Polymorphs........ 1,786 30.5 13 45.8 
Hosins ey el eees eee 772 13.15 3.8 26.5 
Masticells= 25522. 52 31 0.59 Ost 12 


44 NORMAL BLOOD IN DOMESTICATED ANIMALS 


Refik-Bey gives the normal number of leucocytes for cattle 
as 7,000-11,000 per cmm., the number of mononuclears (includ- 
ing lymphocytes) as 4,500-6,500 per emm. (57-84%), the number 
of polynuclears as 1,500-3,500 per cmm. 


SHEEP 


The average number of red corpuscles is given by Woltmann 
as 8,000,000 and of leucocytes as 8,000 peremm. Wetzl found the 
red corpuscles in normal sheep to vary from 8,008,000 to 9,272,000 
per cmm. and the amount of hemoglobin to vary from 47 to 63. 
Giltner found higher amounts in two normal males. The red 
corpuscles were 9,120,000 and 11,500,000, the hemoglobin 85 in 
each and the leucocytes 5,330 and 10,900 per emm. Woltmann 
found the following percentages of the several varieties of leu- 
cocytes. Giltner found widely varying percentages in two males. 
Each had many more lymphocytes than were found by Wolt- 
mann. More work is needed on the blood of normal sheep. 


Taste V.—SuMMARY OF EXAMINATIONS OF THE BLoop oF NORMAL SHEEP 
BY DIFFERENT INVESTIGATORS 


Red Corpuscles Leucocytes Hemoglobin| Specific | Size of Red 


canes per cmm., per cent. | Gravity Corpuscles ashore 

9.133 4,140 —— — 3.9-5.9 Bethe. 
12.090 es a —- 4.9 Cohnstein. 

9.1-11.5 5,300-11,900 85 —- we Giltner. 
—————— | ————— a —- 4.79 Gulliver. 
— aa --— 1038 Miintz. 
10.472 1 9 420 oe a —— Storch. 
11.032 2 10,198 ee a —— | Storch. 
1225 7,000 a a Warthin. 

——-— —— — 5 Welcker. 
8-9 .27 So 47-63 ee Wetzl. 
8.0 8.000 ——- — ——— Woltmann. 


1 Adults, ? lambs. 


The percentages of the several varieties of leucocytes of the 
blood of normal sheep obtained by Woltmann are as follows: 


DOG 45 


Average 
gmnnOCytese 8s farce u ore pa eiele sen k S Bele a 40-60% 53% 
aree;mononucleats. a7... -sa 5 40 co ey ics ae ees 3-11 8 
12a) haiti eric oinice atine ob odcag ace Meee nao pST 30-55 37 
iBlosino piles! ree, etree eee er tats e sete 0.2-8 ver | 
IVE ASESCOLS mera were rar rey) Sr ae ce eater erate NA ease aba ea 0-2 0.3 


GOAT 


Not enough examinations have been made of goats’ blood to 
know what the normal is. The red corpuscles are high, the aver- 
age apparently 9-10 millions. The hemoglobin has not been 
determined for normal animals. Mohler and Washburn state that 
they were unable to obtain correct hemoglobin readings on ac- 
count of the color of the plasma. We have had no difficulty, how- 
ever, using Dare’s hemoglobinometer. 

The leucocytes are about 10,000 per emm. More work needs 
to be done to determine them and the numbers of the several 
varieties. 


Taste VI.—SumMary OF EXAMINATIONS OF THE BLoop or NorMAL GOATS 
BY DIFFERENT INVESTIGATORS 


Red Cor- 


a ee | ee ee eae 
per cmm. 
——. ———. ——— 3.94 Gulliver. 
19.0 30,000 —— ——— 4.25 u Hayem. 
18.0 ——. —— 3.5 Malassez. 
9.9 9,200 —— — Mohler and 
Washburn. 
14°52) 12057 ——. —— - —_— Storch. 
10.12) S91,358 ——— —---- Storch. 
9-10.0 —— —— 1042 4.14 Sussdorf. 
16.0 8,000 === Warthin. 
—- ——- —_—— 4.14 Welcker. 


1 Goats, ? kids. 
DOG 


The red corpuscles are normally from about 5 to 8 millions with 
an average of about 6 millions. The hemoglobin has been found 
to vary from 55 to 104. The average is about 90. Considerable 
variation in the normal number of leucocytes has been found by 
different investigators. Six thousand to 12,000 with an average of 
about 8,000 seems to be the normal for adults. The percentages 


46 NORMAL BLOOD IN DOMESTICATED ANIMALS 


of the several varieties are approximately these:—lymphocytes 
11-29, average 20; large mononuclears 3-10, average 6; polymorphs 
60-76, average 68; eosins 1-10.5, average 6 and mast cells rare. 


Taste VII.—SumMmary oF EXAMINATIONS OF THE BLOOD oF NorMAL Docs 
BY DIFFERENT INVESTIGATORS 


Red Cor- 
purer | lager ene et ae aoe 
per cmm 
7.0 ——_—_— Uff ——— —— | Breuer und y. 
Seiller. 
5.9 8,221 90 ——— —— | Burnett and 
Traum. 
Gie2 9,526 ~ ——. —— | Busch and 
Van Bergen. 
6,000-10,000 | ——— —— —— |Courmont et 
Lesieur. 

ez 19,300 87 — —— | Dawson. 
4.75-5.5 | 11,200-31,200 | 75-110 | ——— —— | Goodall. 

15,800 —. —— |Goodall, Gul- 
land and Pa- 
ton. 

se -- 7.17 | Gulliver. 

6.6 10,000 ae —— 7.2” | Hayem. 

(hs 21,058 Ss — —— | Hinerfauth. 

7.4 11,757 —— —_— ——— | Lyon: 

——— —— 6.95 «| Manassein. 

7,762 —— —— —— | Nicholas et Cot. 

6:11 14.08 — — | Otto. 

5.71 a 13272 —— —— .||\Otto: 

14,182 —— —— | Pohl. 

7:3 8,686 117 1063 —— | Rieder. 

6.2 7,440 93 —— | Sabrazés et 

Muratet. 

5.5 9.438 58 1058.8 —— |Sherrington. 
4.0-5.6 —— |Stéltzing. 
—— — 1060 7.3 | Sussdorf. 
—— | 8,100-15,800 | —— —— | Tallqvist und 

v. Willebrand. 
4.4 as we a 7.3 | Vierordt. 
= ~ ——— 7.3 | Welcker. 
4.8-8 ——— 55-104 —_— —— | Wetzl. 
6.4 — - os —— | Worm-Miiller. 
6.1 7,000 97 —— | Zenoni. 


1 Male, 2 female. 


CAT 47 


Taste VIII—Nuvumsers or LevucocyTES AND PERCENTAGES OF THE 
VARIETIES IN THE BLoop oF NorMAL Docs 


Percentage of Varieties 
Leucoeytes | AAA  — ee 


per cmm. |, i |. ar IV. v. 
Lympho | Large M | Polymor| Eosins Mast 
8,221 19.4 6.3 | 68 6.1 rare | Burnett and Traum. 
9,526 | 21 G28 Oded 5.3 rare |Buschand Van Bergen. 
6-10,000 ——— | 69 ae Courmont et Lesieur. 
19,300 | 22.17 | 4.42 | 64.56 | 8.55 | ——— | Dawson. 
19,500 30 63 iG ——— | Goodall. 
15,800 | 18.5 Geom OOnS 14.5 | ——— | Goodall, Gulland and 
Paton. 
25-36 75-80 ——— | Kriiger. 
7,762 | 26.6 4.2 | 69 0.2 | —— | Nicholas et Cot. 
9,699 10 Wists || 7A 3.3 | —— | Nicholas et Dumoulin. 
7,440 | 33.12 1.32 | 51.07 | 13.97 | ——— |Sabrazés et Muratet. 
9,438 17 75 7.8 Sherrington. 
12,409 5-10 | 10-15 | 70-80 | 4-8 -0.5 | Tallqvist und v. Wil- 
lebrand. 
7,000 28 62 10 ——— | Zenoni. 
CAT 


There are but few examinations of the blood of normal cats re- 
ported. The normal number of red corpuscles seems to be from 
4.8 to 7.6 millions per emm. with an average of about 6.5 millions. 
Goodall found the normal to vary from 7.28 to 8.6 millions with 
an average of 8 millions. The leucocytes range from 7,000 to 
19,000 with an average of 13,300. Goodall found higher numbers 
of leucocytes. He reports the normal as from 15,800 to 38,800 
with the average as 18,000. He reports the following percent- 
ages :—mononuclears 37, polymorphonuclears 54, and eosinophiles 
9. 


48 NORMAL BLOOD IN DOMESTICATED ANIMALS 


TaBLe 1X.—SuUMMARY OF EXAMINATIONS OF THE BLoop or NorMAL Cats 
BY DIFFERENT INVESTIGATORS 


Red 
Corpuscles | Leucocytes | Hemoglobin Specific Size of Red ‘AGih 
Millions per cmm. per cent. Gravity Corpuscles oe 


per cmm., 


6.6 13,331 ——. — |Busch and Van Ber- 


gen. 
7.28-8.6 18,000 65-80 ——_——— —— |Goodall. 
13,500 aaa — Goodall, Gulland 
and Paton. 
—- wes 5.76 |Gulliver. 
9.9 7,200 oe ——-- 6.2 » |Hayem. 
ae —-—— 5.77 |Manassein. 
7.9 14,000 6 5.49 |Mikrukow. 
6.8 14,017 ABS 1052.6 Sherrington. 
1054 6 Sussdorf. 


OM 
6.5 |Welcker. 


The percentages of the varieties of leucocytes in the blood of 
normal cats obtained by Busch and Van Bergen are as follows: 


Tasmallamononuclears aes eerie 34.38% 


4 . 3 /O 
Dy barce;mononuclearcmress ain eerie reer 4.89 
IIIa. Polymorphonuclear without granules......... 54.15 ) 55.5 
Illb. Polymorphonuclear with fine granules........ 1.36 i 
IVa. Polymorphonuclear with large coarse rod- 
shaped oxyphile granules............... 0.9 
IVb. Polymorphonuclear with large medium round t 5.2 
oxyphulejpranules rap ani eee 4.35 
Vis WMlasticells® Sister, ate earns tee crass tate ee roe 0.035 


In making two varieties each of polymorphs and eosins, Busch 
and Van Bergen have followed Hirschfeld. There does not seem 
to be sufficient reason for giving the eat more varieties of leucocytes 
than the other mammals. In other animals than cats one can 
find polymorphs in which the granules are indistinguishable or 
barely visible. Very slight differences in the technic of staining 
have been observed to produce similar differences in the staining 
of these granules. The great majority of eosins contain rod-shaped 
granules, though round and oval forms may be found in the cells 
containing mostly rod-shaped granules. Variations in the shape 
of the granules are seen in other animals than cats. 


SWINE 49 


SWINE 


A great deal of variation is reported by different investigators 
in the blood of normal swine. Some of the variation is probably 
due to the different age and sex of the animals examined. The 
normal count of red corpuscles seems to be about 8 millions. It 
is less for young pigs. The average hemoglobin value is about 85. 
The leucocytes seem to average about 19,000 with more than 
half of them lymphocytes. Gititig found normoblasts numerous 
in some of the four weeks old pigs examined by him. 

The following tables, X and XI, give the results of examinations 
by different investigators: 


TABLE X.—SUMMARY OF EXAMINATIONS OF THE BLOOD oF NORMAL SWINE 
BY DIFFERENT INVESTIGATORS 


Hed rae Hemoglo- P 3 
eee | ee ce ER te audios 
per cmm. 4 
6.9 7,840 — a 5.28-7.9 «| Bethe. 
7.9 19,000 88 —— Giltner. 
a — as 6K Gulliver. 
29,000 2 =, a 6.2 Giitig. 
3.28-9.6 19,900 83 1059 — | King and Wilson. 
5.4 == = Stéltzing. 
8.0 = —— ——— Storch. 
4.9} 11,518 = Storch. 
—- 1050 6 bw Sussdorf. 
8.6 —— = Wendelstadt und 
Bleibtreu. 
7.0 os 60 a <a - Wetzl. 


1 Pigs, 6-35 days old, ? pigs, 2-6 mo. old. 


50 NORMAL BLOOD IN DOMESTICATED ANIMALS 


TaBLeE XI.—NumBeErs or LEUCOCYTES AND PERCENTAGES OF THE SEVERAL 
VARIETIES IN THE BLoop or NORMAL SWINE 


Percentages of Varieties 


Leucocytes 


er cmm. : _| Large Author 
‘ Meytes [monoau-| rot, | Hosins | Cait 
33-77 18-66 1-12 | — Drake. 
56.4 38.46 5.13 “averages. 
19,000 30-79 .8/0.8-10/13-60 |1.2-11 |0.2-5.6) Giltner. 
Silt Zh} |] SY/ 5.2 1.3 “averages. 
29,000 ! 30-88 |1.5-2 |54-62.5]1.5-2.6] 3.1-5 | Giitig. 
34. WE CAsy |) Stsior? 2. 4. ‘* averages. 
20,6902 |29.3-65/1.2-5 | 32-65 |few-4.8|/few-5.3) Giitig. 
44.2 3. 51.7 2. 9 “averages. 
10,070-39,290) 28-78 |0-22.1| 16-72 |.1-12.4/0-2.5 | King and Wilson. 
19,980 54.2 4.1 35.8 4.5 ef ee ‘“* averages. 


1 Pigs, 2-6 mo. old, ? sucking pigs to 4 weeks old. 


RABBIT 


The red corpuscles vary from five to eight millions with an 
average of six millions. The average hemoglobin value is 96. 
The number of leucocytes ranges from 8,000 to 13,000 with an 
average of 11,000. 

The normal percentages of the varieties of leucocytes are: 
lymphocytes, 45-55; large mononuclears, 2-8; polymorphonu- 
clears, 40-50; eosinophiles, 0.5—-1 and mast cells, 4-8. 


RABBIT 51 


TaBLE XII.—SuMMARY OF EXAMINATIONS OF THE BLOOD oF NORMAL RABBITS 
BY DIFFERENT INVESTIGATORS 


Cees Leucocytes |Hemoglobin Specific Size of Red Author 

Millions per cmm. per cent. Gravity Corpuscles 

per cmm. 

5.16 7,800 -- —_—— 5.3-7.9| Bethe. 

4.8 a —— ——— Cohnstein und 

Zuntz. 

—- 9,000 ——. —— ——— | Courmont et 
Lesieur. 

—— 9,414 a —— —— | Ewing. 

4.5-5.7 | 7-16,000 74 sa Goodall. 

—— a -_— 7.04 Gulliver. 

6.4 6,200 — ———. 7.16 Hayem. 

5.9 11,800 == ——— Hiinerfauth. 
—— _| 75-8,500 | _——— —— ——— | Kinghorn. 

“ol 10,720 —— ed Lowit. 

—- ——- —. — 6.3 Manassein. 

— (000 —. Muir. 

— oe 1046.2 — Miintz. 

——-. G213 ae —_— we Nicholas, Fro- 
ment et Du- 
moulin. 

4.15 —— 9.41 a a Otto. 

5-8 10-14,000 —- —_ — + Prus. 

5.6 8,752 96.5 1059 a Rieder. 

4.8 —- a a Stoltzing. 
—- se a 1049 — Sussdorf. 
——- | 8-13,000 | —— —_—. ——— | Tallqvist und v. 

Willebrand. 

6.0 ~-—- a a 6.9 Vierordt. 


Prus gives the number of blood plates as 400,000 per cmm. 


52 NORMAL BLOOD IN DOMESTICATED ANIMALS 


Taste XIIIl.—NumBers or LeEucocyTES AND PERCENTAGES OF THE 
VARIETIES IN THE BLoop or NorMAL RABBITS 


Percentage of Varieties 
Leucocytes 


per cmm. I. Il. III. IV. v. Batist 
Lympho |Large M | Polymor.| Eosins Mast 
a 45-55 2-8 40-50 | 0.5-1 4-8 | Brinckerhoff and 
Tyzzer. 
9,000 -—- a 45 —- — | Courmont et Lesieur. 
10,500 52 43 225 2.5 | Goodall. 
10,720 47.7 52 — | Lowit. 
oon 40.2 12 47.7 — — | Muir. 
7,213 | 26 2022) | 46rd 1.4 — | Nicholas, Froment et 
Dumoulin. 
11,000 | 20-25 | 20-25 | 45-55 | 0.5-3 | 2-5 | Tallqvist und v. Wille- 
‘ brand. ; 
GUINEA PIG 


The red corpuscles vary from 4.25 to 6 millions with an aver- 
age of 5.25 millions. The hemoglobin varies from 85 to 100 with 
an average of 94. The leucocytes have been found to vary widely 
in apparently normal animals. They vary from 5,000 to 22,000 
with an average of 11,000 to 12,000. Considerable variation in 
the numbers and percentages of the several varieties has been 
obtained by different investigators. A difference in the age of 
the animals examined may explain the variation. My animals 
were six months to a year old. Perhaps those of the investigators 
who found higher numbers of polymorphs and less lymphocytes 
were older animals. 

Webb, Gilbert and Havens found the blood plates in guinea 
pigs to have an average of 350,000 per emm. at sea level and an 
average of 434,000 (364,000-528,000) at Colorado Springs, Colo. 
(an altitude of 6,000 ft.). 


DOMESTIC FOWL 53 


TasLe XIV.—Summary oF EXAMINATIONS OF THE BLOop oF NorRMAL 
Guinea Pics By DIFFERENT INVESTIGATORS 


Red Corpuscles C : ; 
Bailie (ease premiere eee | aie oe 1 8 at 

5.14 7,240 a a 6.69-9.2 «| Bethe. 

5.27 10,897 94.5 1053 T.52 Burnett. 

4.24 a 8.91 aa ~ Cohnstein und 

Zuntz. 
ee a — Calg 2 Gulliver. 

5.85 5,600 —— — 7.48 wu Hayem. 
4.8-6.88 9,170 100 — —_— Goodall. 
——— 12,000 ee —— ——_——- Howard. 

5.78 12,600 —— —— Kurloff. | 

SG —— —- Malassez. 

9,400 — eS Rieder. 


TaBLE XV.—NvuMBERS OF LEUCOCYTES AND PERCENTAGES OF THE 
VARIETIES IN THE BLoop or NorMAL GUINEA PIGs 


Percentage of Varieties 
Leucocytes are 
per cmm. 1G | Te III. : Vi 
Lympho.| Large M. | Polymor.| Eosins Mast 
10,897 47.3 | 10 Slee 10.7 0.37 | Burnett. 
9,170 60 37 3 — Goodall. 
12,000 16-36 | 0.8-6.6 | 43-79 |0.2-33.6) 0-1.2 | Howard. 
- 24 ua 62 2-3 0.7 Kanthack and 
Hardy. 
12,600 | 30-35 | 1ogrs|40-50¢) 10 le | \ieurlofe. 


TaBLE XVI.—NUMBERS OF THE VARIETIES OF LEUCOCYTES PER CMM. IN THE 
Bioop or Norma Guinea Pias 


Mast 


Large Polymorphs Eosins Cells Author 


Lymphocytes Aono 


2,797-10,925 | 473-2,496 | 1,138-6,459 3-2,511 |} 0-108 | Burnett. 


5,080 1,090 3,250 1,175 43 ‘* averages. 
1,600-6,000 | 175-900 /4,800-13,900 | 25-5,846 | 0-124 | Howard. 
3,650 425 8,000 1,390 43 «averages. 


THE DOMESTIC FOWL 


The normal number of red cells has been reported by different 
investigators from 2 to over 4 millions per cmm. The average 
seems to be about three millions. The average hemoglobin value 


54 NORMAL BLOOD IN DOMESTICATED ANIMALS 


is from 75 to 85. The thrombocytes are given by Albertoni and 
Mazzoni as averaging 45,500 and by Mack as 55,200. The leu- 
cocytes apparently have a wide normal variation. Averages are 
reported from 18,000 to 36,000. Warthin found the normal range 
to be from 12,000 to 29,000. Taylor gives it as 17,000 to 30,000. 
Care must be taken in securing blood for examination from any 
bird. The drop used must not be exposed to the air longer than 
necessary as the thrombocytes undergo change quickly. De- 
generated thrombocytes resemble degenerated leucocytes. Films 
for histological examination must be made quickly and in a dry 
place. It is very difficult to make films in a damp place that may 
be used because of the liability of the thrombocytes to change. 


TaBLe XVII.—SumMary OF EXAMINATIONS OF THE BLoop oF NoRMAL 
Domestic Fow.ts BY DIFFERENT INVESTIGATORS 


Red Cor- Throm- |Hemoglo- ; 
‘iit | ere [poten | Chat] Gartute Author 
2.46 32,300 | 45,566 | — —————_ | Albertoni und 
Mazzoni. 
33. 30,000 | —— | 50-65 | ————— | Ellermann und 
Bang. 
ue 19,000 | —— oe ————_ | Goodall. 
- ——- — 12.08x7.32 | Gulliver. 
2.4 26,300 | —— — | 11.5 x7.18#| Hayem. 
4.2 24,000 | —— — —_——— | Hedfeld. 
2.18-3.16 | 20-35,000 | ——— — ——— | Launoy et Levy- 
Bruhl. 
3.0 33,(¢0 | 55,272 | 87.3 PSmlexS ae Mack.! 
Sina! — — 13.5 x6.5 # | Malassez. 
— — — 12.96x7.33 # | Manassein. 
13 .09x7.15 # 
3.6 20,081 —-— — —_—_—_——_ Moore. 
3-4 20-80,000 | ——— | 60-70 ———— | Schmeisser. 
3.8 —— — ————_ | Stoltzing. 
23,675 | —— — ———— | Taylor. 
3.28 36,185 —— — ————— Ward. 
2-3 12-29,000 | ——— —- ———- _| Warthin. 
— -— se — 12.1 x7.2 » | Welcker. 
ore 17,921 | —— — 76 ——_—_——_—— Personal obser- 
vation. 


! This study of Mack’s was made in the laboratory of Comparative Pathol- 


REFERENCES 55 


TasBLeE XVIII.—NuvumBErRS oF LEUCOCYTES AND PERCENTAGES OF VARIETIES 
IN THE BLoop oF NorMAL FowLs 


7 Percentages of Varieties 
ep na Fé Il. IIT. LN / V. ee 
Lympho | Large M. | Polymorphs} LEosins Mast 
30,000 40 23 37 — |Ellermann 
und Bang.? 
19,000 56 37 6 1 Goodall. 
24,000 42 12 30 12 3 Hedfeld. 
33,777 54.9 6.2 Sod PAC 3.3 Mack. 
20-80,000 42.3 19.4 29.6 4.3 PAF: Schmeisser. 
17-30,000 42-60 6-14 25-41 1.9-6.8 | 2.6-4.1 /Taylor. 
23,675 51 9 33 3.6 3 “* averages. 
12-29,000 35.5 14.5 21.5 10 2 Warthin.? 
17,921 58 ios 28.8 eites 4.3 Personal ob- 
servation. 


ogy and Bacteriology of the New York State Veterinary College, Ithaca, 
N. Y., and is as yet unpublished. I wish to express my hearty thanks to 
Dr. Mack for his kindness in permitting me to use this data. 

RT. 

2 Ellermann and Bang report 2.2% of the leucocytes as unclassified. 

3 Warthin found 16.5% of degenerated cells in normal fowls. 


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56 NORMAL BLOOD IN DOMESTICATED ANIMALS 


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oll ee — 


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38. KANTHACK AND Harpy. The morphology and distribution of the 
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45. Lowir, M. Studien zur Physiologie und Pathologie des Blutes und 
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58 NORMAL BLOOD IN DOMESTICATED ANIMALS 


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CHAPTER IV 


VARIATIONS IN THE NUMBER OF RED CORPUSCLES 
AND THE AMOUNT OF HEMOGLOBIN DUE TO GEN- 
ERAL PHYSIOLOGICAL AND PATHOLOGICAL CON- 
DITIONS 


Blood obtained from different parts of the vascular system 
differs but slightly in richness of corpuscles. The capillaries con- 
tain ordinarily a slightly higher number than the veins or arteries 
which under normal conditions have practically the same number. 
Where it is practicable it is better to use capillary blood for ob- 
taining the number of corpuscles. When it is not practicable to 
obtain capillary blood, blood from the smaller veins or arteries 
should be used in preference to that from the larger blood vessels. 

Under certain physiological or pathological conditions local 
or general changes may be present in the blood. The total quan- 
tity of blood varies under different conditions. It is generally ac- 
cepted that it may be increased by proper hygienic conditions and 
is decreased in unhygienic and certain pathological conditions. 
Unfortunately the method of measuring the quantity of the blood 
(Haldane’s method) is too complicated for ordinary clinical use. 
We are forced to rely mainly on the findings of an examination of 
a very small quantity of blood. It must be kept in mind that the 
findings of such an examination should not in all cases be inter- 
preted as though it showed the condition of the blood as a whole. 
Finding that the red corpuscles show an increased number per 
cubic millimeter does not necessarily imply that the total number 
of red corpuscles in the body are increased. For example, after 
the administration of a concentrated solution of saline purgative 
the blood may show a decided increase in the number of red cor- 
puscles per emm., yet there is no reason for thinking that there 
has been an increase in the total number of corpuscles. There 
has been instead a diminution of the fluid part of the blood, leav- 
ing the corpuscles in greater number per cmm. The distinction 
between plethora or increase in the quantity of blood and poly- 

60 


POLYCYTHEMIA 61 


cythemia or increase in the number of red corpuscles per cmm., 
which is found by examining a small quantity of blood, should be 
kept in mind; also the distinction between oligemia or diminution 
in the total quantity of blood and oligocythemia or diminution in 
the number of red corpuscles per cmm. 

Polycythemia. An increased number of red corpuscles per 
cmm. does not, in many eases, indicate that there is an actual in- 
crease in the total number in the body; there are cases where a 
polycythemia is interpreted as indicating an increase in the total 
number. Any condition producing a concentration of the blood 
by withdrawing fluid from it (anhydremia) will produce a poly- 
cythemia. Such a change is produced by profuse sweating, by 
watery diarrhea from the administration of purgatives and in 
infectious diseases, by continued vomiting, by withholding water 
and by rapid exudation. Czerny found that cats kept 36 hours 
in a warm dry room without water lost weight and showed a 
marked increase in red corpuscles, in one case rising to 10,000,000 
peremm. Ina case of cirrhosis of the liver with ascites v. Limbeck 
found 3,280,000 red corpuscles before tapping and removing 18 
liters of fluid. On the following day the red corpuscles were 
5,160,000 per emm., rapid exudation having deprived the blood 
of a large amount of fluid. In conditions in which there is venous 
stasis with increased exudation of fluid from the blood vessels, a 
considerable polycythemia has been observed. Some of these 
conditions are cardiac insufficiency, pneumonia, emphysema and 
thrombosis of the lungs, asphyxia. Well marked examples are 
found in the final stage of pneumonia when the heart has become 
too weak to prevent the blood accumulating in the veins. Very 
high counts are often found in horses moribund or nearly so in 
cases of fibrinous pneumonia, when there is actually an anemia 
present. 

Moore, Haring and Cady found an increase in three horses of 
2,965,000, 3,084,000 and 2,803,000 red corpuscles after complete 
chloroform anesthesia of from one and one-half to two hours. In 
the first two cases operations with considerable hemorrhage were 
performed; in the last case the only operation was puncture of 
the guttural pouch, a trifling one, with no hemorrhage. A local 
polycythemia may be produced by ligating a part or by pressure 
of a tumor producing passive congestion. In cases of partial 


62 VARIATIONS IN NUMBER OF RED CORPUSCLES 


paralysis a higher count of red corpuscles has been obtained from 
the paralyzed part of the body. Cold baths, massage, muscular 
exercise and electricity produce a temporary polycythemia. 
Polyeythemia has been observed after the administration of 
various drugs, as pilocarpin, eserin, phosphorus, Glauber’s salt. 

Age. In general the young have more red corpuscles per emm. 
than older animals. Observations made by different investiga- 
tors are conflicting, in some cases even concerning the same species. 
The subject needs further study. It seems to be true that the 
number of red corpuscles is higher in the young of animals that 
are well developed at the time of birth, while in the young of those 
animals that at birth are undeveloped, as the dog, cat, sheep, 
goat and pig, the number is less than it is later. In the fetus the 
red corpuscles gradually increase till the time of birth. They 
seem to increase in the undeveloped young for a time after birth. 
In the aged the number of red corpuscles seems to be lower than 
in youth and middle age. 

Sussdorf states that the lamb has not less than 13-14 millions. 
The average for adult sheep is given from 8-12 millions. Storch 
found the average for adult sheep 10,472,000, while for lambs he 
found 11,032,000. The same investigator found 7,639,000 in 
adult horses and 9,340,000 in foals (one year); in adult cattle 
6,219,000 and 8,523,000 in calves; in rams 11,183,000, in wethers 
9,839,000, in ewes 9,039,600 and in lambs 1-14 days old 8,833,000, 
in lambs two months old 13,232,000; in adult goats, 14,569,000 
and in kids 10,150,000; in adult swine 8,045,000 and in pigs 
4,923,000. Gutig found an average of 5.2 millions in sucking pigs 
from 2 to 4 weeks old while there were 5.7 millions in pigs 2 to 
6 months old. Hayem gives the average for adult cats as 9,900,000 
per cmm., while for kittens four to eight days old as 5,357,000 per 
emm. Burnett and Traum found the average for dogs to be 
5,967,000 per emm. and 90% Hb, while puppies from less than a 
day to 20 days old had from 3,992,000 to 4,134,000 per emm. and 
Hb percentage varying from 73 to 89. Storch found 4,264,000 
red corpuscles in a cow about 15 years old, and 3,720,000 in a 
cow about 18 years old. 

Sex. The number of red corpuscles and the amount of hemo- 
globin seem to be higher in males than in females. Otto found an 
average of 6,123,700 red corpuscles and 14.08 grams of hemoglobin 


PREGNANCY AND PARTURITION 63 


in 12 male dogs and an average of 5,799,500 red corpuscles and 
13.72 gms. of Hb in 5 female dogs. In 10 male rabbits the same 
investigator found an average of 4,710,760 red corpuscles and 
10.05 gms. of Hb and in 10 female rabbits an average of 3,605,000 
red corpuscles and 8.77 gms. of Hb. Of seven normal horses 
Moore, Haring and Cady found an average of 8,595,000 red cor- 
puscles and 99.3% Hb in three males and 7,532,000 red corpuscles 
and 90% Hb in four females. Sussdorf gives the number of red 
corpuscles in the mare as 6,650,000 and in the gelding as 7,780,000. 
He also states that males are richer in hemoglobin than females 
and that castrated animals have the most hemoglobin. Storch 
found an average of 8,205,000 corpuscles in the stallion, 7,595,000 
in geldings and 7,119,000 in mares; 6,503,000 in bulls, 6,683,000 
in oxen and 5,473,000 in cows; 11,183,000 in rams, 9,839,000 in 
wethers and 10,396,000 in ewes. 

Wiendieck found that there were from 6.9 to 10.3 millions, 
average 8.1, in stallions; from 5.4 to 9.3, average 7.1, in geldings; 
and from 5.9 to 7.5, average 6.9, in mares. In guinea pigs the 
writer found an average of 5,866,000 corpuscles in 10 males and 
an average of 4,972,000 in four females. In man the average of 
red corpuscles is 5,000,000 while the average for woman is 4,500,000. 
The difference between the sexes appears at the time menstruation 
is established. é 

Pregnancy and parturition. The effect in the different species 
of animals has not as yet been determined in a sufficient number 
of cases to warrant making a definite statement for each. Normal 
pregnancy seems not to affect the number of red corpuscles as a 
rule, though Cohnstein found an average of 9,742,000 red cor- 
puscles and 7.8% hemoglobin in seven pregnant sheep and an 
average of 12,090,000 corpuscles and 5.5% Hb in five non-pregnant 
sheep. Thompson gives the following conclusions as the result 
of examinations of 12 pregnant women at different stages of 
gestation. There is a moderate increase in the red corpuscles 
rather early in pregnancy, remaining subnormal throughout the 
middle months and rising again to normal at the termination of 
pregnancy—not, however, in all cases. He found a low percent- 
age of hemoglobin constant throughout the first months, rapidly 
approaching normal as pregnancy draws to a close. 

Parturition seems to lower the count for a short time. Burnett 


64 VARIATIONS IN NUMBER OF RED CORPUSCLES 


and Traum found that the count remained low in a bitch for two 
or more weeks after parturition. In man it has been found that 
the count is lowered at parturition but should return to the normal 
in from 10 to 14 days. 

High altitudes. Though the results obtained by different 
investigators are conflicting, the majority have found that there 
is a considerable increase in the number of red corpuscles and in 
the specific gravity in animals and men living at high altitudes. 
The hemoglobin does not seem to be increased to any extent. 
Mintz found the specific gravity of sheep on the plains was 1038 
while on a mountain it was 1053.2; rabbits on the plains had a 
specific gravity of 1046.2 while on a mountain it was 1066.1. 
Viault found a polycythemia in animals on the Cordilleras. Foa 
reports that animals taken to a height of 4,560 meters show a 
polycythemia within eight hours after their arrival; the number 
decreases to normal within 36 hours after removal to normal 
level. Armand-Delille and Mayer on the contrary obtained con- 
flicting results with guinea pigs and rabbits which they carried 
upon the Alps. Guillemard and Moog found an increase in red 
corpuscles in both peripheral and central blood in rabbits and 
guinea pigs taken from Paris to the summit of Mt. Blanc, but a 
decrease in hemoglobin value. 

Webb, Gilbert and Havens found an increase in the blood plates 
in five guinea pigs taken from sea level to Colorado Springs (6,000 
ft.) from 350,000 per emm. to something less than 450,000. The 
average in twenty-six guinea pigs at Colorado Springs they found 
to be 434,000 per emm. 

Anemia. Anemia from the derivation of the word means 
lack of blood, the sense in which the term is often used by practi- 
tioners. In this sense it may mean a diminution in the volume of 
blood, oligemia, or in the amount of hemoglobin, oligochromemia, 
or a lessened number of corpuscles, oligocythemia. As clinically 
used anemia generally means an oligochromemia, an oligocythemia 
or both. This is the meaning we shall use for anemia. 

Anemia occurs in a variety of conditions, the more important 
of which are—after hemorrhage, after marked exudation, in dimin- 
ished nutrition, in diminished activity of the blood forming organs 
and in increased destruction of red corpuscles. 

After hemorrhage with much loss of blood it takes a con- 


ANEMIA 65 


siderable time for the blood forming organs to make good the sub- 
stance lost. First, there is a lowering of blood pressure followed 
by a transfusion of fluids through the capillary walls, partially 
restoring the volume of fluid in the blood vessels. The composi- 
tion of the blood is changed. There is a diminished amount of 
albumins, a diminished number of red corpuscles and an increased 
amount of salts. Besides the diminution in the number of red 
corpuscles, morphological changes are found after severe or re- 
peated hemorrhages. Nucleated red cells may appear within a 
few hours after rapid hemorrhage. Changes in shape, size and 
staining are generally seen in from two to four days or more, at 
the time of greatest reduction in the number of corpuscles. Punc- 
tate basophilia and polychromasia are observed with marked 
oligocythemia. After repeated bleedings in a cow, Smith found 
20% of the red corpuscles enlarged and 15% showed polychromasia 
and punctate basophilia. 


TasBLe XIX.—TuHE FoLtLtowina SUMMARY SHOWS THE EFFECT OF REPEATED 
BLEEDINGS ON THE RED CorPUSCLES IN A Cow (AFTER SMITH) 


Nou ofied Quantity of 


v8 Corpuscles Withdoown 

Aug. 3 | 6,750,000 | 2.268 kgr. | Blood elements not visibly changed. 

Aug. 4 | 5,000,000 | 2.325 kgr. | Blood elements not visibly changed. 

Aug. 5 | 4,650,000 Blood elements not visibly changed. 

Aug. 6 | 5,220,000 | 3.828 kgr. | Blood elements not visibly changed. 

Aug. 7 | 3,820,000 | 4.251 kgr. | Blood elements not visibly changed. 

Aug. 8 | 3,090,000 | 4.989 kgr. | 2-3% show stained granules, about 10% 
appear enlarged. 

Aug. 10 | 2,250,000 ———— 20% macrocytes, 15% contain stainable 
material chiefly as granules. 

Aug. 11 | 2,140,000. —_—— Same as yesterday. 

Aug. 12 | 2,110,000 ——— Same as yesterday, one erythroblast. 

Aug. 14 | 2,530,000 Numerous macrocytes, about 5% con- 
tain stained particles. 

Aug. 17 | 3,200,000 —_— Macrocytes as before, cells with gran- 
ules rare. 

Aug. 22 | 3,200,000 —_—— Macrocytes as before, no stained gran- 

; ules detected. 
Aug. 29 | 4,300,000 = Only a few macrocytes. 


In small animals the restoration of the volume of blood is rapid 
while in the larger animals it may be 35-40 minutes (v. Limbeck) 


66 VARIATIONS IN NUMBER OF RED CORPUSCLES 


before the increased volume is noticeable. With small animals 
the restoration of the red corpuscles is more rapid, three to four 
weeks, while in the larger animals a longer time is required, 19-34 
days (Lyon). The rapidity of the loss of blood has a marked effect 
on the rate of restoration to the normal, recovery being slower 
after rapid than after slow bleeding. Several hemorrhages though 
smaller in amount than from a single one greatly delay restoration 
and produce a more severe form of anemia. The rapidity of resto- 
ration depends on the state of nutrition of the animal. It has been 
found that recovery is hastened by a full diet, an abundant supply 
of water and is more rapid with transfusion of salt solution. The 
following table taken from Ewing shows that the amount of blood 
that may be lost without a fatal result varies greatly in different 
individuals and species. 


TasBLe XX.—Liuits oF HEMORRHAGE FROM WHICH REcOvERY Has BEEN 
OBSERVED (EWING) 


Percentage} Number of 
: Percentage of Body of Red Red Cor- 

Author Animal, ; Weight Lost Corpuscles puscles 
Remaining} Remaining 


Vierordt dog ————— 50 


Hayem dog 4.33-5.55 
Kireeff dog 4.3 -7.3 
Maydel dog 5.48-6 .57 
average 5.12 
Scram dog 4.58 5.4 5.44 


not even always 
fatal chance fatal 


Landerer dog 4.5 

Feis rabbit 3.0 

Andral, Behier man ——_—_—_— 50 

Laache woman ———_— 32 1,598,000 
1,415,000 

Hayem woman —_—_—— 11 

hemorrhages 
in 6 days 


An anemia sometimes of extreme grade is produced by parasites, 
especially those that live on blood. Strongylus in the respiratory 
and digestive tracts, Uncinaria, Trichocephalus and related round 
worms, trematodes in the liver and Cytodites in fowls are ex- 
amples. In cases of anemia from parasites it may well be that be- 


i 
a 
* 


4 v sols J 


eee 


q 


ANEMIA 67 


sides the loss of blood there is also a toxic effect either from the 
parasites themselves or from substances produced in the digestive 
tract. An anemia may occur in cases of disease complicated by 
single or several hemorrhages, as in malignant tumors and bleed- 
ing ulcers. 

After exudation. The loss of blood from hemorrhagic exu- 
dates may be considerable. With fibrinous and with hemorrhagic 
exudation the loss of blood or albumins may determine a severe 
anemia, as for example in chronic suppuration, exudative nephritis, 
purpura hemorrhagica and malignant endocarditis. 

In diminished nutrition. Again anemia may be due to dimin- 
ished nutrition and defective hygiene, as with improper food, 
diseases of the masticatory apparatus, broken jaw, diseased teeth, 
pharyngeal troubles interfering with swallowing, in severe febrile 
conditions, and in unsanitary surroundings, as dark, damp, poorly 
ventilated stables. Irregularity of feeding and irregular work 
have been thought to be partially responsible for anemia. 

In diminished activity of the blood forming organs. Dimin- 
ished activity of the blood forming organs occurs in many of the 
infectious diseases by the action of toxic substances upon the blood 
forming tissues and by a changed structural condition in them. 
For example, in the leucocytosis of pneumonia (Ewing) there is a 
proliferation in the bone marrow of myelocytes at the expense of 
normoblasts. Intoxication by lead, mercury or arsenic produces 
a lessened activity of the blood forming organs. 

In increased destruction of red corpuscles. An increased 
destruction of erythrocytes occurs in septic processes, septicemia, 
pneumonia, malignant endocarditis, tuberculosis, malignant 
tumors (cancer), anthrax in the cow, azoturia in the horse, Texas 
fever in cattle. The increased katabolism of albumins in febrile 
conditions and also in afebrile cachexias may be a factor in pro- 
ducing anemia. 

The changes in the blood in anemia vary a great deal. In many 
cases there is simply a lessened amount of hemoglobin and a low- 
ered specific gravity, the number of corpuscles remaining prac- 
tically normal. Changes in the size, shape and staining reaction 
of the corpuscles may be seen in less mild cases. Many of the 
corpuscles may show lack of hemoglobin, indicated by the increased 
size of the central clear area. A greater than normal variation in 


68 VARIATIONS IN NUMBER OF RED CORPUSCLES 


size may be observed. There may be several very small corpuscles 
(microcytes) and corpuscles larger than normal (megalocytes). 
In very young animals a much greater variation in size than occurs 
in adults is normal. Some of the corpuscles may show irregularity 
in staining, showing either as a diffuse basophile staining (poly- 
chromasia) or as separate bluish points within the corpuscles 
(punctate basophilia). Corpuscles with deformed shapes may be 
found (poikilocytosis), a commonly occurring form being pear- 
shaped with a pointed projection at one end. These several 
changes may be present in slight or in marked degree. Besides 
the changes mentioned nucleated red cells may be found in the 
circulating blood. Normoblasts with a compact deeply stained 
nucleus situated usually in one side of the cell are the forms or- 
dinarily observed. Megaloblasts usually with large, rather pale 
nucleus sometimes showing irregular karyokinetic figures are 
sometimes observed. Microblasts may occur, but are rare. 


Taste XXI.—TueE Foutowine Cases ILLUSTRATE DIFFERENT GRADES OF 


ANEMIA 

Animal eo Cate ee Hb Leucocytes Disease 
Horse 5 7,200,000 80 6,560 | pleuro-pneumonia. 
Horse 13 7,060,000 61 9,958 | quittor. 
Horse 8 6,100,000 70 29,400 | strangles. 
Horse 6,148,000 69 14,180 | chronic suppuration. 
Horse 8 5,575,000 58 6,650 | asthma. 
Horse 11 4,000,000 62 8,000 | “‘pernicious anemia.” 
Horse 15 3,713,000 38 4,929 | chronic suppuration. 
Horse 9 3,400,000 45 4,200 | “pernicious anemia.” 
Horse 17 2,634,000 40 15,232 | chronic suppuration. 
Horse 13 1,452,000 25 5,000 | “pernicious anemia.” 
Horse 6 1,000,000 25 10,800 | ‘‘pernicious anemia.” 
Sheep 5 mo. 5,600,000. — —— | repeated hemorrhages. 
Cow 3% 3,916,000 = —— _| Texas fever. 
Cow 3 1,285,000 — —— | Texas fever. 
Dog 3,050,000 — 4,133 | tuberculosis. 

REFERENCES 


1. ARMAND-DELILLE ET Mayer. Expériences sur l’hyperglobulie des 
altitudes. Journ. d. Physiol. et Path. gen., vi, 1904, p. 466. 

2. Burnett, 8. H. A study of the blood of normal guinea pigs. Journ. of 
Med. Research, xi, 1904, p. 587. 


REFERENCES 69 


3. BURNETT AND TrAuM. The clinical examination of the blood of the 
dog. Proceed. Am. Vet. Med. Assn., xlii, 1905, p. 349. 

4. CoHNsSTEIN, J. Blutveriinderung wihrend der Schwangerschaft. Arch. 
f. gesamm. Physiol., xxxiv, 1884, S. 233. 

5. Czerny, A. Versuch iiber Bluteindickung und ihre Folge. Arch. f. 
exper. Path. u. Pharm., xxxiv, 1895, 8S. 268. 

6. Douatas, C. G. A method for the determination of the volume of blood 
in animals. Journ. of Physiol., xxxii, 1906, p. 493. 

7. Foa, C. Les changements du sang sur la haute montagne. Arch. Ital. 
d. Biol., xli, 1904, p. 93, also p. 101. 

8. GuUILLEMARD ET Mooa. Observations faites au Mont Blane sur les 
variations du sang aux hautes altitudes. Journ. d. Physiol. et Path. gen., xix, 
1907, p. 17. 

9. Gitic, K. Ein Beitrag zur Morphologie des Schweineblutes. Arch. f. 
Mikr. Anat., lxx, 1907, 629. 

10. HALDANE AND SmitH. The mass and oxygen capacity of the blood in 
man. Journ. of Physiol., xxv, 1900, p. 331. 

11. Lyon, J. F. Blutkérperzihlungen bei traumatischer Animie. Arch. f. 
path. Anat. wu. Physiol., xxxiv, 1881, 8. 207. 

12. Moorr, HariInG AND Capy. The clinical examination of the blood of 
the horse and its value to the veterinarian. Proceed. Am. Vet. Med. Assn., 
1904, p. 284. 

13. Muntz, A. De l’enrichissement du sang en hémoglobine, suivant les 
conditions d’existence. Compt. rend. Acad. d. Sciences, Paris, exii, 1891, p. 289. 

14. Orro, J. G. Untersuchungen iiber die Blutkérperchenzahl und den 
Hamoglobingehalt des Blutes. Arch. f. gesamm. Physiol., xxxvi, 1885, S. 12, 
36, 57. 

15. Smita, THEOBALD. On changes in the red blood corpuscles in the per- 
nicious anemia of Texas cattle fever. Trans. Assn. Am. Physicians, vi, 1891, 
p. 263. 

16. Strorcn, A. Untersuchungen iiber den Blutkérperchengehalt des 
Blutes der landwirtschaften Haussiugetiere. Inaug. Diss. Bern, 1901. 

17. Sussporr, M. Blut und Blutbewegung. Ellenberger’s Handb. d. vergl. 
Physiol. d. Haussdéugethiere, Bd. II, Th. I, 8. 163. 

18. THompson, W. L. The blood in pregnancy. Bull. Johns Hopk. Hosp., 
xv, 1904, p. 205. 

19. Viautt, F. Sur l’augmentation considérable du nombre des globules 
rouges dans le sang chez les habitants des hauts plateaux de l’Amérique du 
Sud. Compt. rend. Acad. d. Sciences, exi, 1890, p. 917. 

20. Wess, GILBERT AND Havens. Blood platelets and tuberculosis. 
Trans. Natl. Assn. for Study and Prevent. of Tuberc., 10, 1914, 180. 

21. Wrenpreck, K. Untersuchungen iiber das Verhalten der Blutkérper- 
chen bei gesunden und mit croupéser Pneumonie behafteten Pferden. Arch. 
f. wissen. u. prakt. Tierheilk., xxxii, 1906, 113. 


CHAPTER V 


INFLUENCES AFFECTING THE LEUCOCYTES 


LEUCOCYTOSIS 


An increase in the number of leucocytes in the circulating blood 
is known as leucocytosis or hyperleucocytosis. A diminution in 
the number is called leucopenia or hypoleucocytosis. If the in- 
crease involves mainly the polymorphonuclears it is called a 
polynuclear leucocytosis, polynucleosis, or leucocytosis in a restricted 
sense. When the lymphocytes only are concerned it is known as 
lymphocytosis; when the large mononuclears as mononucleosis; 
when the eosinophiles as eosinophilia; when the mast cells as 
basophilia. When more than one variety is increased, it is called 
a mixed leucocytosis. 

Leucocytosis occurs sometimes under physiological gonditions 
and sometimes is due to pathological processes. The more im- 
portant varieties are: 


PHYSIOLOGICAL LEUCOCYTOSES 


Leucocytosis of digestion. 

Leucocytosis of pregnancy and parturition. 

Leucocytosis of the new born. 

Leucocytosis of violent exercise, cold baths and massage. 


PATHOLOGICAL LEUCOCYTOSES 


Inflammatory. 
Post hemorrhagic. 
Ante-mortem. 


Digestion.—The investigations of Pohl, Rieder and Goodall, 
Gulland and Paton on dogs and of Brinckerhoff and Tyzzer on 
rabbits have shown that there is a diminution in the number of 

70 


DIGESTION aE 


leucocytes after a fast of 12 hours or longer and that there is an 
increase after a fasting dog or rabbit is fed. The increase begins 
an hour or more after feeding, usually reaches a maximum in 
about three or four hours and then declines. The kind of food 
seems to exert a considerable influence, a proteid (meat) diet show- 
ing the greatest effect and a carbohydrate or fat diet little or no 
effect. Digestion leucocytosis seems to be absent in herbiverous 
animals, due probably to digestion being slower and going on 
constantly. Food seems to be present in the digestive tract of 
the horse and cow from the time of one feeding to the next one. 
Wiendieck states that horses have a weak digestion leucocytosis 
with an increase of the polymorphs. Goodall, Gulland and Paton 
examined one adult and five young dogs before and after feeding. 
They found an increase in the number of leucocytes, reaching a 
maximum about four hours after feeding. The increase was due 
to a lymphocytosis which they found constantly present and a 
polynuclear leucocytosis present in a majority of cases but variable 
in degree. There was sometimes a preliminary fall in the leuco- 
eyte count. Brinckerhoff and Tyzzer found that in rabbits a fast 
of 12 hours or longer caused a decrease in the leucocytes averag- 
ing approximately one-third the initial count. Feeding fasting 
rabbits caused an increase two to six hours after the beginning 
of feeding. In pregnant rabbits, those affected with “snuffles”’ 
and certain other infectious diseases there was no decrease on 
fasting. Under ordinary conditions, that is when food is not with- 
held for twelve or more hours, a digestion leucocytosis is not to 
be expected in the rabbit. 

The importance of digestion leucocytosis consists in recognizing 
the possibility of a considerable increase in the leucocytes in the 
animals in which digestion leucocytosis occurs, dog and cat, and 
either taking the blood from these animals before feeding or if 
after a meal making allowance for the changes in the blood caused 
by feeding after being without food for 12 hours or more. 

In carcinoma of the stomach in man digestion leucocytosis is 
reported to be absent in about 90% of the cases. In cases of 
benign stenosis of the stomach, ulceration, chronic gastric catarrh 
and carcinomata of other viscera, well marked digestion leuco- 
cytosis seems to be the rule. 

Pregnancy and parturition. During the latter part of the 


72 INFLUENCES AFFECTING THE LEUCOCYTES 


period of pregnancy in woman there is usually a moderate increase 
in the number of leucocytes. It is most marked in primipare; in 
multipare it occurs in about 50% of the cases. It is a mixed leu- 
cocytosis, the percentages remaining unchanged except that the 
eosins may not be increased. At the beginning of labor the count 
is often 16-18,000. After parturition the leucocytes gradually 
decrease, reaching normal usually in four to fourteen days, unless 
there are complications, as lacerations, ete. 

In the domesticated animals the number of observations are 
not sufficient to warrant drawing definite conclusions. Burnett 
and Traum found a leucocytosis in a bitch, reaching 23,000 at 
the time of parturition, then dropping to normal in less than three 
weeks. The following are their counts: Oct. 29, 17,800 leucocytes; 
Nov. 10, 23,600; Nov. 17, 23,300; Nov. 26, 19,100 (gave birth to 
nine pups the night before); Dec. 17, 12,400. Storch found no 
increase in leucocytes in pregnant cows or goats, and only a slight 
increase in a small percentage of the pregnant sheep examined. 
Brinckerhoff and Tyzzer found that leucocytosis of digestion was 
not present in pregnant rabbits. 

New born. In general it may be said that the number of 
leucocytes is high in the young with a high percentage of lympho- 
cytes. In man the leucocytes are high until about the fifth year 
when they reach normal numbers. Rieder obtained the following 
counts: at birth, 14,200-27,400; 24th day, 8,700—-12,400; after 
Ath day, 12,400-14,800. Gundobin gives the following: fetus last 
day 8,053; at birth 19,500; 24 hours 23,000; 48 hours 17,500. 
Hayem gives the average for 48 hours as 18,000; the 3d-4th day 
7,000; after the 5th day 9-11,000. The results of counts in ani- 
mals are not uniform for the different species. Storch obtained 
an average of 14,034 leucocytes in colts one year old. In cattle 
Storch found the following: in a calf three hours old (had not 
suckled) 21,488 leucocytes; in two calves two days old an average 
of 16,600; four days, 15,754; seven days, 14,813; ten days, 12,856; 
fifteen days, 12,042. In lambs, 30 hours to 14 days old, he found 
the leucocyte count within normal limits. Kids, 5-11 days old 
and pigs 6-28 days old showed no increase above the normal for 
adult goats and swine. Burnett and Traum found the leucocytes 
in pups from a few hours to 20 days old to fall within the normal 
limits for adults. In cats Hayem found the leucocytes in the new 


INFLAMMATORY LEUCOCYTOSIS 73 


born to be 8,000 per cmm., while the average for adults he gives 
as 7,200. Other investigators give the normal for cats as about 
13,000. 

Violent exercise, cold baths and massage. A considerable 
increase in the number of leucocytes has been found after severe 
muscular exertion. Larrabee examined the blood of four con- 
testants in a twenty-five mile running race before and immediately 
after the finish of the race. He found a leucocytosis of 14,400 to 
22,200, the increase being mainly in the polymorphs (83.8-90.3%). 
The eosins were absent in three cases and much reduced in the 
fourth. A small number of myelocytes and cells intermediate 
between myelocytes and polymorphs were found in three cases. 
Similar results have been obtained by other investigators. The 
character of the leucocytosis is similar to that found in the in- 
flammatory type. 

Winternitz found that after short cold baths there was an in- 
crease in the red corpuscles (maximum of 56 persons 1,860,000 
per cmm.), hemoglobin (maximum 14%) and leucocytes (maxi- 
mum, three times the normal). The maximum is not always 
reached at once, often it is reached after an hour. By two hours 
a decrease was generally found, though sometimes an increase 
was observed. In twenty typhoid patients Thayer found an aver- 
age increase of leucocytes from 7,724 before to 13,170 after short 
cold baths. The increase affected all the varieties. Rovighi found 
that the number of leucocytes is increased in an arm given a short 
cold bath or a prolonged hot one, while a prolonged cold or a short 
hot one decreases the leucocytes in the immersed arm. Becker 
reports that the increase in leucocytes after short cold baths is 
found in capillary blood, but is not seen in venous blood, where 
the number of leucocytes is normal. 

Mitchell observed that the leucocytes, red corpuscles and hemo- 
globin were increased after an hour’s general massage. The leuco- 
cytosis found as a result of thermic influences or massage is gener- 
ally thought to be due to changes in the blood pressure and to 
vasomotor influences producing a change in the size of the per- 
ipheral vessels. 

Inflammatory leucocytosis.— Inflammatory leucocytosis is so 
called from there being present an increase in the number of leuco- 
cytes in many of the acute infectious diseases. It is characterized 


74 INFLUENCES AFFECTING THE LEUCOCYTES 


by a high percentage of polymorphonuclears and a lessened per- 
centage of the other varieties. In cases where exudation is present 
it is pronounced though the increase of leucocytes is not a meas- 
ure of the amount of exudation. It does not run parallel with the 
fever, as there may be a marked leucocytosis with little rise of 
temperature and on the other hand there may be a high fever 
without leucocytosis. It measures more the relation of the severity 
of the infection to the resisting power of the individual. Cabot 
has expressed this well in the following schema: 

(1) Infection mild, resistance good, small leucocytosis, 

(2) Infection less mild, resistance less good, moderate leuco- 
cytosis, 

(3) Infection severe, resistance good, very marked leucocytosis, 

(4) Infection severe, resistance poor, no leucocytosis. 

It is observed in individuals in naturally acquired infection; 
but the course is best seen in experimental cases. In an animal 
inoculated with pyogenic organisms, first, there is a decrease in 
the number of leucocytes, this diminution affecting mainly the 
polymorphonuclears though the large mononuclears are also af- 
fected (Ewing). Usually after one-half hour to two hours, the 
leucocytes increase, the increase being principally in the poly- 
morphonuclears which may attain 85-95°9%; the eosinophiles are 
diminished or may disappear entirely from the peripheral circula- 
tion. After reaching a maximum the leucocytes gradually decrease 
to the normal number and normal proportions of the several varie- 
ties are reached. The eosins reappear at the time of the crisis of the 
disease and may reach higher than the normal percentage during 
convalescence and recovery. 

In cases of severe infection with poor resistance of the animal 
the initial leucopenia may persist. This is often seen in cases of 
septicemia naturally acquired. Inoculating rabbits with virulent 
cultures of Pneumococcus lanceolatus produces a septicemia with 
a progressive decrease of leucocytes in the blood. Inoculating 
attenuated cultures of the same organism produces a leucocytosis 
and the animal recovers (Tchistovitch). The initial decrease is 
observed sometimes in cases of naturally acquired infection; but 
this stage is generally not observed by the practitioner, the case 
having passed beyond this stage of the disease before the patient 
comes under the practitioner’s care. Absence of leucocytosis is 


EXPERIMENTAL LEUCOCYTOSIS 75 


a bad sign as showing lack of resistance on the part of the patient. 
The increase of leucocytes occurs more rapidly in cases where the 
course of the disease is more favorable. Ordinarily leucocytosis 
is established within one-half to two hours after the initial decrease. 

Inflammatory leucocytosis has been observed in strangles, in- 
fection with pyogenic organisms, fistulous withers, wound infec- 
tions, abscesses, quittor, suppurations, pneumonia (croupous, 
pleuro, gangrenous and broncho), pleuritis, muscular rheumatism, 
tetanus. In man it occurs in a large number of diseases some of 
which are: Asiatic cholera, relapsing fever, typhus fever, scarlet 
fever, diphtheria, tertiary syphilis, erysipelas, bubonic plague, 
dysentery, pneumonia, smallpox (suppurative stage) and vaccina, 
malignant endocarditis, multiple abscesses, pyemic and septicemic 


TABLE XXII.—EXAMPLES OF INFLAMMATORY LEUCOCYTOSIS 
7 a ug Eos- | Mast 
Animal Age | Leucocytes | ocytes saree Polyn..| “ing | Gells 


Gelding B * 12 | 20,333 {19.4 2.1 | 75.9 | 2.5] 0.1 | fistulous 


withers. 
Mare MHC 3144] 20,000 /14 2.4 | 81. | 2. | 0.6 | suppuration 
jaw. 
Gelding MHC | 14 | 11,000 8.4 1.4 | 90. | 0. | 0.1 | pneumonia. 
Gelding MHC} 18 | 20,108 [15 2. 805 42.41» \nilam: Sof 
sheath. 
Gelding M 8 | 26,970 8.1 4.3 | 87.4]0. | 0. | strangles. 
Gelding M 11 | 23,090 6. ai oo.e | 0-7 | O croupous 
pneumonia. 
Mare M 514 | 20,600 8.1 2.5 | 89.3 |}0. | 0. | muscular 
rheumatism. 
Mare M 18 | 24,689 Al 0.9 | 94.8 )0. | 0. | tetanus. 


* The letters following the animal refer to the investigator reporting the 
case;—B for Buffington, M for Meier, M H C for Moore, Haring and Cady. 


conditions, actinomycosis, glanders, acute articular rheumatism, 
gonorrhoea, cerebro-spinal meningitis, osteomyelitis, whooping 
cough, abscesses, inflammation of serous membranes, gangrenous 
inflammation. 

Experimental leucocytosis. Besides natural infections, leu- 
cocytosis may be induced by many influences. A large number 
of chemical substances and mixtures, organic principles, bacterial 


76 INFLUENCES AFFECTING THE LEUCOCYTES 


proteins or their products and bacterial cultures have been found 
to produce a greater or less grade of leucocytosis. Only a few of 
the great number of investigations can be cited. Pohl found that 
the aromatic extracts and oils (oil of anise, peppermint, fennel), 
vegetable bitters (absinthe, extract of gentian), certain alkaloids 
(piperin, strychnine and others) caused in fasting dogs a distinct 
increase in the number of leucocytes (40-120%) which appeared 
within one-half hour and disappeared in two hours. Winternitz 
studied the effect of a variety of drugs as to the relation between 
the grade of local action on the tissues and the degree of intra- 
vascular leucocytosis. He observed (1) that by subcutaneous 
injection neutral salts and simple irritants, such as free acids and 
alkalis, induced slight local disturbance with moderate leucocytosis 
and fever and (2) that turpentine, oil of mustard, croton oil, 
sapotoxin, digotoxin, silver nitrate, cupric sulphate, mercurials 
and antimonials produced aseptic suppuration and more marked 
leucocytosis. He found that the amount of leucocytosis is propor- 
tional to the intensity of the local reaction. Wilkinson obtained 
a diminution followed by an increase of leucocytes after the injec- 
tion of potassium iodide, camphor, quinine, antipyrin, salicin, 
salicylic acid, nuclein and pilocarpin. Rieder found an increase 
of leucocytes after the administration in dogs of pyrodin per os 
to seven times the normal, NaCl solution, intraperitoneal injec- 
tion, to twice the normal, bacterial cultures, bacterial proteins, 
tuberculin, alkaliprotein (Buchner), pyoecyaneus alkaliprotein, 
glutenocasein in rabbits, peameal pulp. The leucocytes were in- 
creased 11-12 times the normal after three daily injections of 
pyocyanin. Injections of hemialbumose, peptone, pepsin, nu- 
cleinic acid, nuclein, urea, sodium urate, curare, pyocyanin and 
tuberculin produce a leucopenia followed by leucocytosis in ani- 
mals (Léwit). Goldschneider and Jacob obtained similar results 
from the injection of glycerin extracts of spleen, thymus and bone 
marrow; but obtained negative results from extracts of thyroid, 
liver, kidney and pancreas. After the intravenous and sub- 
cutaneous injection of a solution of ether, Derouaux found a 
transient leucopenia followed by a polynuclear leucocytosis last- 
ing several days succeeded by a secondary mononucleosis. In- 
halation of ether he found followed by polynuclear leucocytosis. 
Harvey found that a lymphocytosis occurred after the injection 


EXPERIMENTAL LEUCOCYTOSIS v7 


of pilocarpin, muscarin and barium chloride. This was of purely 
mechanical origin, due to contraction of plain muscle in the spleen 
and lymphatic glands, as it may be inhibited if atropine precedes 
the incorporation of any drug which stimulates plain muscle. 

Von Limbeck injected cultures of bacteria into the knee joints 
of fasting dogs and found the maximum leucocytosis was reached 
6-24 hours after the injection, with ordinarily two to three times 
the normal number of leucocytes of which 88-93% were poly- 
morphs. Pyogenic staphylococci were the most active, increas- 
ing the leucocytes to 6-7 times the normal number.  Strepto- 
coccus pyogenes was next and Friedlander’s pneumococcus third 
in activity. Rieder repeated v. Limbeck’s experiments on dogs 
and rabbits and found an increase in leucocytes preceded by a 
temporary decrease. In some cases the injection was followed by 
leucopenia and the death of the animal. Bacterial proteins pro- 
duced a decrease one to two hours after injection followed by an 
increase, or occasionally persistent leucopenia. A number of 
experiments has shown that nearly all of the pathogenic bacteria 
induce leucocytosis. The duration of the stage of leucopenia and 
the grade of leucocytosis vary with the different bacteria, the 
virulence of the cultures used and the resistance of the animal. 

Some of the substances that have been found by various inves- 
tigators to produce leucocytosis are: sodium chloride solution, 
salts of mercury and of antimony, arsenic trisulphate, dilute acids 
and alkalis, silver nitrate, cupric sulphate, potassium iodide, 
sodium salicylate, salicylic acid, acetic ether, ether, chloroform, 
camphor, turpentine, oil of peppermint, oil of mustard, croton oil, 
oil of anise, oil of fennel, oil of cinnamon, sodium cinnamate, tinc- 
ture of myrrh, extract of gentian, absinthe, digitalis, quinine, 
pilocarpin, morphine, salicin, piperin, strychnine, sodium urate, 
uric acid, urea, sapotoxin, digotoxin, curare, antifebrin, anti- 
pyrin, phenacitin, nuclein, nucleinic acid, albumose, peptone, pep- 
sin, sodium albuminate, egg albumin, hemoglobin, lecithin, spermin, 
fibrin ferment, extracts of spleen, thymus and bone marrow, leech 
extract, ground wheat, gluten casein, peameal, filtered yeast cul- 
tures, pyocyanin, tuberculin, mallein and antitetanic serum. With 
some of these other investigators have obtained negative results. 
A practical application to be made of therapeutic leucocytosis 
is that when examining the blood during the administration of 


78 INFLUENCES AFFECTING THE LEUCOCYTES 


some substance that produces a leucocytosis allowance in inter- 
preting the results must be made for the effect of the substance 
administered. 

Post hemorrhagic leucocytosis. A distinct leucocytosis occurs 
following hemorrhage (after traumatism or other causes). Huner- 
fauth found in six dogs with a loss of blood amounting to about 
4% of the body weight that there was first a slight decrease 
in the number of leucocytes after operation followed by a 
marked increase on the following day (maximum 43,700) which 
persisted two or three weeks. Lyon in experimental hemorrhage 
in dogs found that there was an initial decrease within a few min- 
utes after operation, followed soon by a marked increase which 
reached a maximum in six to eight hours, decreased rapidly after 
three to four days but persisted in moderate degree for days or 
weeks. The majority of the leucocytes during leucocytosis Rieder 
found to be polynuclear, as high as 97%. Rieder repeated the 
experiments on three dogs, finding a leucocytosis except in one 
case where there was no increase. In Rieder’s cases the amount 
of blood lost had been replaced by injections of an equal volume 
of sterile salt solution. In general the transfusion of salt solution 
seems to increase the amount of the leucocytosis. The grade of 
leucocytosis varies with the amount of blood lost, there being a 
greater increase with a greater loss of blood. It varies with the 
powers of regeneration of the individual and is greater with severe 
than mild hemorrhage and with rapid than slow loss of blood. 


POST HEMORRHAGIC LEUCOCYTOSIS 79 


TABLE XXIIJ.—TuHE FoLLowInG SHows THE Errect or HEMORRHAGE ON 
THE Bioop or Two Dogs (RIEDER) 


Dog I. 8,150 grams 


Date Leucocytes | Red Corp. Hb. 
Mar. 27 8 A.M. 8,600 7,808,000 | 120% | fasted 18 hours. 
Mar. 27 3P.M. withdrew 420 cc. blood 
from carotid, infusion 
420 ce. sterile salt soln. 
into jugular vein. 
Mar. 27 4Pp.M. 13,300 5,660,000 70 
Mar. 28 8 A.M. 10,200 5,450,000 70 
Mar. 30 3P.M. 14,600 5,860,000 75 


May 1 9a.m.| 7,100 | 7,656,000 | 125 


Dog III. 28,000 grams 


Wcte 2a) Pont: 7,200 | 6,400,000 fasted 24 hours. 

Oct. 27 4P.M. withdrew 1,450 ce. blood 
from femoral artery, in- 
fusion 1,450 ce. sterile 
salt soln. into jugular 
vein; 3 ctgm. morphine 
sub cut. 

Oct. 28 9a.m.| 34,000 | 3,530,000 | 61 

Oct. 29 Q9a.m.]} 26,200 | 2,071,250 | 45 

Oct. 30 9a.m. | 31,000 | 2,550,000 | 49 


Ante mortem leucocytosis. With slow prolonged dissolution 
there is often a marked increase in the number of leucocytes. In 
a case in man reported by Rieder the leucocytes increased within 
two days from 7,800 to 59,300 of which 87.5% were polymorphs. 
In pernicious anemia in man cases have been observed with high 
leucocyte counts on the day of death. Cabot reported a case 
with about 60,000 leucocytes, 91.7% of which were small lym- 
phocytes. In cases of fowl typhoid reported by Moore, the leuco- 
cytes were much increased just preceding death. In one case the 
leucocytes increased from 56,000 the day before death to 115,000 
the day of death; in another case they rose from 80,000 to 245,000 


80 INFLUENCES AFFECTING THE LEUCOCYTES 


ina day. With rapid or sudden death the ante-mortem increase 
does not occur. Ordinarily the increase is in the polymorphs; 
sometimes it is mainly in the lymphocytes. Small numbers of 
myelocytes and erythroblasts have been found in the circulating 
blood. 

The leucocytosis is believed to be due in the majority of cases 
to terminal inflammation or stasis. V. Limbeck considered that 
the cause, as a rule, is an inflammation of the respiratory passages, 
since he was always able to find such a cause, e. g., patches of 
pneumonia or broncho-pneumonia, septic bronchitis, or hypostatic 
pneumonia. 


LYMPHOCYTOSIS 


In the young the lymphocytes are generally present in greater 
numbers than in adults. In puppies 3-20 days old, there were 
20.8-30.7% while the average for adults is 19.4%. A lymphocy- 
tosis is constantly present (Goodall, Gulland and Paton) during 
digestion. There are several pathological conditions in which 
there is a relative or absolute increase of the lymphocytes. In 


anemia (secondary or pernicious), most splenic tumors, some 


cases of lymphoma, and in infectious diseases associated with 
acute hyperplasia of the lymphatic tissue, there is a relative or 
absolute lymphocytosis. An increase of lymphocytes has been 
found after injections of thyroid extract, tuberculin, pilocarpin, 
quinine hydrochlorate, extract of carcinomatous tissue, and after 
splenectomy. A relative lymphocytosis due to the decrease of the 
polymorphonuclears is found during the early (leucopenic) stage 
of inflammatory leucocytosis. The most marked lymphocytosis 
occurs in lymphatic leukemia in which nearly all the leucocytes 
are lymphocytes. In man, lymphocytosis is found in cases of 
whooping cough, congenital and acquired secondary syphilis, 
typhoid fever, malaria, some cases of scurvy and hemophilia, and 
v. Jaksch’s anemia. 


EOSINOPHILIA 


A slight increase of eosinophiles has been observed in man after 
coitus. In a cow in the early stage of cestrum, Knight found 
9,444 leucocytes of which 18% were eosinophiles. The normal 
number of leucocytes for this cow was 5,600 of which 17.3% were 


= a 
st ie a tl sa 


. = = Gc 
ee ee ee 


Saat 


EOSINOPHILIA 81 


eosins. During the early stage of cestrum she showed a moderate 
absolute and relative eosinophilia. Two other cows examined by 
Knight six hours and three hours after copulation had respectively 
8,166 with 10.4% eosins and 14,846 leucocytes with 12.5% eosins. 
The average percentage of eosins in cattle as determined by Dimock 
and Thompson is 13.1%. In the young in man the number of 
eosins is usually high. In four pups from less than a day to 20 
days o'd, Burnett and Traum found the percentage of eosins rather 
high, 11.8% in a pup less than a day old, 17.1 in one not three days 
old, 11.8 in one not four days, 9.7 in one not six days, 5.9 in one 
fourteen days, 6.6 in one fifteen days, and 6.6 in one twenty days 
old. In calves, ten days to three weeks old, Knight found the 
percentage of eosins small (1.4-1.8%). 

The eosins have been found increased in cases of helminthiasis. 
Bicklers from observations in man states that “all varieties of 
helminthides, from the harmless oxyurides to the pernicious 
ankylostoma, may bring about an increase of eosinophiles in the 
blood, often to an enormous extent.’ Moore, Haring and Cady 
in horses infested with Sclerostoma equinum found an eosinophilia 
of from 7.1 to 13.3%. 

In some cases of follicular and of sarcoptic mange in dogs and 
cats there is usually an increase in the number of leucocytes and 
in the number and percentage of eosinophiles. In 8 severe cases 
of follicular mange in dogs Welch found the eosinophiles from 400 
to 1,664 per emm. (5 to 11%) which was an increase above the 
normal except in one case. In four light cases he found no in- 
crease. In six severe cases of sarcoptic mange in dogs and cats 
there was an eosinophilia in all cases, 640—-1,630 per cmm. in the 
dog and 7,020 per cmm. in the cat. 

Welch also found an increase in the eosinophiles, 860 to 2,750 
per cmm., in six cases of eczema in dogs. He found that the 
eosinophilia in the cases of mange and eczema depends more 
upon the intensity of the dermatitis, that is the amount of pruritis 
and irritation, than upon the nature and extent of the disease. 
In acute and chronic skin diseases in man the eosins have been 
found increased. After the crisis in diseases having an inflam- 
matory leucocytosis the eosins may increase to more than normal 
numbers. Voswinkel states that they are increased in all cases of 
severe ovarian disease excepting during the febrile stages and in 


82 INFLUENCES AFFECTING THE LEUCOCYTES 


eases of cancer of the ovary. The greatest numbers of eosins 
have been found in cases of mixed celled leukemia. 

The eosins are diminished during severe muscular exertion, after 
castration (Neusser), in the febrile stages of diseases having in- 
flammatory leucocytosis, in the moribund state, in malignant 
disease and generally after hemorrhage. 


BASOPHILIA 


The greatest numbers of mast cells recorded have been found 
in mixed celled leukemia. Individual cases of increased mast cells 
have been reported; but these cells are not constantly increased 
in any particular condition so far as has been observed. 


OCCURRENCE OF MYELOCYTES 


Myelocytes have been observed in the largest numbers in mixed 
celled leukemia in which from 20-60% of the leucocytes are finely 
granular myelocytes. A small number of myelocytes may some- 
times be found in cases of infectious diseases having a polynuclear 
leucocytosis. The presence of the myelocytes indicates hyper- 
plasia and hyperemia of the bone marrow. Sometimes after severe 
mechanical disturbances of the circulation, as in uremia, asphyxia 
and acute mania, a few myelocytes may be found in the circulating 
blood. Ewing has observed a few myelocytes in ante-mortem 
leucocytosis. They have also been found in some cases of second- 
ary and of primary anemia. 

Kosinophilic myelocytes occur in greatest abundance in leu- 
kemia, and have been observed rarely in a few other conditions, 
myxedema (Mendel), v. Jaksch’s anemia, in some infectious dis- 
eases (Tark), pernicious malaria (Bignami). 


LEUCOPENIA (HYPOLEUCOCYTOSIS) 


In leucopenia the several varieties of leucocytes are not neces- 
sarily affected alike, very frequently some are lessened much more 
than others. With the reduction in the total number there may 
even be an increased number of some variety. Leucopenia occurs 
in a variety of conditions, as fasting, malnutrition, after short hot 
or prolonged cold baths, often during the initial stage of inflam- 
matory and experimental leucocytosis, in many cases of anemia, 
often in non-septic tuberculosis, and following the injection of 


REFERENCES 83 


ergot, tannic acid, sulphonal, atropine, agaricin, picrotoxin, pep- 
tone, diastase, and eel serum. 

Neegeli states that leucopenia occurs in the following conditions: 
(1) with lessened activity of the leucopoetic organs following a 
lessened demand on the function, e. g., leucopenia in complete 
inanition and the small leucocyte count in embryonal blood; 
(2) in lessened activity through insufficiency of function, e. g., 
through the action of toxins, in typhus and in many cases of 
cirrhosis of the liver and of anemia, and preagonal diminution; 
(3) in lessened function through anatomical destruction of con- 
siderable mases of functional tissue, e. g., the lessened lymphocyte 
count in tuberculosis of the lymphatic system and in destruction 
of tissue following prolonged action of roentgen or radium rays; 
(4) through the action of capillary attraction after injections of 
toxins and certain other substances, the materia peccans being 
taken up by the leucocytes in the pulmonary and hepatic capil- 
laries, thus producing an unequal distribution in the body which 
lasts a short time, until an increased activity of the leucopoetic 
organs supervenes; (5) with negative chemotaxis. 


REFERENCES 


1. Becker. Deutsch. Arch. f. klin. Med., |xx, 1901. 

2. Bianami. Cited by Ewing. 

3. BRINCKERHOFF AND TyzzER. On physiological leucocytoses of the 
rabbit. Journ. of Med. Research, vii, 1902, p. 191. 

4. Bucuner, H. Die chemische Reizbarheit der Leukocyten und deren 
Beziehung zur Entziindung und Eiterung. Berlin. klin. Woch., xxvii, 1890, 
Nr. 47. 

5. Bucxuers. Ueber den Zusammenhang der Vermehrung der eosinophilen 
Zellen im Blute mit der Vorkommen der Charcot’ chen Krystalle in den Fiices 
bei Wurmkrankheiten. Miinch. med. Woch., xli, 1894, S. 22. 

6. Burrincton, R. M. Clinical examination of the blood of the horse. 
Thesis, N. Y. State Vet. College, 1905. 

7. Burnett anpD Traum. The clinical examination of the blood of the 
dog. Proceed. Am. Vet. Med. Assn., xlii, 1905, p. 349. 

8. Derovaux, J. Sur quelques modifications du sang sous l’influence de 
Véther. Arch. d. med. exper., xix, 1907, p. 478. 

9. Dimock AND THompson. Clinical examination of the blood of normal 
cattle. Am. Vet. Rev., xxx, 1906, p. 553. 

10. GoLDSCHNEIDER UND Jacos. Zeitschr. f. klin. Med., xxv, H.5/6. 

11. GoppaLL, GULLAND AND Paton. Digestion leucocytosis in normal and 
in spleenless dogs. Journ. of Physiol., xxx, 1903, p. 1. 


84 INFLUENCES AFFECTING THE LEUCOCYTES 


12. Gunposin. Jahrb. f. Kinderheilk, xxxv, 1893, S. 187. 

13. Harvey, W. H. Experimental lymphocytosis. Journ. of Physiol., 
xxxv, 1906, p. 115. 

14. HtownerrautH, G. Einige Versuche iiber traumatische Animie. 
Arch. f. path. Anat., Ixxvi, 1879, 8. 310. 

15. Knicut, R. F. The condition of the blood in pregnant, newborn and 
rutting animals. Thesis, N. Y. State Vet. College, 1907. 

16. LARRABEE, R. C. Leucocytosis after violent exercise. Journ. of Med. 
Research, vii, 1902, p. 76. 

17. v. Limpecx, R. R. Klinisches und Experimentelles iiber die entzund- 
liche Leukocytose. Zeitschr. f. Heilk., x, 1889, 8. 392. 

18. Lowir, M. Studien zur Physiologie und Pathologie des Blutes und der 
Lymph. Jena, 1892. 

19. Lyon, J. F. Blutk6érperchenzihlungen bei traumatischer Animie. 
Arch. f. path. Anat., lxxxiv, 1884, S. 207. 

20. Meter, Pau. Beitrige zur vergleichenden Blutpathologie. Zeitschr. 
f. Tiermed., x, 1906, S. 1. 

21. Menpet. Cited by Ewing. 

22. MircHe.., J. K. Am. Journ. Med. Sciences, evii, 1894, p. 502. 

23. Moors, V. A. Infectious leukemia in fowls. 12th and 13th Ann. Rep. 
Bur. Anim. Ind., U.S. Dept. Agr., 1895-96, p. 185. 

24. Moorr, Hartna anp Capy. The clinical examination of the blood 
of the horse and its value to the veterinarian. Proceed. Am. Vet. Med. Assn., 
1904, p. 284. 

25. Pout, J. Die Vermehrung der farblosen Zellen im Blute nach Nahrung- 
saufnahme. Arch. f. exper. Path. u. Pharmak., xxv, 1889, 8. 31. 

26. Rreper, H. Beitrige zur Kentniss der Leukocytose. Leipzig, 1892. 

_ 27. Rovieut. Arch. Ital. d. clin. med., xxxii, 1893, p. 3. 

28. Srorcw, A. Untersuchungen iiber den Blutkérperchengehalt des 
Blutes der landwirtschaften Haussiiugetiere. Inaug. Diss. Bern., 1901. 

2S. Tcuistovircu, N. Contribution 4 l’étude de la pathogénie de la crise 
dans la pneumonie fibrineuse. Ann. d. l’Inst. Past., xviii, 1904, 304. 

30. TuHayrer, W.S. Note on the increase in the number of leucocytes in 
the blood after cold baths. Bull. Johns Hopk. Hosp., iv, 1893, p. 37. 

31. Ttrk. Blutuntersuchungen bei Infectionskrankheiten. 1895. 

32. VoswinKEL. Monatschr. f. Gelnirtsh. u. Gyndkol., 1898, 8. 413. 

33. Wetcu, Howarp. Blood examinations of dermatoses in dogs. Rep. 
N.Y. State Vet. College, 1909-1910, 146. 

34. WrenpiEck, K. Untersuchungen iiber das Verhalten der Blutkérper- 
chen bei gesunden und mit croupéser Pneumonie behafteten Pferden. Arch. 
f. wissen. u. prakt. Tierheilk, xxxii, 1996, 113. 

35. WinTERNITz, R. Ueber Allgemeinwirkungen 6rtlich reizender Stoffe. 
Arch. f. exper. Path. u. Pharmak., xxxv, 1895, 8. 77. 

36. Winrernitz, W. Neue Untersuchungen iiber Blutveriinderungen 
nach thermischen Hingriffen. Centralbl. f. klin. Med., xiv, 1893, 8. 1017, also 
SAL i 


CHAPTER VI 


SPECIAL DISEASES OF THE BLOOD 


PERNICIOUS ANEMIA 


This term has been applied to an entirely different condition 
in horses from the affection known by the same name in human 
medicine. In human medicine the distinction between anemia of 
the pernicious type and secondary anemia, is based on several 
criteria, of which the more important are the high Hb index, the 
presence of a large number of megalocytes (at least 33%) or, when 
erythroblasts are present, an excess of megaloblasts over normo- 
blasts. Pernicious anemia has been defined as a severe anemia for 
which the cause is unknown or wholly inadequate to produce so 
serious results in the organism. More recently it is defined by the 
blood picture which shows a greater number of megaloblasts than 
normoblasts or at least 339% megalocytes. The essential lesion is 
a megaloblastic hyperplasia of the lymphoid marrow. The term 
has been applied to a disease in horses producing a severe anemia 
of which the cause is obscure. The blood picture is, however, 
quite different from that presented by pernicious anemia in man, 
being rather that found in a secondary anemia. 

In pernicious anemia in man the red corpuscles are much 
diminished in number. Megalocytes with increased hemoglobin 
comprise from 33-90% of the red corpuscles; but may be few dur- 
ing the periods of remission. Megaloblasts are few or numerous, 
but are more numerous than normoblasts; microblasts are scarce. 
The hemoglobin index * varies but is usually one or higher. It 
may be below the normal during remissions or in the early stages 
of the disease. Coagulation is slow, rouleaux do not form, and 
there is lessened resistance of the red corpuscles. Poikilocytosis, 


* The hemoglobin index, or color index, is the relative amount of hemo- 
globin contained in each corpuscle and is obtained by dividing the percentage 
of hemoglobin by the percentage of corpuscles. In human blood the normal 
number of corpuscles is considered as 5,000,000, which is 100%. 


85 


86 SPECIAL DISEASES OF THE BLOOD 


schistocytosis, punctate basophilia and polychromasia are usually 
marked. The leucocytes are, as a rule, diminished with relative 
lymphocytosis. The eosinophiles are usually few in number; 
myelocytes may be present in small numbers. 

The cause of these changes in the blood in many of the cases 
seems at present to be unknown. Besides what may be called 
the cryptogenic cases, there are also others with similar changes 
in the blood but in which the cause is known. Thus pernicious 
anemia has been observed in cases of certain intestinal parasites 
(Bothriocephalus, Ankylostoma), syphilis and malaria. Certain 
gastro-intestinal disturbances have also been considered as im- 
portant factors in producing this condition. In short, the con- 
dition known as pernicious anemia in man is one shown to be due 
to various causes but presenting characteristic changes in the 
blood and in the blood forming organs. 


percentage of hemoglobin 


Hb index = 


fete oe eels no. of corpuscles 
ercentage oO U = eee 
7 : of 5,000,000 
Examples: (1). In a case of secondary anemia in man 2,650,000 red cor- 
puscles and 40% Hb. were found on examination. The color index is 
2,650,000 40 
40 + —_— = — = .75 the color index. (2). Ina case of perni- 
5,000,000 53 
cious anemia 840,000 red corpuscles and 18% Hb were found. 18 + - 
840,000 18 


5,000,000 16.8 
4,100,000 red corpuscles and 32% Hb were obtained. 32 + 


= 1.07 the color index. (3). In a ease of chlorosis 


4,100,000 32 
—_—__—. = — = .39 the color index. 
5,000,000 82 


In dogs, Uncinaria is said to produce a pernicious anemia. A 
disease in horses in France and Switzerland has been called per- 
nicious anemia; but the condition of the blood differs widely from 
that in man. Meier has reported several cases. The changes in 
the blood are: The presence of many microcytes, poikilocytosis, 
polychromasia, megalocytes in some cases, usually no erythro- 


LEUKEMIA 87 


blasts but when present normoblasts and microblasts. The hemo- 
globin index is low, that of secondary anemia. In fact all the 
changes described are those belonging to secondary anemia as 
shown by the following descriptions of Meier’s cases. 

No. 18, great variation in size and shape of erythrocytes; few 
megalocytes, many microcytes, many poikilocytes, no erythro- 
blasts. 

No. 14, poikilocytosis; many megalocytes and microcytes, no 
erythroblasts. 

No. 15, normo- and micro-blasts; many microcytes and small 
poikilocytes. 

No. 16, many micro- and poikilocytes, small erythroblasts. 

No. 17, poikilocytosis and endoglobular degeneration of ery- 
throcytes; many microcytes, small erythroblasts. 

No. 18, moderately many poikilocytes, many microcytes and 
megalocytes, no erythroblasts. 

No. 19, marked deformation of erythrocytes; poikilocytosis, 
megalocytes, microcytes and normoblasts, uneven staining of 
erythrocytes. 


LEUKEMIA (LEUCOCYTHEMIA) 


Leukemia is a primary disease of the blood and blood-forming 
organs. It is in the majority of instances a chronic disease char- 
acterized by the presence of an enormous number of leucocytes 
in the circulating blood, associated with anemia, though the essen- 
tial characteristic is not so much the large number of leucocytes 
as the varieties and proportions of these which are found. 

Two varieties of leukemia are described, (1) the mzzxed-celled 
(myeloid, myelogenous, myelogenic, spleno-medullary, myelemia) 
and (2) lymphatic (lymphoid, lymphemia), which are differen- 
tiated by the condition of the blood and the blood-forming organs. 

(1). In mixed-celled (myelogenic) leukemia the circulating 
blood usually contains an excessive number of leucocytes, many of 
which are of varieties not found in the normal circulating blood. 
In typical cases the red corpuscles are diminished. In 47 cases in 
man, Cabot found an average of 3,120,000 per emm. Toward 
the end of the disease or with intercurrent disease the number 
may be much reduced, 2,000,000 or less. The hemoglobin is re- 
duced in the early stages more than the number of red corpuscles; 


88 SPECIAL DISEASES OF THE BLOOD 


later the Hb index is nearly normal though there is considerable 
difficulty in obtaining the amount of hemoglobin owing to the 
changed color produced by the excess of leucocytes. Changes in 
the size, shape and staining of the red corpuscles are found corre- 
sponding to the degree of anemia present. As a rule many ery- 
throblasts are found, even in cases showing no external signs of 
anemia. In nine cases DaCosta found from 748 to 12,913 ery- 
throblasts per cmm. with an average of 5,931 perecmm. Of these 
the majority were normoblasts. Megaloblasts occur, but in 
smaller numbers. Erythroblasts with mitotic nuclei are found 
occasionally. 

The most characteristic changes are found in the leucocytes. 
Their number is generally excessively increased. The average 
number in Cabot’s cases was 385,000 per cmm., maximum 
1,072,000, minimum 98,000 per cmm. In acute cases the number 
may not be greater than in cases of inflammatory leucocytosis. 
The appearance of a stained preparation is characteristic. Of the 
leucocytes a large number are myelocytes, mostly metamyelocytes 
and the variety with fine acidophile granules with a comparatively 
small number of eosinophilic myelocytes in chronic cases. All 
stages between myelocytes and polymorphonuclears are en- 
countered. Polymorphonuclears occur in large numbers but with 
smaller percentages than in normal blood. Lymphocytes are 
present in small percentages. Eosinophiles occur in large numbers 
but in about the normal proportion. Mast cells are usually found 
in rather large numbers. In different cases considerable variations 
are found especially in the mast cells and eosinophiles. Cabot 
obtained the following average percentages in 41 cases: myelocytes, 
32.5%, polymorphs, 47.5%, small lymphocytes, 5.2%, large 
lymphocytes, 5.4%, eosinophiles, 4.4%, and mast cells, 5%. De- 
generative changes in the leucocytes are commonly seen. The 
nuclei of some cells may appear pale and swollen; hydropic nuclei 
sometimes are found. In others the nuclei may be fragmented, the 
parts staining deeply. The granules of the polymorphs and 
myelocytes may be few or absent. Variations in the size and 
staining of the fine acidophile granules are often seen. 

With intercurrent infection the character of the blood may be 
greatly altered. The number of leucocytes has been observed to 
fall from excessively high numbers to normal or even below the 


PLATE IV 


Leukemia 


1. Lymphatic, homo. Leucocytes 200,000 per emm., mainly small lym- 
phocytes, a normoblast in the center of the figure. 

2. Mixed celled (myelogenic), homo. Leucocytes 178,000 per emm. Note 
the finely granular myelocytes and the eosinophilic myelocyte. 


LEUKEMIA 89 


normal numbers. With the decrease in numbers there is often a 
change in the proportions of the varieties, the polymorphs being 
relatively increased, so that the blood picture resembles that of 
an inflammatory leucocytosis. 

Pathological anatomy and histology. The primary change is 
found in the bone marrow which undergoes a cellular hyperplasia. 
The red marrow of ribs, vertebree, etc., usually is lighter colored 
and of a firmer consistency. There is an extension of lymphoid 
marrow in the shafts of long bones and an atrophy of fat. In long 
standing cases there may be a considerable increase of connective 
tissue. The hyperplasia consists of a marked increase in the finely 
granular myelocytes together with the eosinophilic myelocytes 
and in lymphocytes, large mononuclear and polynuclear leucocytes 
and nucleated red cells. 

The spleen is much enlarged. It is often rich in cells, sometimes 
both follicles and pulp cords being equally increased, sometimes 
one more than the other. The boundaries between them are less 
distinct or are sometimes indistinguishable. The stroma is often 
much increased, rendering the organ much more firm. In these 
cases it is less rich in cells. The spleen pulp contains many mye- 
locytes, finely granular and eosinophilic, and large non-granular 
leucocytes, lymphocytes and polymorphs, in addition to which 
nucleated red cells are also found. 

The liver is usually enlarged. The capillaries are widened and 
contain many leucocytes. In the interlobular tissue and in the 
lobules there is often a diffuse infiltrative growth and many 
metastatic foci composed of myelocytes with lymphocytes and 
polymorphonuclear leucocytes held in a meshwork of. delicate 
ground substance. Numerous cells, mainly myelocytes and lym- 
phocytes, may be found undergoing mitotic division. 

The lymph glands show a cellular hyperplasia. The boundaries 
of follicles and medullary cords are commonly apparent though 
sometimes indistinct. The lymph sinuses and blood vessels con- 
tain many leucocytes. The reticulum is sometimes thickened, 
making the gland more firm. The follicles are composed mostly 
of lymphocytes but also contain, especially in their peripheral 
portions, finely granular and eosinophilic myelocytes, which are 
especially abundant in the medullary cords. 

(2). In lymphatic or lymphoid leukemia the circulating blood 


90 SPECIAL DISEASES OF THE BLOOD 


usually contains an excessive number of leucocytes, a large pro- 
portion of which (85-99%) are small lymphocytes. The red 
corpuscles are diminished. Cabot found an average of 3,170,000 
per cmm. and 40% hemoglobin in 16 cases in man. In the acute 
cases the red corpuscles are usually much diminished, often less 
than 1,000,000 per emm. during the last days. Normoblasts are 
usually present in much smaller numbers than in mixed-celled 
leukemia and are sometimes absent even with very low red counts. 

The leucocytes are increased, though not so much, as a rule, 
as in mixed-celled leukemia. Cabot found an average of 240,000 
leucocytes (maximum, 1,480,000, minimum, 30,000) in 16 cases. 
The majority of the leucocytes in chronic cases are small lym- 
phocytes, 92-99%, average, 95% (Sternberg). Other varieties of 
leucocytes are relatively scarce; occasionally myelocytes are found 
in small numbers. In acute cases the predominating cell is a very 
large lymphocyte with rather pale nucleus; in other cases varying 
proportions of small, medium and large lymphocytes are found. 
In acute cases the large cells are more abundant. In lymphatic 
leukemia, degenerative changes may be found in the lymphocytes. 
It is not uncommon to find small lymphocytes with cell bodies so 
small as to be seen with difficulty. 

Pathological anatomy and histology. The pathological changes 
found are in general very similar to those occurring in mixed- 
celled leukemia. There is hyperplasia of the bone marrow, spleen 
and lymph glands and growths or collections of cells in various 
organs. Not infrequently hemorrhages occur in the central nervous 
system, the subdural spaces and also in the several internal organs. 
Hemorrhages are more common in acute cases. 

The bone marrow is involved in all cases in which it has been 
examined (Pappenheim). It is rich in cells and in blood. The 
cells are mainly lymphocytes. Large non-granular mononuclear 
cells, finely granular and eosinophilic myelocytes, polymorphonu- 
clear leucocytes and erythroblasts are present in small numbers. 

The spleen is usually much enlarged. Sometimes it is very cellu- 
lar, but follicles and pulp cords are generally clearly distinguish- 
able. The follicles are composed almost exclusively of small lym- 
phocytes; large non-granular mononuclear cells occur in small 
numbers and a few finely granular and eosinophilic myelocytes 
are sometimes found. The trabeculsee are not much increased in 


woten Bp 


Pers et 


LEUKEMIA 91 


size though there is often a considerable increase in the reticular 
connective tissue. 

Any or all of the lymph glands may be enlarged. In the en- 
larged lymph glands there is a diffuse hyperplasia of lymph cells, 
so that the distinction between follicles and lymph cords is lost. 
The reticulum is often obscured by the great mass of lymphocytes. 
The walls of the blood vessels are composed of collections of lym- 
phocytes which sometimes break through into the lumen. In 
many cases a few myelocytes are found in the lymph sinuses. The 
capsule is often infiltrated with lymphocytes. 

In the liver the capillaries are widened and contain many lym- 
phocytes. The interlobular tissue is infiltrated with lymphocytes 
as circumscribed growths or as a more or less diffuse infiltration. 
Sometimes a reticulum may be distinguished in these masses of 
lymphocytes; often the reticulum is obscured by the mass of cells. 

Masses of lymphocytes occur in other organs, as the kidney, 
skin, serous membranes, central nervous system, ete. They appear 
as small grayish nodules, composed of lymphocytes arranged as 
in the organs described. 

Occurrence. Leukemia has been observed in the domesti- 
cated animals in comparatively few cases. Nocard, in 1880, cited 
43 cases, nine in horses, five in cattle, four in swine, twenty-two 
in dogs and one ina cat. In the Prussian army from 1890 to 1895, 
there were 26 horses reported as having leukemia. Other cases 
are reported, mostly in dogs. The disease is doubtless a rare one, 
but is probably not so rare as the number of recorded cases would 
lead one to suppose. All of the cases reported in the domesticated 
animals in which histological examinations have been made have 
been of lymphatic leukemia. Authentic cases of mixed-celled leuke- 
mia have not, so far as I am aware, been observed. In the majority 
of cases reported, merely the proportion of leucocytes to red cor- 
puscles, the post-mortem appearances, and the symptoms in part 
of the cases are given. 

Weil and Clere reported a case of lymphatic leukemia in a dog 
weighing 15,500 grams. There were 2,110,000 red corpuscles, 
320,000 leucocytes and 36% hemoglobin. The differential count 
of the leucocytes gave lymphocytes and small mononuclears 88%, 
large mononuclears 3%, polynuclears 8%, and plasma cells 1%. 
Warthin has reported two cases, Kon has found another and six 


92 SPECIAL DISEASES OF THE BLOOD 


have been examined in this laboratory of lymphatic leukemia in 
the common fowl. Warthin examined the blood of one of his 
cases during the life of the fowl and found 450,000 red cells and 
280,000 leucocytes, of which there were 1.59% small lymphocytes, 
84.5% large lymphocytes, 11.5 polymorphonuclears ‘crystalloid 
eosinophiles,” 2% degenerating white cells and 0.59% mast cells. 

Ellermann and Bang have reported three cases of leukemia in 
fowls. One of them they succeeded in transmitting to other fowls 
by the inoculation of an emulsion of the organs, bone marrow, 
liver and spleen. In some of the later transmissions they used 
blood, in some an emulsion filtered to remove the cells. They 
report transmitting the disease to six generations. In both the 
spontaneous and the experimental cases they found the increase 
in leucocytes to be in the “large mononuclears.”’ Schmeisser also 
has reported a case of spontaneous leukemia in a fowl which he was 
able to transmit to other fowls, to the fifth generation. His ex- 
perimental cases are reported to show an increase in leucocytes, 
131,200 to 210,000, the majority (86%) of which were “large 
mononuclears.”’ Mitoses were common in these. The red cells 
were lessened in number, in one case to 620,000. The hemoglobin 
was diminished, often to 10 or 15 per cent. just before death. His 
spontaneous case, from which the experimental cases developed, 
differs from these in that the majority (52%) of the leucocytes, 
which were in the proportion of 1: 1.3 red cells, are stated to 
be “mononuclear myelocytes with eosinophilic granules.” If 
Schmeisser’s interpretation is correct, his case is a new variety of 
leukemia. 


PSEUDOLEUKEMIA (HODGKIN’S DISEASE, LYMPHADENOMA 
LYMPHOMA) 


This disease cannot be differentiated from lymphatic leukemia 
anatomically or histologically if the blood be excepted. The 
blood is practically normal except during the later stages when it 
may show secondary anemia. A relative lymphocytosis often, 
though not always, is found. The proportion of leucocytes to red 
corpuscles is generally normal, though there is occasionally a 
moderate increase in the number of leucocytes. 

There is marked enlargement of the lymph glands and lymph 


PSEUDOLEUKEMIA 93 


tissue throughout the body and often marked enlargement of the 
spleen. Foci of lymphoid cells or lymphoid infiltration are 
found in the liver, less often in the kidneys, lungs, digestive tract, 
bones and other organs. The histological structure of these is 
essentially the same as in lymphatic leukemia except that the blood 
vessels are not crowded with lymphocytes. 

Cases have been observed in horses, dogs, swine, calves, cattle, 
cats and in domestic fowls. Data as to the frequency of the occur- 
rence of cases is not at hand. Friedberger and Fréhner state that 
according to their experience it is by no means rare in dogs and 
it has sometimes been seen in horses. There is a good deal of con- 
fusion as to the diagnosis. Hyperplasias of the lymph glands or 
spleen due to other causes, as tuberculosis or glanders or malignant 
tumors (lympho-sarcoma) affecting lymph glands, may have been 
mistaken for this disease, while many cases may have escaped 
diagnosis. 

Relation of pseudoleukemia to leukemia and sarcoma. The 
histological changes in lymphatic leukemia and in pseudoleukemia 
are very similar. Many investigators consider them different 
stages of the same disease. Cases of pseudoleukemia are recorded 
in which there has been a marked increase of lymphocytes shortly 
before death (Paltauf, Pappenheim and others). On the other 
hand the great majority of cases of pseudoleukemia run a chronic 
course showing no tendency to change to leukemia. 

Lympho-sarcoma and pseudoleukemia are distinguished by 
lympho-sarcoma having a tendency to infiltrative growth and the 
formation of true metastasis. In lympho-sarcoma the lymph 
glands have lost their characteristic structure and are composed 
of a diffuse growth of lymphoid cells of varying size and often also 
of giant cells. Transitional forms between chronic pseudoleukemia 
and the rapidly growing infiltrating lympho-sarcoma with true 
metastases have been reported. 

The liver is the organ best adapted to distinguish by histological 
examination, leukemia and pseudoleukemia from generalized 
lympho-sarcoma. The characteristic collections of cells found in 
pseudoleukemia and leukemia do not occur in sarcoma. The 
abundant blood vessels of the liver render it easy to distinguish 
between leukemia and pseudoleukemia. 


94 SPECIAL DISEASES OF THE BLOOD 


REFERENCES 


1. Burrerrietp, E. E. Aleukemic lymphadenoid tumors of the hen. 
Folia haematol., ii, 1905, p. 648. 

2. ELLERMANN, V., UND Bana, O. Experimentelle Leukiimie bei Hiihnern I. 
Centralbl. f. Bakt., 1st Abt. Orig., xlvi, 1908, 595. 

3. ELLERMANN, V., UND Bana, O. Experimentelle Leukiimie bie Hiihnern 
II. Zettschr. f. Hyg., lxiii, 1909, 231. 

4. FRIEDBERGER AND FROHNER. Veterinary Pathology, trans. by Hayes, 
Vol. i, 1904, p. 437. 

5. Kon, Juraxa. Uber Leukimie beim Huhn. Arch. f. path. Anat., exe, 
1907, S. 338. 

6. Meter, P. Beitrige zur vergleichenden Blutpathologie. Zeitschr. f. 
Tiermed., x, 1906, S. 1. 

7. Nocarp, E. Leucocythémie. Nouveau Dictionaire pratique de Medecine, 
de Chirurgie et d’ Hygiene veterinaires, xi, 1880, p. 542. 

8. Pauatur. Lymphosarkom (Lymphosarkomatose, Pseudoleukimie, 
Myelom, Chlorom). Lubarsch und Ostertag’s Ergebnisse der allgemeinen 
Pathologie, ii, 1896, S. 652. 

9. PApPENHEIM, A. Zeitschr. f. klin. Med., xxxix, 8. 171. 

10. PappennerM, A. Folia hematol., i and ii, 1904-05. 

11. Pappennerm, A. Uber Pseudoleukiimie und verschiedene verwandte 
Krankheitsformen. Arch. f. klin. Chirur., Ixxi, H. 2. 

12. ScumetsseR, H. C. Spontaneous and experimental leukemia of the 
fowl. Journ. Exper. Med., xxii, 1915, 820. 

13. StrernBerG, C. Primirerkrankungen des lymphatischen und hiima- 
topoétischen Apparates. Lubarsch und Ostertag’s Ergebn. d. allgem. Path., 
ix, Abt. II, 1903, S. 360. 

14. Warruin, A. 8S. Leukemia of the common fowl. Journ. of Infect. 
Diseas., iv, 1907, p. 369. 

15. Wartuin, A. 8. The neoplasm theory of leukemia. Trans. Assn. 
Am. Phys., xix, 1904, 421. 

16. Wein er Cierc. Contribution a |’étude de la leucémie chez les ani- 
maux. Arch. d. med. exper., xvi, 1904, p. 462. 


CHAPTER VII 


GENERAL AND INFECTIOUS DISEASES 


General considerations. In the various diseases the changes 
in the. blood, when changes are found, depend on the character 
of the pathological processes present and also on the nature of 
the exciting cause. In acute exudative inflammations we find 
as a rule an increase in the number of leucocytes, a large per- 
centage of which are polymorphonuclears. The inflammation 
may be in the lungs, in the testes, in muscle, glands, peritoneum, 
pleura, in other organs; the disease may be a wound infection, 
pleuro-pneumonia, strangles, tetanus and the like; polynuclear 
leucocytosis has been found in all of these. The effect on the 
blood has been found to vary with the nature of the exciting 
cause. The character of the lesion produced may vary with 
the cause. For example, the same cause may in one instance 
produce an exudative inflammation as pneumonia, in another 
instance a septicemia may result. Again different effects may 
be observed in the course of the same disease in different stages, 
e. g., when an acute inflammation becomes a chronic productive 
inflammation, as is sometimes observed in strangles. 

In certain of the infectious diseases substances may be found 
in the blood that are characteristic of the particular disease, the 
character of the pathological process or the particular organ 
mainly affected not having a noticeable effect on these substances. 
In glanders, streptococcic infections, typhoid fever, malta fever 
and bacillary dysentery, specific agglutinins or precipitins or both 
have been found in the blood of affected individuals. Some of 
these substances are valuable aids for the diagnosis of the particu- 
lar affection of each. 

Changes produced in the blood in acute febrile disorders. 
Certain changes have been observed in the blood common to 
the acute febrile disorders. In fevers the number of red cor- 
puscles is reduced, though the anemia may not be apparent for 
a time. During the earlier stages there is a contraction of the 

95 


96 GENERAL AND INFECTIOUS DISEASES 


arterioles (Maragliano) followed by a dilatation as the fever 
disappears. The contraction of the peripheral vessels together 
with the increased loss of water during pyrexia tends to pro- 
duce a concentration of the blood. The anemia is usually masked 
during the earlier stages by the concentration of the blood. As 
the fever disappears the number of red corpuscles often drops 
suddenly, the rapidity of the decrease in numbers being propor- 
tional to the rapidity of the fall in temperature. The diminution 
in the number of red corpuscles is due according to some investi- 
gators to an actual destruction (Mobitz, Gerhardt, Hoppe-Seyler, 
Salkowski), while others regard the diminution as due to unequal 
distribution in the body (Breitenstein, Maragliano and others). 
An increase in specific gravity was found by Stein during the 
period of rise in temperature and a lowered specific gravity during 
defervescence. Loss of albumins has been found during fever by 
several observers. 

Concerning the alkalinity of the blood, observations are con- 
flicting. Léwit concludes that the alkalescence of the blood may 
be increased at one time and diminished at another period of an 
infectious disease, that this property is not dependent in any 
large measure upon the leucocytes, and that its significance is still 
unexplained. The coagulability of the blood varies in different 
stages, but has not been shown to be dependent on the tem- 
perature. 

Simple (non-specific) infections.—lFor convenience the in- 
fections not of a specific character are grouped together. The 
group includes the wound infections, pleuritis, pericarditis, peri- 
tonitis, various suppurations, septicemia and so on, due for the 
most part to pyogenic bacteria, streptococci, micrococci, colon 
bacilli and various bacteria not producing a specific infectious 
disease. 

The changes in the blood differ with the character, extent and 
stage of the inflammatory process. With serous exudation of 
small extent, there is usually but little change found in the blood. 
With serous inflammations of greater extent, pleuritis, pericarditis, 
peritonitis, there is usually a moderate increase in the number of 
leucocytes during the febrile stage of the disease. With more 
severe inflammation there is more pronounced leucocytosis. Von 
Limbeck found a leucocytosis of about 18,000-19,000 in a case of 


SIMPLE INFECTIONS 97 


sero-fibrinous pleuritis with a temperature rising to 38.8° C. and 
remittent in type. 

With simple exudative or catarrhal inflammation, there is usually 
no or but slight leucocytosis. DaCosta states that in 45 cases of 
simple appendicitis without pus, gangrene or peritonitis less than 
nine per cent. had a leucocyte count of more than 15,000, the 
maximum was 17,100, the average 8,987. 

With purulent inflammations the changes in the blood are as a 
rule more marked. The red corpuscles may show slight or marked 
decrease. With local suppuration in wounds, empyema, and so 
on, there is usually but slight or no change except in long standing 
cases. Red corpuscles show diminution so long as the discharge 
continues. Fibrin is increased in cases with suppuration (Cabot). 

In cases of septicemia there is usually a rapid loss of red cor- 
puscles. The hemoglobin is ordinarily more affected than the 
number of red corpuscles. The leucocytes as a rule show a marked 
increase, the increase affecting the polymorphs mainly. In a cer- 
tain class of cases it should be borne in mind that the leucocytes 
may show a decrease. These are very severe cases, those in which, 
owing to the virulence of the infecting organisms or the lack of 
resistance of the individual, the leucocytic reaction does not occur. 
In such cases the loss in leucocytes is in the polymorphs. The 
iodine reaction often gives valuable aid in septic cases with leuco- 
penia, glycogenic degeneration being often present. Locke and 
Cabot state “no septic condition of any severity can be present 
without a positive reaction.” Barnicot does not consider that 
the reaction should be given so much value as this; but states that 
“when accumulation of pus is suspected the absence of the re- 
action is of very great negative value.” 

When an abscess becomes walled off or ceases to spread the 
leucocytes decrease slowly; with opening or evacuation of the 
pus the leucocytes promptly decrease if there is free drainage. 
With the formation of pockets of pus the number rises again. 
This was well shown in the case of a horse with shoulder abscess. 
Operations to secure complete drainage were made every few days 
extending over a considerable time. The formation of new pockets 
of pus was shown clearly by the leucocyte count. After drainage of 
_ the pus that had formed, the leucocyte count promptly decreased, 
only to rise again after a day or two due to the formation of other 


98 GENERAL AND INFECTIOUS DISEASES 


pockets. With chronic productive inflammation during suppura- 
tion there is usually a moderate leucocytosis with a high percentage 
of polymorphs. The eosins are usually present in normal or some- 
what increased proportion. The red corpuscles and hemoglobin 
are often reduced, the hemoglobin more than the number of red 
corpuscles. 

The following few cases show the condition found in some of 
the kinds of non-specific infections. The letters in the first column 
are abbreviations of the author reporting the cases: B for Buffing- 
ton, M for Meier, MHC for Moore, Haring and Cady. 


Taste XXIV.—Examp.es or Non-speciric INFEcTIONS 


Varieties of Leucocytes 


. Age|Red Cor-| yp. TSCUCOs | eran ice | aa | GE Pathological 
eearnel = puscles 4 cytes I II III | IV Vv condition 

Geld 12 {5,385,000} 58 | 7,677/38. | 0.9] 57.] 3.8] 0.3] chronic lymphangitis. 

MHC No. 35 

Filly tendo-vaginitis, no 

MHC No. 13} 3 16,560,000] — | 16,266/39.1] 3. |52.6] 4. | 1.3]  suppuration. 

Mare 7 14,880,000} 59 | 19,500}49.1) 4.3/40.8] 4.8] 0.8 fymphangihe, abscess 
ater. 

Mare 14 |8,050,000} 100 | 15,000)12.2] 3.8/83.2) 0.5 Mar. 27 pleuritis, sero- 

M No. 46 fibrinous. 

Mare 6,100,000} 85 | 14,600]/11.3) 4.8/81.5] 1.9 Mar. 28. 

M No. 46 

es te 7,760,000} 95 | 28,800) 4.1] 3. |91.7] 0.5 Apr. 2, died Apr. 2-3. 

{1 No. 

Geld. 14 16,098,000) 78 | 11,000] 8.4] 1.4/90. | 0. | 0. | inhalation pneumonia 

MHC No. 19 and abscesses. Dec. 
U7, WA. 

Geld. 5,578,000} 70 9,722] 8.6] 2.5/88.8] 0. | 0. | Dec. 17,4 P.M. 

MHC No. 19 

Geld. a — — |4 0.8/95.2] 0. | 0. | Dee. 18, 11 a.m. Died 

MHC No. 19 10 Pp. M. 

Horse 13 17,976,000] 86 | 32,555] 6.8] 2.1/90.6] 0.2] 0.2} Nov. 24 thought to be 

B No. 9 acute rheumatism. 

ae : 7,828,000} 84 | 19,558} 8.8] 0.5)90.7] 0. | 0. | Dee. 1. 

3 No. § 

Horse 5,562,000] — | 10,667/11.7] 2.4/84.5] 0.9] 0.5} Dee. 8 diagnosed as 

B No. 9 fistulous withers. 

Horse 5,870,000} 86 8,722/15.6| 5. |76.5] 1.7] 1.2] Dec. 15. 

B No. 9 

Geld. 12 15,750,000] 61 | 20,300]/19.4] 2. 175.9] 2.5] 0.1] fistulous withers. 

Mare 10 |7,900,000| 68 | 12,166]11.8] 4.3/83.5] 0.1] 0.1] fistulous withers. 

Mare 314|8,987,000} 90 | 20,000)14. | 2.4|81. | 2. | 0.6] suppuration, lower 

MHC No. 25 jaw. 

Mare 13 |7,060,000} 61 9,958]16.7} 4.8]/69. 8.5] 0.7] quittor. 

Geld. 7 |7,767,000} 98 HSralZOe |) Qe72e eo. i) Le i equxttor. 

MHC No. 30 

Pig — 16,782,000] 55 | 20,833/18.1] 3. |78.8] 0. | 0. | submucous abscesses, 
gangrene of lip. 

Mare 13 |6,148,000| 69 | 14,180]28.6] 3.5/67.2] 0.7] 0. | chronic suppuration, 
turbinated bones. 

Geld. 12 |6,576,000 20,555/23.4| 0.5/69.5] 6.3] 0.3] fistulous withers both 

B No. 2 shoulders. 

ale 11 17,928,000] 79 | 10,333/26.6] 0.4|70.1} 2.6] 0.3] quittor. 

No. 10 


REFERENCES 99 


REFERENCES 


1. Barnicot, J. The iodine reaction in the leucocytes. Journ. of Path., 
xix, 1906, p. 304. 

2. BREITENSTEIN. Cited by Ewing. 

3. Burrincton, R. M. Clinical examination of the blood of the horse. 
Thesis, N. Y. State Vet. College, 1905. 

4. GerHarpT. Ueber Hydro-bilirubin. Jnaug. Diss. Berlin, 1889. 

5. Hoppr-SeyLter, G. Ueber die Ausscheidung des Urobilins in Krank- 
heiten. Arch. f. path. Anat., exxiv, 1897, 8. 30. 

6. Locke anp Casot. Iodophilia. Journ. of Med. Research, vii, 1902, 
Pp. 25. 

7. Lowit, Die Lehre von Fieber. Jena, 1897, 8. 164. 

8. MaraGuiano. Berlin. klin. Woch., xxiv, 1887, 8. 797. 

9. Meter, P. Beitriige zue vergleichenden Blutpathologie. Zeitschr. f. 
Tiermed., x, 1906, S. 1. 

10. Mosirz. Inaug. Diss. Dorpat, 1883. Cited by Léwit. 

11. Moore, Harina anp Capy. The clinical examination of the blood of 
the horse and its value to the veterinarian. Proceed. Am. Vet. Med. Assn., 
1904, p. 284. 

12. Satkowski. Cited by Ewing. 

13. Stern. Centralbl. f. klin. Med., 1892, Nr. 23. 


CHAPTER VIII 


SPECIFIC INFECTIOUS DISEASES DUE TO BACTERIA 
AND FUNGI 


STRANGLES 


In this disease the blood shows the changes seen in inflammatory 
leucocytosis. With mild cases the red corpuscles and Hb may show 
only slight change. When the temperature is high, the changes 
seen in febrile cases are found in this disease. There may be con- 
centration of the blood. Usually there is moderate anemia with 
a greater relative diminution of hemoglobin. 

The leucocytes are increased (maximum of 13,600—29,400 in 
eight cases reported by Meier). There is a relative and absolute 
increase of polymorphonuclears (maximum 78.2-92.3 in the same 
eight cases). The other varieties are lessened. The eosinophiles 
are decreased or absent during the active stage of the disease. 
After the discharge of the abscess the leucocytes gradually return 
to normal. | 


TasBLte XXV.—CasEs oF STRANGLES (MEIER) 


Varieties of Leucocytes 
Animal SS eee 


Mill. A Fa ae rN 8 

SSS Se ee ee re 
Geld No. 22 4 40C. 8.68 115 5,700 |18.7| 8.8|72.3 June 23. 
Geld No. 22 39.6 6.5 75 15,820 |15.5| 6.6)76. 1.6 June 29. 
Geld No. 22 38.7 6.85 90 14,500 July 2. 
Geid No, 22 37.8 CP? 95 20,000 | 9.3] 2.7/87.2| 0.5 July 5. 
Geld No. 22 38.6 8.4 100 11,700 |24.2| 6. |67.9) 1.1 July 7. 
Geld No. 20 8 38.5 6.8 75 20,000 | 9.1; 3.3)87.5 Oct. 21. 
Mare No. 21| 7 39.2 6.15 80 19,320 | 7.3) 3.1]88.3} 0.7) Oct. 5. 
Mare No. 24] 4 38.2 7.6 75 16,400 |15.8 1.7)80 2,2, Feb. 22. 
Geld No. 25 8 38.9 7.078 90 15,000 | 9.6) 4.2/85 3 0.4 Nov. 4. 
Geld No. 27 8 39.3 8.23 13,900 | 5.1) 2.4/92.3) 0.1) Dec. 10. 
Mare No. 29} 5%} 40.5 7.43 100 20,000 |} 4.3] 8.1/87.4 Dec. 3. 
Mare No. 29 39.6 11.9 115 18,300 | 6.3) 5. |88.6 Dee. 5. 
Mare No. 29 40.3 13. 1 125 26,170 | 3. 5. 191.7 Dec. 7. 
Mare No. 29 39.5 13.76 150 21,400 | 3.8 6.2/90.1) Dec. 10. 
Mare No. 29 40.8 | 18.8 155 | 14,720 | 2.5] 3.4\94: | Dec. 12. 


The above table shows the changes in the blood in cases of 
strangles. In No. 22 there was a hard and painful swelling of the 
throat glands on June 29th. On July 2d the swelling was cireum- 

109 


CROUPOUS PNEUMONIA IN HORSES 101 


seribed and about the size of an apple. The case was discharged 
from the hospital on July 10th as recovered. Nos. 20, 21, 24, 25 
and 27 show the condition of the blood at the height of the leu- 
cocytosis. No. 29 was a case of strangles with necrotic pneumonia; 
died Dec. 13th. Note the excessive polycythemia. 


CROUPOUS PNEUMONIA IN HORSES 


Though an anemia is shown in cases of pneumonia the diminu- 
tion in red corpuscles and Hb is not as a rule shown during the 
early stages of the disease. Often a considerable polycythemia is 
evident, due to the concentration of the blood by the fever, by 
exudation and vasomotor influences. In five fatal cases reported 
by Meier the polycythemia continued to the time of death and 
reached 9,760,000—13,400,000 corpuscles; 110-125% Hb. Four of 
these were necrotic or gangrenous. The other case was a double 
sided pneumonia. In Meier’s non-fatal cases a lesser grade of 
polycythemia occurred in five cases and was of shorter duration 
than in the fatal cases. In four cases there was no polycythemia. 
In all of the non-fatal cases but one an anemia was shown during 
the latter part of the disease. In most cases the anemia was 
moderate, to 65 or 70%; in one case, chronic pleuro-pneumonia, 
the red corpuscles were reduced to 3,600,000 with 50% Hb. 

Leucocytosis appears very early in the course of the disease 
except in very severe cases in which the leucocytes instead of 
increasing show a diminution. In such cases the prognosis is bad. 
In a case reported by Meier there was a stage of leucopenia pre- 
ceding that of leucocytosis, but in the majority of cases reported 
there was leucocytosis at the time of the first examination. In 
man leucocytosis appears very early, at the time of the chill 
(Klein), preceding the exudation (v. Limbeck). The degree of 
leucocytosis is usually considerable, 12,000-59,600 in Meier’s 
eases. Leucocytosis does not run parallel with the rise of tem- 
perature as is shown by the following cases. V. Limbeck pointed 
out that the extent of exudation has much more influence. The 
polymorphs are much increased relatively and absolutely. Meier 
found 75.6—92.59% polymorphs. The lymphocytes are correspond- 
ingly decreased. The large mononuclears are usually within the 
normal percentages, but are sometimes both relatively and abso- 


102 SPECIFIC INFECTIOUS DISEASES 


lutely increased. In none of the cases recorded have they been 
absolutely diminished. The eosinophiles are usually few in num- 
ber or absent during the height of the leucocytosis. As the leu- 
cocytosis declines the percentage of polymorphs diminishes while 
that of the lymphocytes shows a corresponding increase. 


Tarn_e XXVI.—Crovpous Pneumonia IN Horses (MEIER) 


Varieties of 


os Age Red Cor. Leuco- Leucoevtes 
Animal sa Temp. Mill Hb. erten y 
I LP) LN tg 
Geld. No. 35 6 40.8 7.6 90 15,500/11.9} 6.1/81.9 Feb. 2 

40.6 6.4 ThCK 15,700}12.2) 5.3}82.2 Feb. 4 

40.1 6.4 75 23,000} 8. 4. |87.4] 0.4] Feb. 6. 

40. 5.5 67 23,300] 8.5} 0.7/90.1} 0.3] Feb. 10. 

38. 6.7 77 12,870]19.5] 1.7|77.5| 0.7| Feb. 16, dis- 
charged on 
Feb. 18 as 
cured. 

Geld. No. 37 6 40. 7.06 17,240]13.7| 7.8|78.1 July 19. 

39.2 6.6 85 20,100]12.9]10.1/82. | 0.4} July 21. 

38.4 6.4 85 16,500]13.5}) 7. |77. | 2.3] July 22. 

37.8 6.56 90 10,000}18.8} 3.8|74 3.8] July 25, dis- 
charged. 
July 26. 

Mare No. 38] 13 11.4 115 5,400 Jan. 24. 

40.9 13.4 125 5,000 Jan. 25, died 
during the 
night. 

Mare No. 42 5 40.5 10.25 120 12,000)26.5] 4.4/68. Jan. 30 

41. 9.6 125 13,500|20 3} 5.4174. |0.07| Feb. 1 

40. 9.8 115 13,700}25.3} 4.9/69. 3} Feb. 2 

39.9 9.94 115 42,240] 9.3] 4.3/86.2 Feb. 4. 

40.1 10.05 120 59,600] 7.1] 3.3]/89.4| 0.1] Feb. 6, died 
during the 
night. 


TAKOSIS 


Mohler and Washburn in the investigation of this disease made 
a few examinations of the blood. One goat examined during the 
later stage of the disease had 11,208,000 red corpuscles. This 
animal was suffering from profuse diarrhea. In two experimental 
cases, suffering from profuse diarrhea, the first had 11,190,000 red 
corpuscles and 20,560 leucocytes and the second 12,160,000 red 
corpuscles and 18,420 leucocytes. The leucocytosis in both cases 
was due chiefly to an increase in the polymorphs and eosinophiles. 
In another case, natural infection, the red corpuscles were 
10,208,000 and the leucocytes 14,860. Mohler and Washburn give 
the normal number of red corpuscles for the goat as 9,976,000 and 
of leucocytes 9,200. Storch gives the normal numbers as 14,567,000 
and 12,057. But little change in the number of red corpuscles is 
apparent from the examinations made. With violent purgation 


FOWL CHOLERA 103 


one would expect to find a polycythemia. The clinical symptoms 
would lead one to expect an anemia to be present, the effect of 
which is masked by the effect of purgation. Mohler and Washburn 
state that poikilocytosis is shown in the later stages of the disease. 
A greater number of examinations and a more detailed study of the 
blood in the various stages of the disease are needed. 


FOWL CHOLERA 


In this disease the changes in the blood in the cases of natural 
infection in which examinations have been made are those of 
anemia with moderate leucocytosis. In two cases naturally in- 
fected Ward reports the following: 


Fowl A red cells 1,710,000 leucocytes 58,000. 
“ B« “ 1995000 “ 45,000. 
In three cases infected by ingestion he obtained the following 
counts: 
No. 3 red eaU8 2,290,000 leucocytes 23,000 3 days after exposure. 


No.3 “ 2,800,000 20,000 4 days after exposure. 
No.6 “ “ 3,980,000 “s 37,000 3 days after exposure. 
No.8 “ “ 4,490,000 oe 87,000 3 days after exposure. 
INoxse +. — “2°960:000 cK 101,000 4 days after exposure. 


In five cases inoculated with cultures of fowl cholera bacteria, 
Ward found the following conditions: 


TaBLeE XX VII.—ExXPpERIMENTAL Cases OF Fowi CHOLERA (WARD) 


No. Red Cells Leucocytes 

11 2,980,000 24,000 normal. 

11 3,380,000 19,000 23 hours after inoculation. 

13 3,300,000 12,900 before inoculation. 

13 3,310,000 14,200 24 hours after inoculation. 

13 3,046,000 25,700 died following day. 

16 3,920,000 61,000 normal. 

16 1,880,000 15,000 36 hours after inoculation. 
died night following. 

17 2,380,000 30,000 normal. 

17 1,590,000 22,750 30 hours after inoculation. 

17 1,700,000 14,500 48 hours after inoculation. 


A study of the variety of leucocytes was not reported. 


104 SPECIFIC INFECTIOUS DISEASES 


FOWL TYPHOID (Infectious leukemia in fowls) 


Examinations of the blood in cases of this disease were made in 
experimental cases by Moore and later by Taylor. They both 
found that there is a progressive decrease in red cells and a steadily 
increasing number of leucocytes. That is, there is ‘a leucocytosis 
accompanied by a marked anemia. Taylor made differential 
counts of the varieties of leucocytes. The increase in leucocytes 
is in the polymorphonuclears. The high number of leucocytes 
found in the last stage of the disease is interesting. Death seems 
to have been a gradual dissolution. Evidently the high leucocyto- 
sis is an antemortem one. 


Taste XXVIII.—Fow.t TypHorw (Moore) 
Fowl lRed Cells 


et Date | Temp. Millions Leucocytes 
82 6- II | 107.4 3.7 21,222 | inoculated 6-II. 
7 II | 109. 3.4 26,087 apparently well. 
8— II | 108.2 Ded 55,000 | apparently well. 
9- II | 108.4 2.8 76,925 apparently well. 
11- II | 107.4 3.4 90,909 feathers ruffled; refuses 
food. 
13- II | 110.2 2:1 100,000 | very quiet, comb pale. 
14— II | 108 250 140,000 | died later in the day. 
501 | 26-III | 106.2 3.5 18,940 | fed culture 26-III. 
28-III | 110 2.4 70,000 | eats very little. 
2-IV | 110.6 1.6 80,000 | blood very pale, fowl weak, 
refuses food. 
3-IV | 106 Wht 245,000 very weak. 
4-IV found dead. 
80 108.7 2.0 11,636 | 2nd day after inoculation. 
109 1.38 56,000 | 5th day after inoculation. 
109.5 15 115,000 | 6th day after inoculation. 
died during night. 
83 106.5 3.7 14,474 inoculated same day. 
109.7 2.2 83,333 3d day after inoculation. 
OR Z WAGE 150,000 6th day after inoculation, 
died next day. 
500 106.1 4.5 26,666 fed culture same day. 
108 .2 2.9 94,166 | 4th day after. 
107 3.6 42,000 10th day after, recovered. 
507 111.6 an 1325383 6th day after fed culture. 
110.4 1.8 138,000 Sth day after fed culture, 


died during night. 


La 
: 


adbeedibecetad 


ANTHRAX 105 


TasLe XXIX.—DIFFerRENTIAL Leucocyte Counts IN EXPERIMENTAL CASES 
or Fowt TypHor (Taytor) 


Varieties of Leucocytes 
Fowl | Red Cells Leu- 


No. | Millions | cocytes Large Poly- : Mast 
ESE Mono. | morphs LEGSHES Cells 

I 2.592 89,440 23.2 4.2 67.2 1.8 3.5 
Il 2.392 192,000 18.3 rae | Ohok 0.4 1.5 
Ill 2.017 74,680 31.6 7.8 53.1 5.7 1.8 
EY: 1.72 138,670 21.2 3.6 88.1 2.2 4.8 
V 2.068 ~ 72,300 20.5 15.7 63.5 0.1 0.1 


In the above table the counts of red cells are given at the time 
of the greatest diminution while the leucocytes are at the time of 
the greatest increase. These occur on the same date. Cases I 
and III recovered. The examinations of the other cases were made 
No. II six days before death, No. IV the day before death and 
No. V six days before death. 


ANTHRAX 


- In cattle and sheep the blood is extensively invaded by anthrax 
bacteria a short time before death; in the horse microscopical 
examination will reveal the bacteria in the blood in the great 
majority of cases, while in the pig death occurs in a large proportion 
of cases while the blood is still free from bacteria (M’Fadyean). 
Diagnosis is most readily and surely made in cattle, sheep and in 
the majority of horses by making a microscopical examination of 
the blood. Not finding the anthrax bacteria in cattle and sheep 
at the time of death warrants stating that the case is not one of 
anthrax (M’Fadyean). Anthrax bacteria have been found in the 
circulatory blood of cases that recovered during the early stage. 
of the febrile period. 

The microscopical examination is made of smear preparations of 
blood (peripheral blood is to be preferred to that from the large 
vessels), made in the usual way and stained with Jenner’s, Wright’s 
or M’Fadyean’s methods. Jenner’s stain I have found preferable 
to Wright’s, except where the blood is fresh or from an animal 


106 SPECIFIC INFECTIOUS DISEASES 


that has been dead but a short time. If the blood is fairly fresh, 
the capsules of the anthrax bacteria will show well, while if the 
bacteria show disintegration, violet masses, first described by 
M’Fadyean, will be found lying near the anthrax germs. M’Fad- 


Skee, 
2 


Fic. 11. Blood of case of anthrax, cow, two hours before death. x 650. 


yean’s method is an excellent one and has the sometimes im- 
portant advantage of using a thick smear. A thick smear of the 
suspected blood is made on a slide or cover glass. A slide is pref- 
erable as it is more convenient not to mount the stained specimens. 
The smear should be dried in the air quickly, or over a small 
flame, then should be incompletely fixed by heat. The heating 
should be sufficient to fix the film to the glass; but should not be 
enough to prevent the Hb in the red corpuscles becoming dissolved 
during the subsequent staining and washing. Fixation is secured 
by passing the slide, smear side up, through the flame of a Bunsen 
burner or alcohol lamp for a second and repeating three times. 
The under surface of the slide is just too hot for the hand to bear. 


ANTHRAX 107 


The proper temperature is readily found by a little practice. After 
fixation the smear is stained for a few seconds with an old one per 
cent. aqueous solution of methylene blue, or Loeffler’s alkaline 
methylene blue. An old solution is better than a freshly prepared 
one. The staining solution must contain polychrome methylene 
blue. A one per cent. solution of methylene blue if made from the 
pure stain is apt not to give good results. I have obtained much 
better results from Loeffler’s alkaline methylene blue. The stained 
smear is thoroughly washed in tap water, then blotted to remove 
the excess of water and then dried in the warm air over a flame. 
Drying should be done rapidly. The anthrax bacteria and nuclei 
are stained blue. The characteristic reaction is a violet or reddish 
purple color of the amorphous material about or near the anthrax 
bacteria. 

With any of the stains mentioned, Jenner’s, Wright’s or M’Fad- 
yean’s, the larger putrefactive bacteria having square ends should 
not be mistaken for anthrax bacteria. Where both are present 
in the same specimen the difference between them is seen to be 
considerable. The putrefactive germs stain more deeply and uni- 
formly. When putrefaction has begun, the anthrax bacteria show 
considerable degenerative changes. 

The changes in the blood in cases of anthrax are often slight. 
Schindelka found a constant increase in Hb in horses. An anemia 
has been found in the cases in cattle reported. In an acute case, 
in a cow, which died the day after the first symptom was observed, 
the red corpuscles were 4,072,000 while the Hb was normal. 
Hemoglobinuria was not observed in this case; but there may have 
been Hb in the blood plasma. In a cow that died the third day 
after the first symptom appeared, the red corpuscles were 5,156,000, 
the Hb 48%. In four cows that recovered, both the red corpuscles 
and Hb were diminished moderately during the febrile period. In 
a cow examined two hours before death, temperature 106.6°F., 
the leucocytes numbered 20,000, the lymphocytes and _ eosins 
showed an absolute increase, while the polymorphs and large 
mononuclears showed both a relative and absolute increase. This 
leucocytosis was probably an antemortem one as in another fatal 
case examined the day before death, temperature 107.6, there were 
7,222 leucocytes, which is within the normal limits for cattle. In 
this case the polymorphs were in less than the normal proportion. 


108 SPECIFIC INFECTIOUS DISEASES 


Taste XXX.—ExXaMINATIONS OF Two Fatat AND Four nor Fatat Cases oF ANTHRAX 


IN CATTLE 
Red Varieties of Leucocytes 
No. Date | Temp. Cor Hb sae 
Mill MST OG ea nai 
1 9-VII | 106.6 4.07 60 20,000}35.4}11. |35.6]17.6} 0.4] first symptom 8-V1I, 
died 2 hrs. after exam. 
2 28-VII | 107.6 5.15 48 7,222|67.7| 6.1] 9.8)15.5) 0.7 piri a ee 26-VII, 
ied 29-VII. 
3 14-VII | 101.2 4.16 57 5,222|64.2} 5. 127.8] 2.8] 0.2) first symptom 29-VI, 
recovered. 
4 9-VII |} 104 3.87 50 8,222]47.8] 3.6]41.8] 6.3] 0.5) first symptom 7-VII, 
Bact. anth. in blood. 
11-VII 3.95 60 5,210/43.9] 6.5]/40.6] 8.3] 0.7 
13-VII | 101.8 40.1] 4. |47.2| 7.8] 0.7 
14-VII | 101.2 3.48 47 5,666/50. | 2.1/39.2) 7.6) 1.1 
19-VII 54 8,777|42.7| 3. |31.9]22. | 0.4 
24-VIT Srila 63 11,888|50.7] 5.8}26.2/16.3] 0.7] recovered. 
5 10-VII | 106.2 27.4) 5.2/64.8] 2.8] 0.2] first symptom 10-YV. 
11-VII 5.47 56 4,814|34.7| 7.1/45.7/11.4] 1. 
13-VII | 103 3.4 38 3,444/41.6] 7.6]48.4]) 2.2) 0.2 
19-VII 50 9,876]43.1] 2.7]47.5] 6.4] 0.1] recovered. 
6 16-VII | 103.8 53 8,111]43.5] 1.9}37.4|16.4| 0.8] first symptom 15-VII. 
Bact. anth. in blood 
on 15-VIL. 
17-VII | 101. 58 5,333/53.1) 4.8]29.4)12. | 0.7 
18-VII | 102. 8,163})78.1) 1.7)11.2| 9. 
19-VITI 5.94 11,000|60.1| 2.3)23.5)13.6] 0.5 
24-VII 61 10,767|54.9] 4.5]20.3)19.5] 0.8] recovered. 
GLANDERS 


There is generally more or less anemia present in cases of 
glanders. In some cases, serious ones, the anemia may be masked 
by a polycythemia due to concentration of the blood by loss of 
fluid from it. 

Mikrukow found in horses and cats that the red corpuscles are 
diminished in two to three days after infection and sink toward 
the end of the disease to one-third the normal number, that the 
hemoglobin decreases gradually and that the red corpuscles are 
of smaller size in glandered than in healthy animals. Schindelka 
includes glanders among the diseases in whose course there is a 
decrease of hemoglobin. Prus reports that the red corpuscles are 
diminished to 4-5 millions and that the blood plates are increased 
to 700,000-1,600,000 per emm. Burnett and Pearce found a 
moderate anemia in the greater number of their cases. In one of 
their cases, a very pronounced one, there was a moderate poly- 
cythemia. The animal, an aged mare, was much emaciated. Evi- 
dently the polycythemia was due to withdrawal of fluid from the 
blood by exudation. Mielke did not find the red corpuscles dimin- 
ished in any of his cases except one which also had petechial fever. 


GLANDERS 109 


The number of red corpuscles is high in most of his cases, highest 
in the cases with the highest leucocyte count. Probably the 
polycythemia in these cases was due to anhydremia, but not 
enough of the clinical condition of the cases is given to enable one 
to tell. 

There is a polynuclear leucocytosis in active cases. Mild cases 
may have no increase in the leucocytes. Other varieties of leu- 
cocytes are usually not increased. The more severe the case the 
greater is the increase in the polymorphonuclears. In severe, 
actively progressive cases, the eosinophiles may be absent or 
present in very much smaller number. The condition is an in- 
flammatory leucocytosis. In non-clinical cases there may be no 
increase in the number of leucocytes. Macchia found the leu- 
cocytes increased twenty four hours after inoculating an ass. The 
third day there were 17,500 per cmm., the sixth day 31,250, the 
eighth day 34,792, the ninth day 60,000. The fourteenth day the 
ass died of acute glanders. Mikrukow examined glandered horses 
and cats and found that the leucocytes increased till toward the 
end of the disease when they were at least three times the normal 
number. Noniewicz examined three glandered horses and found 
the leucocytes increased, in a case of chronic farcy in the propor- 
tion of one leucocyte to twenty red corpuscles and in a case of 
chronic glanders, early stage, in the proportion of one to thirty. 
Prus found that the leucocytes were increased in glandered horses 
to 20,000—60,000 and that the polymorphonuclears were in greater 
than normal numbers and percentages. He obtained the following 
percentages: eosins 3 per cent., mast cells 2 per cent., basophile 
cells 5 per cent., neutrophiles 75 per cent., small lymphocytes 10 
per cent., large lymphocytes 2 per cent. and transitional cells 3 
per cent. Bidault found a polynuclear leucocytosis in horses. 
Mielke examined 19 glandered horses and found a polynuclear 
leucocytosis in each case. The leucocytes varied from 14,000 to 
48,200 per cmm. The polymorphs ranged from 11,802 to 42,271 
per cmm. 

Burnett and Pearce found a polynuclear leucocytosis in severe 
cases of glanders in horses. Mild cases did not have an increase 
in the leucocytes. A summary of Burnett and Pearce’s cases is 
given in tables XX XI and XXXII. Christot and Kiéner report a 
leucocytosis in acute glanders in man, horse and guinea pig, and 


110 SPECIFIC INFECTIOUS DISEASES 


in chronic cases in two horses and a guinea pig. In acute glanders 
in man a polynuclear leucocytosis has been observed: Cabot found 
11,600—13,600 leucocytes of which 86% were polymorphs, Coleman 
and Ewing found 13,000 and Wherry found 21,000—23,400. 

Mallein was observed by Bidault to produce a leucocytosis 
which is preceded by a moderate leucopenia. The leucocytosis 
was essentially polynuclear though in non-glandered horses the 
mononuclears also were increased. In glandered horses, the poly- 
nuclear leucocytosis was much more pronounced. Burnett and 
Pearce and Mielke found the leucocytes increased in glandered 
horses following the administration of mallein. The polymorphs 
were uniformly affected, the other varieties sometimes increased 
and sometimes decreased. 


Taste XXXI.—SummMary or EXAMINATIONS OF THE BLOOD OF GLANDERED 
Horses (BURNETT AND PEARCE). 


Red Cor- 

Case} ., Temper-| puscles Leuco- 

No. | 5° Age ature | Millions |°Ytes Pe Remarks 
per emm,| °™™- 

1 | G. +) old || fluct: 6.14 6,640 | No symptoms except off feed. 

Ze Gan eel Omepersis: 6.17 9,555 |Submax. gl. enlar., nasal dis- 
charge. 

Sue woldel OD: Gate 20,750 | Emaciated; lymph gland en- 
largement, ulcers, nasal dis- 
charge. 

4/F. |} old | 103. 6.5 6,000 | Symptoms, 1 mo. later no dis- 
charge. 

Dy Gree aa PaO Ze 6.5 9,422 | Few farcy buds. 

GaeG. |) vo.) L022 7.14 7,600 | No clinical symptoms. 

Ch WCC OS oh is) 6.3 12,000 | No clinical symptoms. 

i 105.4 6.28 15,000 | During mallein reaction. 

8 | F. | old | 104.5 6.0 16,000 | Ulcers, enlar. gland, nasal disch. 

OAiG, 5 | norm. 6.5 6,500 | No clinical symptoms, no mal- 
lein reaction. 

10 | G. 5 | 103. 6.4 14,000 | Submaxillary gland enlarged. 

11 | G. | old | 104. 4.19 8,666 | Much emaciated; farey. 

12 re Olde Ope 5.6 25,000 | Acute case. 

13) Ge elo | LOSn> 4.7 8,000 | Nasal discharge, sears. 

14 seth Le? 7.42 12,000 | No clinical symptoms. 

15" | Golds) 103; 6.5 10,000 | Lymphatic swellings. 

16 | °G. 8 | norm. 6.97 8,444 | Nasal discharge, indur. lymph 
gland. 


TUBERCULOSIS 111 


TaBLE XX XII.—TueE LevcocyTes IN CASES OF GLANDERS IN Horses (BurR- 
NETT AND PEARCE). 


Varieties of Leucocytes 
Case} Leuco- 


No. | cytes per Lymphocytes|Large Mon.} Polymorph. | Eosins_ |Mast Cells 


cmm. % No. eNO: Cr aeNO: % No.|% No. 
1 6,640 | 30 1,992} 5.8 385|/61.5 4,084/2. 133] -4 27 
2 9,555 |18 WPA)! Be Sn yey. M7 Ah) Bae || ail 10 
3 | 20;750 |15. 3,118) 4.5 934) 80. 16,600 ae 
4 6,000 | 30 1,800 | 11. 660) 58. 5 35480) 29 54) -3 18 
5 9,422 |22. 2,074) 10. 9AD6D. G6 124 12 94) .1 9 
6 C00 | 2625" 976 a8. 5938) 55. 4.180) 92 61455 38 
7} 12,000 | 14. - 1,680] 4.7 564/79. 9,480)1.3 156] .3 36 
eel OOO pi 2 ease Ie SOOl is 3: 450/84. 12,600} .09 14] .16 24 
Sie GO OOOhs Miles 1760) 5: SOONS2) 135120) (45) 72)|25 80 
9 6,500 |} 24. 1,560] 6.9 449/61. 3,965|6.3 410) .59 38 
HOD) 14.000) | 19 = 2'660)) (3.7 S18) 745 103560) 27 98-7 98 
vil 8,666 | 23. OOS | ORON eAWG | OSeam a 894)| le 2a OAs 7 61 
eo OOF Ore 22250) ort te S50r | Soa2 216250 
13 8,000 | 23. 1,840} 5.7 456/68. 5,440)2.2 176) .5 40 
14 | 12,000 |} 13. ILo0)|| 4b GSP. CHOON sey (at) 8? 36 
15 | 10,000 | 12. 1200} set 340) Sle 200) eon OOl el Onl 
16 8,444 123.8 2010] 5.2 439)]67.6 5,708|3.2 270) .2 17 


TUBERCULOSIS 


Much fewer cases of blood examination have been reported for 
tuberculosis in animals than for glanders. An anemia usually 
moderate but occasionally very severe is ordinarily found in un- 
complicated eases of the chronic disease. The Hb suffers relatively 
greater diminution than the red corpuscles. In man the majority 
of the cases of chronic phthisis show but little change in the 
number of red corpuscles and amount of Hb, though the patient 
may be pale and emaciated. In such cases the normal counts are 
explained by there being a loss of fluid from the blood which 
masks the loss of red corpuscles and Hb. This oligemia is due 
(Ewing) ‘‘to the specific lymphogogic action of the toxins of the 
tubercle bacillus, by which there is established a continuous 
excess in the balance of fluids which leave the tissues through the 
lymphatics.” ‘In the majority of cases of well-advanced phthisis 
(in man) therefore, approximately normal blood indicates con- 


112 SPECIFIC INFECTIOUS DISEASES 


siderable absorption of the toxins of the tubercle bacillus” (Ewing). 

In cases of tuberculosis with secondary infection the blood 
may exhibit the changes found in infection with pyogenic or- 
ganisms. These, however, are not so common in the domesticated 
animals as in man. Ordinarily only slight changes in the size 
and form of the red corpuscles are seen. Poikilocytosis and 
marked changes in the size of the red corpuscles may be found in 
cases of severe anemia. Nucleated red cells are as a rule not found. 
The fibrin is not increased except in cases of secondary infection. 
The blood plates were found by Webb, Gilbert and Havens to be 
increased in guinea pigs to 468,000-776,000 with an average of 
622,000 per cmm. in eleven cases. 

Ordinarily the number of leucocytes is diminished with a 
relative lymphocytosis. In a proportion of generalized cases the 
leucocytes may be increased, though as a rule there is leucopenia. 
The proportion of polymorphs is sometimes above the normal. 
In a dog with generalized disease I found 3,050,000 red corpuscles 
and 4,100 leucocytes. A differential count of the leucocytes gave 
15.6% lymphocytes, seven per cent. large mononuclears, 74.4% 
polymorphs, 2.8% eosins, and 0.2% mast cells. Courmont and 
Lesieur found 88% polynuclears in a tuberculous dog. Webb, 
Gilbert and Havens found the leucocytes increased in tuberculous 
guinea pigs to 10,000-15,000 with an average of 13,200 per emm. 
in eleven cases. Moore and Ward examined the blood of tuber- 
culous fowls and found from 1,010,000—2,600,000 red cells and 
from 35-70% hemoglobin. The leucocytes appeared to be slightly 
increased. Ellermann and Bang state that there is ordinarily an 
increase in the number of leucocytes in tuberculous fowls. The 
increase is in the polymorphonuclears. 

Arloing and Courmont found that the serum from tuberculous 
subjects would agglutinate cultures of tubercle bacilli. Similar 
results have been obtained by other investigators; but agglutina- 
tion could not be obtained by several others. At present the 
agglutination test has not been sufficiently elaborated to be of 
clinical value. 


TETANUS 


In two cases in the horse (Meier) and in three in man (Cabot) 
a leucocytosis was present. In the horse the red corpuscles and 


ACTINOMYCOSIS 113 


hemoglobin were normal. In the human cases the hemoglobin was 
moderately reduced. The following table shows the result of 
the examinations in Meier’s cases: 


TaBLE XXXIII.—TerTaNus 1n Horses (Meter) 


@ Red | re | nee Varieties of Leucocytes 
ss eatahe Pall al Area | RS eh ebb Te how 
Mare No. 51} 25-X 2138.5} 7.0 90; 12,400 dischargedas 
: cured 3-XI. 
1-XI 8.65 |115) 12,240)25.2] 4.4/68.8] 1.2 
Mare No. 52| 3-XII |18 9.47 |110| 24,698] 4-1] 0.9/4.8] | —_ died 14-XIL. 


Three fatal cases in man treated with antitoxin showed the 
following (Cabot) : 


Pee Pe as Pea go kG d Seo 6, 21-VI 11,100 70 
23-VI 11,900 
0 ai cea a 19,600 
ja) [LT Weg anos Ae Baier 18,200 80 
ACTINOMYCOSIS 


In a case of actinomycosis of the jaw in a cow, Dimock and 
Thompson found 5,443,000 red corpuscles, 58% Hb. and 7,222 
leucocytes. Of the leucocytes there were 43.6% lymphocytes, 
0.36% large mononuclears, 53.1% polymorphs, 2.27% eosins, 
and 0.54% mast cells. Ewing found 21,500 leucocytes in a case 
of pulmonary actinomycosis in man. Bierfreund found marked 
anemia of chlorotic type with 30-50% hemoglobin in man. Cabot 
examined the blood of four cases in man and obtained the following 
counts of leucocytes: 


IMGseICHeMAIC seit e mee, oe base: 31,700 18-VI 

28,400 19-VI 

28,200 25-VI autopsy. 
Nos 2 spulmonainy. meen 4) aie 20,800 Apr. 

23,000 Aug. autopsy. 
IPT ONS fe) 072 Oe 12,500 
INGs: 4; pUlMOnaye cise oucvels. cece 12,200 11-VIII 


21,000 15-VIII 
26,000 17-VIII 


114 SPECIFIC INFECTIOUS DISEASES 


BOTRYOMYCOSIS 


In two cases of extensive botryomycosis of the skin in horses, 
reported by Mielke, the red corpuscles were 8 and 8.8 millions and 
the leucocytes 24,000 and 23,200 per cmm. Mielke states that 
the red corpuscles were normal. In one case the varieties of leu- 
cocytes per cmm. were, lymphocytes 5,208, large mononuclears 
none, polymorphs 18,408 and eosins 384; while in the other case 
there were, lymphocytes 3,016, large mononuclears 464, poly- 
morphs 19,720 and no eosins. There were no mast cells in either 
case. These two cases showed a polynuclear leucocytosis. 


HERPES TONSURANS 


Meier reports a case in a gelding five years old, with 8,120,000 
red corpuscles and 8,500 leucocytes. Of the leucocytes there were 
16.1% lymphocytes, 3.5% large mononuclears, 75% polymorphs, 
and 5.4% eosins. 


REFERENCES 


1. ARLOING ET CourmontT. Etude sur la recherche et la valeur clinique 
de l’agglutination du bacille de Koch par le serum sanguin de homme. Con- 
gres pour l'étude de la tuberculose, 1898, p. 586. 

2. Bipauut, C. Recherches sur les leucocytes du sang du cheval et sur 
certains leucocytoses experimentales. Arch. d. med. exper., xvi, 1904, p. 354. 

3. Brerrreunp. Arch. f. Chirurg., xli, cited by Ewing. 

4. BurNeTT AND Pearce. A clinical examination of the blood of glandered 
horses. Proceed. Am. Vet. Med. Assn., 1908, 270. 

5. Curisror rT Kifiner. De la présence des bactéries et de la leucocytose 
concomitante dans les affections farcino-morveuses. Compt. rend. Acad. d. 
Sciences, Paris, xvii, 1868, p. 1054. 

6. CoLEMAN AND Ewrna. A ease of septicemic glanders in the human 
subject. Journ. of Med. Research, ix, 1903, p. 223. 

7. CourmMonT ET LesteuR. La polynucléose de la rage. Journ. d. Physiol. 
et d. Path. gen., iii, 1901, p. 599. 

8. Dimock AND THompson. Clinical examination of the blood of normal 
cattle. Am. Vet. Rev., xxx, 1906, p. 553. 

9. Duvau, GASNE ET GuILLemMor. Observations de morve aigue humaine. 
Arch. d. med. exper., viii, 1896, p. 361. 

10. Kiern. Cited by Ewing. 

11. V. Limpeck. Klinisches und Experimentelles tiber die entzundliche 
Leucocytose. Zeitschr. f. Heilk., x, 1889, S. 392. 


REFERENCES 115 


12. Maccnta. Untersuchungen uber Leucocytose. Il nuovo Ercolani, 
1903, p. 468. Abstr. in Jahresbr. Vet. Med., xxiii, 1903, S. 38. 

13. Merer, P. Beitrage zur vergleichenden Blutpathologie. Zeit. f. 
Tiermed., x, 1906, 8S. 1. 

14. Mre.xr, Geore. Blutkérperchenzalungen bei Rotz und differential- 
diagnostisch in Betracht kommenden Krankheiten des Pferdes. Monats. f. 
prakt. Tierheilk, xxiv, 1913, 1. 

15. M’Fapyran, J. A peculiar staining reaction of the blood of animals 
dead of anthrax. Journ. of Compar. Path. and Therap., xvi, 1903, p. 35. 

16. M’Faypean, J. A further note with regard to the staining reaction of 
anthrax blood with methylene blue. Journ. of Compar. Path. and Therap., 
xvi, 1903, p. 360. 

17. M’Fapyran, J. Preliminary note on the sero-diagnosis of glanders. 
Journ. of Compar. Path. and Therap., ix, 1896, p. 322. 

18. Mixruxow. Ueber die Veranderungen der Zahl, Form und Wider- 
standsfahigkeit der rothen Blutkérperchen unter dem Einfluss des Rotz- 
contagiums. Compt. rend. Chark. Vet. Inst., 1891 (abstr. in Jahresbr. d. Vet. 
Med., xi, 1891, S. 33.) 

19. Monier aND WasHpurN. ‘Takosis, a contagious disease of goats. 
Bull. 45, Bur. Anim. Ind. U.S. Dept. Agr., 1903. 

20. Moors, V. A. Infectious leukemia in fowls. 12th and 13th Ann. Rep. 
Bur. Anim. Ind., U. S. Dept. Agr., 1895-96, p. 185, also Path. of Infect. Dis- 
eases, 3d edn. 1908, p. 114. 

21. Moore, TayLor AND GitTNER. The agglutination method for the 
diagnosis of glanders. Am. Vet. Rev., xxx, 1906, p. 803. 

22. MoorE AND WarD. Avian tuberculosis. Proceed. Am. Vet. Med. Assn., 
1903, p. 169. 

23. Nonrewicz. Bakteriologische Untersuchungen des Blutes beim Rotz. 
Arch. f. Vet. Med., 1891 (abstr. in Jahresbr, Vet. Med., xi, 1891, S. 34.). 

24. Prus, J. Uber die Wirkung des Malleins auf das Blut und iiber seinen di- 
agnostischen Werth. Oesterreich. Zeitschr. f. wissen. Tierheilk., vi, 1894, 8. 106. 

25. ScHinpELKA, H. Hamometrische Untersuchungen an gesunden und an 
kranken Pferden. Oesterreich, Zeitschr. f. wissen. Tierheilk., ii, 1888, 8. 119. 

26. Scuntrer. Zur diagnostischen Verwerthung der Rotzagglutination. 
Centralbl. f. Bakter., xxxix, 1905, S. 180. 

27. Scuttz unp Miessner. Zur Serodiagnose der Rotzkrankheit. Arch. 
f. wissen. Tierheilk., xxxi, 1905, 8. 353. 

28. Srorcu, A. Untersuchungen tiber den Blutkérperchengehalt des 
Blutes der landwirtschaften Haussiugetiere. Inaug. Diss., Bern, 1901. 

29. Taytor, W. J. A report upon an outbreak of Fowl Typhoid. Journ. 
Am. Vet. Med. Assn., xlix, 1916, 35. 

30. Warp, A. R. Fowl cholera. Bull. 156, Agr. Exp. Sta., Coll. of Agr. 
Uni. of Cal., 1904. 

31. Wess, GitBeERT AND Havens. Blood platelets and tuberculosis. 
Trans. Natl. Assn. for Study and Prevent. of Tuberc., 10, 1914, 180. 

32. Wuerry, W. B. Glanders: its diagnosis and prevention. Bull. 24, 
Bur. Govt. Lab. Dept. of Interior, Phil. Isl., 1904. 


CHAPTER IX 


INFECTIOUS DISEASES DUE TO PROTOZOA 


SPIROCHETOSIS 


Launoy and Levy-Bruhl infected fowls intramuscularly with 
cultures of Spirochaeta gallinarum. Spirochetes appeared in the 
peripheral blood in 48 hours. ‘The septicemia lasted three days 
when virulent cultures were used and five days with attenuated 
cultures. There was an early very intense anemia followed by 
regeneration of the red cells in the cases that recovered. The 
greatest anemia they found to be usually at about the fifth day. 
The following are examples of their experimental cases, showing 
the changes in the number of red cells, given in millions per emm. 
The first one (R‘) was infected with strong virus, the second (Z) 
with weaker. 


After Infection 


Before 

Infection | 2 days | 3 days | 4 days | 5 days | 6 days | 7 days | 9 days 
Re Sy 2.27 1.96 — — 2.76 2.85 
Z 2.89 | 2.54 


2.28 == 1.47 1.26 == — 


The leucocytes were increased, from 35,000 to 40,000, excep- 
tionally to 50,000. In some fatal cases the leucocytes reached 
80,000. The leucocytic formula is reported to vary but slightly 
in different fowls. There seems to have been an increase in the 
polymorphs during the period of septicemia followed by an in- 
crease of lymphocytes. A few myelocytes were observed during 
the height of the septicemia. The eosinophiles decreased during 
the septicemia. The following table shows the changes in the 
leucocytes in the case reported by Launoy and Levy-Bruhl. 
What they call ‘“polynucléaires pseudo-éosinophiles” and ‘“neo- 
polynucléaires”’ are evidently polymorphonuclears. 

116 


RABIES 117 


TaBLE XXXIV.—Fowt INrecteD Marca 6 wits 0.2 cc. or A CULTURE OF SPIROCHAETA 
GALLINARUM INTRAMUSCULARLY (LAUNOY AND LEvy-BRUHL) 


Condition of infection 0 + +H | tit 0 

ee ES --——- — | — — —- 

Variety of leucocytes ise if 8 9 | 10 11 12 14 17 19 
Lymphocyte......... 49 29 22 16 14 34 56.5] 63 59 45 
Medium mononuc.....} 14 8.5 il 24 25 35 31 15 18 11 
Large mononuc....... ite 1 2 1 5 & 0.5 0 0 0 
Polynucl. pseudo eosino| 24 56 24 10 6 2 0 0 15 35 
Polynucel. eosino...... 7 S250 ae5 0 1 ff) ft) 1 8 8 
Neopolynucliaires..... | 0 0 39 47 48 23 11 20 9 0 
Basophiles) 25252: =<: 5 Z 0.5 2 0 1 1 1 1 1 
Myelocytes.......... 1 
Leucocytes, total no. . .|20,500}21,000 24,000)21,000 24,000/ 21,000) 27,000) 36,000) 32,000) 25,600 


RABIES 


Courmont and Lesieur made a study of rabies in three cases 
in man and five cases in the dog of natural infection and also 
experimental cases in dogs, guinea pigs and rabbits. They found 
the percentage of polymorphonuclears high in all cases, beginning 
in experimental cases with the appearance of symptoms. The 
total number of leucocytes was increased in nearly all cases. In 
a woman 29 years old, 83 days after having been bitten and one 
hour before death, there were 3,300,000 red corpuscles and 24,800 
leucocytes of which six per cent. were lymphocytes, three per 
cent. large mononuclears, three per cent. intermediate forms, and 
88% polymorphs. In a child ‘six years old, not given Pasteur 
treatment, the percentages of leucocytes were, lymphocytes 13.5, 
large mononuclears 0.5, intermediate forms two, and polymorphs 
84. 

In a man 49 years old the leucocytes were: 


29 hours before death 5,000 with polymorphs 84%. 


2D ce “ce ‘e 7,000 ce ins 83%. 
8 “ce ce “c 12,000 “c cc 5%. 
1 “ce “ “c 21,000 “ “ 85%. 


In five cases of natural infection in dogs they found the following: 


Dog No.1 2 hours before death 98% polymorphs. 
2 2 oe “ ce 88% ce 
3. al 13 iT: bc 93% 6c 
4 1 “cc “cc “cc 96% “ee 
5 1 “ce “c “c 90% “c 


118 INFECTIOUS DISEASES DUE TO PROTOZOA 


In experimental cases in dogs the total number of leucocytes 
increased suddenly on the appearance of symptoms, reaching 
15,000-19,000, then falling somewhat on the day of death. The 
percentage of polymorphs exceeded 90% from the time of the 
appearance of symptoms to death. In experimental cases in 
rabbits and guinea pigs there was a polynuclear leucocytosis 
from the time symptoms appeared and an increase in the number 
of leucocytes in some of the cases. In some there was no increase 
in the number of leucocytes, in a few there was a leucopenia. 


TEXAS FEVER 


The protozoon causing this disease was first observed by Babes 
(1888) in Roumania in the blood of cattle affected with hemo- 
globinuria. In 1889, Smith found the organism in the blood of 
cattle suffering from Texas fever and named it Pyrosoma bige- 
minum. The generic name has been changed to Babesia. 

In the acute form of the disease the parasites may be found in 
the circulating blood during the febrile period. When the fever 
subsides and the number of red corpuscles has been found greatly 
reduced, the parasites disappear rapidly from the peripheral 
blood, the reduction of temperature usually coinciding with the 
more or less rapid disappearance of the parasites. An occasional 
parasite may be found for some days or even a week after recovery 
has set in (Smith and Kilbourne). Kossel and Weber report that 
the parasites are abundant during the time hemoglobinuria is 
present. When hemoglobinuria disappears the parasites disappear 
or are very scarce in the circulating blood. In one case Kossel 
and Weber found individual large typical pyriform parasites in 
the blood seven days after the disappearance of hemoglobinuria. 

In acute cases the parasites appear in fresh blood as two pale, 
pear-shaped bodies situated within red corpuscles. The broader 
end of the parasite is rounded, the other end long and tapering. 
The tapering ends are directed toward each other and are ordinarily 
close together. Sometimes a thin film of protoplasm may be made 
out connecting the two tapering ends. The broad ends may 
occupy various positions as regards each other; sometimes they 
are rather close together so the pyriform bodies lie nearly parallel, 
then they may point away from each other, the pyriform bodies 


TEXAS FEVER 119 


forming a straight line. The smaller forms appear as a rule 
homogenous, the large forms contain a minute spherical body, not 
over 0.1-0.2 in diameter, which appears darker than the re- 
mainder of the body of the parasite. In the largest pyriform bodies, 
a larger rounded or oval body 0.5-1.0u in diameter may be ob- 


10 


Fic. 12. Babesia bigemina. 1, blood obtained postmortem; 2, before death 
(Smith and Kilbourne); 3-10, different forms of the parasite (Kossel). 


served situated in the center of each broad rounded end. The 
infected red corpuscles show crenated margins and may be darker 
than the uninfected corpuscles; they have lost their flexibility, 
retaining the disc form even after uninfected corpuscles have 
become shrivelled and folded in preparations that have been made 


120 INFECTIOUS DISEASES DUE TO PROTOZOA 


for some time. Besides the pyriform parasites a considerable 
number of single forms somewhat irregular in outline may be 
found. These forms undergo ameboid movement. 

Alkaline methylene blue stains the parasites a blue color leaving 
the red corpuscles unstained. Methyl violet gives much the same 
result. The parasites are stained by carbol fuchsin; but this stain 
also stains the corpuscles deeply. Much better results are obtained 
by using the Romanowsky method of staining or one of its modi- 
fications. Chromatin bodies within the parasites are brought out 
by the use of one of these stains. With the Romanowsky method 
of staining the smallest forms appear as very small rings about 
one-eighth the diameter of a corpuscle. The periphery of the 
ring takes a red color in a greater or less extent, while the re- 
mainder appears blue. Other very small parasites have a very 
irregular outline and contain two, sometimes four, chromatin 
bodies of a red color. In the large double pyriform parasites a 
red chromatin body is found usually at the broader pole, some- 
times in the middle (Kossel). Ziemann observed forms with the 
chromatin bodies at the pointed end. The remainder of the body 
of the parasite stains blue. The chromatin body is ordinarily 
rounded. 

The number of infected corpuscles is usually about one-half 
to one per cent. of the entire number of red corpuscles. Some- 
times a long search is necessary to find a parasite. When the 
number becomes larger, death may be expected within 24 hours. 
Toward the fatal termination five to 10% infected corpuscles 
may be found. Very rarely large numbers of parasites may be 
present and yet the animal recover. Smith and Kilbourne ob- 
served one such case (No. 49), in which hemoglobinuria was 
present. Parasites are present in the internal organs in much 
larger numbers than in the peripheral circulation. The distribu- 
tion of the parasites is well shown in one of Smith and Kilbourne’s 
cases, No. 163. This cow was killed when the temperature was 
107° F., red corpuscles 2,645,000 per ecmm. Four days before 
the temperature was normal, the red corpuscles numbered 5,000,000 
per cmm. Before she was killed there were two to three per cent. 
infected corpuscles in the peripheral blood. Examination of the 
internal organs showed 50% in heart muscle and hyperemic fringes 
of the omentum, 10-20% in liver and in kidney, five per cent. in 


id 
BY 
fi 
PS) 


4 
# 
te 

| 


ee 


TEXAS FEVER 121 


spleen, two to three per cent. in blood of left heart and lung, 
very few in marrow of sixth rib and in skeletal muscles. At post- 
mortem examination the corpuscles have a rounded form. Free 
forms of the parasite were not observed by Smith and Kilbourne 
in the peripheral blood; but were found in the blood from the 
heart. 

In the mild type of the disease the parasites are as a rule in- 
visible in fresh blood, rarely one may be observed on the edge 
of a corpuscle as a pale spot about 0.5 in diameter. In prepara- 
tions stained by alkaline methylene blue, they appear as round 
coccus like bodies 0.2—0.5u in diameter, situated within red cor- 
puscles. Ordinarily but one is found in a corpuscle. In many cases 
division of the parasite was observed into two (Smith and Kil- 
bourne). This form of the parasite is characteristic of the mild 
autumnal form of the disease. Smith and Kilbourne found that 
three groups of animals have this type of the disease, (1) those 
exposed late in the season (October and November), (2) those 
that have passed through an acute attack earlier in the season; 
the second attack or relapse in October or November, (3) those 
that contract the mild form during or previous to the season of 
the acute form of the disease. In groups 1 and 2 the disease is 
mild and may pass unnoticed. Infected corpuscles appear in the 
blood as the number of red corpuscles begin to diminish and dis- 
appear as the number of red corpuscles begin to increase. Rarely 
a corpuscle containing a large pyriform parasite is found. A few 
animals (group 3) showed infected corpuscles several weeks before 
fever appeared, the disease changing into the acute type with 
pyriform parasites instead of those of the coccus form. In the 
mild type of the disease there may be five to 50% of the red cor- 
puscles in the circulatory blood infected for a period of one to 
five weeks. 

Changes in the blood.—There is a progressive loss of red cor- 
puscles until an extreme oligocythemia is reached. In some cases 
as high as 1,000,000 corpuscles have been lost per day. In many 
cases the count of red corpuscles decreases nearly to 1,000,000 
to 2,000,000 per emm. Counts, taken from Smith and Kilbourne, 
are given of two cases,—one fatal, the other recovering. With 
the reduction in the number of corpuscles marked changes are 
found in their size and staining. When the number of corpuscles 


122 


INFECTIOUS DISEASES DUE TO PROTOZOA 


TaBLeE XXXV.—Texas Fever (SMITH AND KILBOURNE) 


Date 


Steer No. 56 20-IX 


22-IX 
29-IX 
9-X 

22-X 
25-X 
30-X 
6-XI 
8-XI 
13-XI 
15-XI 


17-XI 
21-XI 
26-XI 
2-XII 
11-XII 
7-VII 
13-VIII 
14-VIII 
15-VIII 
16-VIII 
18-VIII 
19-VIII 


Cow No. 95 


20-VIII 


22-VIII 


25-VIII 


31% 


104. 


104. 


100. 
104. 


“J 


Red C 
: Mill 


PRO Ne 


own wo ek, WO Ff 


36 


.09 


or. 


Parasites 


negative 
negative 
negative 
negative 
10-20% peri- 
pheral cocci. 
10-20% peri- 
pheral cocci. 
10-20% peri- 
pheral cocci. 
20-30% peri- 
pheral cocci. 
30% peripheral 
cocci. 
10% peripheral 
cocci. 
10% peripheral 
cocci. 


1-2% periph- 
eral cocci. 

a few periph- 
eral cocci. 

negative 

negative 

1% peripheral 
cocci. 


5% peripheral 
cocci. 

20% peripheral 
cocci. 

20% peripheral 
cocci. 

15% peripheral 
coccl. 

10% peripheral 
cocci. 

10% peripheral 
cocci. 

10% peripheral 
cocci. 

144-1% large 
parasites. 

10% peripheral 
cocci, 44-1% 
large 
parasites. 

10% peripheral 
coccl. 

144-1% large 
parasites. 

5% large para- 
sites; 5% 
peripheral 
cocci. 


exposed 8-IX. 


many macrocytes; some 
punctated red corpuscles 
30% macrocytes; 10-20 
% tinted corpuscles. 
30 macrocytes; 10-20 
% tinted corpuscles. 
some erythroblasts. 


20% macrocytes; 10% 
punctated; 5% tinted 
corpuscles. 

5% tinted and punctated 
corpuscles. 


some macrocytes. 

some macrocytes; recovery 
complete so far as ap- 
pearances go. 

exposed 4-VII. 


a few punctated corpuscles. 


1% macrocytes; some 
punctated corpuscles. 
some punctated corpuscles. 


many macrocytes; some 
punctated corpuscles. 


many macrocytes; some 
punctated corpuscles. 


evidently dying; some 
macrocytes; both tinted 
and punctated corpus- 
cles. 


has fallen to about 3,000,000, enlarged corpuscles (six to eight in 
diameter), showing punctate basophilia and polychromasia, are 


found. 


When the number falls to 2,000,000 erythroblasts appear. 


The amount of hemoglobin seems not to have been determined. 
While the rapid destruction of red corpuscles is going on hemo- 
Hemoglobinuria, however, is 


globin may appear in the urine. 


not present in all cases. 


CANINE PIROPLASMOSIS 123 


It has been found by Hibbard and Neal that there are changes 
present in the blood in mild chronic cases of Texas fever, as in 
cattle raised within tick infested regions or that have been im- 
munized by having mild attacks of the disease. The red cor- 
puscles and hemoglobin are diminished by mild attacks, but 
increase to normal or nearly so after a time. The leucocytes are 
increased and remain higher than normal. The increase is mostly 
in the lymphocytes. Examinations of 41 cattle in the general 
herd of the Mississippi Agricultural College showed the red cor- 
puscles 4.5-7.8 millions, average 6.05; the hemoglobin 50-98, 
average 83; and the leucocytes 4880—26,220, average 12,360. The 
varieties of leucocytes were: lymphocytes 3,218—24,622, average 
9,578; the large mononuclears 0-851, average 155; the poly- 
morphonuclears 440-5,052, average 1,456; the eosinophiles 60- 
3,320, average 947 and the mast cells 0-249, average 59 per cmm. 

The following table shows the results of examinations of five 
yearling heifers before treatment and after inoculation with Texas 
fever organisms. The animals had recovered from three attacks 
and been passed on as in good condition a month before the 
second examination (Nov. 18th) was made. 


TABLE XX X VI.—EXAMINATIONS OF THE BLoop oF FIVE YEARLING HEIFERS - 
IMMUNIZED TO TEXAS FEVER (HIBBARD AND NEAL). 


After Treatment 


Betore. er eS See 
Treatment | Nov. 18 Dec. 1 Jan. 31 Apr. 14 

Red corp. millions 7.3 ee 9.3 72 6.64 
Hemoglobin 97 90 86 865.5 88.5 
Leucocytes 8,950 24,444 | 22.804 | 23005 | 21,721 
Lymphocytes 7,163 20,280 19,003 18,243 15,994 
Large mononuclears 171 383 700 858 519 
Polymorphs 1,443 2,384 2,310 3,444 _ 2,930 
Eosins 253 586 756 1,296 2,215 
Mast cells 37 52 —— 87 68 


CANINE PIROPLASMOSIS (MALIGNANT JAUNDICE IN THE DOG) 


The specific cause of this disease, Babesia canis, first described 
and figured in 1895, by Piana and Galli-Valerio in Italy, is a 
hematozoan found in the blood of diseased dogs. It occurs mostly 


124 INFECTIOUS DISEASES DUE TO PROTOZOA 


within red corpuscles though parasites are found free in the blood. 
Parasites were found by Nocard and Motas within 36 hours after 
inoculation in the most rapid case, usually, however, it was two 
days before they were found even after intravenous inoculation; 
after subcutaneous or intermuscular inoculation it was usually 


Fiaq. 13. Babesia canis (Nuttall and Graham-Smith). 


five or six days before the parasites were found. Robertson did 
not find them before the fourth day after inoculation though the 
blood from a dog three days after inoculation proved to be virulent. 
Nuttall and Graham-Smith found that the parasites made their 
appearance in appreciable numbers in the peripheral blood im- 
mediately before the onset of fever. In one case parasites were 
first found in films on the sixth day of the disease; in most of their 
other cases parasites appeared between the eighth and twelfth 
days after infection. 

Babesia canis has a striking resemblance to the parasite of 
Texas fever. Piana and Galli-Valerio from its morphology named 
it Pyrosoma bigeminum var. canis. Nocard and Motas state that 
morphologically the hematozoan is identical with that of cattle. 


bat ct: iil 


CANINE PIROPLASMOSIS 125 


The changes which the parasite undergoes in ameboid movement 
are best seen during the febrile period. The most varied ameboid 
forms are found toward the end of the febrile period (Nocard and 
Motas). The infected corpuscles are larger and paler than other 
corpuscles. The parasites appear as small rounded bodies having 
a dark contour and refractive central part. Very soon after the 
febrile period the parasites lose their ameboid properties, take on 
a rounded form and remain immobile in the center of the affected 
corpuscles. At the beginning of the disease only a single parasite 
is found in each infected corpuscle; later infected corpuscles often 
contain several parasites, when pyriform parasites may be found, 
though they are rare (Nocard and Motas). Though the parasites 
may be found in fresh blood when they are numerous, they are 
much more readily found in stained preparations. Some one of 
the modifications of the Romanowsky method is_ preferable. 
Nuttall and Graham-Smith obtained excellent results using Leish- 
man’s modification. With this stain the parasite appears as a 
blue body containing usually a single homogenous chromatin body 
(karyosome) which stains a bright red. In larger forms the cell 
- body has frequently a vacuolated or trabecular structure and 
appears condensed at the periphery. Small spherical forms often 
appear as rings, resembling young malarial parasites in man. In 
dividing forms a delicate protoplasmic thread may for some time 
join the daughter cells. With pyriform parasites the connecting 
thread is usually at the pointed ends, with other forms the con- 
necting threads are somewhat irregularly situated. The chro- 
matin body is usually spherical and is usually centrally situated, 
though it is sometimes eccentric or peripheral. In dividing forms 
the chromatin body becomes elongated and separates into two 
portions, immediately followed by division of the cell body. Both 
spherical and pyriform parasites undergo division (direct division). 

In the acute form of the disease several parasites, two to 16, 
may be found in a corpuscle; in the chronic form it is rare to find 
several parasites in the same corpuscle. Corpuscles may be found 
containing one to 16 or even more parasites. In the very beginning 
of the disease only a single parasite is found in a corpuscle, later 
the infected corpuscles often contain several. Those containing 
several parasites, eight to 16 or more, are found more often in 
blood from the internal organs, brain, lymphatic glands, bone 


126 INFECTIOUS DISEASES DUE TO PROTOZOA 


marrow, etc. The parasites are smaller in the corpuscles contain- 
ing many. Free parasites are also found, especially in advanced 
stages of the disease (Robertson). Graham-Smith reports that 
free forms are seldom seen in the earlier stages of the disease but 
later become more numerous. On the day of death he found one 
free parasite to 18 infected corpuscles. 

The number of infected corpuscles varies considerably. They 
are more abundant in the acute form, in which they are in con- 
siderable numbers during and immediately after the febrile period. 
The following table shows the percentage of infected corpuscles 
and the duration of the disease in 11 cases of the acute and sub- 
acute forms of the disease (from Graham-Smith). 


TaBLE XXXVII.—CaNINE PiropLasmosis (GRAHAM-SMITH). 


Percentage of Infected Corpuscles 
Duration of Disease 


Day Before Death Autopsy 
Dog VI 6% 4% 13 days 
VII 4 5 32 days. 
I 1.4 1 25 days. 
x 1.4 B 23 days. 
II 8 2.8 23 days. 
XI 5 12 17 days. 
Iil 4 8 22 days. 
Ix 3 at 24 days. 
VIII 2 4 47 days. 
IV a 4 23 days. 
V t 05 13 days. 


In dog I, the proportion of infected to non-infected corpuscles 
varied from .3-.6% from the first appearance until the day before 
death. In dog II, only .05% were infected five days before death, 
two days later .8% were infected. 

In the chronic form the parasites are often scarce. Usually 
examinations made on successive days will reveal their presence. 
In some cases it is necessary to inoculate several c.c. of blood from 
the suspected case into a young dog which will often develop an 
acute case in which the parasites may easily be found. The 
parasites are more numerous at autopsy in the capillaries of the 
internal organs. In the majority of cases Graham-Smith found 


- 


CANINE PIROPLASMOSIS 127 


parasites in great numbers in the small capillaries of the internal 
organs, in kidneys 95% of the corpuscles were infected, while in 
the larger vessels there was a small proportion of infected cor- 
puscles. 

Changes in the blood.—A severe, progressive anemia is the 
chief feature of the disease. From the time of the appearance 
of the first symptoms the number of red corpuscles decreases slowly 
and regularly, then at the time of the hemoglobinuric crisis falls 
suddenly to two millions and below (Nocard). The Hb decreases 
parallel to the red corpuscles from 12-13%, the normal, to six to 
four and three and one-half per cent. The greatest reduction 
found by Wright was from 110-18%; the smallest amount. of 
Hb 17%. Nocard and Motas give the following as a typical acute 
case: 


Day Red Corpuscles 
5,240,000 intravenous inoculation 2 c.c. virulent blood. 
5,560,000 well. 
5,960,000 temperature 40° C, few parasites. 
5,240,000 many motile parasites. 
2,600,000 35.6° C, hind limbs paralyzed. 
2,200,000 33.5°C, worse. 
found dead. 


aon fr Wh = 
Db 
ee 


The following are two cases reported by Wright: 


TasBLeE XXXVIII—Two Casrs or CANINE PIROPLASMOSIS (WRIGHT) 


Dog III 
Bed Leu- | Varieties of Leucocytes 
Day| Temp : SSS SSS SS 
Corpuscles cocytes| 7; | 17 |tIr/1v | Vv 
15 | 104.2 | 5,050,000 20,000 | 18 | 10 | 70 | 2 
16 | 104.3 18,570 
17 | 104.2 | 4,800,000 12,500 
18 | 103.3 | 3,800,000 13,000 
19 4,800,000 10,000 
20 | 105.7 | 4,400,000 11,000 parasites 
found, 
Ze ed OD: 1,300,000 9,900 
22) 104.3 | 1,850,000 17 10,000 | 15 | 11 | 74 


128 INFECTIOUS DISEASES DUE TO PROTOZOA 


Dog XI 
6} 103. 4,900,000 | 100 28 70 | 2 
7 | 106.5 
10 | 103. 4,000,000 | 70 | 4,500 
14 |} 101.8 | 1,800,000 | 32 | 50,000 parasites 


found. 
16 | 101.4 | 1,400,000 26 | 59,000 
17 | 100.8 950,000 18 | 49,000 23 76 1 


The blood is pale as if diluted with water. Coagulation is 
slower than in normal blood. The serum is tinted with Hb. 
The red corpuscles present considerable changes, some are larger 
(from one-third to two-thirds) and paler than normal; some are 
smaller than normal. At the time parasites appeared erythro- 
blasts were also found present (Wright). Erythroblasts in some 
cases are present in large numbers. 

The leucocytes are usually much increased. Nocard found 
as high as 40,000. Wright found nearly 52,000 in one and 60,000 
in a second case. In one dog Wright found that the leucocytes 
dropped gradually from 20,000 on the 15th day to 10,000 on the 
22d day. The increase, according to Nocard and Motas, is nearly 
always in the polymorphonuclears. In Wright’s case both poly- 
morphonuclears and mononuclears were increased. 

In the chronic form of the disease there is marked anemia, the 
red corpuscles decreasing to about two millions. In one of Nocard 
and Motas’ cases they fell to 1,200,000. The return to normal is 
very slow. They are scarcely returned to normal before two or 
three months (Nocard and Motas). As recovery progresses the 
number of red corpuscles increases; erythroblasts become rare. 
The Hb suffers much less than the red corpuscles. In one of 
Nocard and Motas’ cases with only 2,760,000 red corpuscles there 
was 914% Hb. Thechanges in the size and staining of red corpuscles 
are more marked than in the acute form. Some corpuscles are 
two or three times the normal diameter and stain less deeply. 
Many erythroblasts are present at the beginning of the decrease 
in red corpuscles. 

The number of leucocytes is increased, ordinarily from 15-30,000. 
Nocard and Motas record one case where they reached 54,000. 
The leucocytosis involves polynuclears and mononuclears equally. 


EQUINE PIROPLASMOSIS 129 


Phagocytosis of infected red corpuscles is frequently observed in 
the days following the febrile period. The phagocytes are exclu- 
sively mononuclears. _ 

The following is a case, dog No. 61, given by Nocard and Motas 
as typical of the chronic form of the disease: 


TABLE XX XIX.—CuHrRoniIc CANINE Prropuasmosis (NocarD AND Moras). 


Red Cor- | 


Day ices Leucocytes 
1 5,840,000 temperature 38.7° C. 
, few parasites found. 
33 more parasites. 
4 numerous motile parasites. 
6 4,040,000 few parasites; mucosz pale. 
8 | 2,820,000 very few parasites; profound anemia. 


10 1,520,000 54,000 | erythroblasts numerous. 
15 1,200,000 10,000 ‘| no parasites found. 


18 | 2,120,000 slight improvement; no parasites. 

20 =| 2,480,000 few erythroblasts; distinct improvement; no 
parasites found. 

25 | 4,380,000 improving rapidly; mucose pink; no para- 
sites found. 

ae 5,100,000 one parasite found. 


dog considered cured. 


EQUINE PIROPLASMOSIS; EQUINE MALARIA; SOUTH AFRICAN HORSE 
SICKNESS 


The specifie cause, Babesia equi, discovered by Guglielmi, 
closely resembles Babesia bigemina. The parasites are found 
without difficulty in the peripheral blood during the febrile period 
but disappear later. They are transmitted as shown by Theiler 
by Rhipicephalus evertsi. 

The parasites appear as small spherical or elongated, oval or 
rarely pyriform bodies and are nearly always within red corpuscles. 
It is not common to find them free in the plasma. The parasites 
are from .56-2)4mu in diameter, the most common being 1-1)p. 
Stained by Romanowsky’s or Laveran’s method the cell body 
takes a bluish tint, the karysome a red-violet color. The following 
forms of the parasite are described by Bowhill: (1) large and small 


130 INFECTIOUS DISEASES DUE TO PROTOZOA 


spherical forms, karysome situated at edge of parasite; (2) large 
and small pyriform parasites single and in pairs; (3) large and 
small rod-like bodies, some of them extending across the entire 
diameter of the corpuscle, sometimes in pairs; (4) rosette form, 
consisting of four bodies connected in center by fine threads, 
each body usually containing a karysome at its extremity; (5) 
flagellate forms.* 

Laveran found multiplying forms more common in the spleen 
than in peripheral blood. Multiplication is by direct division, 
usually into two, sometimes into four bodies. The karysome 
elongates, then divides into two parts; these separate, followed 
by division of the cell body. The two parasites often divide giving 
four, within the red corpuscle. Sometimes the karysome divides 
into four parts before the protoplasm divides. The disposition 
in fours is one of the most striking morphological characters of 
Babesia equi (Laveran). 

The number of parasites in the peripheral blood varies a great 
deal. They are present during febrile stages but disappear after 
the fall of temperature. During the stage of high fever they are 
numerous. Theiler has found them in unstained blood as abundant 
as a parasite to five to 40 red corpuscles. Williams states that the 
number of parasites in the peripheral blood is proportional to 
the severity of the disease and that from one to 10% or up to 30% 
of the corpuscles may be infected. Baruchello and Mori found 
50-60% of the red corpuscles infected in some cases; they state 
that the parasites are found most easily during the early stages of 
the disease. The “rosette” form is present in varying numbers. 
Sometimes the parasites are so scarce as to be found only after a 
long search. After the administration of quinine the rosettes are 
very scarce (Theiler). With the fall of temperature the number of 
parasites decreases from day to day; by the time the temperature 
has fallen they can be found only with difficulty. 

Changes in the blood.—The disease is characterized by a 
progressive anemia. In the beginning of the disease the infected 
red corpuscles ordinarily show no microscopical change; they are 


* Nuttall and Graham-Smith observed dumb-bell forms and flagella like 
processes while studying canine piroplasmosis. They found that these forms 
and processes were due to overheating the red corpuscles and were able to 
produce similar forms by overheating films of normal blood. 


BABESIA MUTANS, THEILER 131 


infrequently larger than the non-infected corpuscles. Later when 
the anemia is marked very many relatively large, pale corpuscles 
are found (Theiler). Williams found variation in the size and 
shape of red corpuscles, (megalocytes, microcytes, poikilocytes) 
and polychromatophilia and an increase of mononuclear and 
polymorphonuclear leucocytes; in some smears also a marked 
increase in the eosinophiles. Counts were not given. 


OVINE PIROPLASMOSIS (CARCEAG) 


Babesia ovis, Starcovici, discovered by Babes in 1892, is very 
similar to Babesia bigemina. The form of the parasite is round 
or pyriform. It is not rare to find two to four in the same red 
corpuscle. The liver seems to be the principal depot of the para- 
sites, which occur within red corpuscles and free (Motas). Divid- 
ing forms are frequent in the capillaries of the liver. The injection 
of a large quantity of virulent blood into cattle, goats, dogs, cats 
and rabbits was without effect (Motas). 

Complete examinations are not recorded. The number of red 
corpuscles falls from eight or nine millions to four millions or less. 
There is a marked diminution in the amount of hemoglobin, from 
13 and 14 grams per 100 cc. to seven or eight grams per cubic 
centimeter and a lessened coagulability (Motas). The red cor- 
puscles vary greatly in size (Bonome). 


BABESIA MUTANS, THEILER 


Theiler has recently described another species of Babesia in the 
blood of cattle in South Africa. He named the parasite causing 
it Piroplasma mutans. The organism is found, though never 
present in large numbers, in the peripheral blood of the affected 
animals. In the cases observed by Theiler, B. bigemina has also 
been present. The disease is moculable, thus differing from East 
coast fever. Theiler inoculated 15 calves with the blood of cattle 
immune to red water and obtained reactions with small organisms 
in the blood from the 25th to the 41st day after inoculation, be- 
tween the secondary and tertiary reactions due to B. bigemina. 
The parasites were present in the blood in small numbers. The 
importance of this disease is that it is liable to be mistaken for 


132. INFECTIOUS DISEASES DUE TO PROTOZOA 


Hast coast fever, a much more serious disease, from the similarity 
of the parasites. Theiler states that B. mutans may easily and 
has constantly been mistaken for Th. parva. Tor diagnostic 
purposes where small numbers of piroplasmata are found in the 


Fic. 14. Babesia mutans (Theiler). 


blood, the examination must be repeated. In East coast fever 
the organisms will usually increase rapidly in numbers, whereas 
B. mutans increases slowly and is never present in large numbers. 
Examinations of the blood, except for parasites, were not given. 


EAST COAST FEVER (RHODESIAN FEVER) 


East coast or Rhodesian fever is a destructive disease of cattle 
in parts of South Africa caused by Theileria parva, Theiler. A 
disease very similar, if not identical, has been reported in Tunis 
(Ducloux) and in Egypt (Bitter). The parasites during the first 
stages of the disease appear as very small rod-shaped or ring forms. 
Exceptionally, larger and pyriform parasites are found (Schilling). 
The parasites are found usually in large numbers in the circulating 
blood. The disease is not inoculable by blood containing the 
parasites, but is transmitted by ticks. 


TRYPANOSOMATOSIS 133 


‘ 


Notwithstanding the large number of parasites in the blood, 
anemia is not very marked. Often the red corpuscles remain at 
the normal number, in some cases fall to not less than 4,500,000, 
in only one case fell to 2,380,000 (Koch). 

Dschunkowsky and Luhs have described a disease of cattle in 


Fig. 15. Theileria parva (Theiler). 


Transcaucasia, due to an organism very similar to Th. parva, 
which Dschunkowsky named Piroplasma annulatum. The para- 
sites have been found in large numbers in the blood in the acute 
form of the disease, up to 95% of the red corpuscles containing 
from one to eight parasites. The disease may be transmitted by 
the inoculation of blood containing the parasites. In the chronic 
form from 10-40% of the red corpuscles contain parasites. Anemia 
is marked in chronic cases, as low as 800,000 red corpuscles having 
been found. 


TRYPANOSOMATOSIS 
The organisms causing the several varieties of trypanosomatosis 


are so similar in morphology that a description of one with slight 
modifications will serve for the others. The trypanosomes are 


134 INFECTIOUS DISEASES DUE TO PROTOZOA 


unicellular organisms found in the blood of the animals infected 
by them. The body of a trypanosome is fusiform, provided with 
a lateral undulating membrane, the thickened free border of which 
terminates in the posterior part of the body in a centrosome or 
blepharoplast and is prolonged anteriorly as a free flagellum. The 
nucleus is generally in the anterior part of the body. Multiplica- 
tion is by longitudinal division and by segmentation, which differs 
only in that the cell body divides much more slowly than the 
centrosome (blepharoplast) and nucleus, thus four, eight or 16 
small trypanosomes are formed attached by their anterior ends. 
Conjugation is at present undetermined. ‘Trypanosoma lewisi 
was cultivated by MacNeal and Novy in 1903. Since then several 
other species have been cultivated by them and others. 

A positive diagnosis is made by finding the trypanosomes. In 
the majority of cases this may be done without difficulty by 
making a microscopical examination of the blood of the affected 
animal. The parasites are most numerous in the blood during 
the febrile periods. During the intermissions the blood is virulent 
though the parasites may be so few as to escape even a careful 
microscopical examination. Several preparations should be made 
and carefully searched. The blood may be examined in the fresh 
condition for living parasites, or smears may be made and stained, 
preferably by one of the modifications of the Romanowsky method. 
When the parasites are scarce it is of advantage to centrifuge the 
blood or fluid to be examined. If blood, the red corpuscles may 
be rendered invisible by the addition of dilute acetic acid (one- 
third per cent. glacial). If the organisms are not found the exam- 
ination should be repeated each day for several days. Consecu- 
tive examinations each day for six or seven days will usually 
reveal the parasites; but in some cases their presence is more 
easily determined by inoculating a susceptible animal with some 
of the blood (from a few drops to one cc.) of the suspected case. 
Mice, rats or dogs are the most susceptible to nearly all of the 
trypanosomes (not for Tr. theileri), the disease running an acute 
course in them. The parasites will be found in large numbers in 
the blood of these animals inoculated with blood or infective 
material containing pathogenic trypanosomes. 

At the present time opinions differ as to whether the disease 
occurring in different countries is caused by different species of 


SURRA 135 


trypanosomes. A discussion of the relationship of the several 
trypanosomes is outside the scope of this work. The following 
diseases caused by trypanosomes affect the domesticated animals: 


TABLE XL.—TRYPANOSOMATOSES 


: : . Geographical Animals 
D db 
BaSeae Specific Cause |iscovered by Distribution Affected 
Tr. evansi Evans 1880 | India, Indo- Horse, ass, 
Surra Steel (1885) China, East mule, 
Indies, Persia, camel, 
Philippines, elephant, 
Mauretius, dog. 
North Africa. 
Nagana Tr. brucei Bruce 1894 Africa Horses and 
(Plimmer most 
and Brad- mammals 
ford 1899) 
Dourine Tr. equiper- Rouget 1894 | N. Africa, Per- Horse, ass 
dum (Dof- sia, Turkey, 
lein 1901) South France, 
North Spain. 
Mal de Tr. equinum | Elmassian S. America Horses, dogs 
Caderas (Voges 1901)| 1901 
Gambian Tr. dimorphon| Dutton and | Senegambia Horses 
horse (Dutton and| Todd 1904 
sickness Todd 1904) 


In all of these, except dourine, transmission is supposed to be 
by means of biting insects; in dourine the disease is transmitted 
by copulation. 


SURRA 


The greatest losses from surra are among horses, mules and 
asses. It is also naturally acquired by the camel, elephant, dog 
and cat; cattle, buffaloes and caraboa are less susceptible. The 


136 INFECTIOUS DISEASES DUE TO PROTOZOA 


disease is transmissible by inoculation to nearly all mammals, rats 
and mice being the most susceptible. 

Tr. evansi is a motile trypanosome 20-30 p in length, including 
the flagellum, by one to two p in breadth, somewhat blunt at the 
posterior end and tapering gradually at the anterior end. The 
undulating membrane is well defined, beginning at or near the 
centrosome (blepharoplast) in the posterior 
portion of the parasite and ending anteriorly 
in a long, free flagellum. 

The parasites are transmitted by flies, 
Tabanus tropicus (Rogers), Stomxys calcit- 
rans, (Curry), possibly other flies and by 
fleas (Musgrave and Clegg). 

In the majority of cases the parasites are 
easily found in the peripheral blood. They 
are usually seen during the febrile periods; 
but decrease in numbers during the afebrile 
periods so that a prolonged search may be 
required or the microscopical examination 
may even fail to reveal the trypanosomes. 
The periods during which the parasites are 
scarce or are not found on microscopical 
examination vary from one to six days 
(Lingard); but the blood is virulent as 
shown by inoculation into susceptible ani- 
mals. Mice, rats and dogs are the most 
suitable for inoculation. In mice and rats 
the parasites are present in the peripheral 
blood, two to three days after subcutaneous inoculation, 24 hours 
after intraperitoneal inoculation and increase in numbers till death, 
which occurs three and one-half to five days after subcutaneous 
and two and one-half to three days after intraperitoneal inocu- 
lation. 

Changes in the blood.—There is a progressive diminution in 
the number of red corpuscles and in the amount of hemoglobin. 
Smith and Kinyoun state that in a horse sick seven days there 
were 3,500,000 red corpuscles and 14,500 leucocytes, and in an- 
other, sick six weeks, 3,200,000 red corpuscles and 13,900 leu- 
cocytes per emm. The hemoglobin was slightly diminished, 


Fia. 16: Trypanosoma 
evansi, rat’s blood (Nocht 
and Mayer). 


NAGANA 


137 


about 85%. Hemoglobinuria has been observed in some cases. 
Musgrave and Clegg state that it may occur temporarily in the 


first stage of the disease. Leucocy- 
tosis is given as being constantly 
present. A detailed study of the 
changes in the blood has apparently 
not been made. 


NAGANA 


Trypanosoma brucei is very similar 
to Tr. evansi. Laveran and Mesnil 
consider that there are certain differ- 
ences,—that Tr. evansi is more slender, 
has a longer flagellum and is more ac- 
tively motile in hanging drop and that 
animals immunized to one are not to 
the other species. 

The parasites are present in the 
blood in sufficient numbers to be 
found on microscopical examination 
during the febrile periods; but during 
the intermissions may be very scarce. 
Inoculation of susceptible animals 
however, shows them to be present 
even when the microscope fails to re- 
veal their presence. Toward the end 
of the disease they are often present 
in both febrile and afebrile periods 
in considerable numbers. There may 
be 50,000-70,000 per cmm. on the day 
of death (Theiler). 

Kanthack, Durham and Blandford 
found the trypanosomes present in 


Fic. 17. Trypanosoma 
brucei, rat’s blood (Nocht and 
Mayer). 


the right inguinal lymph glands in animals inoculated subcutane- 
ously in the right side one to three days before they were dis- 


coverable in the blood. 


138 INFECTIOUS DISEASES DUE TO PROTOZOA 


TasLe XLI.—NuMBER OF TRYPANOSOMES IN THE BLoop (AFTER SAUERBECK) 


ee Kanthack, Durham and Laveran and Mesnil, Proportion 
a Blandford of Parasites to Red Corpuscles 

Horse scarce 

Dog 300,000 1:50-1:100 

Mouse, | 2-3,000,000 tel 

Rat } 

Guinea pig 500,000 

Rabbit 60,000 1:50 


Changes in the blood.—The disease is a progressive anemia. 
Bruce reported a diminution of red corpuscles in one horse from 
5,000,000 to 3,800,000 and in another case from 5,500,000 to 
2,500,000. The red corpuscles decrease while the parasites be- 
come more numerous. As low as 848,000 red corpuscles are 
reported in the dog on the day of death. Erythroblasts are often 
present. Schilling found a reduction of red corpuscles to 2,270,000 
and of hemoglobin to 25%. The red corpuscles lose the power 
of forming rouleaux and form clumps; the serum of such blood 
mixed with normal blood of the same species of animal caused the 
red corpuscles to clump (Kanthack, Durham and Blandford). 
According to Kanthack, Durham and Blandford leucocytosis is 
not constant. The highest number they found was 15,000-34,000. 
Schilling found a slight increase, 11,000 per emm. 


DOURINE 


This disease affects equines, mainly horses. Asses are less sus- 
ceptible. Infection occurs naturally by coition. Dogs, rabbits, 
rats and mice are easily infected by inoculation. 

Trypanosoma equiperdum closely resembles Tr. evansi and Tr. 
brucei. Laveran and Mesnil state that the most important dif- 
ference is in the absence of the protoplasmic granules such as are 
present in Tr. brucei. Baldrey states that Tr. equiperdum is 
smaller than Tr. evansi, the posterior extremity is not so long 
and is less sharp, and the centrosome and nucleus are more 
elongated. 

The parasites are found most easily in blood taken from the 


MAL DE CADERAS 139 


center of newly formed plaques. If the plaques are old (24 hrs.) 
there may be no parasites visible; the further removed from the 
center the puncture is made the 
fewer are the parasites likely to 
be (Baldrey). Before the forma- 
tion of plaques diagnosis is diffi- 
cult. The parasite may often be 
found by making a microscopical 
examination of scrapings of the 
urethra in males or the vulva in 
females (Baldrey). The parasites 
are present in the blood in small 
numbers. Ordinarily they are 
found only by inoculating a sus- 
ceptible animal. They are pres- 
ent in the exudate of the male 
urethra and of the vagina, in the fyg. 18. Trypanosoma equiperdum, 
seminal fluid and in the fluid of blood, horse (Rouget). 
edematous swellings. 

Changes in the blood.— Detailed examinations of the blood 
have apparently not been made. From the time of the appearance 
of the plaques there is a progressive anemia which seems to be 
more rapid from the time of the appearance of nervous symptoms. 
There is an increase in the number of leucocytes. Pease states 
that there is a large increase in the number of eosinophiles. 


MAL DE CADERAS 


Trypanosoma equinum is similar in form and size to the other 
pathogenic trypanosomes, but is readily distinguished morpho- 
logically by the apparent absence of a centrosome, which is so 
inconspicuous that its existence has been denied by some. In 
Tr. equinum the centrosome measures about one-fourth to one- 
third p. 

The number of trypanosomes in the peripheral blood varies a 
good deal in cases of natural infection. Sivori and Lecler state 
that in cases of progressive anemia they are nearly always found 
and are numerous, while in cases of parexia they are found from 
time to time in small numbers, and in cases of paraplegia they are 


140 INFECTIOUS DISEASES DUE TO PROTOZOA 


not generally found on microscopical examination. When not 
found on microscopical examination the injection of blood into 
susceptible animals (horses, dogs, mice, rats) proves their ex- 
istence. 


Fia. 19. Trypanosoma equiperdum, blood, mice; a, four days after inoculation, 
b, eight days after inoculation (Rouget). 


Changes in the blood.—There is a progressive diminution in 
the number of red corpuscles and in the amount of hemoglobin. 
The red corpuscles may fall to 3,000,000 or less some days before 
death. Voges found them reduced to 800,000 in one ease. The 
hemoglobin may be reduced to five or six per cent. (grams per 
100 ce.). The leucocytes appear to be increased. Sivori and 
Lecler found 10,000 on the fourth day after inoculation. Of these 


MAL DE CADERAS 141 


there were 70% polymorphs, 20% large and medium mononu- 
clears, five per cent. lymphocytes, four per cent. eosinophiles and 
one per cent. transitionals. Before inoculation the same horse 
had an average of 54.5% polymorphs, 31.25% large and medium 


& 
= 


Fic. 20. Trypanosoma equinum, horse (Sivori and Lecler). 


mononuclears, nine per cent. lymphocytes, 3.25% eosins and two 
per cent. transitionals. The leucocytes vary corresponding to the 
appearance and increase of the trypanosomes in the blood. At the 
end of the disease they found 10% myelocytes. The following 
case illustrates the progressive diminution of the red corpuscles 
and of the hemoglobin. 


142 INFECTIOUS DISEASES DUE TO PROTOZOA 


TasBLe XLII.—Mau pre Capreras (EXPERIMENTAL Horse No. 3 Stvorit AND 


_———?}———<——— | — ————————— |__| —_—________ 


Date Temp. | Temp 
A. M. P.M 

16-VIII 37. By eel 
17-VIII 38. 38. 

18-VIII 38. 39.6 

19-VIII 39. 39.3 


— 


20-VIII 38.8 39. 
22-VIII 37.1 37. 
24-VIII 36.5 39. 


1-IX 38. 37.6 

6-IX 39.4 40.6 
8-IX 37.2 38.5 
15-IX 37.5 37.9 
10-X 37.5 o7.7 
14-X 38.6 39.3 
19—X 37.8 38.4 
25-X 38. 38.5 

4-XI 38. 38.1 
17-XI 39.4 38.3 
22-XI 


LECLER) 

Red Cor- Hb. % Trypanosomes 
puscles 
6,000,000 | 14. 

5,900,000 | 14. 


5,800,000 | 14. 2-3 per field, first seen. 
5,500,000 15.5 | 2-3 per field. 
6,100,000 14. 2-3 per field. 
5,500,000 10.5 | none observed. 


5,400,000 | 10.2 | none observed. 
4,900,000 9.8 | none observed. 
5,000,000. 9.8 | 1 per field. 
4,500,000 8.8 | none observed. 
3,400,000 7.9 |1 to 2-3 fields. 
3,000,000 6.7 | 5-10 per field. 
2,800,000 6. 10-20 per field. 
2,500,000 6. 1-2 per field. 
2,300,000 5.7 | none observed. 
2,000,000 4.5 | none observed. 
1,800,000 3.5 | 5-10 per field. 


5-10 per field, died. 


GAMBIAN HORSE SICKNESS 


Horses are affected naturally; horses, rats, mice, guinea pigs, 


Fig. 21. Trypanosoma dimor- 
phon (Laveran and Mesnil). 


rabbits, dogs, cattle and goats may 
be given the disease by inoculation. 

Trypanosoma dimorphon was 
found by Dutton and Todd in three 
forms: (1) in the beginning of the 
disease small forms 11-13 by 0.8-1 p, 
with very small undulating mem- 
brane, short flagellum and blunt pos- 
terior end; (2) long form 26-30 by 
1.6-2 p, with very long flagellum; 
(3) “stumpy form” 16-19 by 3.4- 
3.5 @, with short thick body and 
very long flagellum. Transitional 
forms between these occur. The 


long form (2) is very numerous during the last stages of the dis- 
ease. Laveran and Mesnil did not find the ‘‘stumpy form” 


TRYPANOSOMA THEILERI 143 


and found that the long form had no free flagellum, but that 
in the long and short forms the protoplasm extended to the end 
of the flagellum. The parasites are found in small numbers (to 
10 in a field of the microscope) in the peripheral blood, or are not 
found for several days at a time. 


TRYPANOSOMA THEILERI 


The parasite, named Trypanosoma theileri, was found by 
Theiler in 1902 in the blood of cattle. It is the largest of the 
pathogenic trypanosomes, measuring 20-70 by 2-6 p, and is di- 
morphic. In the ordinary form (Theiler) the centrosome is situ- 
ated at the posterior end of the body at some distance from the 
nucleus; morphologically it resembles Tr. brucei except that it is 
much larger. In the rarer form the centrosome is near or even 
attached to the nucleus. This form is broader and shows ab- 
normal shapes,—round, oval, lacerated, etc., while the nucleus is 
larger and generally less compact. 

The parasites are most quickly found in living blood. They 
are present in the blood a varying length of time. The longest 
period observed by Theiler was 13 days, the shortest one day, the 
average nine days. The number of parasites in 
the peripheral blood varies a good deal. In one 
case Theiler found 30 per field (objective No. 6 
Zeiss); in other cases none could be found on 
microscopical examination. Theiler considers 
about five per field as a fair average. 

Frequently the parasites have been transmitted 
in the process of immunizing cattle against 
rinderpest, the blood injected containing the 
trypanosomes. Theiler showed experimentally 
that flies, Hippobosca rufipes and H. maculata,  F'6- 22. Try- 
may transmit the disease. Tr. theileri is at pres- ?@”080"@ Mee 

: Z . (Theiler). 
ent regarded to have very little if any pathogenic 
properties. A similar trypanosome, perhaps the same species, has 
been found in the blood of apparently healthy cattle in America. 

Changes in the blood.—The effect on the animal varies greatly. 
In some cases no symptoms are produced; in others there is a 
marked reduction in the number of red corpuscles. In one of 


144 INFECTIOUS DISEASES DUE TO PROTOZOA 


Theiler’s experimental cases the red corpuscles fell from 6,780,000 
to 3,000,000 per emm. Poikilocytosis was observed. In more 
severe cases the number may be reduced still lower, with marked 
pathological changes in the red corpuscles, the presence of numer- 
ous corpuscles showing punctate basophilia, many erythroblasts 
(normoblasts and megaloblasts), microcytes and megalocytes. 
In cases of light infection the number of leucocytes is scarcely 
increased; but when the trypanosomes are frequent, the leucocytes 
seem to increase in direct proportion. The eosinophiles are usually 
increased in number and are sometimes very numerous (Theiler). 


REFERENCES 


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3. Bases, V. L’étiologie d’une enzootie des moutons denommée Carceag 
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5. BARUCHELLO UND Morr. Untersuchungen iiber die in Italien vorkom- 
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6. Brrrer. Cited by Theiler. 

7. Bonomr, A. Ueber parasitiire Ietero-Hematurie der Schafe. Beitrag 
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8. Bownttu, T. Equine piroplasmosis. Journ. of Hyg., v, 1905, p. 7. 

9. Bruce, Davin. Preliminary report on the tsetse fly disease or nagana 
in Zululand. Durban, 1895. 

10. Brucr, Davin. Further report on the tsetse fly disease or nagana in 
Zululand. Ubombo, Zululand, 1896. 

11. Bruce, Davip. Note on the discovery of a new Trypanosoma. Pro- 
ceed. Roy. Soc. London, |xix, 1902, p. 496. 

12. Courmont ET Lesteur. La polynucléose de la rage. Journ. d. Physiol. 
et d. Path. gen., iii, 1901, p. 599. 

13. Crawtey, H. A Trypanosome which appears in cultures made from 
the blood of American cattle. U.S. Dept. of Agr., Bur. Anim. Ind., Bul. 119, 
Oct. 1909. 

14. Curry, J. J. Report on a parasitic disease of horses, mules and caraboa 
in the Philippine Islands. Am. Med., iii, 1902, p. 512, also Vet. Journ., liv, 
p. 292. 

15. Dortern, F. Die Protozoen als Parasiten und Krankheitserreger, 
Jena, 1901. 


REFERENCES 145 


16. Dortern, F. Lehrbuch der Protozoenkunde. 3te Auf. 1911. Gustav 
Fischer, Jena. , 

17. DscHUNKOWSKY UND Luus. Die Piroplasmosen des Rindes. Centralbl. 
f. Bakt., I Abt. Orig., xxxv, 1904, S. 486. 

18. Ductoux, E. Sur une piroplasmose bacilliforme de bceuf en Tunisie. 
Compt. Rend. Soc. d. Biol., lvii, 1905, p. 461. 

19. Durron anD Topp. Researches on trypanosomiases in West Africa. 
Brit. Med. Journ., 1903, II, p. 650. 

20. Exmasstan, M. MaldeCaderas. Anal. d.l. Univ. Nacional, Asuncion, 
i, 1901. 

21. Eumasstan, M. Mal de Caderas. Berlin. tierdirtz. Woch., 1901, S. 
604. 

22. Evans, GrirritaH. Report on “surra” disease in the Dera Ismail 
Khan district. Military Dept., Nov. 13, 1880. 

23. Evans, Grirrtid. On a horse disease in India known as ‘‘surra,”’ 
probably due to a Hematozoan. Vet. Journ., xiii, 1881, pp. 1, 83, 180, 326 
and xiv, pp. 97, 181. 

24. GrawaM-Smitu, G. S. Canine piroplasmosis III, morbid anatomy. 
Journ. of Hyg., v, 1905, p. 250. 

25. GueuieLmr. Un caso di malaria nel cavallo. La Clinica veterinaria, 
1899, p. 220. 

26. Hipparp anp Neau. Some observations on the blood of dairy cows 
in tick-infested regions. Journ. Inf. Dis., ix, 1911, 324. 

27. KanTHACK, DURHAM AND BLANDForRD. On nagana or tsetse fly disease. 
Proceed. Roy. Soc. London, |xiv, 1898, p. 100. 

28. Kocu, Ropertr. Rhodesian investigations. Agr. Journ. Cape of Good 
Hope, xxiv, 1904. 

29. Kocu, Rosperr. Vorliufige Mitteilungen iiber die Ergebnisse einer 
Forchungreise nach Ostafrica. Deutsch, med. Woch., xxxi, 1905, S. 1865. 

30. Kosset, H. Die Haimoglobinurie der Rinder. Handb. d. path. Mikroog. 
von Kolle u Wassermann, Bd. I, 1903, S. 841. 

31. KossEL unp WesBer. Ueber die Himoglobinurie der Rinder in Fin- 
land. Arbeit. Kais. Ges-Amt., xvii, 1900. 

32. Launoy eT Livy-Bruuxu. Les variations numériques et morphologiques 
des globules blanes chez les poules infectées de Spirochaeta gallinarum. Compt. 
rend. Soc. d. Biol., xxiv, 1913, 754. 

33. Launoy, L. et Lfivy-Bruat, M. Sur L’anémie observée chez la poule 
au cours de l’infection par la Spirochaeta gallinarum. Compt. rend. Soc. d. 
Biol., lxxv, 1913, 250. 

34. LaveraNn, A. Contribution a l’étude de Piroplasma equi. Compt. 
rend. Soc. d. Biol., liii, 1901, p. 385. 

35. LAVERAN, A. Sur un nouveau trypanosoma des bovidés. Compt. rend. 
Acad. d. Sciences., exxxiv, 1902, p. 512. 

36. LAVERAN ET Mesniu. Recherches morphologiques et expérimentales 
sur le trypanosome du nagana ou maladie de la mouche tsetse. Ann. d. 
UInst. Past., xvi, 1902, p. 1. 

37. LAVERAN ET Mesniu. ‘Sur un trypanosome d’Afrique pathogéne pour 


146 INFECTIOUS DISEASES DUE TO PROTOZOA 


les équidés. Tr. dimorphon Dutton et Todd. Compt. rendes Acad. d. Sciences, 
exxxvill, 1904, p. 732. 

38. LaverRAN AND MeEsniu. Trypanosomes and trypanosomiases, transl. 
by D. Nabarro. London, 1907. 

39. Lincarp, A. Annual report of Imperial Bacteriologist, 1900-1901, 
Calcutta, p. 3. 

40. MacNrnau anp Novy. On the cultivation of Trypanosoma lewisi. 
Contributions to medical research, dedicated to Vaughn, 1903, p. 549. 

41. Moras, C. 8. Contribution a |’étude de la piroplasmose ovine (Car- 
coag). Arhiva Veterinara Bucarest, 1904. Abstr. in Fol. Ham. i, 1904, p. 607. 

42. MusGraAvE AND Cieca. Report on trypanosoma and trypanosomiasis, 
with special reference to surra, in the Philippine Islands. No. 5, Bur. of 
Govt. Laboratories, Manila, 1903. 

43. Nocarp, E. Sur la fréquence en France et sur le diagnostic de la piro- 
plasmose canine. Bull. d. l. Soc. centr., 1xi, 1902, p. 716. 

44. Nocarp ret Atmy. Une observation de piroplasmose canine. Bull. d. 
l. Soc. centr., Ix, 1901, p. 192. 

45. Nocarp ET Moras. Contribution a l'étude de la piroplasmose canine. 
Ann. d. UV Inst. Past., xvi, 1902, p. 257. 

46. Nocut unp Mayrr. Trypanosomen als Krankheitserreger. Handb. 
d. path. Mikroorganismen, Kolle und Wassermann, Erst. Ergdnzsungsbd., 
1907, S. 1. 

47. Nurrauy, G. H. F. Canine piroplasmosis I. Journ. of Hyg., iv, 1904, 
p. 219. 

48. NurraLL AND GRAHAM-SmiTH. Canine piroplasmosis. Journ. of 
Hyg., v, 1905, p. 237; vi, 1906, p. 586 and vii, 1907, p. 232. 

49. Pease, H. T. Surra and dourine. Vet. Journ., N.S., ix, 1904, p. 187. 

50. Prana BT GALLI-VALERIO. Su di un’ infezione del cane con parassiti 
endoglobulari nel sangue. Jl moderno Zooiatro, 1895, p. 163. 

51. PLimmer AND Braprorp. A preliminary note on the morphology and 
distribution of the organism found in the tsetse fly disease. Proceed. Roy. 
Soc. London, |xv, 1899, p. 274. 

52. Roperrson, Wm. Malignant jaundice in the dog. Journ. of Compar. 
Path. and Therap., xiv, 1901, p. 327. 

53. Roacrrs, L. The transmission of the Trypanosoma evansi by horse 
flies, ete. Proceed. Roy. Soc. London, \xviii, 1901, p. 163. 

54. Roucrr, J. Contribution a l'étude du trypanosome des mamiféres. 
Ann. d. UInst. Past., x, 1896, p. 716. 

55. SauperBEcK, E. Die Trypanosomiasis vom Standpunkt der allgemeinen 
Pathologie. Lubarsch und Ostertag-Ergebnisse der allgem. Path., 10te Jahrg., 
1904-05, S. 305. 

56. Scuriytinc, C. Piroplasmosen. Kolle und Wasserman. Handb. d. 
path. Mikroorganismen, Erst. Ergdnzungsbd., 1907, 8. 76. 

57. ScuriuiNG, C. Bericht iiber die Surra-Krankheit der Pferde. Centralbl. 
f. Bakt., xxx, 1st Abt. Orig., 1901, S. 545. 

58. Stvort prt Lecter. La surra américain ou mal de Caderas. Anal. d. 
Minist. d. Agr. Argentina, i, No. 1, 1902. 


REFERENCES 147 


59. SmitH, THEOBALD. Preliminary observations on the micro-organism 
of Texas fever. Med. News, Dec. 21, 1889. 

60. SmitH AND KILBOURNE. Investigations into the nature, causation and 
prevention of Texas or Southern cattle fever. Bull. No. 1, Bur. An. Ind., 
U.S. Dept. of Agr., 1893. 

61. SmirH AND Kinyoun. A preliminary note on a parasitic disease of 
horses. Army path. laboratory, Manila, P. I., 1901. 

62. Starcovict, C. Bemerkungen iiber den durch Babes entdeckten Blut- 
parasiten und die durch denselben hervorgebrachten Krankheiten, etc. Cen- 
tralbl. f. Bakt., xiv, 1893, S. 1. 

63. STEEL, J. H. An investigation into an obscure and fatal disease among 
transport mules in British Burma. 1885. 

64. THemerR, A. Die Pferde-Malaria. Schweizer-Arch. f. Tierheilk., xliii, 
1901, S. 253. 

65. THEILeER, A. Die Tsetse-Krankheit. Schweizer-Arch. f. Tierheilk., 
xliii, 1901, S. 97, 153. 

66. THEmLeR, A. A new trypanosome and the disease caused by it. Journ. 
of Compar. Path. and Therap., xvi., 1903, p. 193. 

67. THeILER, A. Piroplasma mutans noy. sp. A new species of piroplasma 
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70. Wricut, J. A. Canine piroplasmosis IV. On certain changes in the 
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71. ZreMANN, H. Ueber Malaria und andere Blutparasiten u. s. w. Jena, 
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CHAPTER X 


DISEASES WHOSE CAUSE HAS NOT BEEN DEFINITELY 
DETERMINED 


DOG DISTEMPER 


Sabrazes and Muratet examined the blood of four cases of dog 
distemper at Bordeaux where the nervous form of the disease is 
frequently observed and is very severe, the mortality exceeding 
60%. The counts of red and white corpuscles and the amount of 
hemoglobin were not reported. In one case there were signs of 
anemia with normoblastic reaction. In another case there were 
slight anisocytosis and polychromatophilia. The changes in the 
leucocytes were more pronounced. Polynucleosis with lessened 
number of eosins was the rule. The absolute number of leucocytes 
was increased in three cases. The iodine reaction was present each 
time it was made (three cases). The following table gives the 
differential counts in the four cases examined. 


Taste XLIII.—Doc Distemper (SABRAZES AND MURATET) . 


2 
. | Age Large ain 
T ar , = = 
No. |Sex Mo. Lymph. Maes Polym. | Eos. 38 
I m| 10 5.% |11.% | 83.5% |0.54% symptoms for 24 hrs. 
Te et 6.) 27AL |S OA ee 0.85 |0.41 |sick 6 hrs. temp. 39.2° C. 
IV |m]} 3 6. St 91. sick 5 days; temp. 37.6°. 
V f | 14 } 138.84 85. 0.84 |sick 114 months. 
RINDERPEST 


Though the specific cause of rinderpest has not been determined, 
the blood of animals sick of the disease is virulent. Jobling states 
that it has been proven experimentally that 0.1 ce. of blood from 
a sick animal injected subcutaneously will produce the disease. 

148 


RINDERPEST 149 


Nicholle and Adil-Bey have shown that the virus is able to pass 
through a Berkefeld filter. The changes in the leucocytes in the 
course of the disease have been studied by Réfik-Bey. He found 
that in cases of fatal infection there is an initial increase in the 
number of leucocytes followed by a decrease, constantly present; 
then there is a secondary increase, constantly present. The initial 
increase takes place the second or third day after inoculation; the 
number may reach 18,300 per emm. The mononuclears, including 
the lymphocytes, increase in about half the cases, maximum ob- 
served 12,300 percmm. Réfik-Bey states that the normal number 
of mononuclears in cattle is from 4,500 to 6,500 per emm., 57-84%; 
the normal number of polynuclears 1,500 to 3,500 per emm. Gen- 
erally the polynuclears take part in the initial increase, maximum 
observed 8,000. Sometimes the eosinophiles are increased, maxi- 
mum observed 3,500. 

The number of leucocytes commences to decrease the fourth 
day (sometimes the third), the minimum being ordinarily reached 
the fifth day (sometimes the fourth, exceptionally the sixth or 
seventh). The lowest count obtained was 2,000. The minimum 
is generally observed the day of the rise of temperature, rarely the 
day before and sometimes the second or third day of fever. In 
this stage all the varieties are diminished. The minimum number 
of mononuclears observed was 1,000 per emm., of polymorphs 200 
per cmm., of eosinophiles 200 per emm. The eosinophiles then 
disappear and do not reappear. 

The secondary increase begins generally the eighth day, some- 
times the seventh and exceptionally the ninth. Usually the tem- 
perature falls at this time; rarely it has fallen the day before or 
falls the day following the increase. The leucocytes in the cases 
observed have increased, exceeding the normal; in one case there 
were 45,000 per cmm. Toward the time of death the leucocytes 
commence to decrease. The mononuclears increase, in half the 
cases observed not reaching the normal; in the other half reaching 
or exceeding the normal, maximum 27,000 per cmm. The poly- 
morphs increase, sometimes simply returning to the normal 
number and sometimes exceeding it. The polynucleosis is more 
marked when life is prolonged, maximum observed 18,000 per 
cmm. 


150 DISEASES WHOSE CAUSE IS UNKNOWN 


HOG CHOLERA 


The cause of hog cholera has been determined to be a virus that 
will pass through a bacteria proof filter. King, Baeslack and Hoff- 
mann state that they have constantly found by dark field examina- 
tion a spirochete in the blood of hogs (40 cases) affected with hog 
cholera but did not find it in the blood of hogs (48 cases) not 
affected with hog cholera. The spirochetes were not found in 
large numbers, but were found with less difficulty in the acute 
form of the disease and when it was at its height. The spirochete, 
which they named Spirochaeta su7s, later Sp. hyos, is relatively 
large, averaging from 5-7 micra in length by one micron in width. 
The blood was drawn aseptically from the caudal artery into 
sterile sodium citrate solution and kept in the incubator until the 
examination was completed. Dilution was in the proportion of 
about one part of blood to ten or fifteen of citrate solution. 

The changes occurring in the blood in hog cholera were studied 
by King and Wilson. They found the red corpuscles and hemo- 
globin decreased. The red corpuscles varied from 2.8 to 9 millions 
with an average of 5.84 millions. “The hemoglobin varied from 50 
to 82, average 72. There was an increase of ore minute in the 
average time of coagulation. 

The leucocytes were decreased. The number varied from 7,200 
to 23,600 with an average of 15,515. The decrease was in the 
lymphocytes, polymorphonuclears and eosinophiles. The large 
mononuclears and mast cells were increased. The lymphocytes 
varied from 16.5 to 74.2 per cent., average 50.3; the large mononu- 
clears 2 to 42 per cent., average 11.3; polymorphonuclears 10 to 70 
per cent., average 31.8; eosinophiles 0 to 16 per cent., average 3.5 
and mast cells 0 to 18.1, average 3.5. 


EQUINE INFECTIOUS ANEMIA 


The cause of equine infectious anemia has not been discovered. 
It is so minute it will pass through a bacteria proof filter (Carrée 
and Vallé). The disease may be transmitted by the inoculation 
of blood or urine (Carée and Vallé, Francis and Marstellar and 
others) of a diseased animal. It is probable that the disease in 
America known as swamp fever is the same. 


EQUINE INFECTIOUS ANEMIA 151 


Infectious anemia was at one time called ‘pernicious anemia” 
because of the profound anemia produced by it. The red corpuscles 
and hemoglobin are much reduced. As low as one million red 
corpuscles and 25 per cent. hemoglobin are reported (Meier). 
Marked changes in the size, shape and staining of the red cor- 
puscles are found in the more marked cases of the disease. Many 
poikilocytes, microcytes and megalocytes may be found. Nu- 
cleated red cells sometimes occur, normoblasts and microblasts. 
Megaloblasts have not been observed. 

The leucocytes are decreased. Sometimes they are increased, 
but possibly the leucocytosis is due to some other condition. The 
polymorphonuclears do not seem reduced so much or so constantly 
as the lymphocytes. Further investigation is needed to determine 
the changes in the leucocytes. The following tables are of cases 
in Switzerland reported by Meier. 


TaBLeE XLIV.—Cases or Equine Inrectious ANEMIA (MEIER) 


ae Date = Sex ape gh Hb. Leucocytes 

13 13 g 1.452 25 5,000 
14 10-X-04 5% m 1.8 25-30 5,880 
11-X 1.9 25-30 6,200 
17-X 1.74 25-30 5,500 
15 13-I-05 11 m 4.0 60 8,000 
17-1 3.22 45-50 20,600 
16 7-IlI a m 1.76 30 4,500 
17 3-XI hs m 2.376 30-35 21,870 
26-XI 2.4 30-35 6,600 
8-XIT 1.3-1.9 30 4,026 

10-XII 2.4 30 50-7,812 

11-XII 3.3 62-5,312 
12-XII 10,920 
18 9-VI 9 m 3.4 45 4,200 
19 10-VI 6 g 1.0 25 10,800 


152 DISEASES WHOSE CAUSE IS UNKNOWN 


TaBLE XLV.—Tue LevucocytTes IN Cases oF Equine INFEcTIOUS ANEMIA 
(MErER) 


L VARIETIES OF LEUcocyTES, NUMBER AND PERCENT 
euco- 


No. | Date ee 
cytes |T,ympho.|Large Mon.|Polymorphs| Eosins |Mast Cells 
13 5,000 | 1,640 587 2,675 
42.8 1157 33.5 
“14 | 11-X| 6,200] 389 375 5,439 39. 
6.2 5.4 87.7 «|) 1086 
| 17-X |} 5,500) 389 223 4,865 10. 
7.0 4.0 88.4 | 0.17 
“15 | 13-1] 8,000 | 2,249 1,435 4,160 21. 
28.0 17.9 52. 0.2 
~~ | 17-1 | 20,600 | 3,333 1,517 15,610 
16 7.2 tise lee 
16 | 7-IIl| 4,500] 932 151 3,406 7 
20.7 Pa 75.60 | 0.1 
“17 | 26-X1] 6,600 | 1,485 704 4,400 11 
22.5 10.6 66:6. |. ===") ene 
| 12-X1T | 10,920 | 3,594 1,168 6,136 
32.91 10.7 ae a es 
“1g | 9-VI| 4,200] 946 295 2,956 
22.5 6.8 70S | eee 
“19 | 10-VI | 10,800 | 5,810 614 4,150 ive 
53.8 5.6 58.4. | 0001 
RHEUMATISM 


There are but few cases reported in animals in which examina- 
tions of the blood have been made. In man there is an oligo- 
cythemia in some cases. Cabot in 163 cases had 13 with less than 
4,000,000 red corpuscles. The lowest count was 2,528,000 with 
45% hemoglobin. The average number for the entire series was 
4,300,000. The hemoglobin suffers more than the red corpuscles. 
In Cabot’s cases the average was 63% with a color index of .73. 
The fibrin is much increased. There is usually a moderate leu- 
cocytosis but in mild cases without exudation there is usually no 
inerease in the leucocytes. The average number of leucocytes in 
243 cases reported by Cabot was 13,800. Turk insists that when 


REFERENCES 153 


the leucocytes reach or exceed 20,000 it is nearly always due to 
complications (pleuritis, peritonitis, pneumonia). Ewing supports 
Turk’s statement. When the leucocytes do not exceed the normal 
limit, there is little change in the proportion of the varieties; but 
with distinct leucocytosis, there is an absolute increase in the 
polymorphs. The eosinophiles are scanty or may be absent during 
the very early stages, but later are present in moderate numbers. 
After defervescence the eosins are usually increased. 

Meier reports a case of muscular rheumatism in a mare, five 
and one-half years old, with 8,420,000 red corpuscles, 90% hemo- 
globin, and 20,600 leucocytes, of which there were 8.1% lym- 
phocytes, 2.5% large mononuclears, and 89.3% polymorphonu- 
clears. 

Dr. Ward Giltner, in a personal communication which he has 
kindly permitted me to use, gives the counts in a gelding about 15 
years old, taken with acute inflammatory rheumatism. On Nov. 
9th, with a temperature of 105° F., there were 5,250,000 red cor- 
puscles and 20,000 leucocytes, of which 2.6% were lymphocytes, 
three per cent. large mononuclears and 94.4% polymorphs. No 
eosins were found. Two days later the animal was much improved; 
eosins were present in normal numbers. On Dec. 19th, the disease 
had changed into the chronic form; the horse was down, unable to 
rise. There were 6,200,000 red corpuscles, 11,000 leucocytes and 
70% hemoglobin. Of the leucocytes 13.6% were lymphocytes, 
one per cent. large mononuclears, 84.8% polymorphs, 0.4% eosins 
and 0.2% mast cells. The horse died the following day, the post- 
mortem showing lesions of articular rheumatism, ulcers on the 
articular cartilages and fibrosis of left biceps. 


REFERENCES 


1. Francis AND MarsTeELuarR. Infectious anemia of the horse. Tezras 
Agr. Exp. Sta., Bul. 119. 

2. Josyine, J. W. A preliminary report on rinderpest of cattle and carabaos 
in the Philippine Islands. Bull. No. 4, Bur. of Govt. Lab., Manila, 1903. 
3. Kina, Barstack AND HorrMaNN. Studies on the virus of hog cholera. 
Journ. Inf. Dis., xii, 1913, 206. 

4. Kine, W. E. anp Witson, R. H. Studies on hog cholera and preventive 
treatment. Kans. State Agr. Col. Exp. Sta., Bul. 171, 1910. 

5. Kina anp Witson. Spirocheta suis, its significance as a pathogenic 
organism. Journ. Inf. Dis., xii, 1913, 463. 


154 DISEASES WHOSE CAUSE IS UNKNOWN 


6. Mack, W. B. Equine anemia. Univ. of Nev., Agr. Exp. Sta., Bul. 68, 
Mar. 1909. 

7. Metigr, P. Beitriige zur vergleichenden Blutpathologie. Zeitschr, f. 
Tiermed, x, 1906, S. 1. 

8. NicHOLLE ET ApiL-Bry. Etudes sur la peste bovine. Ann. d. l’Inst. 
Past., xvi, 1902, p. 56. 

9. Rérik-Bry. Modifications leucocytaires dans la peste bovine. Ann. 
d. lV Inst. Past., xvi, 1902, p. 163. 

10. SaBprazis ET Muratet. Contribution a l’étude du sang et du liquide 
cephalo-rachidien dans la ‘‘ Maladie” des chiens. Rev. gen. d. Med. Vet., viii, 
1906, p. 663. 

11. TurK. Klinisch. Untersuchungen. Wien, 1897. 

12. VauLtfe eT Carr. Sur la nature infectieuse de l’anémie du cheval. 
Compt. rend. Acad. d. Sc., exxxix, 1904, 331 and 1239. 

13. VaLLie UND Carr. Die infektidse Natur der Animie der Pferde. 
Berl. tierartz. Woch., Aug. 18, 1904. 

14. VaLLfie eT Carrté. Recherches expérimentales sur |’anémie pernicieuse 
du cheval (Typho-anémie infectieuse). Rev. gen. med. vet., viii, 1906, 593. 


5 
4 
4 
: 
et 
j 
Pa 


Pa eee 


CHAPTER XI 


DISEASES DUE TO ANIMAL PARASITES 


Acariasis.—<An increase in the leucocytes and in the number 
and percentage of eosinophiles has been found in severe cases of 
follicular and of sarcoptic mange in dogs and cats. The greatest 
increase was in a eat affected with sarcoptic mange in which there 
were 7020 (27%) eosinophiles per emm. Welch found that the 
greater the amount of itching and irritation the greater was the 
eosinophilia. He states that the eosinophilia depends more upon 
the intensity of the dermatitis than upon its extent. 


TaBLe XLVI.—SEVERE CasEs or FoLLicuLAR MANGE IN Docs (WELCH) 


Varieties of Leucocytes, Number and Per Cent. 
Leucocytes 
No. per cmm. 


Lympho Large Mono.| Polymorphs Eosins Mast Cells 

1 | 10,000 16% 3% 70% 11% 0 
1,600 300 7,000 1,100 0 

2 8,000 30 5 60 5 0 
2,400 400 4,800 400 0 

3 12,000 23 4 60 8 0.4 
2,760 480 7,200 960 48. 

4 14,000 26 3 62 8 0 
3,640 420 8,680 1,120 0 

5 —— 38 2 56 5 0 

6 12,800 22 1 64 13 0.4 
2,810 128 8,200 1,664 50. 

Zi 20,000 30 5 59 4 0 
6,000 1,000 11,800 800 0 

8 18,000 38 2 51 8 0 
6,200 360 . 9,180 1,440 0 


| 


155 


156 DISEASES DUE TO ANIMAL PARASITES 


TaBLE XLVII.—Severe Cases or Sarcoptic MANGE (WEtcnH) 


Varieties of Leucocytes, Number and Per Cent. 


Leucocytes ps a eee 
SS er Lympho. Large Mono.| Polymorphs Eosins Mast Cells 
No. 1 20% 1% 53% 27% 1% 
_cat_ 26,000 5,200 260 1,380 7,020 260 
No. 2 20 2 72 6 0 
dog 14,600 2,900 290 11,500 876 0 
No. 3 14 4 74 8 0 
dog 8,000 1,120 320 5,920 640 0 
No. 4 36 1 44 17 0 
dog 13,000 4,600 130 5,720 2,200 0 
No. 5 8 1 83 9 0 
cat | 18,200 1,450 182 15,106 1,630 0 
HELMINTHIASIS 


A large number of observations are recorded showing the value 
of blood examinations in cases of intestinal helminthiasis in man. 
In certain helminthiases an anemia of a very severe type occurs, 
notably with Bothriocephalus latus and Uncinaria duodenale, in 
which the anemia may closely simulate that of cryptogenic per- 
nicious anemia. Severe anemia is also sometimes produced by 
other intestinal worms, as Trichocephalus dispar and Oxyuris 
vermicularis. In many of the intestinal helminthiases a pro- 
nounced eosinophilia is present. Brown reported an eosinophilia 
of 68.2% (11,070 per emm.) with a leucocyte count of 17,700 per 
cmm. in a ease of trichiniasis. Bucklers found as high as 9.89% 
eosins in a case of ascariasis, 8.2% with Tenia solium and 10% 
with Teenia saginata. 

There are many parasites that produce anemia in the domes- 
ticated animals. The anemia is so marked in some of these that 
it is known as “pernicious anemia,” for example Uncinariasis in 
dogs and in cats. Thiroux and Teppaz found a profound anemia 
(1,750,000 red corpuscles per emm.) present in dogs infested with 
Uncinaria trigonocephala. Sheep and cattle also have a very 
severe anemia due to different species of Uncinaria. Some of the 
other worms producing serious anemia are: Distoma hepaticum, 
Tenia fimbriata, Echinococcus, Sclerostoma, Oxyuris, Strongylus 


4 
: 
! 
‘ 


HELMINTHIASIS 157 


and others. Unfortunately but few detailed examinations of the 
blood of clinical cases have been made; but from those made it 
seems that an examination of the blood is of considerable diag- 
nostic value. Of course a positive diagnosis of helminthiasis is 
to be made by finding the specific worms, larve or eggs in each 
ease. The value of the blood examination consists in giving a 
clue as to the cause of trouble; it is a symptom that may be of 
great value in doubtful cases. 

Sclerostomatosis.— Moore, Haring and Cady found that in 
horses having extensive aneurisms in the mesenteric arteries, 
caused by Sclerostoma bidentatum, there was a decided increase 
in the eosinophiles. They state “‘our results suggest that the 
examination of the blood of horses troubled by frequent attacks 
of colic, of which the cause is obscure, would be of some diagnostic 
value in determining whether or not the attacks were caused by 
this parasite.’ This is a conservative statement as the other 
troubles showing colic produce a quite different effect on the 
blood. In acute indigestion there is no increase of eosinophiles 
and in acute inflammation of the bowels there is a polynuclear 
leucocytosis. Further. studies have strengthened the value of 
these findings. In a more extended investigation, as yet unpub- 
lished, Dr. V. A. Moore found that aneurisms might be present 
in the arteries without an accompanying eosinophilia; but that 
a marked eosinophilia was present in subjects having numerous 
worms present. The eosinophilia indicates not the presence of 
aneurisms but an active infestation with the parasites. The fol- 
lowing cases were reported by Moore, Haring and Cady. The 
animals were dissection subjects and had many aneurisms in the 
mesenteric arteries, each containing many worms. 


Tapie XLVIII.—Scterostomatosis (Moore, Harine anp Capy) 


Red Cor- Leuco Large Mast 
No.| Age | Sex miiscles Hb. ayics Lymph Ton. | Polym Eos Cells 
20 | aged | geld. ».4 62 | 10,303 | 22.3% | 6.1% | 63.9% ALG 0.4% 
21 | aged | mare 6.7 95 4,807 | 33.3 6.6 50.8 Sul 12 
22 | aged | geld. 6.7 60 20.6 PE 61.3 13.3 2.1 
23 | aged | mare 1.4 82 6,555 | 14.2 LS 74.6 8.3 1.4 


Trichinosis.—In trichinosis in man there is a marked rela- 
tive and absolute increase in the number of eosinophiles during 
the acute stages of the disease; but in cases of long standing or 


158 DISEASES DUE TO ANIMAL PARASITES 


quiescent the eosinophilia may disappear (Cabot). Cabot states 
that the characteristic blood lesions change trichinosis from the 
position of a disease very difficult and uncertain of diagnosis 
(without excision of a bit of muscle) to one whose recognition is 
usually easy. Opie in an experimental study fed pork containing 
different numbers of trichina larve to guinea pigs and obtained 
the following results: “‘The administration of trichina spiralis to 
the guinea pig causes an increase of the eosinophile leucocytes 
in the blood, comparable 
to that which accompanies 
human infection. There is 
no constant alteration of 
the number of these cells 
until the end of the second 
week after infection, when 
their relative and absolute 
number rapidly increases 
and reaches a maximum 
at the end of the third 
week. At this time em- 
bryonic trichine are in 
process of transmission 
from the intestinal mucose 
by way of the lymphatic 
vessels and the blood through the lungs to the muscular system.”’ 
Drake examined the blood of 15 swine, the muscle of which he 
had found contained larval trichinse, and found that there was 
no increase in the numbers of eosinophiles. The blood contained 
the following percentages of leucocytes: lymphocytes 53-72, aver- 
age 63.2; polynuclears 26-42, average 32.7; eosinophiles 0.5-10, 
average 4.03. He concludes that there is in swine trichinosis no 
increase in the percentage of eosinophiles. Another explanation, 
however, is possible, that his examinations were made ina stage 
too late to show the increase. 

FiJariasis.—In an old dog much emaciated and showing marked 
ascites, Burnett and Traum found larvee of Filaria immitis in the 
peripheral blood. The blood examination gave the following: red 
corpuscles 2,642,000, hemoglobin 57, leucocytes 24,590. Of the 
leucocytes there were lymphocytes 8%, large mononuclears 7%, 


Fic. 23. Filaria immitis in blood, dog. 


HELMINITHIASIS 159 


polymorphs 85%, and eosinophiles 2%. There were 72 erythro- 
blasts per emm. The larve averaged about one per cubic milli- 
meter. At the postmortem many adult worms, Filaria immitis, 
were found in the right auricle, vena cava and pulmonary artery. 
The changes in the blood are evidently not due to the filariz. In 
another dog they found larve, probably of Filaria lewisi. In this 
ease the blood had 6,235,000 red corpuscles, 104% hemoglobin 
and 7,716 leucocytes of which there were 13.6% lymphocytes, 
4.2% large mononuclears, 78.1% polymorphs, and 4.2% eosino- 
philes. In the reported cases of filariasis in man it seems that 
eosinophilia is present in recently acquired cases. Calvert in 
one case found leucocytosis present, 18,000—26,600, with the 
eosinophiles varying irregularly between 22.2 to eight per cent. 
In a second case of much longer duration he found the leucocytes 
varying between 7,600—14,000; the eosinophiles from six to 20%. 

Teniasis.—In cases of Tzenia solium, T. saginata and T. nana 
in man, Bucklers found the eosinophiles increased (5 to 10%). 
Launois and Weil found eosinophilia in cases of T. inermis. Cabot 
states that in the ordinary cases of tape worm many of which he 
has examined he has not usually found eosinophilia. 

Uncinariasis.—In most cases in man there is moderate anemia 
with the hemoglobin more affected than the red corpuscles. In 
many cases anemia of the pernicious type with megalocytes, 
microytes, megaloblasts and increased color index is seen. A 
moderate leucocytosis is frequently found. Ashford, however, 
regards leucocytosis when it occurs as due to complications. The 
eosinophiles are nearly always increased and are sometimes very 
numerous. As high as 72% is recorded. 

Trichocephalus, Strongylus and Oxyuris.—In 12 cases in man 
in which Trichocephalus was the only worm found in the feces, 
P. F. Brown found that the eosinophiles rarely fell below five 
per cent. 

In sheep infested with Strongylus contortus, Law states that 
there is a deficiency of red corpuscles with many peculiar cells 
larger than normal red corpuscles and distorted (poikilocytosis). 
Counts were not given. 

Runeberg observed a case of pernicious anemia in man due to 
Oxyuris. Butcklers reported a case of Oxyuris in man with 16% 
eosinophiles and in another case of Oxyuris and Ascaris there was 


160 DISEASES DUE TO ANIMAL PARASITES 


19% eosinophiles. In four cases of Ascaris in man Bucklers re- 
ported three with increase of eosinophiles, 7.4-9.8% while in one 
there was no increase, 1.8%. 


REFERENCES 


1. AsHrorp, B. K. Ankylostomiasis in Puerto Rico. N. Y. Med. Journ., 
Ixxi, 1900, p. 552. 

2. Brown, P. K. The report of three cases in which embryos of the strongy- 
loides intestinalis were found in the stools. Bost. Med. and Surg. Journ., 
exlvili, 1903, p. 583. 

3. Brown, T. R. Studies in trichinosis. Bull. Johns Hopk. Hosp., viii, 
1897, p. 79. Also Journ. of Exper. Med., iii, 1898, p. 315. 

4. Buckiers. Ueber den Zusammenhang der Vermehrung der esoinophilen 
Zellen im Blute mit der Vorkommen der Charcot’chen Krystalle in den Fices 
bei Wurmkrankheiten. Miinch. med. Woch., xli, 1894, 8. 22. 

5. BurRNETT AND TrAuM. The clinical examination of the blood of the dog. 
Proceed. Am. Vet. Med. Assn., xlii, 1905, p. 349. 

6. Catvert, W. J. A preliminary report on the blood in two cases of 
filariasis. Bull. Johns Hopk. Hosp., xiii, 1902, p. 23, also p. 133. 

7. Drake, A. K. Trichinosis. Journ. of Med. Research, viii, 1902, p. 255. 

8. Launots ET Wetu. Eosinophilie et parasitisme vermineux chez l’homme. 
Sem. med., xxii, 1902, p. 378. 

9. Law, James. Veterinary Medicine, vol. v, 1903, p. 254. 

10. Moore, Harina anp Capy. The clinical examination of the blood of 
the horse and its value to the veterinarian. Proceed. Am. Vet. Med. Assn., 
1904, p. 284. 

11. Opin, E. L. An experimental study of the relation of cells with eosino- 
phile granulation to infection with an animal parasite (Trichina spiralis). 
Am. Journ. Med. Sciences, exxvii, 1904, p. 477. 

12. Opin, E. L. The occurrence of cells with eosinophile granulation and 
their relation to nutrition. Am. Journ. Med. Sciences, exxvil, 1904, p. 217. 

13. RuneserG. Deutsch. Arch. f. klin. Med., xli, 1887, 8. 304. 

14. Tarroux ET Teppaz. Sur l’ankylostomiase du chien au Sénégal. 
Compt. rend. Soc. d. Biol., viii, 1906, ii, p. 265. 


15. Wetcu, Howarp. Blood examinations of dermatoses in dogs. Rep. 


N.Y. State Vet. College, 1909-1910, 146. 


INDEX 


Abscess, 75, 97. 
Acariasis, 155. 
Actinomycosis, 113. 
Age, effect on blood, 62. 
Agglutinins, 26, 95, 112. 
Alphanaphthol-pyronin method, 20, 
34. 
Altitude, effect on blood, 64. 
Ameboid movement, 30. 
Anemia, 64. 
Pernicious, 85. 
Anesthesia, 61. 
Anhydremia, 61. 
Animal parasites, diseases due to, 
155. 
Ankylostoma, 81, 86, 156, 159. 
Antemortem leucocytosis, 79. 
Anthrax, 105. 
M’Fadyean’s method for stain- 
ing, 106. 
Aseariasis, 156, 160. 
Ascaris, 156, 159. 


B 


Babesia, 118-132. 

bigemina, 118. 

canis, 123. 

equl, 129. 

mutans, 131. 

ovis, 131.° 
Bacteria, diseases due to, 100. 
Bacteriological examination of blood, 

26. 

Basophile cells, 33. 
Basophilia, 70, 82. 
Blepharoplast, 134, 136. 
Blood dust, 37. 


Blood plates, 36. 

Counting, 9. 

Morphology of, 36. 
Bogg’s coagulometer, 25. 
Bothriocephalus latus, 86, 156. 
Botryomycosis, 114. 


Cc 


Carceag, 131. 
Cats, normal blood of, 47. 
Cattle, normal blood of, 42. 
Centrosome, 134, 136, 138. 
Cleaning apparatus, 7. 
Coagulation, time of, 25. 
Bogg’s method, 25. 
Hinman and Sladen’s method, 25. 
Wright’s method, 25. 
Coagulometer, Bogg’s, 25. 
Wright’s, 25- 
Coarsely granular basophile cells, 33. 
Coarsely granular oxyphile cells, 
33. 
Coition, 80. 
Cold baths, 73. 
Computation, 7, 8. 
Counting blood plates, 9. 
Counting chamber, 3. 
Thoma, 3. 
Turck, 4. 
Zappert-Ewing, 4, 8. 
Counting leucocytes, 8. 
Counting red corpuscles, 2. 
Croupous pneumonia in horses, 101. 
Cytodites, 66. 


D 


Daland’s hematocrit, 24. 
Dare’s hemoglobinometer, 13. 


161 


162 


Degenerative changes in leucocytes, 
35. 

Dermatitis, 81, 155. 

Differential counting of leucocytes, 21. 

Digestion, leucocytosis of, 70. 

Diluting fluids, 3. 

Distoma hepaticum, 156. 

Dog distemper, 148. 

Dogs, normal blood of, 45. 

Domestic fowls, normal blood of, 53. 

Dourine, 138. 

Drugs, effect of, 76, 80, 83. 

Dust, blood, 37. 


EK 


East coast fever, 132. 
Echinococcus, 156. 
Eczema, 81. 
Eosin and methylene blue stain, 19. 
Eosinophiles, 33. 
Eosinophilia, 70, 80, 155-160. 
Eosinophilic myelocyte, 34, 82, 88. 
Equine infectious anemia, 151. 
Equine malaria, 129. 
Erythroblasts, 30, 88, 128, 138, 144, 
159. 

Erythrocytes, 29. 
Estimation of hemoglobin, 11. 
Experimental leucocytosis, 75. 
Exudation, 96. 

Catarrhal, 97. 

Purulent, 97. 

Sero-fibrinous, 97. 

Serous, 96. 

Simple, 97. 


F 


Fat, test for, 23. 

Fever, changes in the blood in, 95. 
Filaria immitis, 158. 

Filariasis, 158. 

Finely granular oxyphile cells, 32. 
Fixation of smears, 17. 

Fleam, 2. 

Fleischl-Miescher hemometer, 15. 


INDEX 


Follicular mange, 155. 

Fowl cholera, 103. 

Fowl, domestic, normal blood, 53. 

Fowl, domestic, polymorphonuclears, 
32. 

Fowl typhoid, 104. 


G 


Gambian horse sickness, 142. 

General and infectious diseases, 95. 

Giemsa’s stain, 19. 

Glanders, 108. 

Glycogen test, 22. 

Glycogenic degeneration, 35. 

Goats, normal blood of, 45. 

Gower’s hemoglobinometer, 12. 

Graham’s alphanaphthol-pyronin 
stain, 20, 34. 

Guinea pigs, normal blood of, 52. 


H 


Haldane’s hemoglobinometer, 13. 

method, 13. 
Hammerschlag’s method, 25. 
Hasting’s stain, 18. 

Hayem’s fluid, 3. 
Helminthiasis, 81, 156. 
Hematoblasts, 37. 
Hemotacrit, Daland’s, 24. 
Hematocytometer, 3. 
Hemoglobin, estimation of, 11. 
Hemoglobin index, 85. 
Hemoglobinometers, 11. 

Dare’s, 13. 

Fleischl-Miescher’s, 15. 

Gower’s, 12. 

Haldane’s, 138. 

Sahli’s, 13. 

Tallqvist’s, 11. 
Hemoglobinuria, 122, 127, 137. 
Hemokonia, 37. 

Hemometer, Fleischl-Miescher’s, 15. 
Hemorrhage, 64, 78. 

Herpes tonsurans, 114. 

Hinman and Sladen’s method, 25. 


INDEX 


Hippobosca maculata, 143. 
Hippobosea rufipes, 148. 
Histological examination, 16. 
Hodgkin’s disease, 92. 

Hog cholera, 150. 

Horse, normal blood of, 40. 

Horse sickness, South African, 129. 
Hyaline cells, 31. 
Hyperleucocytosis, 70. 
Hypoleucocytosis, 70, 82. 


I 


Ictero-hematuria in sheep, 131. 
Infections, simple, 96. 
Infectious diseases, 100, 116. 

Due to bacteria, 100. 

Due to protozoa, 116. 
Infectious leukemia, 104. 
Inflammation, 95, 96. 

Catarrhal, 97. 

Exudative, 97. 

Purulent, 97. 

Serous, 96. 

Simple, 97. 

Inflammatory leucocytosis, 73. 
lodine reaction, 22, 35, 97, 148. 
Todophilia, 35. 


J 


Jenner’s stain, 17. 


K 


Karysome, 130. 

Kemp and Calhoun’s method of 
counting blood plates, 10. 

Kurloff bodies, 31. 


L 


Large mononuclears, 31. 

Leucoblasts, 34. 

Leucocytes, counting, 8. 
Differential counting, 21. 
Morphology, 30, 33. 


163 


Leucocytosis, 70. 
Antemortem, 79. 
Experimental, 75. 
Inflammatory, 73. 
Mixed, 70, 73. 

Of cold baths, 73. 

Of digestion, 70. 

Of massage, 73. 

Of new born, 72. 

Of parturition, 71. 

Of pregnancy, 71. 

Of violent exercise, 73. 

Polynuclear, 70, 71, 73, 74, 78, 

79. 

Post hemorrhagic, 78. 
Leucopenia, 70, 77, 82, 97, 101. 
Leukemia, 87. 

Lymphatic, 87, 89. 

Lymphoid, 87. 

Mixed celled, 87. 

Myelogenie, 87. 

Occurrence, 91. 

Spleno-medullary, 87. 
Limit of error, 7. 
Lymph-adenoma, 92. 
Lymphatic leukemia, 89. 
Lymphocytes, 31. 
Lymphocytosis, 70, 71, 72, 76. 
Lymphoma, 92. 
Lympho-Sarcoma, 93. 


M 


Mal de caderas, 139. 
Malaria, canine, 123. 
Malaria, equine, 129. 
Malignant jaundice in the dog, 123. 
Mallein, 110. 
Mange, 81, 155. 
Follicular, 81, 155. 
Sarcoptic, 81, 155. 
Massage, 73. 
Mast cells, 33, 82. 
Megakaryocytes, 36. 
Megaloblasts, 30, 68, 85, 88, 144. 
Megalocytes, 29, 68, 85, 131. 
Metamyelocytes, 34, 88. 


164 INDEX 


Methods of examination, 1. 
M’Fadyean’s stain, 106. 
Microblasts, 30, 68, 85. 
Microcytes, 29, 68, 131, 144. 
Mixed celled leukemia, 87. 
Mixed leucocytosis, 70, 73, 128. 
Monocytes, 31. 
Mononucleosis, 70. 
Morphology, 29. 

Of blood dust, 37. 

Of blood plates, 36. 

Of leucocytes, 30. 

Of red corpuscles, 29. 

Of thrombocytes, 36. 
Myeiemia, 87. 
Myelocytes, 34, 82, 90, 116. 

Eosinophilic, 34, 82. 


N 


Nagana, 137. 
Neutrophiles, 32. 
New born, 70. 
Newton’s rings, 6. 
Normal blood, 40. 
Cats, 47. 
Cattle, 42. 
Dogs, 45. 
Domestic fowls, 53. 
Goats, 45. 
Guinea pigs, 52. 
Horses, 40. 
Rabbits, 50. 
Sheep, 44. 
Swine, 49. 
Normoblasts, 30, 68, 85, 90, 144. 
Nucleated red cells, 30. 


O 


Occurrence of myelocytes, 82. 
Oestrum, 80. 

Oligemia, 61, 64. 
Oligochromemia, 64. 
Oligocythemia, 61, 64. 

Oxygen capacity of the blood, 23. 
Oxyuris, 81, 156, 159. 


P 


Pappenheim’s stain, 20. 
Parasites, animal, diseases due to, 
155. 
Parturition, 63, 71. 
Pernicious anemia, 85, 156. 
In horses, 68, 85. 
In man, 85. 
Phagocytosis, 129. 
Piroplasma annulatum, 133. 
bigeminum, 118. 
canis, 123. 
equi, 129. 
mutans, 131. 
ovis, 131. 
parvum, 132. 
Piroplasmosis, 118. 
Bovine, 118. 
Canine, 123. 
Equine, 129. 
Ovine, 1381. 
Plasma cells, 34. 
Plates, blood, 36. 
Plethora, 60. 
Pneumonia, 101. 
Poikilocytes, 30. 
Poikilocytosis, 30, 85. 
Polychromasia, 30, 65, 86, 122. 
Polychromatophilia, 30, 131. 
Polyeythemia, 61. 
Polymorphonuclears, 32. 
Polynuclear leucocytosis, 70, 71, 73, 
74, 78, 79. 
Polynuclears, 32. 
Polynucleosis, 70. 
Posthemorrhagic leucocytosis, 78. 
Pratt’s method of counting blood 
plates, 9. 
Precipitins, 26, 95. 
Pregnancy, 63, 71. 
Preparation of site of puncture, 1. 
Procuring blood, 1. 
Protozoa, diseases caused by, 116. 
Pseudoleukemia, 92. 
Punctate basophilia, 30, 122. 


INDEX 


Puncture, 2. 
Pyrosoma (see Babesia). 


R 


Rabbits, normal blood of, 50. 

Rabies, 117. 

Red corpuscles, counting, 2. 

Morphology, 29. 

Reizungsformen, 34. 

Relation of pseudoleukemia to leu- 
kemia and sarcoma, 93. 

Relative volume of corpuscles and 
plasma, 24. 

Rheumatism, 152. 

Rhipicephalus evertsi, 129. 

Rhodesian fever, 132. 

Rinderpest, 148. 


S 


Sahli’s hemoglobinometer, 13. 
Sarcoma, relation to leukemia, 93. 
Sarcoptic mange, 155. 
Sclerostoma bidentatum, 81, 
157. 

Sclerostomatosis, 157. 
Securing the blood, 2, 54. 
Septicemia, 74, 97, 105. 
Sex, effect on blood, 62. 
Sheep, normal blood of, 44. 
Simple infections, 96. 
Simple inflammation, 97. 
Site of puncture, 1. 
Smears, method of preparing, 16. 
Soundness, examination for, xvi. 
South African horse sickness, 129. 
Specifie gravity, 25. 
Specific infectious diseases, 100, 116. 
Spindelzellen, 36. 
Spirochaeta, 116, 150. 

Gallinarum, 116. 

Hyos, 150. 

Suis, 150. 
Spirochetosis, 116. 
Staining smears, 17. 
Stains, 17. 


156, 


165 


Stains, Eosin and methylene blue, 19. 
Giemsa’s, 19. 
Graham’s, 20. 
Hasting’s, 18. 
Jenner’s, 17. 
Laveran’s, 129. 
Leishman’s, 125. 
M’Fadyean’s, 106. 
Pappenheim’s, 20. 
Romanowsky, 120, 125, 129, 134. 
Wright’s, 18. 

Stimulation forms, 34. 

Stomyx calcitrans, 136. 

Strangles, 100. 

Strongylus, 66, 156, 159. 
Contortus, 159. 

Suppuration, 97. 

Surra, 135. 

Swamp fever, 150. 

Swine, normal blood of, 49. 


A 


Tabanus tropicus, 136. 
Taenia fimbriata, 156. 
Inermis, 159. 
Nana, 159. 
Saginata, 156, 159. 
Solium, 156, 159. 
Takosis, 102. 
Tallqvist’s hemoglobin scale, 11. 
Teniasis, 159. 
Test for agglutins, 26, 112. 
Fat, 23. 
Glycogen, 22. 
Tetanus, 112. 
Texas fever, 118. 
Theileria parva, 132. 
Thoma’s hematocytometer, 3. 
Thrombocytes, 36. 
Time of coagulation, 25. 
Toisson’s fluid, 3. 
Total volume of blood, 23. 
Transitional leucocytes, 34. 
Trichina, 156, 157. 
Trichinosis, 156, 157. 
Trichocephalus, 156, 159. 


166 INDEX 


Trypanosoma, 133. Uncinaria, Trigonocephala, 156. 
Brucei, 137. Uncinariasis, 156, 159. ; 
Cultivation of, 134. 
Dimorphon, 142. Vv 
Equinum, 139. 
Equiperdum, 138. Value of blood examination, xv. 
Evansi, 135. Violent exercise, 73. 
Lewisi, 134. Volume of blood, 23. 
Staining of, 134. 
Theileri, 143. Ww 
Trypanosomatosis, 133. 
Tiirek ruling, 4. Wright’s coagulometer, 25. 
Typhoid, fowl, 104. Wright’s stain, 18. 
Wright and Kinnecutt’s method, 10. 
U 
Z 
Uncinaria, 66, 86, 156, 159. 
Duodenole, 156. Zappert-Ewing ruling, 4. 


Printed in the United States of America 


HE following pages contain advertisements of a 
few of the Macmillan books on kindred subjects. 


Practical Veterinary Pharmacology 
and [herapeutics 


By HOWARD JAY MILKS, 


Professor of Therapeutics and Small Animal Clinic, New York State 
Veterinary College, Cornell University. 


Svo. Preparing. 


This book is designed as a text-book for students and practitioners in 
veterinary medicine. In addition to the usual discussion on the action 
and uses of drugs there are chapters on the method of action of drugs, 
incompatibilities, solubilities, prescription writing and biologic prepara- 
tions. 


Drugs are grouped according to their therapeutic indications or uses and 
the general therapeutic considerations are taken up just before the 
members of the group are discussed in detail. Thus the general actions 
and uses of the group and the detailed study of the drugs belonging to 
it are discussed in the same chapter. This plan differs from many texts 
in which the various therapeutic groups are discussed briefly in the 
first part of the book and to which no reference is made under the de- 
tailed discussion of the drugs. 


Included under the discussion of the various drugs are the common 
and official names, synonyms, derivation, preparations, doses in both 
metric and apothecary’s systems, action upon the various systems of 
the body including poisoning and its treatment, and the uses. The 
action and uses of the drugs are correlated so far as is possible. 


That part of the book devoted to drugs has been brought up to date and 
made to conform to the last revision of the United States Pharmacopceia. 
Representative prescriptions involving the use of different drugs in 
various combinations are profusely scattered throughout the book. 


The chapter on serums, antitoxins and viruses was prepared by Dr. 
C. P. Fitch, Professor of Bacteriology, New York State Veterinary Col- 
lege, Cornell University. It deals with the method of preparation of the 
different products as well as their application and should be especially 
valuable to those practitioners who have been out of college for some years. 


THE MACMILLAN COMPANY 
Publishers 64-66 Fifth Avenue New York 


Diseases of the Dog and Aids to 


Treatment and Management 


By FRANK TOWNSEND BARTON, M.R.C.V.S. 
(Captain At Wee) 
255 pages, $1.50 


FROM THE PREFACE 


“ Diseases of the Dog and Aids to Treatment and Manage- 
ment ” is primarily intended to serve as a First Aid for those who 
have the charge of dogs either in health or in sickness. It is not 
always convenient to obtain professional assistance, but when such 
aid is within reach it should always be obtained as speedily as pos- 
sible, as unskilful treatment, no matter however well directed, fre- 
quently leads to disappointment and much useless suffering to the 


patient. 


By skilled assistance we mean the employment of a qualified 
practitioner, and not that of the empiric, whose knowledge is based 
upon no scientific training and whose treatment may be on entirely 
wrong lines. 

There are minor ailments and accidents which can be effectively 
dealt with by the novice, and the Author has endeavored to incor- 
porate in this work the needful instructions for carrying out the 


elementary principles of canine medicine and surgery. 


THE MACMILLAN COMPANY 
Publishers 64-66 Fifth Avenue New York 


The Pathology and Differential 


Diagnosis of Infectious Dis- 
eases of Animals 


Fourth Edition, revised and enlarged. 


Be VERANUS- ALVA MOORE, B:S., M.D. 


Professor of Comparative Pathology, Bacteriology and Meat Inspection, and 
Director of the New York State Veterinary College, Cornell University, 
ithacal Ne Ye 


Cloth, 8vo, 560 pp., with 120 ill., $4.00 


This edition has been carefully revised, much of it rewritten and 
numerous additions made. It has been kept, however,. within the 
limits of a text-book. Two appendices have been added, one on 
the requirements for interstate shipment of live stock and the other 
on the Federal regulations for the veterinary inspection of meat. 
These may be of much assistance to veterinarians. The diseases 
not indigenous to, or imported into, this country have been accorded 
much less space than those existing here. The desire is to empha- 
size the nature of the diseases our veterinarians are liable to en- 
counter and, at the same time, give the characteristics of the others. 
The same plan of presenting the subject and of grouping the dis- 
eases according to their etiology, that was followed in the previous 


editions, has been retained in this. 


THE MACMILLAN COMPANY 
Publishers 64-66 Fifth Avenue New York 


Medical and Veterinary 
Entomology 


By WILLIAM B. HERMS 


Associate Professor of Parasitology in the University of California; 
Consulting Parasitologist for the California State 
Board of Health, etc. 


Cloth, 8vo, illustrated, $4.00 


A work of interest to physicians, veterinarians, health 
officers, and sanitarians as well as to students. Herein is 
contained a discussion of all the more important insects and 
arachnids relating to disease and irritations of man and beast. 
The author has placed special emphasis on control and pre- 
vention. He has aimed to familiarize the student with the 
specific parasite treated in a chapter, its identity, life history, 
habits, relation to disease transmission or causation, and to 
indicate methods for its control and prevention. There are 
228 illustrations in the text, largely made from original 


photographs or drawings. 


* 


THE MACMILLAN COMPANY 


Publishers 64-66 Fifth Avenue New York 


SF Burnett, Sammel Howard 

ath The clinical pathology of 
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f 1917 animals 2d ed., rev. and enl. 


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