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LIBRARY OF CONGRESS.
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PRESENTED BY_

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HOG CHOLERA:

ITS HISTORY, NATURE, AND TREATMENT,

AS DETERMINED BY

THE INQUIRIES AND INVESTIGATIONS

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THE BUREAU OF ANIMAL INDUSTRY.
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WASHINGTON:
GOVERNMENT PRINTING OFFICE.
1889. :
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TABLE OF CONTENTS.

Page.
INTRODUCTION AND SPREAD OF HOG CHOLERA IN THE UNITED STATES ......- 9
EWE SMEATION ORNS WINE DISASUS: .ccc.-c.cs cas. ccccec case mceves sauces ace 14
SYMPTOMS AND POST-MORTEM APPEARANCES IN HoG CHOLERA..--...--- Boa ap
“esions produced by hog cholera ...-.-- si eaterai Pae(ceintels aeVaistle aa/eeie Sa tance oS 34

(a) Acute type.----. olan aatteeate SO OO eee Seah seee cece e 3
(b) Chronic forms...-.- 3 ASO DED ORR BoD Oe SOB AR ES mee eens i ete 335,

HIsToRY AND AUTOPSY NOTES OF AN OUTBREAK OF HoG CHOLFRA......--- 37)

DISEASE IN HEALTHY PIGS CAUSED BY MATERIAL FROM THIS EPIZOOTIC.-.- 50
BRIEF SUMMARY OF THE IMPORTANT FEATURES OF THIS EPIZOOTIC ....---- 52
Eien MEMO LOSTONG =e aaietee steals isle accel snoe sa enem a Sceeons etadientes 4 52
WileeRaLimepleSiONSes foc caSewe clase see cased OSS IAS OAD Ses Be 6 Bassoon Be 53
Complications -....-- Se ee 9 SRC EES ET RISERS Oe aE OR one irae nen eae 54
PMMOPLOSIOHS = oe Saccce ceceeaeme 5: i Paar ae Biss Moree eee Oe ale seer 54
EACPURTOLOGTICAT, OBSERVATIONS Sars = 2s s220 seas cices a. ccicemnee ieerteic Sac. 5}
iin CAUSATION OR: ETIOLOGY OF HOG CHOLBRA! ..-<..<-<ca ccc ccc cee wcoaec 6:
eeouacelugion nes whOlorar y= 0. 22 = sacks ace 2 Ses Sasa cecdat seve Sue's cock 63
SiaMinovahhos-CholenanlaGhentas mln oi tae me clei ew ee cre crac isoclsyeisen cere 65
Esiotory of the hor-cholera bacillus. <.20..-- .2.6- ooo ocne ees een cot ene eee 66
(a) Diagnostic characters ....-...- 3: StS See a RESIS AB SSS AC CORES 66
iayoumer physiolotical characters. * of...) 2 52h ecrshs. t. pote cee. ese 69
Tue DiIaGNoOsis OF HOG CHOLERA BY MEANS OF INOCULATION... .-.-.---.-- 69

VITALITY OF HOG-CHOLERA BACILLI AND THEIR RESISTANCE TO VARIOUS
OTST SONA ECT) 7 WEN DEN (CIDE (se Ae Perce i a ae = ne ene near as 75
Resistance of hog-cholera bacteria to heat in liquid media........-...-.-- 75
Vitality of hog-cholera bacteria in ordinary water ............-....--...- 75
Resistance to continuous drying at ordinary temperatures ........-.-.---- 73

SoME EXPERIMENTS ON THE LENGTH OF TIME DURING WHICH HoG CHOL-
MRAwVMIRUSERMITAING ATL VR ENi DEM SOUL... sss nscecceseccecs vane Sees 80

A FEW ADDITIONAL OBSERVATIONS AS TO THE VITALITY OF HoG CHOLERA
VIRUS IN THE SOIL AT THE EXPERIMENT STATION ..-.-----..-- Be seers ; 86
THE EFFECT OF SOME DISINFECTANTS ON THE VIRUS OF HOG CHOLERA... 87
Mercuric chloride.:..... ..... seers es a Secnt ae Sa ete, ae sate was seen 88
Carbolic acid -..-- SESSA NS mas noe bs 5 SORE ee Soe Ae eee oe ae 2 88
Iodine water.. --. ee ee Sieh AOE EES Stars ay ee one Serra eciz scissor 89
Peoaaneanate of Patasil..xoa2srs sce ossceen evens ccess sence ceastaee es Spee 89
Mercuric iodide ...--- Be es Bp See no ten ees ears Se ate a eneie eae oct : 89
Salplieie! Gly COpPer-s cea. 2--kecs cecanann-- Saree ere Cae oe TS 3 90
Eivdinochloricr acre oa.) ne ee eee on as Pee ees A. Ae Pe steele 90
Cinloriderotazin Clos so. noe a eee ee ee oe ee Rey pare Ay ee See ae 90
SUL PEC, oe Sea yen Tet oc, 1s) kod ie son ge a ne 90

(CHROMSIES> (ESTES TENE NENG Lee ece ee eR IRE SS So a ee ee eee 91
3

4

ORDINARY LIME AS A DISINFECTANT FOR HoG CHOLERa ...---. .-- Peshotee
DISINFECTION OF THE SOIL WITH LIME ...----.- Sree Laake aa as 1 A
Is THERE ANY RESISTANT SPORE STATE IN THE Lire HISTORY OF THE Ba-
CIETUS ON SHOGMCHOLERA .ene er eee eee SorMeeCSnGoas
WAYS IN WHICH SWINE BECOME INFECTED. ....---.-.---- eS Sisco ane Soe J
By way of the digestive tract ..............-- S Snes eee See ee ewes

a. Feeding diseased viscera... -. Sa Re Sees Gee eee Saks mis Janene

b. Feeding pure culture of Hog Cholera bacilli. -.........-......--- an
Subcutaneousnocwlation =. ese. ee se. sess oho ic ee = Se eee ae Se
Intra-venous inoculation ..5.25...--. ..- Ee ee ons Se ae A Goods
Imfectious by: way ot theslino st ssee sere eeiee eee eb cee met oo eee
SoME OBSERVATIONS ON THE PATHOLOGICAL ACTION oF HoG CHOLERA BaAc-
THRDA ct cc o Hess aes cee eee eee ees e Sete RE SSE Oe eee ee eee is
BACTERIOLOGICAL INVESTIGATIONS OF HOG CHOLERA 1N NEBRASKA, ILLI-
NOUS ANID MUAVREN A AGNGD reer teetare po mtoasocs eseceal ds dysiets BE en ier seme
DIFFERENTIAL CHARACTERS OF THE HoG CHOLERA BACILLUS -..-.....---<.<
Bacillus frome@Nebraska. soe. o weseence sss hee see eerie ee cee eee wuldaes cates
Bacillus from Wlimois: <4cs. cote ones sctacee wines seca tas eme Reece ee eee eee
Bacillus from Maryland......- agaiciewmlaps Bem atlas cid teerate sie mns ete ete Ie eee eer
RELATION OF HOG CHOLERA TO. TH PUBLIC EmALEH <=. er eee eee eae 2
PREVENTION OF HoG CHOLERA -....-. -=-------+------.--- wart 2 shiec eee eee is
ISOLATION, DISINFECTION, AND CLEANLINESS AS PREVENTIVE MEASURES....
TROAEMENT ORE OG CHORMRA Ss ceercee ies cen coe ee been eee eases See 3

EXPERIMENTS ON THE PREVENTION OF HOG CHOLERA By INOCULATION ..-..
J. Inoculation of small doses of strong virus in the form of liquid culture...

Il. The effect of feeding small quantities of cultures on immunity----.----
III. Injection of sterilized culture liquid to produce immunity-.------------
Tests with sterilized cultures on pigeons. ...- oxeceteeeeee Bi AG OS

Tests with sterilized cultures on pigs .-...----------- Stinsis, s1oi> Syeie e :

EXPERIMENTS ON THE ATTENUATION OF THE HoG CHOLERA BACILLI BY HEAT
Hog CHOLERA OR DISEASES CLOSELY ALLIED TO IT IN OTHER COUNTRIES -.

In Great Britain’ 2.2. BEE she ote ee hig and aes A ee pe te) eee ice atoee
In Sweden and Denmark ..--- UF PR Ey Se Pee Pee = Oe te Occ 3
MUIR agiiee = os csc eediecccecivaice oe eae wion cc od sew eavdoees cee eee

ILLUSTRATIONS.

INVESTIGATION Or HoG CHOLERA: ae
PuaTEs I, II, III, and IV. Illustrating necrosis and ulceration of the mu-
cosa of the large intestine, more particularly the cecum ....-.-- 194
ive SHOWS Hleere mt Ghemilewy Poo 5 hss 2.02.2 cc cies. a's alaeatrs eee 194
Min showie hemorrhagic kidney. 525. Soha <aieanls ermaine Sane Sed a 194
MEL SHO Whe HOMOEE NAO UG ING: 22s cceisd s\aewe ates Soeur aoa 194
VIE SHOWiie HeMOLlineie Heath. 2. < ras esse su. Se we cle ake be 194
IX: Collapse’and broncho-pneumonia........-. .... 22-22. cee---e- 194
X. Microscopic characters of hog cholera bacilli. ....- Sisieiets cet eie 194
XI, XII. Growth of hog cholera bacilli in various culture media.. 194
XIII. Spleen and liver of rabbit inoculated with hog cholera ba-
CN aE Rice SE Soe EE eh Es and ae eee ee ee EN ag 104
XIV, XV, XVI. Photomicrographs of hog cholera bacilli, showing
variation due to growth in different media. ................---- 194

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LETTER OF TRANSMITTAL.

WASHINGTON, D.C., January 18, 1889.

Srr: I have the honor to submit herewith a report upon the history
nature, and treatment of the disease known in the United States as
hog cholera. Our knowledge of this pest has been developed almost
entirely by the inquiries and experimental investigations of the Bureau
of Animal Industry; and while much of the information contained in
this volume has been published in the reports of the Department of
Agriculture, a systematic and complete statement of the facts has never
before been made in a connected manner.

It has been discovered in the course of these investigations that there
are two very different and distinct epizootic diseases of swine in this
country which are widely prevalent, and which had previously been
spoken of under the one name of hog cholera or swine plague. These
two names had, therefore, been used synonymously previous to 1886,
when the differences between the diseases were pointed out in the re-
ports of this Bureau. It was then deemed best to apply the term hog
cholera to that disease in which the intestines were found most af-
fected, and in which the symptoms would come nearest to justifying
the appellation. The other malady appeared identical, not only in
symptoms and lesions but in the microbe which caused it, with the
disease recently described in Germany by both Léffler and Schiitz un-
der the name of Schweineseuche, or swine plague. For this reason it
- was considered best to call this affection swine plague in the reports,
and thus preserve uniformity and prevent confusion of ideas in refer-
ence to the diseases of swine in different countries.

This volume treats exclusively of hog cholera, as it is the malady
which has been longest under investigation; but the material is on hand
for an almost equally complete volume on swine plague, which we hope
soon to submit for publication. There are, of course, many other dis-
eases of swine, some of which are communicable in a certain degree,
but none of which are so widespread and fatal as the two that have been
named. Someof these, especially the parasitic ones, are receiving at-
tention, and may in the future be treated at length in the bulletins of
this Bureau.

The greater part of the detailed study of the disease, the planning of
experiments, and the bacteriological investigations have been carried

7

8

out by Dr. Theobald Smith, while the conducting of the experiments,
the care of the experimental animals, and the general management
of the experiment station have been under the direction of Dr. F. L.
Kilborne. I can only speak in the highest terms of the untiring in-
dustry and skill displayed by both of these gentlemen.

The experiments in regard to prevention and medical treatment are
being continued, but it is confidently believed that an understanding of
the facts detailed in this volume will enable the owners of hogs to pre-
vent or even arrest the great majority of outbreaks. It should be un-
derstood, however, that the measures indicated must be enforced
promptly, energetically, and thoroughly.

D. E. SALMON,
Chief of the Bureau of Animal Industry.
Hon. NoRMAN J. COLMAN,
Commissioner of Agriculture.

THE INTRODUCTION AND SPREAD OF HOG CHOLERA IN THE
UNITED STATES.

In the early days of hog-raising in the United States these animals
were comparatively free from disease, and wide-spread epizootic mala-
dies among them appear to have been unknown. A circular letter of
inquiry was recently sent from the Bureau of Animal Industry to the
correspondents of the Department and to swine-breeders in all parts of
the country, asking the date of the first appearance of hog cholera in
the respondent’s county, and a statement as to the health of swine pre-
vious to that time. More than a thousand replies have been received,
many of them so carefully written as to be of much interest and value.
Nearly all agree in stating that at one time the swine industry was not
subject to the periodical losses from epizootics which now cause such
discouraging losses. From the first appearance of this class of diseases
the outbreaks became more numerous and more wide-spread until nearly
all parts of the country are now subject to frequent invasions.

The correspondence on this subject can only be briefly summarized
in this bulletin. The first outbreak of disease supposed to be cholera
that was referred to occurred in Ohio in 1833. It is reported from one
county in South Carolina in 1837, and from one in Georgia as having
existed in 1838. It existed in 1840 in one county in Alabama, one of
Florida, one of Illinois, and one of Indiana. In 1843 it is reported from
one county in North Carolina. In 1844 one county in New York re-
ports being affected. Its presence in 1845 is only mentioned by one
correspondeat from Kentucky.

The thirteen years, from 1833 to 1845, inclusive, form a period in
which but ten outbreaks of swine disease, supposed by the writers
to have been hog cholera, were mentioned in these replies. It is evi-
dent that during this period hogs were generally healthy throughout
the country, and that the losses from disease were not sufficient to at-
tract very much attention. The nature of the disease referred to as
existing so long ago may, of course, be questioned at this day, and we
have no means of deciding whether or not any particular outbreak was
cholera or some non-contagious malady due to local conditions. It is
reasonable to conclude, however, that the correspondents are correct in
their opinion in most cases, because since 1845 the outbreaks mentioned
became more numerous year by year until we find nearly the whole

9

10

country involved. This rapid increase of the number of affected sec-
tions would seem to indicate that a contagious disease had been intro-
duced and carried to widely separated sections of the country, from
which it extended until, with a year favorable to its propagation, we
find a sudden and alarming increase.

Turning again to the number of outbreaks reported, we find, in 1846,
that there were two in North Carolina, one in Georgia, one in Ilinois, one
in Indiana, and one in Ohio. In 1847 four are given in Tennessee and
one in Virginia. In 1848 we hear from it in one county in Ilinois, two
in Indiana, two in Kentucky, one in North Carolina, and one in Virginia.
In 1849 it is mentioned as in one county in Tees and in one county
in Ohio. In 1850 we have accounts of three outbreaks in Georgia, one
in Pennsylvania, one in Indiana, two in Kentucky, one in North Caro-
lina one in Ohio, and two in Tennessee. In 1851 there were outbreaks
in Ilinois, Indiana, and Tennessee. In 1852 there were two reported
in Illinois, two in Indiana, one in Missouri, and one in Ohio. In 1853
it invaded two new counties in [linois, two in Indiana, two in Kentucky,
one in North Carolina, four in Ohio, two in Tennessee, cne in Texas,
and one in Virginia. In 1854 it appeared in one more county in Ili-
nois, four in Indiana, five in Kentucky, two in North Carolina, two in
Ohio, and one in Tennessee. In 1855 it is found in six counties in Ili-
nois, five in Indiana, one in Kansas, four in Kentucky, one in Missouri,
two in Tennessee, and one in Virginia.

The number of outbreaks mentioned by correspondents, it will be
seen, 1s not less than ninety-three for the ten years from 1846 to 1855
inclusive. As compared with the ten outbreaks reported for the pre-
vious thirteen years this is an enormous increase. ‘There can be little
doubt that it was during the period from 1846 to 1855 that hog cholera
became scattered over the country and fairly began that work of ae
struction which has become so familiar to us in later years.

Below will be found a tabulated statement of the replies from nearly
eight hundred and fifty of our correspondents. The figures show the
number of original hog-cholera infections reported for the different pe-
riods from the first recorded appearance of the disease in this country
to 1887. Of course there have been many counties infected within that
time which are not referred to in these communications, but the large
number that were mentioned gives as perfect an idea as can now be
obtained cf the development and spread of this contagion. It is to be
remembered that the outbreaks mentioned are not secondary infections,
but are the first outbreaks of the disease in the correspondent’s local.
ity, andin most cases the first which occurred in his county. In nearly
all cases it is stated that previous to the outbreak referred to the health
of hogs had always been good, and the losses from disease had been
confined as a rule to a single animal at a time.

sal

Number and dates of original infections with hog cholera and swine plague, as compiled
JSrom recent correspondence.

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DLN S Sa te eee GS Os Se. cee ssdaecd Ae dheed pagscc ce teerkcosd larncerns Vices. 1 1
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PB OGD INE seme on decien <== 1 5 13 13 7 Ee petatan Mc 1 1
it eee 1 14 40 | 14 7 8 7 Tip| rerace 5
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SENS aie oe a Se ies o's 6 o' [vine ole mine Nacia clare ais 7 15 1l 11 V7 13 3
PRCERRGM See me ce cs oc ora See=|enielonccs 1 Di eymcatote ares iets note ‘DDI 12 26 6
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MERSROU Bi se atlameaetelts lee iaere= | =a =e 2 6 8 16 8 8 2
LMG ORT et 535 See epo oe Mapceeec Geanaane ye sire if 2 3 15 3
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North Carolina...........- 1 7 4 10 9 3 4 2) | awn ek <
SEROI MEER seston wate eee nicl Some eens |vaiemesa- 6) se ecemsn| ce e-ciatlascceess|~ eae Waterers
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IPENMSVLVANNA 2 occne ~~ - nate |scmecen. 1 3 Dh \oretetarestars 2 4 3 1
South Carolina ............ 1 1 3 5 hl eee Ti lieaaases pee coeele caceres
PEERNENSCOse=<25 sacs s.2 25 c|t em enon 12 18 10 5 Soviene aches eee ec aeee 1
PED RAN EE ea ee eee ana anc cel|sacrecas|Se.cdeeoclteaedae nel: oes sices|e-c'leeinn 2 GN ectatcnead 2
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VG Wahl tse) e Se ee ee ee “2 2 ad Pet ae 4 1 1
“WEIS DTT SS OS BPE ae ae Ree i | ee eaten olG Pees Se 4 13 2

Whether the outbreak which occurred in Ohio in 1833 was the first
introduction of hog cholera in this country or not, can not now be de-
termined. It seems reasonably certain, however, that the contagion
was imported from Europe with some of the animals that were brought
from there to improve our breeds of swine. The investigations made
in England and on the continent during the last year demonstrate that
the swine fever of Great Britain is identical with our hog cholera, and
that this disease is also widely scattered over the continent of Europe.
This being the case, it would appear much more likely that the conta-
gion was imported from there, as we know occurred with the contagion

12

of pleuro-pneumonia of cattle, than that it appeared spontaneously or
was developed by the conditions of life in this country. Having been
once introduced it spread gradually, following the lines of commerce
and being for a long time confined to them, until, extending step by step,
it has at one time or another invaded every section of the country in
which swine raising is a prominent industry.

Dr. George Sutton of Aurora, Ind., in 1858, wrote as follows:

I have seen notices of this disease prevailing in the States of Illinois, Kentucky,
Indiana, Ohio, New York, Massachusetts, Pennsylvania, and Maryland. It has pre-
vailed extremely in Indiana, particularly in Dearborn, Ohio, Ripley, Rush, Decatur,
Brown, Bartholomew, Shelby, Johnson, Morgan, Marion, Boone, Posey, and Sullivan
Counties. It has also prevailed in Campbell, Kenton, Boone, Gallatin, Carroll, Breck-
inridge, Bullitt, Bath, Henry, Henderson, Nicholas, Livingston, Union, and Crittenden
Counties, Kentucky. It has also prevailed in Hamilton, Butler, Clinton, Fayette,
and Clermont Counties, Ohio. Also in different portions of Illinois, and very severely
in Wayne, White, and Gallatin Counties. It has also prevailed in the State of New
York. The Ohio Farmer for January 3, 1857, quoting from the Buffalo Republic the
extensive prevalence of the disease, says that ‘‘in western New York especially we
learn it has been very fatal, but is now over. In conversation with one of the most
extensive dealers in the neighberhood, a day or two since, he informs us that about
six weeks ago he lost about four hundred in a very short space of time. A distiller
in Jordan, during the month of September, lost fourteen hundred, which cost, in ad-
dition, over $1,000 to have them buried. In Rochester, at all the principal points,
and even among the farmers, the mortality has exceeded anything ever before heard
of. A butcher in this city not long since purchased $500 worth of fat hogs, but they
died so rapidly on his hands that he scarcely realized $75 on the investment.” The
Worcester (Mass.) Spy reports that many farmers in that city and vicinity are losing
their swine by the mysterious and fatal disease known as the hog cholera. In the
southeast part of the town it prevails in a greater or less extent upon nearly every
farm.

In most cases the disease is traced to Western hogs that have been sold by the
drivers the present season, and which seem to have communicated the contagion to
the other inmates of the sties in which they have been kept. It is known that of
many droves of Western shoats that have been sold at Brighton this season, and ped-
dled about the State, nearly all have died. The disease has, no doubt, prevailed ex-
tensively in other parts of the country, of which I have seen no notice. In this sec-
tion of the country it has been extremely fatal. Over portions of Dearborn County
it spread from farm to farm, and some of our farmers lost from 70 to 80 ont of 100 of
their hogs. At the distilleries the mortality has been very severe. I received infor-
mation that more than 11,000 died at the distillery in New Richmond, in the summer
and fall of 1856. The owners of the distillery at Aurora inform me that they have
lost between 6,000 and 7,000. A gentleman informs me that he lost in 1856, at Ingra-
ham’s distillery, in Cincinnati, from the 1st of August up to the 24th of October,
1,285, losing 1,152 out of a lot of 2,408. Another gentleman informs me that at the
distillery in Petersburgh, Ky., he lost from the 1st of June up to the 18th of October,
1856, 2,576. Ihave also received information from several other distilleries where
the losses were large.*

According to Dr. Sutton, this disease first appeared in Dearborn
County, Ind., in July, 1850.

* George Sutton, M. D., Observations on the supposed relations between epizootics
and epidemics, and experimental researches to ascertain the nature of the recent epi-
zootic among the swine, and the effects which diseased meat may have on human
health. The North American Medico-Chirurgical Review, May, 1858, pp. 483-504,

Dr. E. M. Snow writes that—

During the last five years this disease has been seen, from time to time, in portions
of the more eastern States, sometimes, as in western New York in 1856, proving quite
severe and fatal in comparatively limited localities. Butin the Eastern States it has,
to a great extent, originated with and has generally been confined to hogs imported
from the West. I think that in no State east of Ohio has the disease prevailed ex-
tensively, or attained the character of a wide-spread epidemic.

In the vicinity of Providence, R. I., it has prevailed to some extent, more particu-
larly among large herds of swine during each of the last five winters, but has been
mostly confined to hogs brought from the West, and has usually disappeared with the
approach of warm weather. During the last winter it was more severe than in any
preceding, and was not confined to Western hogs. Neither did the disease, as here-
tofore, cease with cold weather, but it continued until August, having destroyed
more than 500 hogs in Providence and in the adjoining towns during the first seven
months of the present year, 1861. I havealso heard of its prevalence in various towns
in Massachusetts during the same period.*

The losses from hog cholera in the United States have been enormous.
Estimates have from time to time been made from carefully-compiled
data, and these have, so far as the writer is aware, never been less than
$10,000,000, and have reached $25,000,000 annually. The inclusion of
losses from other diseases is, however, unavoidable in such estimates,
and consequently some allowance must be made for these. The recent
identification of an epizootic pneumonia of hogs by the Bureau of Ani-
mal Industry, a disease which appears to be identical with the Schweine-
seuche of German writers, shows that the varieties of swine diseases in
this country are more numerous than has been supposed. The erysipe-
las of Europe (French, rouget ; German, Rothlauf), and charbon have
not yet been identified as occurring in an epizootic or enzootic form
among swine in the United States but the existence of these diseases is
not impossible, as the investigations have not yet been sufficiently nu-
merous to reveal the nature of all such outbreaks. The diagnosis of
such diseases has been very uncertain in the past, because the symp-
toms were not clearly defined, and not always sufficiently characteristic.
The most reliable means of discrimination between these maladies at
present is the isolation of the microbes which produce them. The char-
acteristics of these organisms are now so well known that the bacteri-
ologist has no difficulty in distinguishing between them. —

* Edwin M. Snow, M. D., Hog Cholera. Annual Report U. 8. Department of Agri-
culture, 1861, p. 147.

THE INVESTIGATIONS OF SWINE DISEASES,

Among the first to investigate these diseases in the United States
from a medical point of view was Dr. George Sutton, of Aurora, Dear-
born County, Ind. In the extensive epizootics which prevailed in that
county from 1850 to 1858 he had abundant material for’ study, and he
noted the more salient features of the plague in a very clear and com-
prehensive manner. While it is extremely difficult at this day to de-
cide whether the outbreaks studied by Dr. Sutton were hog cholera or
swine-plague, or a combination of the two, his observations are very in-
teresting and bring out many important facts. Of the symptoms, post
mortem appearances, and nature of the malady, he says:

This disease presents a great variety of symptoms. In January, 1856, when this
epizootic was at its height in this section of country, I published a short notice of it
in the Cincinnati Gazette. The syniptoms which I then described I have found upon
amore extensive observation to be correct. The hog first appears weak, his head
droops, and sometimes in a few hours after these symptoms diarrhea commences.
There is frequently vomiting. In some cases the discharges were serous and clay-
colored, sometimes dark, also bloody, and mucus resembling those of dysentery. The
urine at first was genérally small in quantity and high colored, but as the animal re-
covered it became abundant and clear; this was one of the symptoms by which the
men who were attending the hogs at the distillery ascertained that they were recover-
ing.

In a large number of cases the respiratory organs appeared to be principally af-
fected; there was coughing, wheezing, and difficult respiration. In some instances
the animal lost the power of squealing, and the larynx was diseased. There was
frequently swelling of the tongue and bleeding from the nose. In those cases where
the respiratory organs were the principal seat of the disease there was generally no
diarrhea or dysentery. In many instances the disease appeared to be principally con-
fined tothe skin; sometimes the nose, the ear, or the side of the head were very much
inflamed; the ear swollen to twiceits usual thickness. This inflammation would spread
along the skin, sometimes over the eye, producing complete blindness. Sometimes
one or more legs were inflamed and swollen, and the inflammation also extended
along the body. The skin where w as inflamed was red and swollen. Some had
large sores on their flanks or sides from 3 to 6 inches in diameter. In one instance, at
the distillery, the inflammation extended along the fore leg, the foot became ulcerated
and sloughed oft, and the animal recovered. Some appeared delirious, as if there was
inflammation of the brain. I examined the blood of four hogs which had this disease
well marked; they were stuck, and tke blood, arterial and venous, was caught ina
bowl. It was cupped and presented a well-marked buffy coat. Death took place in
from one to ten days after the attack. Sudden changes in the weather, particularly
from warm to cold, appeared to increase the fatality of this disease, The average

14

15

mortality of hogs that were in pastures or fed on slop was from 33 to 45 per cent.,
but it was frequently much more fatal if hogs were fed on corn—in some instances
ranging from seventy to eighty out of the hundred, and in some instances even
higher.

I found on opening the bodies of hogs that had died of this disease that they all
presented evidences of a diffusive form of inflammation. From sixty-seven hogsthat
I have examined I found it was not confined to any particular tissue. Sometimes
this inflammation was confined to one organ; in other cases it attacked several at
the same time. The skin frequently presented patches of inflammation, and often
had a purple appearance. In cutting through parts that were the most inflamed, the
skin was swollen and the cellular tissue was infiltrated with serum. Frequently,
however, the skin was merely discolored, without any swelling whatever. The
stomach was occasionally distended with food, and the mucous membrane in nearly
every instance presented evidence of inflammation, sometimes extending over the
whole stomach, at others only in patches. It was generally of a deep-red color,
thickened, and frequently softened. Sometimes it was covered with a viscid mucus;
in other instances there was an effusion of bloodinto the stomach. The mucous mem-
brane of the small or large intestines, where there had been diarrhea or dysentery
presented in all instances evidences of inflammation; in patches it was red, thick-
ened, sometimes softened, and occasionally ulcerated ; where there had been dysen-
tery there was generally bloody mucus found in the large intestines. The bladder
generally contained urine ; sometimes its mucous membrane was inflamed, and in one
instance there was an effusion of blood into this organ. In a Jarge number of cases
I found evidences of peritoneal inflammation, such as redness of this membrane, ef-
fusion of turbid or bloody serum, adhesions between the intestines and between the
intestines and sides of the body. In three instances blood was effused into the peri-
toneal cavity—in one instance more than a quart; it appeared in this case to come
from the liver. The liver was occasionally the seat of this inflammation, not only
in its investing membrane, but the parenchyma; sometimes there were abscesses,
and in one instance portions of it were gangrenous. The lymphatic glands were gen-
erally of a dark-red color, frequently resembling clots of blood. This disease of the
lymphatic glands was of common occurrence.

The lungs were frequently the seat of this inflammation, portions of one or both
presenting different appearances, from simple congestion to complete hepatization ;
sometimes there was ulceration, and frequently there was a turbid or sero-purulent
or bloody effusion into the pleural cavity ; sometimes there were extensive adhesions
between the lungs and pleura of the ribs. At first I was inclined to believe this
malady to be a form of pleuro-pneumonia, but after I became better acquainted with
it I found that the inflammation was not uniformly confined to any organ. In a
number of instances the mucous membrane of the bronchia was deeply inflamed and
the inflammation extended to the trachea and larynx. In several instances the larynx
was inflamed, resembling laryngitis. One animal that had great difficulty in breath-
ing and could make no noise I had knocked in the head, and on examination I found
the mucous membrane of the larynx and epiglottis inflamed and swollen; also the
tongue was swollen. There were evidences in several instances of pericarditis, which
had produced adhesions between the heart and the pericardium. The brain, from the
difficulty of opening the skull, was examined only in one instance; it was found
healthy, although I feel confident it was frequently the seat of the disease.

From these examinations we sec that it is a misnomer to call this malady cholera.
It is a contagious inflammatory disease, the inflammation being confined to no par-
ticular tissue, sometimes attacking only one, at others several, in the same animal.
Evidences of this inflammation were found in the dermoid, the cellular, the serous,
the mucous, and glandular tissues. I consider it a diffusive form of inflammation
from the manner in which I have witnessed it spread along the skin. In one night I
have seen it extend from the eye to the ear—the ear becoming inflamed and swollen,

16

Although we have not been able to show that thisis a cholera epizootic, still the facts
elicited may be of interest and remove doubts at some future period. But, then, if
this malady does not resemble cholera, does it resemble any of the diseases to which
the human system is subject? I think not. Like the specific eruptive diseases, it is
highly contagious; the infection has a period of incubation of from twelve to twenty
days, and one attack appears to exempt the animal from a second. But in this dis-
ease, although petecchix and an eruption may appear on the skin, its principal char-
acteristic is a diffusive form of inflammation which may attack nearly every tissue
and spread like an erysipelas. But then, again it differs from this disease, as it is well
known that in erysipelas one attack does not exempt the system from a second; and
although erysipelas may be contagious, still it is doubtful whether the period before
the eruption shows itself is so uniform as in this disease, and while erysipelas is gen-
erally confined to the skin this inflammation most frequently attacks the lungs and
mucous membrane of the alimentary canal. This disease appears to be intermediate
between the specific eruptive diseases and erysipelas, partaking of the nature of each,
and probably not having its exact resemblance among the diseases to which the human
system is subject.*

Of his experiments and observations on the contagiousness of the
disease and the manner of its spread he writes:

When the disease made its appearance in this section of country, in the summer of
1850, and we saw it spreading from farm to farm, the question was suggested whether
it did not spread by contagion, for it was not known at that time (July) that the
malady was contagious. Feeling much interest in watching the progress of this dis-
ease, from the large numbers of animals that were dying, I suggested to the owners of
the distillery at Aurora, Messrs. Graffs, that we should try a series of experiments to
ascertain the nature of the disease, and whether it was propagated by contagion.
To this they readily assented, and as they were constantly receiving fresh hogs,
there was a fine opportunity to make any experiments we saw proper. I am indebted
to Mr. J. J. Barkman, of Aurora, for seeing that the following experiments, with the
exception of the last, were carefully made. The hogson which the experiments were
made were known to be healthy:

(1) Six hogs that had been exposed to the malady by being in contact with dis-
eased hogs were put into a yard by themselves and fed on slop and corn; on the four-
teenth day from the time they were exposed to the disease they were all unwell; 3
died within a week afterwards, the rest recovered.

(2) Ninety hogs were exposed to the disease, then put into a yard by themselves
and fed on corn and water (no slop given); in thirteen days disease made its ap-
pearance among them, and they continued to die until 60 out of the 90 died.

(3) Fifty hogs were put into a pen by themselves, and fed on slop; they had not
been exposed to the disease ; for six weeks they continued heaithy. ;

(4) One hundred hogs that had not been exposed to the disease were put intoa
yard by themselves, and fed on corn and water; for thirty days no symptoms of dis-
ease appeared among them. They were then put into a pen with diseased hogs; on
the thirteenth day they began to show symptoms of the malady, and the disease
rapidly spread among them, until 40 died.

(5) Thirty-three hogs, out of a lot of 263, were put into a pen by themselves; for six
weeks they continued healthy. The remaining 230 were put into a pen adjoining in
which were diseased hogs; in thirteen days disease made its appearance among them,
and continued until one-half died.

(6) Four young and healthy hogs were put into a pen in which, four days previous,
diseased hogs had been; they were fed on corn and water. On the fourteenth day
they were all unwell; and one died on the fifteenth day, and in five days more they
were all dead. This experiment shows that the infection may be retained in a pen
several days.

* North American Medico-Chirurgical Review. 1858, II, 496,

ed

17

(7) Linoculated, on the 28th of October, five healthy hogs with the blood taken
from the inflamed tissues of hogs that had died of this disease. On the fourteenth
day (November 11) they were all unwell, and all died with the exception of one,
In three inflammation spread from the point where they were inoculated, along the
skin and down the legs, which became very much swollen. I can not say that this
inflammation was caused by the inoculation, for it did not appear until the fourteenth
day, and many hogs had this external form of disease.

From these experiments I think that we not only ascertained that this disease was
infectious, but that the infection had a latent period of from twelve to fifteen days.
Observations have since led me to consider the latent period as varying from twelve
to twenty days. These experiments also showed that the hogs in the pens were not
dying from strychnine in the slop. A statement was going the rounds of the papers
about this time that strychnine was used in making yeast at the distilleries, and was
poisoning the hogs at these places in large numbers.

The manner in which this disease in many instances spread among hogs from farm
to farm also showed most conclusively that it was infectious. One farmer had 75
hogs that he turned into a corn-field to fatten. These hogs had been exposed to the
disease, had become sickly, and numbers had died. He bought 36 more; these were
all healthy; they were put into the same field with the diseased hogs; in two weeks
they were unwell, and numbers died. He bought 45 more, all healthy, and put them
in the same field; in two weeks they began to show symptoms of disease, and in a
few days after a number died. Finding that he was likely to lose all his hogs, he
sold 50 of the fattest that were left to the butchers in Cincinnati, at a reduced price,
as diseased hogs. These hogs, it was said, were purchased for their fat, to be used
in the manufacture of lard oil. After deducting the 50 he sold, he lost out of the
156 all but 10.

A large number of facts could be given, if necessary, to show the contagiousness of
the disease. Hogs that had been once under the influence of this malady appear not
to be susceptible to a second attack. Although placed in pens with diseased hogs
they continue healthy and fatten, and not a single instance can I find of hogs having
this disease twice. There is reason to believe that this malady occasionally prevails
at the distilleries in a mild form, as the old hogs at many of these places did not take
the disease. But why it should suddenly have assumed so malignant a character is
as difficult to account for as that scarlatina, from being at one time the mildest of dis-
eases, at another becomes one of the most malignant. On the farms the old and young
hogs appear to be equally susceptible to the disease.

In 1861 Edwin M. Snow, M. D., of Providence, BR. I., contributed a
paper on hog cholera to the Annual Report of the United States De-
partment of Agriculture (pp. 147-154). The symptoms of the disease he
gives as follows:

The symptoms, as described by persons unaccustomed to such observations, are ex-
tremely various. By combining the information obtained from others with results of
our own observations the symptoms, as seen during the life of the animal, are nearly
as follows :

(1) Refusal of food.—This is the first symptom usually noticed by those who have
the care of the animals, though, as will be seen hereafter, this sympton by no means
indicates the beginning of the disease. The refusal of food, after it is first noticed,
generally continues through the whole sickness, and food of every description is
mostly refused.

(2) Great thirst.—This is constant, and large quantities of cold water will be swal-
lowed if it can be obtained. Even after the animal is unable to stand alone it will
drink cold water with eagerness.

(3) After a time, the length of which varies very much, the animal begins to show
signs of weakness; reels, staggers, and, in attempting to walk, often falls down,

15612 HC 2

18

(4) In most cases there is a diarrhea, with copious fluid discharges of dark, bilious,
and very offensive matters. In a few cases there is no diarrhea, but evacuations of
hard black balls; but in some of these cases the fluid offensive matter is found in
the intestines after death.

(5) In a few cases there is vomiting; but this is not often severe, nor is it contin-
uous for any length of time.

(6) The external appearance of the animal is at first paler than usual, but towards
the last of the sickness purple spots appear, first on the nose and sides of the head.
These extend along the sides of the belly and between the hind legs, after which the
animal soon dies.

(7) In many eases, perhaps a majority, ulcers are found on the different parts of
the body. These were particularly noticed on the inside of the lips and gums, and on
the feet, and were often quite deep and excavated. In some cases these ulcers were
seen in the nostrils, and in one case there were extensive ulcerations in the back part
of the mouth, on the tonsils.

(8) In some cases the legs are swelled, and the animal is lame ; sometimes the ears
and sides of the head are swelled ané red; sometimes the eyes are sore and inflamed ;
sometimes swellings like carbuncles are seen; and, generally, the glands near the
surface seem to be enlarged.

(9) In most cases the pulse is quickened, the breathing is hurried and difficult, and -.
there is much cough. But insome genuine cases there is no perceptible trouble with
the lungs, and no important signs of disease are found in them after death.

(10) The duration of the disease in fatal cases, after the first symptoms are noticed,
is extremely variable. We have seen some which have died within two or three
hours; others have lived many days. It is difficult, however, to fix the time of the
appearance of the first symptoms. The first noticed is usually the refusal of food;
but it is probable, indeed it is certain, that the sickness is in progress for a consider-
able period before the animal refuses food. Cases like the following are sometimes
seen: A hog refftses to eat; it soon grows weak ; staggers in walking ; turns purple
on the sides and belly, and dies within two or three hours after the first symptom is
noticed. But; on examination after death, extensive disease is found in the intes-
tines, or in the lungs, or in both, ata stage of development which must have required
many days to reach.

The post-mortem appearances are then summarized in the following
language:

Having described the symptoms, as seen while the animal is living, I will now give,
briefly, the appearances found on examination of the bodies after death ;

In the course of our investigations, during the last winter and spring, the bodies of
nine hogs were carefully examined by Drs. G. L. Collins, J. W. C. Ely, and E. T,
Caswell, of Providence, in the presence of several other physicians. A minute ac-
count of each case was prepared by Dr. Collins, and published in the Transactions of
the Rhode Island Medical Society for 1861. It will be sufficient for the objects of this
paper to give a brief synopsis of the diseased appearances which were found in these
examinations :

Lungs.-—-I two cases the lungs were healthy. In the remaining seven cases one or
both lungs were more or less inflamed, having a liver-like appearance, called hepatiza-
tion. In some eases the inflammation was more advanced, and the substance of the
lungs was breaking down into a mass of disease. In all cases where the lungs were
inflamed there was also pleurisy, and the lungs were adherent to the walls of the
chest; the inflammation of the lungs and the pleurisy together constituting true pleu-
ro-pneumonia. In two cases there were tubercles, or consumption in the lungs; but this
is not uncommon in hogs, and is not supposed to have any connection with the Sper
cial disease we are considering.

Stomach.—The stomach and the small intestines were generally healthy. The
stomach was freqently distended with an offensive mixture of food, and in one case.

Lin

the inner surface was ulcerated to some extent. In two cases worms were found in
_ small intestines, but this was probably a merely accidental occurrence, and had no
necessary connection with the disease. ]

Large intestines.—The inner coat of the large intestines was generally inflamed and
softened with ulcerations to a greater or less extent, and they were frequently so
tender as to be easily torn with the fingers. On account of their diseased condition
their inner coat was frequently discolored. The inflammation and ulceration of these
intestines are probably the principal cause of the diarrhea in this disease.

Kidneys.—These organs were, in every case, much more pale and yellow than
natural; this condition was well marked.

The liver and bladder were generally healthy. In some cases water was found in
the cavity of the belly and of the chest, and in the membrane surrounding the heart
(heart-case). In two cases numerous minute purple spots were seen upon the mem-
brane lining the walls of the belly. The urine was often changed from the healthy
condition, containing albumen and other diseased products, not, however, noticeable
to the eye. Ulcers upon the feet and in the mouth were often found, The brain was
not examined, as there were no symptoms observed which seemed to indicate disease
of this organ. It may be at times affected, but is probably more rarely so than the
other organs of the body.

Such are some of the most important appearances which are found on examination
of the bodies of hogs which have died with this disease. It will be noticed that three
of the diseased conditions I have described are prominent, important, and such as
would be readily recognized by the most ignorant observer.

These are, first, the pleurisy and inflammation of the lungs; second, the inflamma-
tion, ulceration, and softening of the inner coat of the large intestines; and, third,
the pale and yellowish color of the kidneys. One or more of these diseased condi-
tions will be found in every case, and in perhaps a majority of cases they will all be
found in the same animal.

While Dr. Snow admitted the disease to be epizootic he did not con-
sider it to becontagious. Indeed, he neither considered epizootic nor epi-
demic diseases to be contagious, but, on the contrary, held that they
were caused by (1) “an epidemic atmospherical poison,” and (2) “ the
local conditions or circumstances adapted to receive and propagate the
poison existing in the atmosphere.”

In 1875 Prof. James Law contributed a paper to the report of the
Department of Agriculture giving his observations upon hog cholera,
or “intestinal fever in swine,” ip which he so completely embraces the
knowledge of our swine epizootics as it then existed that bis paper is
here reproduced in full. It is as follows:

Synonyms.—Typhoid fever, enteric fever, typhus carbuncular fever, carbuncular
gastro-enteritis, carbuncular typhus, pig distemper, blue sickness, blue disease, pur-
ples, red soldier, anthrax fever, scarlatina, measles, diphtheria, erysipelas.

Definition.—A specific, contagious fever of swine, characterized by congestion, ex-
udation, ecchymosis, and ulceration of the mucous membrane of the intestines, and
to aless extent of the stomach; by general heat and redness of the skin, effaceable by
pressure; by small red spots, complicated or not by elevations and blisters; by black
spots and patches of extravasated blood on the integument, the snout, nose, eyes,
mouth, and all other visible membranes, and on internal organs, ineffaceable by
pressure and tending to sloughing; usually by liquid and fetid diarrhea; and by a
very high and early mortality.

The malady has been long known to pig-raisers and pork-factors in the Old World
and the New, but in veterinary works it has been mistakenly placed in the list of
malignant anthrax affections, to which many of its lesions bear a striking resem-

20

blance. Two English works, published within the last year, repeat this time-honored
fallacy. To malignant anthrax it is allied by the altered condition of the blood, by
the solution of the blood-globules, by the imperfect coagulation of the blood in many.
cases, by the occasional enlargement and congestion of the spleen, by the extrava-
sation of the blood out of the vessels (petechiw) into the skin, mucous membranes,
and internal organs, and by the dusky hue of the eye, nose, ete. That it is essen-
tialiy distinct is shown by the fact that its virus, so frightfully contagious and fatal
to pigs, is not communicable to any other domestic animal. The contagion of malig-
nant anthrax, on the other hand, is deadly to all domestic animals, and even to man
himself.

The common American designation of hog cholera has only the diarrhea to support
it, and, as we see outbreaks in which this feature is mainly remarkable for its ab-
sence, the name comes to be an absolute misnomer. In many cases a gelatiniform
exudation takes place on the affected surface of the mucous membrane of the intes-
tines, windpipe, or bronchia, and the disease has accordingly been named diphtheria.
But as such an exudation is by no means constant, a name founded on this peculiarity
would have no actual foundation in a large proportion of cases. Again, the exuda-
tion (see Post mortem No. 1) is mainly composed of cells and granules, with less of
the fibrinous matrix than is usual in diphtheria. Lastly, the intestinal fever of swine
is most virulently contagious, whereas diphtheria is very slightly, if at all, infec-
tious, and is confined rather to certain insalubrious localities or buildings.

From scarlatina and measles it is sufficiently distinguished by the constancy of the
intestinal legions, though it resembles both in its cutaneous rash. With erysipelas
it has no real connection, the one common feature, the redness of the skin, being due
to a condition altogether different in nature, progress, and results.

The constancy of the congestion, specific deposit, and ulceration in the intestines
in the fever of swine, characterize it as perfectly as do the same lesions in typhoid
feverinman. It further agrees with typhoid fever in having a higher evening than
morning temperature and a rose-colored eruption on the skin. To this disease, indeed,
it bears a closer resemblance than to any other disorder of man or beast, so that Dr,
Budd and others with much plausibility call it the typhoid fever of pigs. But in
spite of the similarity of the specific deposits and ulcerations on the intestines, those
of the pig show less tendency to attack the agminated glands (Peyer’s patches) and
the solitary glands than is the case in man. They appear on all parts of the mucous
membrane of the large and small intestines, yet the agminated and solitary glands
rarely escape entirely, and sometimes they alone are the seats of ulceration and morbid
deposit. The skin eruption, too, in the pig-fever is often distinctly raised, and even
vesicular, whereas that of typhoid fever is a simple rash, and, like a blush, may be com-
pletely though temporarily effaced by pressnre. Finally, the contagion is incompara-
bly more virulent and tenacious of life than that of typhoid fever, and the mortality
is greater and occurs earlier in the disease. On the whole, we must look on this
affection of pigs as a disease sui generis, having close affinities with the typhoid fever
of man, yet essentially distinct, and hence the term intestina! fever of swine is more
applicable, as at once expressing its nature and avoiding confounding 16 with other
and distinct affections.

Incubation.—The period of incubation has not been definitely settled. My experi-
ence in Scotland in 1864 would have led me to set it down at from seven to fourteen
days. The infected pigs were four days on the journey from the English market by
rail and seven days on the farm before the disease manifested itself. Again, the
home-bred swine were sound until four weeks after the strange hogs came on the
farm, and three weeks after the latter were generally sick. Pigs, though farrowed
by sick dams, did not show any sign of disease for about a week, although nearly all
eventually died.

In Dr. Budd’s cases, in April, 1865, the first symptoms of illness were shown four
or five days after the pigs were brought from Bristol market, where they may or may
not have been infected.

21

Dr. Sutton’s experiments, made at Aurora, Ind., in September, October, and Novem-
ber, 1848, deserve repetition in this connection. (1) Six hogs, after contact with dis-
eased animals, were placed in a sound pen, and sickened on the fourteenth day. (2)
Of 90, similarly exposed and then put in a sound yard, some sickened on the thir-
teenth day. (3) One hundred, similarly exposed, contracted the disease on the
thirteenth day, (4) One hundred and thirty, placed in a yard adjoining one occu-
pied by diseased hogs, became ill on the thirteenth day. (5) Four young and healthy
pigs, placed in a pen occupied four days previously by diseased hogs, sickened on the
fourteenth day. (6) Five healthy hogs, inoculated with the blood from the inflamed
tissues of diseased swine, were unwell on the fourteenth day.

Further experiments were made by Professor Axe, of London, iu April, May, June,
and July, 1875. (1) Two healthy pigs were (in April) placed for forty-eight hours
in the same house with a diseased one, contact being carefully avoided. One was
dull and off its food on the sixth day and the other on the eighth. (2) On May
15 a pig was inoculated with the liquid cutaneous exudation, which had been kept
on dry ivory points for twenty-six days. On the fifth day there was slight dullness
and heat of skin, and on the sixth the malady was well developed. (3) On June
10 another pig was inoculated with the cutaneous exudation of the last, the opera-
tion being performed by another party and the pig kept apart to avoid all risk of
indirect contagion. On the fifth day temporary redness was noticed on four teais,
and on the sixth day the symptoms were fully developed. (4) Another pig broke into
the pen occupied by the last-named subject and was left there for six days, when it
was taken out seriously ill. In the hot summers of Illinois instances are met with in
which symptoms of the disease are shown in a previously healthy herd under three
days atter the wind has blown from the direction of a sick lot half a mile distant. In
analyzing this apparently somewhat discordant evidence we must bear in mind that
the period during which a poison will remain latent in the system will vary accord-
ing to the amount taken in, the excited or febrile condition of the subject, and the
mode of introduction into the system. Thus an excess of any poison, animal or veg-
etable, will usually show its effects with remarkable rapidity. A feverish state of
the system, whether induced by intense heat, passion, or disease will rouse the poison
into unusually early activity. Lastly, poisons that are inoculated usually act sooner
than those introduced into the system by other channels. These considerations
will serve to reconcile the prolonged latency of the poison in Dr. Sutton’s cases,
observed in cold weather, as compared with Dr. Budd’s, Professor Axe’s, and my own,
in the English summer, and of these in their turn with the prompt development of
the malady in the semi-tropical summer of Illinois,

Symptoms.—The earliest symptoms are slight duliness, with sometimes wrinkling
of the skin of the face as if from headache; shivering or chilliness and a desire to
hide under the litter are not uncommon. Some loathing of food, intense thirst,
elevation of the temperature of the rectum to 104° Fahrenheit and increased heat
and reduess of the skin are usually the first observed symptoms, and occur one or two
days later than premonitory signs above mentioned. The increased heat of the skin is
especially noticeable inside the elbow and thigh and along the belly. By the second
day of illness the whole surface feels hot, and in white pigs is suffused with a red
blush, which may pass successively through the shades of purple and violet. It is
usually more or less mottled at particular points, and a specific eruption appears as
rose-colored spots of from 1 to 3 lines in diameter, sometimes slightly raised so
as to be perceptible to the touch, and either pointed or more frequently rounded.
The redness fades under the pressure of the finger, but only to re-appear immediately.
The eruption is usually abundant on the breast, belly, and haunch, the inner side of
the forearm and thighs, and the back of the ears. It staysout fortwo or three days,
and may be followed by one, two, or more successive crops of the same kind. The
cuticle is sometimes raised in minute blisters, a feature which distinguishes this from
the rash of typhoid fever, and the liquid of such blisters inoculated on other pigs

22,

communicates the disease. In addition to the rash and simultaneously with it, or
soon after, there appear on the skin numerous spots of a dark-red or black color, vary-
ing in size from a line to an inch in Ciameter, on the color of which pressure has no
effect. These are due to the extravasation of blood or of its coloring matter from the
blood vessels into the tissues, and they dry up into thin scabs or sloughs if the ani-
mal survives. Similar petecchial spots appear on the muzzle, in the nose, and on the
eyes, and in some instances they are confined to these parts. The tongue is covered
by a brownish fur.

From the first the animal is sore to the touch, but as the disease develops the handling
of the animal is especially painful and causes grunting and screaming. ‘The pig lies
on its belly, and, if compelled to rise and walk, moves stiffly, feebly, unsteadily,
and with plaintive grunting. This weakness and prostration rapidly increases, and
often ends in utter inability to rise or to support the body on the hind limbs. A wa-
tery discharge from the nose, followed by a white muco-purulent flow, is not uncom-
mon. A hard, barking cough is frequently present from the first and continues to
the last. Sickness and vomiting may be present, but are far from constant. The
bowels are often confined at first, and in certain cases, and even in nearly all the
victims of particular outbreaks, may remain so throughout, nothing whatever being

passed, or only a few small black pellets covered by a film of mucus. These cases

are quickly fatal. More frequently, however, they become loose by the second or
third day, and diarrhea increases at an alarming rate. The passages are first bilious
and of a light or brownish yeilow when not colored by ashes, charcoal, or the nature
of the foo |. But soon they assume the darker shades of green and red, or become
quite black and intolerably offensive. In such cases the elements of blood, inspis-
sated lymph, and membranous pellicles, sloughed off from the ulcerated surfaces, are
usually to be found in thei.

The diarrhea becomes more profuse, watery, and fetid; the pulse sinks so as to be-
come almost imperceptible; the cough becomes more frequent, painful, and exhaust-
ing; the breathing is more hurried and labored; and the weakness increases until
the patient can no longer rise on his hind limbs. At this period the petecchiw become
far more abundant. Before death the animal is often sunk in complete stupor, with, it
may be, muscular jerking or trembling, or sudden starts into the sitting posture, and
loud screams. In the last stages involuntary motions of the bowels are common.

Exceptionally swellings appear on the flank, with extreme lameness, and extensive
sloughs of the skin of the ears or other parts. Palpitations of the heart also occasion-
ally occur as precursors, attendants, or sequels of disease. If the disease should take
a favorable turn, slight causes may make an early and perfect recovery, a complete
convalescence being established in three or four weeks. A considerable proportion
of the survivors, however, linger on in an unthrifty condition for months, evidently
suffering from the persistent ulceration of the intestines or infiltration of the lungs.
The mortality often reaches 80 or 90 per cent. of all swine exposed, and in case of a
certain number of the survivors recovery brings no profit to the owner.

Post-mortem appearances.—The blue color of the skin becomes dgeper and more uni-
versal a few hours after death. The fat beneath the skin is colored more or less
deeply in points corresponding to the discoloration of the integument. The snout is
usually of a deep blue, with ineffaceable black spots (petecchie). The membrane
lining the eyelid,-and to a less extent the skin, present similar black spots of extray-
asation.

The most constant changes are in the mucous membrane lining the alimentary
canal, and especially that of the terminal portion of the small intestine (ileum) and
the commencement of the large (cecum, colon). The tongue is furred, but deep red,
even eroded, at its base, and the pharynx and adjacent parts usually studded with
petecchiw. The cavity of the abdomen generally contains a few ounces of reddish
serum, which coagulates on being heated. The stomach may show no more than a
pink blush, but more commonly it is of a deep red, from congestion, especially to-

28

ward the pylorus, and its mucous membrane is often black throughout from the close
aggregation of petecchie. The small intestines are usually extensively congested,
and of a deep red, in many cases approaching to black, as examined externally.
Their mucous membrane in such parts is equally high colored, studded with petec-
chiz, and in some ‘cases lined by a firm, semi-fibrinous exudation. A more constant
condition is the presence of minute sloughs or erosions in the seat of petecchiw, and
of equally small elevations, due to excessive cell-growth, beneath the epithelium.
These commonly have a whitish center, with a yellowish or red border. Such is the
appearance in cases that prove fatal within two or three days. In those that have
survived longer, extensive ulcers appear, of an inch and upward in diameter, evi-
dently the sequel of the petecchii, and especially of the eruption.

These ulcers are often covered by black scabs or sloughs, have irregular projecting
margins and a variously colored center, consisting of cells in precess of disintegration.
They are sometimes situated on Peyer’s patches, but show no very marked preference
for those over other portions of the mucous membrane. The large intestines present a
similar varying vascularity, discoloration, petecchiw, deposit, softening, and ulcera-
tion. The changes are especially marked in the cecum and colon and in the rectum
close to the anus. The solitary glands are often large and open, but the ulcers show
no particular preference for the points occupied by them. Extensive extravasations.
of blood into the coats of the bowels and among their contents are not infrequent, and
in certain exceptional and advanced cases the peritoneum is inflamed and false mem-
branes bind the bowels together or to other organs, or to the walls of the abdomen.

In the wind-pipe and air-passages within the lungs, the mucous membrane is usually
mottled with black petecchix, or covered by a viscid mucous exudation. The anterior
lobes of the lungs are often soliditied by exudation, but remain bright, red, tough, and
elastic (splenisation). Limited hepatization is also exceptionally met with, and even
false membranes on the pleura or pericardium.

Petecchix are common over the various internal orgaus—on the lungs, pleura, heart,
pericardium, diaphragm, peritoneum, liver, pancreas, kidueys, and bladder. The
spleen is large and dark, as is usual in connection with blood poisons. Both sides of
the heart contain. clots of blood, extending from the auricles and ventricles into the
great vessels. In the worst cases, the clot is black, soft, and somewhat diffluent ;
exceptionally it is firm, and shows a distinet buffy coat. The blood-globules, as seen
under the microscope, are more or less puckered or crenated at their edges, and mixed
with an excess of granular débris and even in some instances spores of a fungus
(micrococcus).

As illustrating the various lesions in different cases, I append from my notes of
post-mortem examinations two that occurred with two years’ interval, near Edin-
burgh and London, respectively :

I.—No. 4. A three months’ old, white Yorkshire pig in excellent condition. Exam-
ined a few hours after death, being still quite warm, rigor mortis had set in strongly.
Along the whole lower surface of the body, from the mouth to the tail, are spots of
dark ref or purple. On the right side of the head and left side of the chest the spots
run into each other, so much that they seem to form a single continuous blush. On
the back the spots are smaller and less numerous. There are no spots nor petecchie
on the snout, but a glairy bloody fluid runs from the right nostril.

The membrane lining the eyelid is congested, having a dark hue, approaching
purple, and a portion of the mucous membrane of the rectum, exposed by the relaxa-
tion of the sphincter, presents the same appearance. Dark red spots and petecchize
exist about the vulva. Under the belly is a subcutaneous layer of fat about an inch
thick, and beneath the purple spots on the skin this is discolored by blood through-
out the entire thickness. |

The abdominal cavity contains 6 ounces of a dark bloody fluid. The intestines
have a deep florid hue externally. The stomach and the greater part of the rectum
are pale and without any lesions of the mucous membrane. Close to the anus this

24

membrane is congested. The stomach contains about two pounds of food (boiled
potatoes, corn, etc.). The small intestines have their mucous membrane thickened,
soft, friable, and very red, the shades being lighter or deeper at different points. It
presents at intervals spots of a much darker hue, approaching purple, and respect-
ively from one to two lines in diameter. The large Peyer’s patch on the ileum seems
hypertrophied and of a deep red, especially close to the ileo-cecal valve, where it
also shows small ulcers. The large intestines have their mucous membrane of a very
bright red, soft, friable, and presenting at intervals small ulcers of about a line in
diameter, and corresponding apparently to the solitary glands. Some of these ulcers
are of a deep red, and appear on the peritoneal coat as dark spots; others are of a
dirty white in the center, with raised red edges, and are not so marked on the perito~
neal surface. A small nodule felt through the outer coats is characteristic of both.
The contents of the large intestines consist of dark semi-liquid feces, with a great
amount of ashes.

The liver is variable in color and very friable. Though still warm, it presents
small bubbles of gas at intervals under its capsule and throughout its substances,
The gall-bladder is half full of a very light-colored yellow bile. The pancreas seem
healthy. The kidneys, bladder, and uterus are normal.

The pleura and lungs appear healthy, excepting a portion of the anterior lobe of
the left lung, which is in a state of splenisation. The bronchia contains bloody
froth, especially in the left lung, and those of the solidified portion contain a white
solid substance, completely filling them, and appearing to the naked eye like a fibri-
nous clot, while under the microscope it is found to be mainly composed of small glob-
ules about the size of blood-cells. It is disintegrated and partly dissolved in a strong
solution of potassa. The mucous membrane of the larynx and trachea is congested
and the tube filled with a white frothy mucus of an exceedingly tenacious consist-
ency.

II.—No. 2. Three months’ old femate pig, large of its age. Dead twelve hours.
Rigor mortis well marked. Skin almost universally of a livid hue, but purple along
the abdomen. Back, white. Profuse eruption over the body, but especially abundant
on the abdomen. The smallest, and evidently the most recent specimens of the
eruption, are individually about a line in diameter, deep purple, and covered by a
delicate, slaty-looking skin. ‘The larger spots have a dark, hard, dead center, which
appears to spread gradually to the whole of the patch; some appear as a large black
scab of one-half to 1 inch in diameter.

Abdomen contains 6 ounces of serum, which fornis a solid copa on being heated.
False membranes bind the large intestines to the lower wall of the belly, also the
two horns of the uterus together and to the bladder, and both to the walls of the
pelvis. The large intestines are the seat of an exudation half an inch thick, from
which a straw-colored fluid escapes on section. The stomach is considerably dis-
colored on its great curvature externally, asif from extravasated blood. The mucous
membrane of the stomach presents numerous petecchiw and ramified redness along
the great curvature. The small intestines show slight branching redness oh part of
the ileum.

Large intestines.—Cxecum has its mucous membrane abnormally vascular; with
abundant petecchix, and ulcers of considerable standing; these appear as white,
raised masses, and have no manifest connection with the sclitary glands. The blind-
gut contains numerous ascarides. The mucous membrane of the colon repeats that
of the cecum, but at one point beneath its serous coat is a blood-clot BREST aS 1
inch by half an inch, and a quarter of an inch thick.

The liver is eatane. The diaphragm has abundance of petecchiz on its posterior
surface, especially on the cordiform portion, and apparently leading in radiating
lines from the center. Beyond the presence of petecchie the organs of the chest seem
to be little affected.

Causes.—Contagion is the main cause of this disease. The introduction of diseased

25

pigs into healthy herds; the placing of healthy pigs in pens, cars, steam-boats, mar-
kets, etc., where diseased swine are then or have formerly been exposed; a fresh
breeze from the direction of a diseased herd, though half a mile distant; the passage of
men or quadrupeds or birds from the diseased to the healthy ; the use of food, litter,
or water that has been in near proximity to the affected animals, have each served to
transmit the fever.

The virus appears to be concentrated in the bowel-discharges and liquids of the
eruption, but doubtless exists in all the liquids and tissues of the body, and is given
off into the air from the skin and exposed mucous membranes. Pigs are often born
sick, and die in twenty-four hours. ‘The feeding-troughs and water, contaminated by
the filthy feet and snouts, are particularly liable to convey the disease.

The malady prevails at all the periods of the year, but it has opportunities for the
widest diffusion in dry seasous and countries, where the virulent matter may be dried
up and preserved unchanged for an indefinite period, and in this state may be car-
ried by winds and otherwise. Wet weather contributes to the decomposition and
destruction of this, as of any other animal poison, but can not influence its propa-
gation by the direct contact of healthy with diseased animals, nor affect its preserva-
tion inside dry buildings.

Unwholesome conditions of life contribute largely to its diffusion, if not to its de-
velopment de novo. The malady frequently appears in pigs that have been carried
several days in succession in crowded boats or cars, among the accumulated filth of
their own bodies and those of their predecessors, and subject to compulsory absti-
nence from food and water. Again, it will occur in fat hogs that have been driven
a number of miles under a hot sun and then cooped up in a filthy, close, ill-ventilated
pen, subjected to the reeking fumes of their own bedies and of long-accumulated
nastiness. Many think that dry-corn feeding and overcrowding on filthy manure
heaps are largely productive of the disease. But it is too much to assume that the
poison is developed de novo in such conditions. Similar unwholesome influences favor
the development of all contagious diseases by loading the blood with effete and dele-
terious organic matter, and bringing about a feverish and susceptible state of the
system. But, on the other hand, such abuse and maltreatment fail, in very many
cases, to induce the affection, so that we are left in doubt in regard to those instances
in which it appears as to whether the virus was not hidden away in the buildings,
cars, etc., and roused into activity by the presence of a fertile field for its growth in
the bodies of the pigs, the blood of which was loaded with organic elements in proc-
ess of decomposition. The important point is this: We know this as a contagious
affection, to the propagation of which all probable insalubrious conditions contribute.
So soon as we concentrate our attention on this point we have the key to its preven-
tion, if not to its entire extinction. But, while admitting the influence of over-
crowding, filth, starvation, and suffering in predisposing to this disease, it ought to
be added that the very highest mortality is often reached among pigs kept in the
best hygienic conditions, but among which the virus has been accidentally intro-
duced, Again, some hogs, and even families, appear to be insusceptible, and resist
the poison which is carrying off all around them. But similar instances of immunity
are met with in all contagious affections.

Treatment.—In a fatal contagious disease like that under consideration it is rarely
good policy to subject to treatment. The enormous increase of the poison in the
bodies of the sick, and the extreme danger of its diffusion through the air, as well as
on the feet of men and animals, render the preservation of the victims eminently un-
safe and unprofitable. Yet, in the case of very valuable animals, and where seclu-
sion, disinfection, and careful nursing can be secured, it may be resorted to.

A dry, airy, well-littered building may be provided, abundantly sprinkled with a
solution of carbolic acid or chloride of lime. Rugs steeped in a solution of one or
other of these agents may be hung up at intervals, and sulphurous acid set free by
burning a pinch or two of sulphur three or four times a day. The dung should be

26

saturated or thickly sprinkled with finely powdered copperas. Any drains will re-

quire disinfection in the same way. If the sick animals are kept in the open air, the
ground must be freely sprinkled with disinfectants, above all where the dung has
been deposited.

The diet should be well boiled gruel of barley, rye, or Graham flour; or, if fever
runs high and the temperature is raised by such food, corn-starch made with boiling
water or milk may be substituted. Fresh, cool water should be freely supplied, either
pure or slightly acidulated with sulphuric acid.

During the early stages, while constipation exists, the bowels may be gently opened
by castor oil (2 ounces for a good six-months’ pig) or rhubarb (1 dram), aided by in-
jections of warm water. The heat of the skin must be counteracted by sponging
with cool or tepid water, as may seem most agreeable to the patient. As the laxa-
tive operates, 20 grains of nitrate of potash and 10 grains of bisulphite of soda may
be given twice a day in the drinking water. Charcoal may also be given to absorb
and neutralize the deleterious products in the bowels. Or the niter may be replaced
by any other neutral salt and the bisulphite by another antiseptic agent. If the pa-
tient survives the first few days and gives indications of ulceration, by tender abdo-
men, diarrhea, and the passage by the bowels of membranous sloughs, oil of turpen-
tine, in doses of 15 or 20 drops, may be given, shaken up in milk or beaten in an egg;
or this may be replaced by similar doses of creosote or carbolic acid, or 3 to 5 grain
doses of nitrate of silver. it may be necessary to give opium to check excessive
purging, or stimulants to sustain the failing strength and very prostrate condition.
‘nfiltrations and inflammaticns of the Jungs and bowels may demand applications of
mustard and turpentine to the chest or abdomen. In short, any complication must
be combated as it appears, and the soundest judgment will be wanted throughout to
adapt the treatment to the various indications. Each case will demand as close at-
tention and as careful an adaptation of remedial measures to its different stages and
phases as would a case of typhoid feverin man. In case of recovery a course of tonics
(gentian one-half dram, sulphate of iron 10 grains daily) will often be beneficial, and
the return to ordinary feeding should be brought about by slow degrees.

Prevention.—A successful system of prevention can only be instituted when we duly
appreciate the fact that almost all cases of this intestinal fever are due to contagion.
And this is precisely what our hog breeders fail to realize. No manin his senses will
affect to deny that the disease is contagious, but the natural tendency is to seek for
other causes in the great majority of cases. Asin the case of all contagious affections

that have attained a wide prevalence, this presents a number of outbreaks which can.

not be traced to contagion from any diseased stock, and these are at once assumed to
be spontaneous, and the cause of the disease is sought in the peculiar treatment of
the herd, and future prevention is attempted by the avoidance of these peculiarities.
In iilustration, I may quote from a letter of Mr. I. F. Hatch, an intelligent Illinois
farmer, and former student of Cornell University :

In former years hog cholera has been local with us except when it first appeared,
some ten or twelve years since. Then, as now, it was general, and swept everything.
But since then it has been confined to a few farms or localities. Sometimes it ap-
peared on a single farm, or perhaps on several farms, 1, 2, or 3 miles apart, all others
escaping. I have a neighbor who has had it every second year since its first apppear-
ance, losing more or less hogs each time, but his is the only case of which I have been
informed where it has been so regular and often.

This irregularity and local appearance deluded us into the belief that we were pre-
venting the disease by extra care and attention, and that salt, sulphur, and ashes
were a preventive ; but we have been effectually undeceived this time, for hogs that
have been doctored thus fared no better than those that had not.

There is one man here whose hogs have escaped the disease entirely, and he has
fed for a number of years once a week, or once in two weeks, corn boiled in the ear
with ashes—lyed corn, as they call it—putting a peck of wood-ashes into a 40-gallon
kettle. He tells me he has had no cholera since he adopted this plan, and his hogs are
certainly good subjects for cholera—poor, half-fed, and sleeping in a pile under the
barn. He says others have tried this plan and successfully warded off the disease.

27

He goes on to quote instances of alleged prevention by feeding house-slops without
corn, and by giving once a week a feed of the boiled jowls and waste parts of the pigs
killed the year previous, and adds:

Generally diseased hogs run, sleep, and eat with the others, it being the general
opinion that they’ll all have it anyway, sono matter. I am of a different opinion.
A few change the yards and sleeping places, but generally they stay in the same
places throughout the disease. No attention is paid to disinfection.

These alleged preventives are doubtless somewhat beneficial by maintaining a
free action of the bowels and kidneys, and favoring the elimination of the poison, as
does diarrhea in the milder cases of the disease. But there need be as little doubt
that, like the salt; sulphur, and ashes, they would all fail in the presence of a strong
dose of the poison. Meanwhile, they are made to serve an evil purpose in diverting
attention from the one effectual means of restricting the disease, the extinction of
the poison. It must be fully recognized that neither contact nor proximity is neces-
sary to contagion. The poison may be carried a certain distance on a stream of water
without losing its vitality. It may be blown a long way by a favorable wind, when
dried, up, on light objects. It may be carried on the boots, hands, etc., of men
(dealers) passing from farm to farm and from district to district. Horses, cattle,
sheep, dogs, fowls, pigeons, und wild animals of all kinds are liable to carry the virus
on their feet and limbs, and to deal out death to the pigs at places widely separated
from each other. It is, therefore, quite impossible to trace all new outbreaks to con-
tagion. But to attribute them to spontaneous evolution of the disease is to beg the
whole question.

It can be freely conceded that a certain number of cases probably originate spon-
taneously every year; but these are few and far between as compared with the enor-
mous mortality caused by contagion. It can be equally conceded that certain seasons
are far more favorable to the propagation and virulence of the disease than others,
yet even in these the great majority of cases are infectious. It can be admitted even
that a wholesome laxative diet is to some extent protective, as well as comfortable
dwellings and antiseptic agents, like copperas, bisulphite of soda, charcoal, or car-
bolic acid. But all such protectives are comparatively limited in their operation,
and, though they seem to have saved a few isolated herds, will fail disastrously if
generally relied on. The epizootic influence, too, though apparently all-powerful in
localities where the poison has already penetrated, fails to produce the disease in the
neighboring States not previously infected. We can not give too much attention to
secure the best sanitary conditions of life for the hogs, but if we allow a few of these
so to engross our attention that our eyes are blinded to the most important of all—
the preventiun of contagion—we shall only spread the poison and increase the de-
struction of our herds. On the other hand, the highest success must attend such
measures as will stop the production of the poison and destroy and render innocuous
what is already in existence. :

Diseased pigs must be removed from the healthy, killed, and buried. A thorough
disinfection of all buildings, yards, and manure must be made. Chloride of lime or
zine, sulphate of iron, or carbolic acid may be used for all solids, floors, troughs,
walls, etc., and for drains; and sulphurous acid or chlorine for the atmosphere... The
sulphurous acid may be produced by burning sulphuryand the chlorine by adding oil
of vitrol to common salt and a little black oxide of manganese. The surviving pigs
must be carefully watched for the first signs of illness. Any unusual sluggishness,
stiffness, or inappetence, or any disposition to leave the herd, demands a careful ex-
amination; and if there is heat or shivering, and, above all, if the thermometer in-
troduced into the rectum indicates a temperature above 103° Fahrenheit, the animal
should be at once separated from the herd, and destroyed as soon as unequivocal
symptoms of the malady are shown. Care should be taken to avoid the possibility of
contamination by water which has passed infected hog-pens or fields. If the malady
exists within a wide radius, the visits of dealers and others must be absolutely for-

28

bidden, and a similar prohibition should attach as far as possible to quadrupeds and
birds, wild and tame. Disinfectants may even be given to the sound animals that
have been exposed to contagion. A table-spoonful of charcoal, animal or vegetable,
may be given daily to each pig in its food. Twenty grains of bisulphite of soda, or
ten drops of carbolic acid, or 10 grains of sulphate of iron may be used instead, and a
tea-spoonful each of sulphur and gentian may be added with advantage. When aherd
has been freed from the disease, a most exhaustive disinfection of the whole premises,
manure, and other products is imperative, and it is usually desirable to change the
site of the hog-pen and run to obviate any future effects of this most virulent conta-
gion. Old and rotten wood work should be burned.

In purchasing pigs, buyers will consult their interests by avoiding markets, and
going rather to the breeders whose stock is known to be healthy, and by seeing per-
sonally to the thorough cleansing and disinfection of loading-banks, cars, boats, ete.,
which they must use in bringing them home. And after all such precautions, newly
purchased swine should invariably be placed in quarantine, at a safe distance from
other hogs, and kept there for three weeks, with separate attendants, until they have
been proved sound.

As in the case of other fatal contagions, this could doubtless be kept in check, or
even completely extinguished, by a uniform system of destruction of the infected,
and disinfection of their carcasses and all with which they have come in contact.
Such a proceeding would imply an amount of governmental supervision and pecuni-
ary outlay that would be profitable in the long run, though the past experience of
the American people have scarcely prepared them to sanction it.

In 1877, a paper written by H. J. Detmers, V.S., giving his obser-
vations of the disease generally called hog cholera, and bis conclusions
as to its nature, was reprinted in the annual report of the Department
of Agriculture. Dr. Detmers proposed to call the malady “ epizootic
influenza of swine,” and he divided it into (1) “the catarrhal rheu-
matic form,” (2) the gastric-rheumatic form,” (3) ‘the cerebro-rheu-
matic form,” and (4) “the lymphatic-rheumatic form.” The causes of
the disease he divided into three classes, and he writes:

As belonging to the first class I look upon everything that will interrupt or disturb
the perspiration ; in the second class I place all such noxious influences and agencies
as interfere directly with the process of respiration; finally, in the third class, I put
all such noxious agencies or injurious influences as tend to aggravate the disease if
already existing, by aiding in making its character more typhoid, or which produce
a special predisposition by weakening the constitution of the animal.

In regard to the contagiousness of the affection he says:

Still I think the epizootic character of the fearful spreading of the disease can be
satisfactorily explained without the existence of a contagion.

The above extracts show the most divergent views among physcians
and veterinarians as to the cause and nature of the epizootics among
swine. At the same time'there were equally wide differences of opinion
among swine-breeders and the contributors to the agricultural press.
In short, there was the greatest uncertainty and confusion of ideas not
only as to the characters of the disease or diseases, but as to the most
elementary principles to be applied for prevention.

It was just at this period (1878) that Congress provided for the first
investigation of swine diseases by making an appropriation of $10,000
for this purpose. The beginning of this investigation, which has been

29

continued with short interruptions until the present time, marks a new
era in our knowledge of swine epizootics and of contagious diseases in
general. It was just at the time when the biological researches of Pas-
teur in regard to fermentation were attracting so much attention, and
had already inspired Lister to make his discoveries in antiseptic sur-
gery, and Koch to institute those researches which definitely connected
the bacillus anthracis with the causation of charbon. The time was
propitious, therefore, for the institution of a new line of researches, in
a direction which even then promised much, and which since has prac-
tically revolutionized the position of medical science as to the nature
of contagion and the methods most important for its control.

The writings of Drs. Sutton, Snow, and Law gave a very correct state-
ment of the symptoms and post mortem appearances of the organs usually
found in the swine epizootics of this country. ‘They covered about all
the points which can be decided by ordinary field observations, but they
left many questions still unsolved which it was necessary to determine
before measures of prevention could be formulated and made successful.

There were many who believed that these epizootics were due to the
ravages of more than one disease, and there were also many who held
that contagion and infection played no part in their extension. As to
the nature of the agent or agents which caused the outbreaks, or the
conditions which were required to prevent their destructive ravages, no
results of value had been obtained, or indeed could be, without a more
systematic and persistent investigation, with all the instruments, ap-
paratus, and laboratory facilities which are required to work out the
obscure problems of pathological science. As with other contagious dis-
eases of men and animals, the instruments of the post-mortem case had
been the means by which a certain amount of information had been
gained, but there were problems which they could not reveal, and for
these the microscope, the culture apparatus, the biological and chemi-
cal laboratories were necessary, and without these a reliable solution
could not be reached.

For the investigations of 1878 nine men were appointed for a period
of two months each, as follows: Dr. H.J.Detmers, Illinois; Dr. James
Law, New York; Dr. D. W. Voyles, Indiana; Dr. D. E.Salmon, North
Carolina; Dr. Albert Dunlap, lowa; Dr. R. F. Dyer, Illinois; Dr. A.
S. Payne, Virginia; Dr. J. N. McNutt, Missouri; Dr. C. M. Hines, Kan-
sas. The researches were to be made in the field in different sections
of the country, and various remedies, suggested as applicable to the
treatment of epizootic diseases, were to be tried. The result of this
investigation may be summed up practically as follows: (1) Swine dis-
eases were found destructive in the most widely separated districts of
the country. (2) The symptoms and lesions enumerated were similar to
those formerly given by Drs. Sutton, Law, and Snow. (3) No evidence
was discovered to show the existence of more than one disease which
prevailed as an epizootic. (4) There was a preponderance of opinion
that the outbreaks were due to contagion and that the disease was com-

30

municable. (5) The remedies tested either produced no effect or were
of doubtful value for the treatment of affected animals or for guarding
against the contagion. .

There were two points of more than usual interest raised in the inves-
tigation. In the course of Dr. Law’s investigations he made inocula-
tion experiments with rabbits, rats, and sheep, which he thought dem-
onstrated the communicability of the disease that he investigated.
Dr. Detmers devoted more of his time to microscopical investigations,
and asserted that he had discovered a specific micro-organism, which
he called the Bacillus swis, and that he had demonstrated its pathogenic
connection with the disease.

Both of these conclusions must now be looked upon as premature and
not supported by the direct and positive evidence which is necessary
to establish such important points. That Dr. Law produced disease in
the experimental animals which he inoculated is not to be doubted for
a moment, but that it was the same disease and caused by the same
microbe which produced the swine epizootics of the country could only
be definitely determined after the microbes of the swine diseases had
been identified and their characters established. Very frequently in
inoculating with the products of disease taken from dead animals, septic
disorders are caused in the inoculated animals which are entirely dif-
ferent in nature from the malady which caused the death of the indi-
vidual inoculated from. ‘To determine, therefore, whether the disease
induced is identical with the disease which we propose to propagate by
inoculation it becomes necessary to determine the microbe which causes
the morbid changes in each case. At that time neither of the microbes
which we have since identified and studied in swine epizooties in this
country had been discovered, and consequently the line of evidence
just indicated was impossible.

Dr. Detmers’s culture experiments were too crude and primitive to be
of any value, even in the condition in which bacteriological science was
at that time; and his descriptions of the germ might be applied with
equal accuracy to many different species of micro-organisms. For this
reason no attempt will be made in this volume to give the details of
either the culture or inoculation experiments which he made. While
failing to obtain the evidence necessary to establish the connection of
any microorganism with the production of this malady, this and sub-
sequent reports of Dr. Detmers had some effect in directing the atten-
tion of investigators in this country to bacteriological researches as a
promising field in which to search for the hidden mysteries connected
with this class of diseases.*

* It is due to justice to state in this connection that, whereas the appointments lim-
ited the work of those selected for the investigations of 1878 to a period of two months,
Drs. Detmers and Law were subsequently given an opportunity to continue their jn-
vestigations for a much longer period. It is also proper to state that several months
before the investigations of 1878 began, Dr. Klein, of London, had published investi-
gations which he believed established the fact that the swine epizootics of Great
Peni caused by a bacillus. See Quarterly Journal of Microscopical Science,

pril, 1878,

31

The investigations of the Department of Agriculture were continued
in 1879 by Drs. Law and Detmers; in 1880 by Drs. Law, Detmers, and
Salmon, and in 1881~82 by Drs. Detmers and Salmon. The efforts of
Dr. Law were largely directed to obtaining a modified virus for prevent-
ive inoculation, a doubly difficult and discouraging task before the mi-
crobes of the diseases had been discovered and studied. While, his
results were more or less encouraging, no conclusions of practical value
as to a method of preventive inoculation were established.

Dr. Detmers continued his microscopic observations and modified his
first descriptions of the microbe so far as to speak of it in later reports
as amicrococcus. The author devoted the greater part of his time during
these years to an investigation of southern cattle fever and fowl cholera,
but incidentally investigated a number of outbreaks of swine diseases.
He found micrococci in the liquids of the affected animals, which he
cultivated and inoculated into other animals, but his results were not
sufficiently positive to demonstrate their connection with the disease.

There was here a period of about four years when the investigations
of swine diseases gave no very decided advance in our knowledge of
the subject. The reason for this was that the investigation had been
carried about as far as was possible by the methods then employed.
To get a better insight into the nature of the epizootics and the pecu-
liarities of the contagion, it was essential that the pathogenic inicrobes
should be discovered and accurately studied. The investigators saw
this and were working in the proper direction, but at that time bacteri-
ological science was young and the methods of research had not been
clearly worked out. Another and equal difficulty was the fact tiat
the investigators were working without proper laboratory facilities and
apparatus for such researches, without assistants, and some of them
were devoting much of their time to other duties. Under-such condi-
tions it is next to impossible to reach successful results in such a diffi-
cult field of study. These difficulties were not fully appreciated either
by the officials of the Department of Agriculture or by the stock-owners
of the country, for the reason that such investigations were new to them
and their requirements but imperfectly understood. It was not expected
that a chemist would go into a sorghum field and discover the propor-
tion of cane sugar in the sorghum cane without apparatus or laboratory
facilities, but it was expected that the veterinarian would make much
more difficult and delicate investigations than these with no other aids
than an ax, a butcher knife, a scalpel, and a microscope.

The author saw that more facilities must be provided for these in-
vestigations, and the work systematized and properly divided, or the
final result would be disappointment and failure. It was through his
urgent representations that a beginning was made in 1885, by securing
an unoccupied room under the roof of the Department building, which
was fitted up as a laboratory, and by obtaining permission to renta
small place in the suburbs of Washington on which to keep experi-
mental animals,

ya2

The year 1883, however, was one in which the necessity of investigat-
ing the prevalence of the lung plague or pleuro-pneumonia of cattle
became too urgent to admit of delay. There were frequent outbreaks
which it'was the duty of the chief of the veterinary division to visit
and give assistance to the State authorities as to their diagnosis and
eradication. This prechided any systematic investigations of swine
diseases. The spring of 1884 brought the extensive outbreaks of ergo-
tism in Kansas, Missouri, and Illinois, which alarmed the whole coun-
try, and which demanded instant attention; and these unfortunately
were followed, in the summer, by the outbreaks of pleuro-pneumonia in
Ohio, Illinois, and Kentucky, which required the constant attention of
the chief veterinarian and prevented scientific researches for several
months.

The investigations during the years 1883 and 1884 were, therefore,
too much interrupted to allow the number of experiments and the thor-
ough working out of details which was desirable. The time was not
entirely barren of results, however, in the investigation of swine dis-
eases. The laboratory was fitted up and suitable microscopic and bac-
teriological apparatus obtained. Able assistants were selected and
placed in charge of the different branches of the work. The lines of
research were marked out and such arrangements made as would per-
mit of the intelligent prosecution of the work, even in the absence of
the chief of the bureau.

This systematization of the investigations, with the employment of a
proper number of persons to keep the different lines of study advancing
uniformly, was followed almost immediately by the most important de-
velopments. In 1885 a motile bacillus was discovered to be the cause
of hog cholera, and its leading characteristics were accurately de-
scribed. In 1886 the production of immunity by chemical products was
demonstrated, the effect of disinfectants on the hog cholera contagion
was thoroughly studied, and the presence of swine plague, a second
epizootic disease of swine, was discovered. These discoveries solve the
most important problems connected with swine epizooties and give a
secure scientific basis from which to work in future. In fact these dis-
eases are now much better understood than are most of the contagious
diseases of people, and the measures applicable, in the present condi-
tion of science, to their prevention are equally as apparent as are those
which are applied to the plagues of mankind.

In the sections of this work which follow the details of the investiga-
tions of hog cholera made since 1884 are given as fully as are consid-
ered necessary to an understanding of the different phases of the sub-
ject. The account of the experiments in regard to swine plague are
reserved for publication in a separate volume, which it is hoped will
appear within a few months.

SYMPTOMS AND POST-MORTEM APPEARANCES IN HOG CHOLERA.

The symptoms are not entirely characteristic, owing to the many
forms which the disease may assume. It is moreover quite trouble-
some to make careful thermometric and other clinical observations on
swine, which enhances the difficulty of exactly determining the course
of the malady. In general we may regard the disease as manifesting
itself in an acute and a chronic or mild form.

Of the acute form very little need be said. The animals die very
suddenly, without having been sick for more than a few hours to a day.
The chronic disease may last from three weeks to several months. The
animals grow stupid and dull, they refuse to eat,and are apt to sepa-
rate themselves from the rest of the herd. They grow weak, and their
movements become slightly tottering. A common symptom is diar-
rhea, which may appear very soon after the animal becomes sick and
last until it dies. In protracted cases the liver may become affected
secondarily through the impaired condition of the large intestine.

The following symptoms, as noted for three or four years by Dr. Kil-
borne at the experiment station of the Bureau, will show how little
there is upon which we can depend for a diagnosis during life.

The temperature of healthy pigs ranges between 101° and 104° F,
With sick animals it may rise from 1° to 3° above the temperature ob-
served in health. Frequently this elevation is absent. During an out-
break elevation of temperature may be considered diagnostic, but ab-
sence of such elevation proves nothing, since an animal may die with-
out having shown any rise of temperature during the disease. There
is rarely any cold or shivering stage. The sick animals are dumpish,
spiritless, and lie quietly in a corner or huddle together, hiding the
head under the litter. They refuse to move even when disturbed, and
are more or less oblivious to surroundings.

There is more or less loss of appetite. They usually continue to eat
a little, however, and often the appetite is scarcely impaired during the
whole course of the disease. Acute cases may be seen feeding before
they are found dead an hour or so later. In most cases the stomach is
well filled after death.

The bowels may be costive at the outset or continue apparently
normal for some time, or they soon become costive, and remain so in
some cases throughout the disease. In the later stages diarrhea of a

15612 H c——3 33

o4

liquid, fetid character appears in many cases. The color of the dis-
charges depends largely upon the feed. In slop or garbage fed pigs
they are usually of a dirty black color. In those fed with grain they
are light yellowish. The diarrhea persists until death. Vomiting is
absent.

Respiration is only oceasionally quickened and labored in the later
stages. The pulse is more rapid than in health, but its determination
unsatisfactory, owing to the struggle of the animals when held. Cough
is infrequent, and then only heard when the animals are aroused, as a
single effort or in paroxysms.

The skin is frequently found reddened on the nose, abdomen, inside
of limbs, the ears, and over the pubic region. The redness is diffuse,
’ varying from a slight blush to a deep bluish red or purple. It increases
as death approaches, and is usually found at the autopsy. A skin
eruption appears ocvasionally, which is followed by crusts or scabs of
rarying size. Reddening of the skin is a sympton common to the other
swine diseases—rouget and swine plague.

The eyes are apt to be watery. This is frequently the first outward
sign. Later the discharge becomes thick, yellowish, often gumming
the lids together.

Towards the end of the disease the animals have a gaunt appearance,
with arched back and staring coat. Emaciation is very rapid. The
weakness manifests itself in a staggering, uncertain gait, as if the
animal were about to fall. Death ensues quietly. Rarely convulsive
kicking is observed. The mortality is very high, usually from 80 to 90
per cent. of those attacked die.

These symptoms vary in intensity, and only a certain number are seen
in one animal at the sametime. In very chronic cases only the autopsy
enabled us to make a diagnosis.

LESIONS PRODUCED BY HOG CHOLERA.—POST MORTEM APPEAR-
ANCES.

(See Plates I-VIII inclusive. )

a. The acute type—This might with equal propriety be called the
hemorrhagic type,inasmuch as the chief and perhaps the only changes
are hemorrhagic in character, and these lesions are seen most clearly
when an animal is examined immediately after death. The spleen is
rariably enlarged, soft, gorged with blood. Sometimes it is twice as
long as the normal spleen (the other dimensions being proportionately
increased), and it may extend across the median line to the right side.
Next to the spleen the lymphatic glands and serous membranes are
most severely involved. The cortex shows, on section, as a hemor-
rhagie line or band, according to the amount of extravasated blood, or
the entire gland may be infiltrated with it. Among the glands most
commonly hemorrhagic are those of the meso-colon (large intestine),

35

those at the root of the lungs (bronchial), and on the pesterior thoracic
aorta. Besides these, the retro-peritoneal and gastric glands (lesser
omentum) may be involved. Most rarely the mesentric glands show
extravasations to aslight extent. Hemorrhages are also quite frequent
beneath the serous surfaces of abdomen and thorax. They are most
abundant under the serosa of the large and small intestines as petec-
chie and larger patches. They are occasionally found under the peri-
toneum near the kidneys, the diaphragm, the costal pleura as extrava-
sations nearly an inch across.

The lungs, in a small percentage of cases, show subpleural ecchy-
moses in large numbers, and on section small hemorrhagie foci are ob-
served throughout the lung tissue. Ina few vases severe hemorrhages,
involving one or more lobes, have been observed. The kidneys are oc-
casionally the seat of extensive hemorrhagic changes. The glomeruli
appear as blood red points; larger extravasations occur in the medul-
lary substance, and blood may collect around the apices of the papil-
le. The subcutaneous tissue over the ventral surface of the body may
be dotted with petecchiz and occasionally collections of blood (haemato-
mata) are found in the superficial muscular tissue. The brain and
spinal cord have not been examined for want of time. In one ease,
however, in which they were laid bare, petecchiz were seen on the cere-
bellum.

The digestive tract usually is the seat of extensive lesions. The fun-
dus of the stomach is as a rule deeply reddened ; there may be more
or less hemorrhage on the surface, giving rise to patches or larger sheets
of blood clots. The small intestine in some cases has submucous ecehy-
moses throughout its entire length. In the large intestine the eechy-
moses may be so numerous as to give the membrane a dark red ap-
pearance. The food is now and then found ineased in sheets of blood
clot due to hemorrhage ou the surface.

b. The chronic form is perhaps the most common, at least in those
epizooties which we have studied. The acute hemorrhagic cases usually
die in the beginning of an outbreak and are apt to be overlooked. Fol-
lowing these are the more protracted, milder cases. In these animals
the disease is apt to be limited in its severe manifestations to the
large intestine. The other organs, however, are not exempt from degen-
erative changes, owing in part to the impairment of the functions of the
large intestine, consequent fermentations and the absorption of poisons
thereby produced, in part to the presence of the specific bacteria in the
spleen and presumably in other organs where they exercise their poison-
ous activity. ;

The lesions of the large intestines are necrotic and ulcerative in char-
acter. The ulcers may be isolated and appear as circular, slightly-pro-
jecting masses stained yellowish or blackish or both in alternate rings.
Or they may be slightly depressed and somewhat ragged in outline,

i

36

When the superficial slough is scraped away many ulcers show a gray-
ish or white bottom. <A vertical section reveals a rather firm neoplastic
growth, extending usually to the inner muscular coat. When sections of
such an ulcer are stained with aniline dyes and examined under the micro-
scope we notice the submucous tissue very much thickened, infiltrated
with round cells, and containing a large number of dilated vessels.
Resting upon this thickened submucosa is a line of very deeply-stained
amorphous matter, and upon this is situated the necrotic mass which
fails to retain the coloring matter and is penetrated by an immense num-
ber of bacteria of various kinds. Frequently ova of trichocephalus are
imbedded in the slough.

The extent of the submucous infiltration depends upon the age of the
ulcer. In old ulcers it contains many newly-formed capillaries, and
evidences of the formation of connective tissue are present. The
capillaries may extend to the very edge of the border where the slough
begins. The latter may have been partly shed, leaving a smooth line
bounding the cicatricial tissue. The submucous infiltration gradually
disappears as we leave the center of the ulcer, and somewhat outside
of the ulcer no inflammation of the membrane is observable. Giant
cells may be seen in some cases in the intertubular tissue at the edge
of the ulcer. In very young ulcers it is frequently possible to observe
the fundi of the tubules intact, while the inner or free half is converted
into an amorphous mass. The depth to which the infiltration extends
is not always limited to the submucosa; it may extend into the muscular
coats and cause inflammatory thickening there and inflammation and
the formation of new vessels in the subjacent serosa.

In some cases the necrosis, instead of appearing in circumscribed
ulcers from one-sixteenth to one-half inch or more across, involves the
whole surface of the mucosa, giving it the appearance of a so-called
diphtheritic membrane. In such cases the walls of the intestine are,
very much thickened and so friable as to be easily torn with the for-
ceps in handling. Such necrosis is rare in spontaneous cases, but it
quite invariably appears in animals which have been fed with pure
cultures of hog cholera bacilli.

The distribution of the ulcers varies but slightly. They appear most
frequently in the cecum and on the ileo-excal valve, as well as in the
upper half of the colon. The lower half is implicated in severe cases
only, and then less extensively. The rectum is only very rarely ulcer-
ated. The lower portion of the ilewm is ulcerated in a small percentage
of animals, especially when they have been fed with hog cholera vis-
cera or cultures. “The stomach is occasionally the seat of slight ulcera-
tion. The lymphatic glands of the affected intestine are usually much
enlarged, pale, tough, whitish on section. The spleen is rarely enlarged;
the liver shows degenerative changes (softening of the parenchyma,
increase of connective tissue). Heart and lungs are usually normal.
The lobular pneumonia frequently found in young pigs in the winter

37

months must be ascribed primarily to exposure rather than to the dis.
ease, as will be shown subsequently.

In some outbreaks theacute and the chronic types of the disease are
not so clearly distinct as given in the foregoing pages. Frequently re.
cent hemorrhagic lesions seem to be grafted upon cases presenting ex-
tensive ulcerations, which certainly are much older than the extravasa-
tions. It may be that the latter are the result of asecondary invasion
of the hog cholera virus, either from the ulcers in the intestine or from
without.

HISTORY AND AUTOPSY NOTES OF AN OUTBREAK OF HOG CHOLERA.

There is perhaps no better way to illustrate this disease than by giv-
ing briefly the history of an outbreak in a single isolated herd. In the
following pages are recorded the autopsy notes and the bacteriological
examination of such an outbreak near the city of Washington during
the months of November and December, 1887. A study of this out-
break was taken up to ascertain more especially the condition of the
lungs inhog cholera. As it is the fifth or sixth which has been observed
during the past three years less attention was paid to careful bacterio-
logical observations. At the same time this phase was by no means
neglected, as the notes will show. The history of the outbreak as far
as could be ascertained was briefly as follows: On October 28, there
were in all one hundred and nineteen swine, chiefly young pigs, weigh-
ing from 50 to 100 pounds. Most of these had been purchased in the
city markets. At this same time some twenty boar pigs were castrated.
Within two weeks these began to die, and soon after the others took
sick, dying at the rate of three to four a day. Less than three weeks
after the first deaths only sixty-seven remained out of the one hundred
and nineteen. At the end of the year only about a dozen were alive out
of the entire herd. These may have acquired immunity.

The animals were kept in pens on the top of a hillock sheltered from
the weather by large boxes. They were swill-fed, and this may account
for their feeble resistance to the disease. In most of them there was a
cirrhosis of the liver, with softening of the parenchyma, which was prob-
ably induced by the feeding. The origin of the epizootic could not be
traced, as the animals had come from various quarters. The city markets
had proved themselves in the past the source of disease in several pur-
chases of pigs for experimental purposes.

The autopsy and bacteriological notes will be given in tbe order in
which the animals were examined, any general remarks being reserved
for tne end. The rapidity with which the animals succumbed to the
disease made any very thorough examination quite impossible, since it
‘seemed more desirable to utilize all the material by examining those
organs most always diseased in hog cholera. Most attention was paid
to the lungs and the digestive tract, while the lungs and the spleen

38

were the only organs examined bacteriologically. These notes will
serve to supplement the autopsy uotes in the reports for 1885 and 1886.

In making cultures from the spleen the following method was usually
adopted. At the autopsy the abdomen was carefully laid open by first
removing the skin and then cutting through the abdominal muscles
with flamed instruments. The flaps laid back, brought into view the
spleen not touched as yet by any instrument. It was then drawn out
with flamed forceps, severed from its attachments with flamed scissors
and placed in a large bottle plugged with cotton wool which had been
previously subjected to a temperature of 150°-160° C. for two hours.
In this way it was taken to the laboratory and either immediately ex-
amined or kept in the refrigerator below 55° F. over night. In making
cultures the spleen was placed on a sterile glass support and the surface
thoroughly charred with a red-hot platinum spatula. This was always
done, although seemingly unnecessary when we consider the momentary
exposure to the air in transferring the spleen from the abdomen to the
sterile bottle. It may, however, destroy any bacteria which have
entered the peritoneal cavity through ulcers. Through this charred
area an incision or rent was made and a platinum wire introduced, and
then a tube of gelatine or beef infusion inoculated with it. When roll
cultures were made a minute bit of spleen pulp was torn away from be-
neath the charred portion and stirred about in the liquefied gelatine.
From this usually a second tube was prepared. Experience of past
years had shown that frequently this is not sufficient to insure the fer-
tility of the cultures. In chronic cases with the spleen but moderately
enlarged, hog cholera bacteria are found in very small numbers. In
such cases bits of spleen are cut out trom the charred area with flamed
scissors and transferred to tubes of gelatine or beef infusion with or
without peptone. Such cultures rarely fail. It might be supposed
that the chances of accidental contamination are very great in this pro-
cess. But along experience with spleens of healthy animals and with
organs in the study of other diseases has demonstrated the entire safety
of this procedure. Salmon culture tubes with bits of organs in the bottom
covered by nutrient liquids have remained sterile for months in the
laboratory. At present the Esmarch tube or roll culture is indispens-
able in such cases.

In nearly all the cases examined both liquid and gelatine cultures
were made. The former permit adiagnosis on the following day, while
the latter require at least two days, usually three or four, before a re-
liable diagnosis can be made. The cultures were always examined un-
stained in a hanging drop, as the bacteria in this way are not deprived
of their power of motility, which is one of the important diagnostic
characters. Staining cultures was also resorted to, but it adds little in-
formation to that gained by a careful examination of the hanging drop.
When gelatine cultures were examined the bacteria were always mixed
with some sterile beef infusion to bring out their motility.

In a number of cases rabbits were inoculated directly trom lung tis-
sue. A small bit, about one half centimeter cube, was torn up with
flamed forceps in a flamed watch glass containing some sterile beef in-
fusion, and the turbid fluid injected beneath the skin of the thigh. The
syringe used was an ordinary hypodermic syringe carefully disinfected
by 5 per cent. carbolic acid above and below the piston for one-half
hour both after and before use, and each time thoroughly rinsed in boil-
ing water. As hog cholera bacteria are destroyed by a 1 per cent. so-
lution of carbolic acid in less than ten minutes, and by a momentary

oo

contact with water near the boiling point the disinfection was certainly
all that could be desired. This method was regarded as less open to
criticism than the insertion of bits of tissue under the skin. We still
stand in need of asyringe which can be disinfected without much trouble,
as the a-ove method is extremely tedious. The syringes devised by
Koch are both unsatisfactory. The joints formed by the glass barrel
and the metal cap in the syringe in which the propelling force is air
were found to leak in five out of six samples. From the fluid injected
into rabbits either plate or roll cultures were made in order to get
an idea of the approximate number and the kind of organisms present.
In every case the portion of lung tissue from which the inoculations
' were made was transferred to sterilized bottles and protected from ac-
cidental contamination as carefully as possible. Unless otherwise indi-
cated, the methods just given were employed throughout the investiga-
tion.

November 16.—Pig No.1, just died and brought to experimental sta-
tion. No skin lesions; heart and lungs normal with exception of a few
collapsed lobules in principal lobe of one lung.* In abdomen omentum
injected so as to appear bright red. Spleen enlarged, soft, dark. Some
lymphatics have the cortex hemorrhagic. Stomach and small intes-
tines normal. In cecum near valve several large superficial yellowish
ulcers and a number of smaller ones, an eighth of an inch in diameter.
Two bits of spleen were cut out and dropped into a tube of gelatine,
and one of beef infusion. The gelatine culture remains sterile. The
liquid culture contains the motile hog cholera bacteria and a large bu-
tyric bacillus growing only in the bottom of the liquid.

No. 2 died last night. Buzzards have eaten into the thorax and
penetrated the coats of the stomach. Only the small ventral lobe
of right lung diseased. Bright red, mottled with pale yellow dots.
(See Plate IX, fig. 2.) The smallest bronchi occluded by cylindrical
plugs. Alveoli likewise occluded. The plugs consist chiefly of cells
and are so dry and firm that they may be removed as small ramifications
or branchings when the lung tissue is torn. away. Bronchial glands
enlarged, hemorrhagic. Spleen enormously enlarged, liver in advanced
stage of cirrhosis. Glands at portal fissure chronically enlarged. In
cecum four superficial ulcers one-half inch across, slough stained yel-
‘low. In upper colon four similar to these and a large number of small
ones about one-eighth inch across with yellowish slough.

A moderate number of bacteria found in cover-glass preparations of
Spleen. A gelatine tube culture contained, after three days about, sev-
enty-five to one hundred colonies of the motile hog cholera bacteria in

*In order to understand the description of the lung lesions, the following brief
outline of the anatomy of the lung and of the terms used may be of service:

The right lung is made up of four lobes; the left has only three. (In text-books
on anatomy the left lung is considered as being made up of only two.)

In both there is a large principal lobe resting upon the diaphragm and against the
adjacent thoracic wall. Thislobe forms the major part of each lung. The remainder,
occupying the anterior (or cephalic) portion of the cavity, is made up of two small
lobes, one extending ventrally (or downward in the standing position of the animal)
and in the expanded state covering the heart laterally; the other extending towards
the head and overlapping the base of the heart. These small lobes may be denomi-
nated the ventral and cephalic lobes, respectively. The right cephalic lobe is longer
and more distinct from the ventral lobe than the corresponding left cephalic. Wedged
in between the two principal lobes and resting on the diaphragm is a small lobe,
pyramidal, belonging to the right lung (azygos lobe). This lobe rests on the left
against the mediastinal membrane, and on the right it is separated from the right
principal lobe by a fold of the pleura passing from the ventral abdominal wali to in-
close the inferior vena cava. This sinall lobe is almost completely shut off, therefore,
from the other lobes by folds of the pleura,

a

A()

each needle track. A liquid culture inoculated simply with the platinum
wire thrust into the spleen pulp contained hog cholera bacteria only.
A rabbit was inoculated from lung tissue as above described; about one-
fourth of a cubic centimeter of the suspension injected. Dead on the
seventh day. Slight fibrinous exudate on coils of intestines. Spleen
very large, soft, dark. Beginning coagulation-necrosis in liver. Bae-
teria very numerous in spleen; both gelatine and liquid cultures contain
only the motile hog cholera bacteria. The plate from lung tissue with
which rabbit was inoculated contains a very large number of identical
colonies, made up of motile hog cholera bacteria.

November 17.—No. 3, male, died yesterday. Buzzards have consumed
pectoral muscles and pierced into thorax and abdomen. Ecchymoses on
costal pleura and entire epicardium, a few under pulmonary pleura. Left
lung hypostatie, slight amount of whitish foam in trachea. Lung tissue
otherwise entirely normal, neither hepatization nor collapse anywhere
to be seen. Bronchial glands and those along posterior aorta with hem-
orrhagic cortex. Hcchymoses in the subcutaneous fatty tissue over en-
tire ventral aspect of body, about one-eighth inch across, beneath peri-
toneum of abdominal muscles and of the entire length of small intes-
tine, from size of pin’s head to one-eighth inch. Congestion in patches
in large intestine, no ulceration. Stomach and intestines contain a yel-
low liquid resembling the yolk of eggs. Spleen but slightly enlarged.
Ecchymoses under serosa of liver. Girr hosis moderate. A bit of spleen
tissue dropped -into a tube of beef infusion gave rise to a culture of hog
cholera bacteria. In each needle track of a gelatine culture countless
colonies of the motile bacteria appear.

November 18.—No. 4, medium sized male, died this morning. Super-
ficial inguinal glands enlarged, cortex slightly hemorrhagic. Some
fibrils on coils of intestine. Petecchise under serosa of small intestine ;
extensive hemorrhage between mucous and muscular coat of stomach
along fundus, forming a clot about one-half inch thick. Spleen very
large, friable, blackish, extends beyond median line into right side.
Petecchie on liver, whicl-is considerably cirrhosed ; mucosa of stomach
along fundus blackish ; closely set petecchize under mucosa of small in-
testine ; contents liquid, blood-stained. A dark hemorrhagic patch
near valve in large intestine. Colon studded with petecchix, no ulcera-
tion. Small number of petecchiz on surface and throughout cortex of
kidneys. No bacteria seen on a cover-glass preparation of spleen tissue.
Beef infusion inoculated with a wire thrust into spleen remains sterile.
A bit of spleen dropped into a tube of gelatine gives rise to about a dozen
colonies of hog cholera bacteria.

November 18.—No. 5, male, 75 pounds, three to four months old, died
last night. Inguinal glands enlarged, pale. Left cephalic, ventral,
and about one-third of principal, right cephalic and ventral lobes of
lungs solidified, bright red, mottled with minute yellowish dots, 7. e.,
same as No. 2. ’Costal pleura covered with a very thin whitish exudate.
Solidified portion of principal lobe adherent. On epicardium a very
delicate papery deposit. Spleen much congested. Inflammatory ad-
hesion of liver to diaphragm. Mesenteric glands nearly as large as
hen’s eggs, mottled, pale red. About twelve ulcers one-quarter to one-
half inch across in lower ileum; base depressed and covered with a thin
yellow layer; outline irregular; not connected with Peyer’s patches.
Valve thickened and ulcerated. Several ulcers in cecum; a large
projecting slough attached to one of them. A gelatine and a liquid cult-
ure from the spleen contain hog cholera bacteria only. <A liquid cHlnns
from the pleura remains sterile.

.

Al

A rabbit inoculated from the hepatized lung tissue died on the eighth
day. Slight fibrinous exudate on intestines, diffuse coagulation necrosis
in liver, spleen much congested. Immense number of hog cholera bac-
teria in spleen and liver. Cultures pure. <A plate made from the same
bit of (pig’s) lung tissue contains about fifty colonies resembling hog
cholera.

No. 6, large black male, died last night. Extensive sero-fibrinous
infiltration of subeutis from axilla to pubis and over right thigh. The
subcutis has a gelatinous aspect. Spleen much congested. Lungs nor-
mal. In cover-glass preparations from spleen large bacilli, with ends
square. Cultures in gelatine and beef infusion remain sterile. Animal
probably died of malignant cedema.

November 21.—No. 7, medium sized male, died yesterday. Tempera-
ture of air varying from 26° to 50° F. Omentum deeply reddened.
Spleen enlarged, soft; small hemorrhages under capsule one-eighth
inch across. Liver imparts a sensation of grittiness when cut. Cortex
of kidneys dotted with hemorrhagic points. The patch of mucous
crypts about valve in cecum dark, pigmented; no ulceration. Mucosa
of stomach hemorrhagic in fundus. Thorax half full of blood-stained
serum and some fibrin stretching from lung surface to walls; small
quantity of fibrin in pericardial cavity. Lung tissue infiltrated with
blood (pulmonary hemorrhage). Two ventral lobes collapsed; subpleu-
ral hemorrhagic patches. <A cover-glass preparation from spleen con-
tains numerous hog cholera bacteria. In each needle track of a gela-
tine culture, countless colonies. A liquid culture from a bit of spleen
tissue contains hog cholera bacteria only.

No. 8, small female, died yesterday. Patches of skin on ventral as-
pect of limbs and groin reddened. Minute petecchiz under serosa of
ventral abdominal walls. Spleen very large, congested. Some delicate
fibrils stretched over coils of intestine. Liver cirrhosed. Glands of
mesentery and meso-colon enlarged; cortex hemorrhagic. Fundus of
stomach moderately congested. In cecum are black pigment spots
resembling former hemorrhage, chiefly on the summit of folds. In
upper colon ulcers about three to a square inch, each one-fourth inch
in diameter, and covered by a convex, projecting yellowish slough.
Ulcers found down to rectum. Small quantity of clear serum and a
few fibrils in pleural cavities and pericardium. Left ventral and tip of
right cephalic lobe collapsed. A gelatine and a liquid culture made
from a bit of spleen tissue contain hog cholera bacteria and a butyric
bacillus which slowly liquefies the gelatine.

No. 9, small male. Diffuse reddening of ventral aspect of body es-
pecially markedon limbs. Spleen, lymphatics, and kidneysnormal. A
small abscess in pelvis attached to bladder, probably caused by castra-
tion. Venous congestion of vessels of meso-colon. The transverse
folds of mucosa of colon covered by very thin yellowish patches of ne-
crosis. Feces hard, distending the large intestine. Cephalic and ven-
tral lobes of left lung solid, plainly mottled. The bronchioles and
alveoli filled with consistent plugs of cellular exudate. Remainder of
lungs normal. Owing to small size of spleen, two liquid cultures were
made, each with a bit of spleen tissue. In both, hog cholera bacteria
alone appeared. <A rabbit inoculated with hepatized lung tissue re-
mains well for weeks after. A plate culture therefrom is liquefied in
two days.

No. 10, small castrated male, died yesterday. Has been sick for some-
time according to overseer of farm. Spleen notenlarged. Inflammatory
changes in pelvis due to castration. Stomach. slightly reddened and

42

bile stained, One large ulcer on ileo cecal valve one-half inch across,
black, with yellowish margin. A few very superficial ulcers in czcum.
Lungs normal, left somewhat hypostatic. Two cultures made with bits
of spleen contain both hog cholera bacteria and butyrie bacilli.

No. 11, dying, killed by being bled from brachial vessels. Lungs
normal. Spleensmall. Liver slightly cirrhosed. Two ulceres in cecum;
slight superficial necrosis in colon. <A liquid culture made from a bit of
spleen contains hog cholera bacteria on following day.

November 23.—No. 12, small white male, died: yesterday. Median
line of ventral aspect of body much reddened, limbs slightly so; ex-
travasation under skin and into muscular tissue over sternum. Much
blood-stained serum in peritoneal cavity; spleen very large, dark.
In kidneys, cortex and base of pyramids deeply reddened. In cecum,
slight traces of superficial necrosis. Anterior and cephalic lobes of
both lungs collapsed. Blood-stained serum in pericardium. Numer-
ous hog cholera bacteria on cover-glass preparations of spleen pulp.
In a gelatine culture from the spleen countless colonies appear in each
needle track. <A liquid culture made with platinum wire contains hog
cholera bacteria on following day. A rabbit inoculated from the col-
lapsed lung tissue died on the tenti day. Spleen engorged ; numerous
foci of coagulation necrosis in liver, involving each one or more acini;
extensive necrosis along border of left lobe. Eechymosis of pyloric
valve and duodenum; hemorrhagic foci in lungs, about fifteen in each
lung, one eighth inch to three-sixteenths inch in diameter. Examina-
tion of tbe spleen shows numerous hog-cholera bacteria. <A’ gelatine
culture contains countless colonies in each needle track.

Number 13, small female, died yesterday. Skin on ventral aspect of
limbs and over pubis reddened. Spleen greatly enlarged, congested.
Lungs normal. <A few lobules in ventral and right cephalic lobe eol-
lapsed. Liver slightly cirrhosed. Stomach distended with food. Large
patch of mucosa in fundus reddened. Czecum and eclon contain numer-
ous ragged depressed ulcerations. Valve entirely encircled by ulceration.
Contents of intestine liquid, yellow. <A gelatine and a liquid culture
inoculated with a platinum wire thrust into spleen remain sterile. No
bacteria seen in cover-glass preparations.

No. 14, smail female, weight about 50 pounds. Considerable redden-
ing of the skin over ventral aspect of body and limbs; especially marked
along median line. Superficial inguinals enlarged, of a mottled pale
and deep red on section. Spleen very large, 12 inches long, 2 inches
broad, and five-eighths to three-fourths inch thick at hilus; gorged
with blood, friable. A smail number of punctiform hemorrhages in
cortical portion of kidneys. Glands of mesentery and of colon en
larged and congested. Deep reddening of several square inches of
mucosa in fundus of stomach. Large intestine contains a semi-liquid
mass, chiefly earth. Four large ulcers in cecum, one of them at least
1 inch across, covered by ayellowish slough; the pcritoneum covering
it is thickened and inflamed. In upper colon there is considerable ne-
crosis, involving the epithelium in patches. Lungs normal, excepting
the right ventral lobe, which is solid. Bronehiand air cells of this lobe
completely occluded by plugs as with No. 2; surface bright red, mottled
with yellowish points—the ultimate air cells filled with the cellular ex-
udate. Subpleural eechymoses over both lungs. From the spleen a
liquid and a gelatine culture contained only hog-cholera bacteria. They
were very numerous in cover-glass preparations from this organ.

A rabbit, inoculated from the consolidated lung tissue died on the
seventh dxy. At the point of inoculation a pasty mass extends to ab-

48

domen, only subcutis involved. Spleen engorged. Single acini and
groups in the liver are completely necrosed, yellowish w hite. In both
organs, hog-cholera bacteria. Cultures from spleen pure.

‘November 25.—No. 15, black and white male, died yesterday morn-
ing. Redness of skin of abdomen, throat, and limbs. Superficial in-
guinals hemorrhagic. Spleen very large, gorged with blood. Lungs
normal, excepting a few lobules at the caudal border of principal lobes,
which are red, collapsed, and contain lung worms. Pericardium con-
tains deep- colored serum and coagula; left auricle dotted with petecchiz.
Bronchial lymphatics hemorrhagic. Liver slightly cirrhosed. Cyst in
right kidney one-half inch in diameter. Fundus of stomach intensely
congested, similarly the cecum and colon; no ulcers. Lymphaties of
meso- colon hemorrhagic. A beef-infusion culture from a bit of spleen
contains the motile hog-cholera bacteria only. A gelatine culture be-
came liquefied by the heat of the laboratory; no bacteria seen on a
cover-glass preparation of spleen.

No. 16, black and white female, died last night. Skin and spleen as
in previous case. Thesmall ventral lobe of both lungs collapsed, lungs
otherwise normal. Liver in advanced stage of sclerosis; stasis of por-
tal circulation. Lymphatics of abdomen asin No. 15. Fundus of stom-
ach slightly reddened; one ulcer three-fourths inch across. Extensive
necrosis of mucous membrane in colon and rectum, slight in cecum ;
wherever the membrane is free from a slough it is deeply congested.
Numerous hog-cholera bacteria and some large (butyric) bacilli in spleen.
A beef infusion and a gelatine culture contain them. From a bit of
collapsed lung tissue a plate culture is made and a rabbit inoculated.
The plate contains in two days about six to seven liquefying and a
large number of non liquefying colonies, the latter made up of motile
hog-cholera bacteria; the rabbit died on the seventh day. Spleen very
large, friable; contains large numbers of hog cholera bacteria. On
left lobe of liver an area of necrosis one-fourth inch by three-fourths and
one-sixteenth inch deep. On the right lobe only three or four acini
necrosed. Pylorus and duodenum covered with hemorrhagic dots and
patches. Culture from spleen pure.

November 26.—No. 17, female of medium size; died suddenly this
morning without previous illness. Subcutaneous fat abundant. Spleen
moderately congested. Petecchiz in cortical portion of kidneys. Fundus
of stomach slightly reddened. In lower ileum patches of congestion.
Scattered petecchize in mucosa of large intestine; contents normal.
Glands of mesentery and meso-colon with cortex hemorr hagic. Large
quantity of blood-stained serum in thorax. Fibrinous deposit on pleura;
lungs partly expanded ; cephalic half of right lung solid, blackish; air-
tubes and alveoli filled with extravasated blood. Interlobular tissue
distended with blood-stained serum (pulmonary hemorrhage). Left lung
in the same condition. Trachea full of reddish foam. Blood and fibrin-
ous coagula in pericardial cavity. Beef infusion, into which a bit of
spleen was placed, remains sterile; also a tube of gelatine inoculated
from the spleen with platinum needle. In a cover-glass preparation of
the spleen large (butyric?) bacilli.

No. 18, small female, died last night. Buzzards have consumed thigh
muscles, Diffuse reddening alone median line of abdomen. Hemor-
rhagic spots one-eighth to one-fourth inch across, subepidermal, chiefly
on ventral aspect of limbs; subcutaneous and subperitoneal eechymoses.
All abdominal lymphatics with cortex infiltrated with blood. Serosa
of large intestines as if sprinkled with fresh blood; several subserous
hemorrhagic spots one-half inch across on diaphragm, along inferior

14

vena cava, common bile duct, and gall bladder; also, under mucosa of
the whole length of small intestine, throughout cortical portion and be-
tween pelvis and medullary portion of kidneys. Fundus of stomach
one mass of petecchi and larger extravasations. One ulcer in cecum,
old, with indurated base. Valve and the patch of mucous crypts at its
base ulcerated; depth of ulcer indurated, consisting of a tough, pale
tissue. Small old ulcersin upper colon. Lungs dotted with small hemor-
rhages, chiefly subpleural. Three or four hemorrhagic patches under
costal pleura of each side. Lung tissue normal, excepting the base of
right ventral and the tip of left ventral lobe, which are collapsed. Hemor-
rhages under epicardium over entire heart; left auricle one mass of ec-
chymoses. Coagula of fibrin in auriculo-ventricular groove.

Through an oversight the cultures from this animal and the one fol-
lowing were both numbered the same, so that it was impossible to
identify them. <A liquid culture from each was made by adding a bit of
spleen tissue. A gelatine culture from each was made simply with
platinum wire. One tube of infusion contains hog cholera and butyri¢e
bacteria; one tube of gelatine contains immense numbers of hog-cholera
colonies. The other two tubes remain sterile. A rabbit inoculated
from the collapsed lung tissue remained well fora month after. A plate
culture from the same contained about six colonies, evidently of hog-
cholera bacteria.

No. 19, small male, died last night. Diffuse reddening on abdomen
along median line. Superficial inguinals very large, pale, cedematous;
peritonitis; feeble adhesion of coils of intestine to ventral wall and of
lobes of liver to one another. Slight fibrinous deposit on intestines.
Liver sclerosed. Lymphatics hemorrhagic. Cortex of kidneys dotted
with extravasations. Mucosa of large intestines of a dark slate color;
it is dotted with closely-set conical elevations, tough, whitish, about one-
eighth inch high and one-sixth across. When scraped away a depressed
pale pink, sharply-outlined spot remains. Microscopic examination of
the intestine showed that these elevations correspond to amorphous
masses, which failed to become colored on applying the ordinary stain-
ing agents. They covered portions of the mucosa which were either
wholly or partially necrosed and incapable of being stained. In some
places the outline of the tubules could still be discerned. On applying
Weigert’s fibrin stain, long meshes of fibrin corresponding in general to
the outline and position of the destroyed tubules appeared. Valve
thickened and completely covered by ulceration. Cephalic half of both
lungs airless, affected with broncho-pneumonia; catarrhal exudate filled
alveoli and air tubes. Epicardium dotted with hemorrhagic points.
Slight, feeble, pleural adhesions.

For cultures from spleen, see No. 18. A rabbit inoculated with lung
tissue died on the fifth day. Spleen slightly enlarged; contains many
hog-cholera bacteria. Gelatine culture contains very many colonies of
the same.

No. 20, alarge female. No skin lesions; a few strings of coagula over
coils of intestine; spleen small; base of pyramids of kidneys much
reddened; ileum dotted with subperitoneal hemorrhagic points and
patches ; mucosa not affected; mesenteric glands with cortex hemor-
rhagic. Large intestine empty, scattered ulcers one-eighth to one-fourth
inch across. Liver sclerosed.

A beef-infusion culture inoculated with a bit of spleen tissue contains
hog-cholera bacteria and butyric bacilli. A gelatine-tube culture con-
tains a few hog-cholera colonies.

November 29.—No. 21, small Jersey red, female, died last night. Skin

45

deeply reddened along median line of abdomen. Large quantity of
blood-stained serum in peritoneal cavity. Serosa of ileum and the
mesentery completely covered with hemorrhagic points and patches.
Lymphatics of abdomen hemorrhagic throughout their substance. Pe-
tecchiz in cortex of kidneys. Mucosa infundus of stomach hemorrhagic.
Mucosa of lower ileum a confluent layer of necrosed tissue. Numerous
‘round ulcers in cecum and colon; slough projects slightly. Lungs hypo-
static, interlobular spaces distended with coagulated blood, most marked
in dependent lobes. Simple collapse of both ventral lobes and of the
right principal near the root. Ventricles of heart dotted with petecchi,
auricles black, covered with clotted extravasated blood. Hog cholera
bacteria present in cover-glass preparations from spleen and in both
gelatine and liquid cultures.

No. 22, male, Jersey red, died last night. Glands of abdomen with
cortex infiltrated with blood. Spleen engorged. A few hemorrhagic
patches in fundus of stomach. In cecum and colon ulcers about three-
eighths inch across ; very thin, adherent, yellowish slough. About one
ulcer to 4 square inches of surface. Considerable blood-stained serum
in pleural cavities, hemorrhage in anterior half of left lung, which is
solid, blackish on section. Clots and reddish foam in trachea and
bronchi; hemorrhage seems somewhat older than in No. 21. Pleura
of right lung roughened and parts adherent to chest wall. Ventral
lobe solid, bronchioles firmly plugged with dry catarrhal secretion.
Hog cholera bacteria on cover-glass from spleen pulp and in a gelatine
and liquid culture made therefrom; only five to ten colonies in each
track of the platinum wire. <A rabbit was inoculated from a bit of the
solidified lung tissue and a plate culture mace. The latter develops
numerous colonies of hog cholera bacteria. The rabbit died on the thir-
teenth day. Numerous hog cholera bacteria in both organs. <A gela-
tine culture from the spleen contains the same organisms.

No. 23, small black male. Buzzards had removed pectorals of one
side. Lymphatics congested, not hemorrhagic. Crowded petecchiz in
subeutis and beneath peritoneum of ventral abdominal wall. Spleen
very large, congested. Four or five small hemorrhages on diaphragm.
Mucosa of cecum and upper colon ulcerated in large patches. In
lower colon the ulcers are small, yellowish, depressed areas embedded
in a very dark mucosa dotted with numerous punctiform ecchymoses.
At root of left lung there is some collapse, extending slightly into all
lobes. Of rightlung the ventral and cephalic lobes are collapsed, with
occasional emphysematous lobules interspersed. Lungs otherwise nor-
mal. Extensive hemorrhage of both auriclesin the form of diffuse patches
and petecchie. A gelatine and aliquid culture from the spleen remain
sterile. A plate culture made froma bit of collapsed lung tissue con-
tainsa considerable number of colonies, which are made up of bacteriare-
sembling those of hog cholera, but differing from them in their manner of
growth on gelatine, in. beef infusion, and in the absence of motility. A
rabbit inoculated from the same bit of lung tissue remains well. A
plate culture from a bit of normal tissue from the same lung contains
but one colony.

No. 24 died yesterday; medium-sized female. Spleen very large,
extends beyond median line. Lungs normal, excepting collapse of a
small portion of the right ventral lobe. Lymphatic glands in general
with hemorrhagic cortex.. Ceecum and colon very much congested, ul-
ceration superficial and slight. Entire fundus of stomach of a uniform
deep wine color. A gelatine and a liquid culture from the spleen con-
tain only motile hog cholera bacteria. In the former the colenies are

46

very numerous. The bacteria are demonstrated in cover-glass prepara-
tions from spleen pulp.

No. 25, medium sized black male, died yesterday. Spleen very large.
Subperitoneal tissue fuil of peteechiz. Lymphaties with hemorrhagic
cortex. Hemorrhages under serosa of duodenum and common bile duet.
Valve completely ulcerated. Intestine otherwise normal and feces —
dry. Lungs contain a large number of subpleural hemorrhages, tissue
normal, epicardium hemorrhagic. Kidneys contain a specimen of kid-
ney-worm (sclerostoma pinguicola). A gelatine and a beef infusion culture
from the spleen became confused with those of another pig (No. 435), to
be described later on. One set of cultures remained sterile; the other
contained hog cholera bacteria. In all probability the sterile cultures
belonged to this animal.

December 2.—No. 26, medium-sized female, died last night. Consid-
erable redness of skin over the ventral aspect of limbs and along me-
dian line of abdomen. Spleen very large, blackish. Several strong
fibrous adhesions betweeen costal and pulmonary pleura. Lung tissue
normal. Left kidney contains a small cyst. Large namber of round
depressed ulcers stained yellow, most numerous in cecum. One ulcer
is one-half inch across, the inflammation extending to serosa. Stomach
very dark, pigmented along fundus. On a cover-glass preparation
from spleen numerous large bacilli (probably butyric). They did not
develop in the liquid and gelatine culture, which latter contained only
hog cholera bactera colonies, very numerous in each needle track.

No. 27, small black male. Superficial inguinals enlarged, pale, cedem-
atous. Superficial ulceration and hemorrhagic changes in cecum,
Lungs normal. Post mortem changes too advanced for cultures.

No. 28, small female, died last night. Superficial inguinals with
cortex hemorrhagic. Spleen slightly enlarged. Minute hematomata
on its surface. Slight sclerosis of liver. Left kidney contains six cysts
one-half inch diameter. Stomach in fundus somewhat congested. In
large intestine, ulcers one quarter to three-eighths inch diameter, with
adherent yellowish, projecting slough, most numerous in cecum. About
one-third of the ventral lobe of each lung and a few lobules of the right
principal lobe collapsed. Lungs otherwise normal. In a beef infusion
culture from the spleen both hog cholera and butyric bacteria were
present. A gelatine culture contained but two colonies. From a bit of
collapsed lung tissue a plate culture was made and a rabbit inoculated.
On the plate about fifteen colonies of hog cholera bacteria appeared.
The rabbit died on the fifteenth day. Bare indications of necrosis in
liver. Spleen very large. Both organs contain a moderate number of
hog cholera bacteria. A roll culture from the spleen is pure.

No. 29, large black male, died about thirty-six hours ago. Tempera-
ture below freezing point. Skin deeply reddened over entire ventral
aspect of body. Superficial inguinals enlarged, slightly congested.
Spleen very large (about 14 inches Jong), very soft and friable. Slight
sclerosis of liver and old perihepatitis. Retro-peritoneal glands with
cortex hemorrhagic. Cyst in right kidney. Slight eechymoses in fun-
dus of stomach. Valveand patch of mucous glands in cecum very dark
with pigment. Slight superficial ulceration in cecum and upper colon.
Lungs and heart normal. Both gelatine and beef infusion cultures con-
tain hog cholera bacteria. In the former the colonies are very numer-
ous.

No. 30, small black male; died thirty-six hours ago. No reddening
of skin. Superficial inguinals and spleen but slightly enlarged. Peri-
tonitis, Petecchiz under serosa of small and large intestines and blad-

47

der. Moderate amount of fibrinous exudate. Valve completely ulcer-
ated, ulcer deep. One near valve has caused thickening of serosa of
intestinal wall. In cecum an extensive patch of ulceration; in colon
a few ulcers and numerous punctiform hemorrhages. Right lung com-
pletely adherent to costal pleura by means of fibrous tissue. A small
ventral portion of principal lobe of left lung is airless, pale red, mot-
tled with yellowish points. Air tubes aud vesicular portion occluded
with dry cylindrical plugs. A culture in gelatine fiom the spleen de-
velops numerous colonies in each track of the wire. <A liquid culfure
contains the butyric bacillus also. A bit of the solidified lung tissue
was used for a plate culture and to inoculate a rabbit. The plate de-
veloped countless colonies of hog cholera bacteria as tested by other
cultures. The rabbit died on the tenth day. The spleen was enlarged,
the liver full of centers of advanced necrosis, involving one to three
acini; hog cholera bacteria very numerous in both organs.

December 3.—No. 31, small black and white female, died yesterday.
Well-marked odor of decomposition. Noskindiscoloration. Spleen but
slightly enlarged. Lymphatics in general with hemorrhagic cortex.
Liver in state of advanced sglerosis. Stomach normal. A few large
old ulcers and a considerable number of small ones throughout cecum
and colon. Mucosa itself pigmented with patches of fresh congestion.
Lungs normal. A liquid culture from the spleen contains only butyric
bacilli.

No. 32, small black and white female. No skin discoloration. Lym-
phaties, including inguinal, bronchial, and peritoneal. with more or less
hemorrhagic cortex. Spleenengorged. Liversclerosed. Kidneys with
numerous petecchize throughout cortical portion. Stomach pale. Sev-
eral large old ulcers in upper colon. Cecum and colon pigmented.
Lungs normal with exception of a few collapsed lobules in ventral lobes.
Both a gelatine and a beef infusion culture contain hog cholera bacte-
ria. Colonies very few.

No. 33, large black and white male; said to have died last night.
Advanced post mortem changes. No examination made, excepting to
see the condition of lungs, which were healthy.

No. 34, medium-sized white, died lastnight. Considerable reddening
over ventral aspect of body. Inguinals reddened on section. Small
quantity of dark-colored serum and numerous yellowish flaky coagula
attached to abdominal organs. Spleen very large, dark, friable. Liver
cirrhosed. Kidneys with cortical portion thickly dotted with petecchiz,
hemorrhage into pelvis. Lymphatics in abdomen with cortex more or
less hemorrhagic. Extensive and deep ulceration in large intestines ;
in cecum and upper colon as large patches, in lower colon as small
ulcers. The mucosa which is not destroyed is deeply congested.
Stomach along fundus deeply reddened. Extensive fibrous adhesions
of left lung to walls of thorax. Collapse involves ventral, cephalic, and
portions of principal lobe of right lung, and small portion of principal
and ventral lobe of left Jung. Extensive muco-purulent secretion in
trachea, bronchi, and subdivisions throughout both lungs. Bronchial
glands with cortex hemorrhagic. A beef infusion culture from the
spleen contains hog cholera and butyric bacteria. In the gelatine cult-
ure each track of the wire contains countless colonies of what are shown
under the microscope to be motile hog cholera bacteria. From a bit of
collapsed lung tissue a plate culture was made and a rabbit inoculated.
The plate develops countless non-liquefying colonies. The rabbit died
on the eighth day. Spleen enlarged. Liver infested with coccidia, A

48

slight amount of coagulation-necrosis. Hog cholera bacteria in both
organs and in cultures from the spleen (both gelatine and liquid).

December 5.—No. 35, small black and white female, died yesterday.
Redness of skin over abdomen and inside of limbs. Spleen enlarged,
slightly congested. Lymphaties with cortex infiltrated with blood.
Large quantity of blood-stained serum in abdomen. Liver sclerosed.
A few scattered petecchiz in cortical portion of kidneys. Mucosa of
colon pigmented ; a few small ulcers present. Lungs normal, with ex-
ception of a few collapsed lobules in ventral lobe of each lung. Dark-
colored serum in pericardial cavity. The spleen contains large num-
bers of butyric bacilli. A liquid culture contains both hog cholera and
butyric bacilli. A gelatine culture remains sterile.

No. 36, large black and white female, died yesterday. Lungs normal.
Spleen very large, dark, friable. Liver sclerosed; lymphatics gener-
ally with cortex congested or hemorrhagic. Large number of ulcers in
cecum and colon; mucosa deeply congested. From spleen countless
colonies of hog cholera bacteria in a gelatine tube culture. In aliquid
culture the butyric bacilli are also found.

No. 37, medium Jersey red and the last_of a lot of seven, dead forty-
eight hours. This animal has been sick for some time; the spleen
was very large, gorged with blood.. Lymphatics pale. Large number

of old ulcers, from one sixteenth to 14 inches across in cecum and colon ; -

mucous membrane generally pale. Of the lungs, both ventral and a
small portion of cephalic lobes with smaller bronchi and alveoli plugged
with dry catarrhal products. <A liquid culture from the spleen contains
hog cholera and butyric baeilli. A gelatine culture contains countless
colonies. The spleen pulp on coverglass preparations shows many.
From the diseased lung tissue a rabbit was inoculated and a plate cult-
ure made. The latter develops a large number of colonies of hog cholera
bacteria. The rabbit died on the eighth day. Spleen enlarged and
friable, contains many hog-cholera bacteria. Slight coagulation-necrosis
in liver, which is infested with coccidia. Cultures from blood and spleen
pure.

December 7,.—No. 38, small white female, died last night. Much ema-
ciated. Subcutaneous and subperitoneal tissue contains numerous ex-
travasations. LLymphaties in general with hemorrhagic cortex. Spleen
moderately congested. Lung tissue normal. Numerous subpleural and
epicardial hemorrhages. Kidneys with cortical portion dotted with
numerous punctiform extravasations. Mucosa of small intestine con-
tains numerous petecchie. One ulcer, one-half inch across, in lower
ileum. Extensiveand deep ulceration throughout whole length of large
intestine. Some of the ulcers over 2 inches across; surface coal-black ;
the inflammation extending through the intestinal walls to serosa, which
is dotted with scattered extravasations. A gelatine tube culture from
Spleen pulp contains countless colonies in each needle track, consisting,
as seen under the miscroscope, of motile hog cholera bacteria. A liquid
culture contains also streptococci and butyric bacilli.

No. 39, black and white female, post mortem changes under way. No
examination made beyond ascertaining that lungs are normal, lym-
phatics with cortex infiltrated with blood, and spleen enlarged and con-
gested.

December 8.—No. 40, small black female, died this morning. Super-
ficial inguinals enlarged but pale. Moderate quantity of straw-collored
serum in abdominal cavity. Spleen enlarged, deeply congested. In
cecum and upper colon a large number of deep broad ulcers; in some
the inflammation extends through intestinal wall to serosa, In lower

a

49

colon, ulcers small and mucosa deeply congested. Numerous hog
cholera bacteria in spleen as shown by a gelatine culture. <A liquid cul-
ture contains also butyric bacilli.

No. 41, small black and white female, died yesterday. Post mortem
changes under way. Large quantity of bload-stained serum in abdomen.
Plastie peritonitis matting together the various organs; spleen enlarged
and congested. Numerous old ulcers in cecum and colon, with adher-
ent slough. Adhesive pleuritis, with large quantity of blood-stained
serum in thorax. Lungs normal, excepting areas of collapse in ventral
and cephalic lobes. <A liquid culture from spleen contains both hog
cholera and butyric bacilli. A gelatine tube culture develops a large
number of colonies in each needle track.

December 10.—No. 42, small black and white male, died yesterday
morning. No discoloration of skin. Spleen very large, congested.
Lymphatics with cortex slightly reddened. Livercirrhosed. A fewex-
travasations in pyramids of kidneys. Mucosa of cecum and upper
colon covered with ulcers, the adherent slough dirty yellowish. Fully
one-half the area of membrane thus involved, the remainder is pale.
Lungs normal. From the spleen, hog cholera as well as butyric bacilli
appeared in a beef-infusion culture. In a tube of gelatine the colonies
were very numerous.

December 12.—No. 43, small black and white male, died December 10.
No discoloration of skin. Spleen very large, friable, gorged with blood.
Inguinals and lymphatics at lesser curvature of stomach hemorrhagic
throughout. ‘Those of mesentery and meso-colon less so. A few
petecchiz on surface of kidneys. Liver slightly cirrhosed. Mucosa of
excum pale, of colon considerably congested. A few small ulcers with
hemorrhagic border. Mucosa in fundus of stomach deeply congested.
Slight hemorrhage in principal lobe of each lung, otherwise both nor-
mal. Bronchial glands hemorrhagic. Hog cholera bacteria quite abun-
dant in spleen, as shown by cover-glass preparations and cultures.

December 15.—No. 44, medium-sized white female, died yesterday
morning. Slight reddening of skin along median line of abdomen, limbs,
and throat. Spleen enlarged and engorged. Inguinal, bronchial, retro-
peritoneal and meso-colic glands with cortex hemorrhagic. Liver badly
cirrhosed. In ezcum one ulcer an inch across, involving entire thick-
ness of wall, and few smaller ones. A few in upper colon. Lungs
cedematous. At least one-half of each lung (most dependent portion)
airless, of ared flesh color. Sprinkled through it in some places more
densely than in others are grayish-yellow areas one-half to two milli-
meters in diameter. Trachea full of foam. Bronchi contain a thick
mucous secretion, most abundant in the diseased region. A roll cult-
ure from the spleen contains numerous colonies of hog cholera bae-
teria. Froma hit of lung tissue a rabbit was inoculated ; a plate culture
from the same shows a very large number of colonies, probably hog
cholera. The rabbit died on the seventh day. Spleenenlarged. Coagu-
lation necrosis in liver, which also contains coccidia. Hog cholera bac-
teria numerous in spleen, as shown by cover-glass preparations and roll
cultures.

No. 45, large black-and-white female, died December 13. Slight red-
dening of skin. Spleen large, congested. Lymphatics in general with
cortex hemorrhagic. Liver badly cirrhosed; surface dotted with hem-
orrhagice points. Kidneys on surface and on section, as well as mucosa
of ceecum and upper colon, dotted with numerous petecchiw. No ulcer-
ation. Large quantity of blood-stained serum and coagula in pleural
sacs, chiefly in the right. Lungs not collapsed, infiltrated with a red-

15612 8 C——4

50

dish serum; left hypostatic. Abundant mucous secretion in bronchi
and smaller air tubes stained with blood. Nohepatization. Roll cult-
ure from a bit of spleen contains a large number of colonies of hog
cholera bacteria. The same may be seen in cover-glass preparations from
the spleen itself.

No. 46. Large black-and-white male, died December 13. Spleen en-
larged and congested. Abdominal lymphatics with cortex more or less
congested. Liver slightly cirrhosed. One large ulcer on valve about 1
inch across; several half as large in the middle of colon. Mucosa
deeply congested in cecum and colon; much pale serum in pleural
sacs. Lungs slightly edematous. Of right lung the principal near
root, ventral and tip of cephalic airless, collapsed. One lobule on ventral
(diaphramatic) surface of principal lobe airless, with faint catarrhal in-
jection of bronchioles and alveoli; of left lung a small portion of the
principal collapsed; the ventral and cephalic emphysematous. The
trachea, bronchi, and branches contain a large quantity of a translucent
viscid mucus; no lung worms present. Bronchial glands enlarged, pale;
those on posterior aorta with cortex hemorrhagic. Extravasations
beneath epicardium. A plate culture from a bit of lung tissue develops
about seventy-five colonies of hog cholera bacteria. A rabbit inoculated
from the same bit remains well. <A roll culture from the pig’s spleen
contains about fifty colonies alike; one examined is made up of motile
hog cholera bacteria.

December 17.—No. 47, small female, died yesterday. Superficial in-
guinals entirely hemorrhagic. Mesenteric glands slightly congested.
Spleen barely congested. Mucosa of lower ileum completely ulcerated.
Similarly that of cecum and upper colon, but more severely so as to
make the intestinal wall very friable. In lower colon the ulcers are
isolated. Lungs and heart normal. In a roll culture from a bit of
spleen tissue about one hundred colonies of hog cholera bacteria ap-
peared.

No. 48, medium-sized black-and-white female, died last night. Super-
ficial inguinals enlarged, pale. Abdominal lymphatics in general
with cortex hemorrhagic. Spleen congested; surface covered with
numerous elevated blood-red points. Liver extensively cirrhosed.
Mucosa of ileum dotted with petecchie. It contains about fifteen ulcers,
not limited to Peyer’s patches, with longer diameter transverse, in some
cases encircling the tube. The ulcer is covered by a thin yellow
slough. One ulcer, one-half inch across, in cecum, and two in colon.
About one-half pint of straw-colored serum and a mass of semi-
gelatinous pale coagulum the size of a fist in each pleural sac. Lungs
but partly collapsed, pleura slightly roughened. Interlobular tissue of
dependent lobes distended with serum, parenchyma cedematous, so as
to sink in water. Bronchi contain a slight amount of reddish fluid. In
aroll culture from a bit of spleen pulp about two hundred colonies of
hog cholera bacteria appear.

December 24,—No. 49, large, black and white. Spleen gorged with
blood. Lymphatics generally pale; liver cirrhosed. Cecum and colon
with walls thickened and very friable; mucosa entirely ulcerated. One
ulcer in rectum. A roll culture from the spleen melted, but found to
contain on examination only hog cholera bacteria.

DISEASE IN HEALTHY PIGS CAUSED BY MATERIAL FROM THIS EPI-
ZOOTIC.

November 21.—Two pigs (Nos. 434, 435), about two months old, fed
with spleens from several of the preceding cases. Two days later a few

Op

more spleens were given them. Both became sick a few days later and
died November 28, about twelve hours apart.

No. 434. Spleen slightly enlarged, full of blood. All glomeruli of kid-
neys show as hemorrhagic points: lymphatics moderately congested.
Stomach along entire fundus deeply congested. Superficial small ul-
cers in cecum and colon; in the cecum they are covered by a project-
ing slough. Right ventral and cephalic lobes collapsed, the former de-
veloped into broncho pneumonia (catarrhal injection of small air tubes
and alveoli). A few lobules of left principal lobe in the same condition.
Hog cholera bacteria in the spleen as determined by a gelatine and a
liquid culture. A rabbit was inoculated with a bit of lung tissue and
a plate culture made. This developed countless colonies, non-liquefy-
ing, alike, shown to be motile hog cholera bacteria. Rabbit dies on sixth
day. Spleen moderately congested; contains many hog cholera bacte-
ria. In liver, minute foci of necrosis. A gelatine culture from the spleen
contains numerous colonies of hog cholera bacteria.

No. 435. Spleen enlarged, covered with hemorrhagie¢ elevations. Kid-
neys hemorrhagic as in No. 434. Stomach near pylorus deeply con-
gested. Czcum and entire colon covered with a dirty yellowish and
blackish slough. Right and left ventral lobes, a small portion of right
principal and left cephalic affected with broncho-pneumonia. Cultures
from the spleen of this animal were confused with those of another pig
(No. 25), but one set remained sterile; the other contained hog cholera
bacteria, and it is highly probable that the fertile cultures belonged to
this animal.

A few additional cases are cited to show the infectious nature of
this outbreak.

No. 436 and No. 437 were placed, November 27, in the infected pen
containing the two preceding animals. They were also fed portions of
hog cholera viscera later on. No. 436 was found dead December 27.
Red blotches on skin of ventral aspect of body. Superficial-inguinals
hemorrhagic. Other lymphatics enlarged but pale. Spleen slightly
congested. Mucosa of cecum and colon deeply congested and dotted
with considerable number of small ulcers. <A roll culture from the
spleen melted, but contains only hog cholera bacteria according to mi-
croscopic examination. No. 437 did not take the disease.

No. 449 and No. 452, placed in the same pen December 17, but not fed
with infectious matter, died December 29. The lesions were somewhat
different from those usually found, and are briefly as follows:

No. 452. Spleen and lymphatics notenlarged. Large quantity of se-
rum and fibrinous coagula in abdomen. Viscera generally agglutinated.
Lungs glued to chest wall by a recent exudate. Pericardium distended
with serum and coagula. Lung tissue not affected. Kidneys deeply
reddened. Mucosa of cecum and colon entirely covered with a thin
layer of diphtheritic exudate; when scraped away a deeply reddened
surface is exposed. Numerous small, deep ulcers present. A roll cult-
ure of spleen, also melted from the heat of laboratory, contains only hog
cholera bacteria. In No. 449 the lesions were the same, excepting the
pericarditis. The ulceration of large intestine less extensive.

Two very instructive cases of hog cholera were caused by simply ex-
posing pigs on an infected asphalt floor in a pen adjoiniug cases of the
disease.

_No. 464 and No. 466, about three and one-half months old, exposed with
six others January 4. No. 464 died January 11. Superficial inguinals

52

normal. Those in abdomen much tumefied and hemorrhagic through-
out. Spleen enlarged, friable, with hemorrhagic points, Several patches
of mucosa in fundus of stomach one-fourth to one-half inch across,
covered with blood clots. In large intestine only a few scattered petec-
chiz on mucous membrane. Some subpleural hemorrhages in lungs;
lung tissue normal. Scattered petecchiz on epicardium of auricles and
ventricles. On cover glass preparations from spleen pulp a moderate
number of bacteria were present. In several roll cultures only colonies
of hog cholera bacteria appeared.

No. 466 died January 13. Skin of ears, throat, nose, limbs, and belly
deeply reddened. Spleen as in No. 464. A few petecchix on epicardium.
Kidneys as in No. 464. Urine contains blood. The mucosa of large intes-
tine in general deeply congested and studded with about fifty ulcers
one-fourth inch across. Meso-colic and retro-peritoneal lymphatics
with cortex hemorrhagic. Stomachas in No. 464. Lungs normal, ex-
cepting collapse of two-thirds of ventral lobes. Roll cultures from a
bit ef spleen pulp gave the same result as in preceding case.

BRIEF SUMMARY OF THE IMPORTANT FEATURES OF THIS EPIZOOTIC.

The high percentage of mortality in epizootics of bog cholera like
the foregoing is the first thing to claim our attention. Out of 119 ani-
mals not less than 100 perished within the brief space of two months,
or over 80 per cent. As no disinfection was resorted to, no isolation of
the healthy attempted, it is difficult to say what number could have
been saved. At any rate, the above figures indicate the mortality of
this disease when left to itself, and it shows that nearly all young
animals, such as weigh between 50 and 100 pounds, are susceptible to
this disease.

Most of the animals died rather unexpectedly. Only a comparatively
small number were visibly diseased some time before death. Since in
many there was more or less ulceration in the large intestine, it indi-
cates that animals may be in a very bad condition and become a source
of infection for others without necessarily showing it.

The swill feeding has already been mentioned as a probable cause of
the cirrhosis of the liver observed in so many of these animals. This
organ was tough and imparted a gritty sensation tothe hand when cut.
The parenchyma was softened and degenerated. It seems reasonable
to suppose that this chronic malady may have meade the herd more
susceptible to the disease.

Hemorrhagic lesions.—At least one-third of the cases examined showed
lesions of a hemorrhagic character. The most common was an infiltra-
tion of the cortical portion of lymphatic glands with blood; sometimes
the entire glandappeared hemorrhagic on section. As regards the rel-
ative frequency of this condition, the bronchial, posterior mediastinal
(aortic), and inguinal glands stood first; next, the retro-peritoneal,
meso-colic glands and those in the lesser curvature of the stomach.
The mesenteric glands were rarely affected. Accompanying this con-

dition of the lymphatics was a very large spleen, its great size being

simply due to an engorgement with blood.

53

Next in frequency were the hemorrhagic lesions of serous membranes,
in the form of punctiform extravasations, larger ecchymoses, and very
rarely of collections of blood infiltrating the muscular layers beneath
the serous membrane. These extravasations were most frequent on the
auricles and ventricles of the heart, under the serosa of the large and
small intestines, beneath the pulmonary pleura, and in the subcutane
ous tissue. In the severest cases blotches appeared on the diaphragm-
and costal pleura. In about 10 per cent. the kidneys were hemor-
rhagic. The glomeruli then appeared as minute blood-red points. To
this may be added hemorrhages in the pyramids and extrayasations col-
lecting around the papille.

The mucous membrane of the stomach in hemorrhagic cases was
deeply reddened in the fundus; in some cases there was hemorrhage
into the membrane, more rarely on the surface. The mucosa of the
small intestine was usually intact, but that of the large intestine in the
acute form of the disease was in the same condition as the stomach. In
older cases, when not covered with ulcers, it was either pigmented or
dark red, chronically congested. This outbreak was characterized by
hemorrhagic lesions more than any other which we haveexamined. Our
experience has been that the early cases are hemorrhagic and are suc-
ceeded by those in which ulceration, cellular infiltration of the lym-
phaties and signs of weakness, such as serous effusions, predominate.

In some of the animals in this outbreak there were most extensive
hemorrhages. In one the mucous membrane of the stomach was sepa-
rated from the muscular coat by an extensive clot one-half inch thick.
In five cases (10 per cent.) the lungs were the seat of extensive hemor-
rhages, which literally converted the most dependent lobes into a blood
clot and filled the pleural sacs with blood-stained serum. In a consider-
able number both peritoneal and thoracic cavities contained much blood-
stained serum.

Ulcerative lesions.—Ulcers of the large intestine were present in 36
out of 49 cases, or 70 per cent. They varied from very slight to very
severe and extensive lesions, involving in a small number nearly the
whole mucous membrane of the cecum and colon. The rectum was
quite invariably free from disease. The age of the ulcers can not
be determined, as the process of necrosis and subsequent ulceration
seems to vary much in rapidity. In afew eases it was not limited to
the mucous membrane, but extended into the muscular wall, produc-
ing considerable local inflammation and thickening of the serous mem-
brane. In rare cases the necrosis and cellular infiltration had made the
intestinal wall so friable that it broke when handled. When the ulce-
ration was slight it was frequently confined to the ileo-cecal valve and
adjacent membrane, which consists of a large patch of lymph follicles
and some mucous glands. The ulceration in this situation was accom-
panied by an extensive neoplastic thickening of the valve beneath the
ulcer, indicating that the ulcer was old. In 5 cases (10 per cent.) the

54

lower ileum was ulcerated (Nos. 5, 21, 38, 47, 48); the ulcers seemed to
have no relation to Peyer’s patches.

Complications.—Peritonitis, pleuritis, and pericarditis were not un-
common complications usually accompanying old ulceration.

Lang lesions.—This epizootic was studied mainly for the purpose of
determining the condition of the lungs in hog cholera. Swine plague
is essentially a disease of the lungs, secondarily of the digestive tract.
It may be possible to find some cases of swine plague in which the
large intestines are primarily diseased. Thus far they have not come
to our notice. From the facts obtained from this epizootic we may
safely assume that hog cholera produces no lesions which may not be
found in the lungs of apparently healthy animals of the same age, and
which may be due to the debility caused by the infectious disease. -We
must accept, however, the hemorrhages found in a small percentage of
cases. Such are co-existent with hemorrhages in most other organs,
and are not specific lung lesions. (See Nos. 7, 17, 21, 22, 43, of autopsy
notes.) The lesions found on post-mortem examination were either sim-
ple collapse or lobular broncho pneumonia following it.

Simple collapse usually involved the two ventral dependent loves,
more rarely portions of the small cephalic and the principal lobes. The
collapsed lobes, or groups of lobules interspersed among emphysematous
lobules, appeared slightly, iv at all, depressed. The color appro:ched
thatof red flesh. In only a few instances could plugs be found occlui-
ing the bronchi. Sections made from lobules in this condition show a
number of interesting features. The alveolar walls are crowded together
in some places till they almost touch one another. Besides the fibrin,
there may or may not be one or several large cells, round, with much
protoplasm inclosing a vesicular nucleus. The bronchi are all open;
the epithelium intact. The alveolar walls are not changed, nor is there
any round cell infiltration to be seen. In circumscribed areas the capil-
lary net-work is distended with blood corpuscles, while all the larger
vessels are similarly filled with these elements. In the alveolar duct
there is now and then considerable fibrillar fibrin well brought out by
Weigert’s stain.

In about 15 per cent. of the animals examined one of the smaller
ventral lobes was airless throughout and moderately enlarged. Viewed
from the ‘surface, the diseased lobe is bright red, dotted with minute,
pale grayish or yellowish points of a diffuse hazy outline, each not more
than 1 millimeter (j. inch) in diameter. They are usually arranged in
groups of four, and represent the ultimate air-tubes filled with cel-
lular exudate. The larger bronchi are also occluded. The exudate is
yellowish white, so firm that it is possible to tear away the lung tissue
with needles without necessarily breaking up the inclosed exudate. It
may thus be teased out in the form of branching cylinders, becoming
smaller, and finally dwindling down to the size of a coarse hair.

In microscopic sections the alveolar walls are found beset with dis-

55

tended capillaries. The alveoli are filled up with cellular masses, fibrin
appearing very rarely. In most alveoli the cells are large, round, with
vesicuiar nucleus, evidently derived from the alveolar epithelium. In
some alveoli and in the smallest air-tubes the cell mass is so dense that
individual elements can only be seen with difficulty, but they appear
to be identical with the cells just described. The process seems to be
accompanied with very little inflammation. The desquamation and
proliferation goes on in the alveoli and smallest air-tubes until they are
occluded by tbe casts described. Of the 49 animals of the same herd,
17 were found with collapse (Nos. 1, 7, 8, 12, 13, 16, 18, 21, 23, 24, 28, 32,
34, 35, 41, 44, 46), and eight with lobular broncho-pneumonia (Nos. 2, 5,
9, 14, 19, 22, 30, 37; see also Nos. 434 and 435). More than one half,
therefore, had some defect of the lungs.

Itmight be questioned whether such lesions as those of broncho-pneu-
monia are not due to swine plague bacteria, since they closely resemble
the appearance found in many swine plague lungs. This question is
effectually disposed of by the inoculation of lung-tissue into rabbits.
From 16 lungs 16 rabbits were inoculated. Of these lungs 8 were in-
volved in simple collapse; 8 in broncho-pneumonia. Of the 16 rabbits
4 survived (Nos. 9, 18, 23,46); the remainder died of hog cholera
(Nos. 2, 5, 12, 14, 16, 22, 28, 30, 34, 37, 44, 434). (The notes on these
rabbits will be found in the autopsy notes of the swine as numbered.)
Of the 4 survivors 3 had been inoculated from collapsed lung tissue,
1 from a broncho-pneumonia. It is interesting to note that of these
rabbits 1 died in six days, 4 in seven days, 3 in eight days, 2 in
ten days, 1 in thirteen days, and 1 in fifteen days after inoculation.
Plate cultures from the corresponding bits of lung tissue showed a vari-
able number of colonies almost invariably non-liquefying, and in many
cases identified as hog cholera bacteria.

These facts lead to the inference that in hog cholera the specific
bacteria will find their way to any diseased portion of lung tissue, and
there multiply to a certain extent. In one case a plate culture from a
bit of normal lung tissue showed but one or two colonies, while a bit of
collapsed tissue from the same lung showed a large number. ‘There is
no doubt that the slight exudate and feeble circulation in collapse and
the abundant partly cellular, partly mucus or fibrinous exudate into
the air spaces in broncho-pneumonia furnish a favorable nidus for
pathogenic bacteria. These may have been carried there by the blood or
they may have been introduced from without. If the latter supposition
prove true, and there are no valid objections to it, diseased lungs in
hog cholera may not only become the means of disseminating the dis-
ease through the mucus and expired air, but they may become the chan-
nel, the weak spot, through which the virus enters the organism.

To elucidate this question, if possible, the following instructive ex-
periment was made:

Two pigs (Nos. 460 and 461), about ten weeks old, received each into

56

the right jung, December 21, 3 cubic centimeters of a beef-infusion-pep-
tone culture two days old, inoculated from a single colony growing in a
roll culture. This had been made from a bit of spleen tissue from No.
46 of the outbreak described in the preceding pages. There were about
fifty colonies in the tube, all alike. To test the culture, a rabbit received
at the same time one-ninth cubic centimeter subcutaneously in the thigh.
It died in five days. The spleen was much enlarged, blackish, friable,
and contained hog cholera bacteria. A roll culture contained numerous
colonies after two days. The liver contained no centers of coagulation
necrosis, as the animal had succumbed too quickly.

No. 460 beeame very weak in its hind limbs in less than a week; res-
pirations short and quick; bowels relaxed. It was found dead on the
ninthday. Superficial inguinal glandsnormal. Petecchiz in the slight
deposit of fatty tissue beneath peritoneum of abdominal muscles.
Spleen about 12 inches long, 14 inches wide, and three-fourths inch
thick at the hilus, blackish, friable. A few petecchize on cortex of
left kidney. One cyst, the size of a large pea, in medulla. <A large
number of small hemorrhages in connective tissue around pelvis of
right kidney ; five small urinary cysts not showing on surface. Glands
in lesser omentum enlarged, hemorrhagic throughout. In cecum and
colon an almost continuous yellow sheet of superficial necrosis, about 1
millimeter thick, covering the mucosa. In lower colon it breaks up into
isolated patches, simulating ulcers. In microscopic sections this layer
is found to consist of necrosed epithelium intermixed with some round
cells. On Peyer's patches in lower ileum a yellow, soft deposit rests,
which is not adherent and migh£ be mistaken for chyle. Lobes of right
lung glued together and to pericardium. Pleura thickened generally ;
serum very slight in amount, blood stained. On lobes of left lung,
which are also glued together, and on right lung, there is a very slight
deposit, about one-half millimeter thick, in the form of a net work.
The pleuritis and exudate is most marked on the most dependent por-
tions of the lungs. Cavity of pericardium normal. Lung tissue not
hepatized anywhere; trachea and bronchi contain a small quantity of
reddish fluid. Bronchial glands and those along posterior aorta hem-
orrhagiec throughout. Cultures from pleural cavities, as well as. those
from spleen, contain only hog cholera bacteria. As shown in roll cul-
tures they were very numerous in the latter organ.

While No. 460 presented such a well-marked case, No, 461, although
presenting at first the same symptoms, slowly recovered. The differ-
ence may have been due to the fact that with No. 460 a 6-inch needle
was used, while with No. 461 one only 3 inches long. In the latter case
the chances for the passage of bacteria into the lung tissue and thence
into the intestines were much poorer.

On July 31, over seven months after inoculation, No. 461 was found
dead. It had continued well and thrifty, and no more attention had
been paid to it. Only the lungs and the liver were brought to the lab-

57

oratory, since all the other organs, including the digestive tract, were
reported normal, excepting the kidneys, which were said to be highly
congested.

Lungs, buat slightly collapsed, dark red. Cephalic and ventral lobes
of both lungs and the azygos lobe solid: to the touch, °f a grayish-red
color, with tortuous injected vessels under the pleura, On section, the
tissue cuts like cold meat. Color grayish to dark red. The cut ends of
bronchi show plugs of a glairy mucus. The marginal portion of the
lobe is grayish, homogeneous, very dense. Towards the center of the
lobes the tissue is more reddish, infiltration not so dense, and speckled
with small masses (one-half millimeter across) of a yellowish-white,
homogeneous, cheesy matter. On the border of the right cephalic love
an encysted mass, cheesy, yellowish, gritty to the kiife, evidently the
result of the inoculation. There were reported adhesions of the dis-
eased lobes to chest wall, indicative of pleuritis.

Bronchial glands slightly larger than walnuts, of a uniform grayish
dense texture. Trachea and bronchi occluded with a blood clot of very
recent origin. In the extremities of the large bronchi lung-worms em-
bedded in the clot.

Heart of normal size, rather flabby. Both auricles and the attached
vessels filled with tarry semi-coagulated blood. In left auricle a white
clot also present. Left ventricle firmly contracted.

Liver small; surface roughened with adherent flakes of tissue, indi-
cating old perihepatitis. Parenchyma tough, resembling in texture
very soft rubber. Acini wit dark ceuter and pale bloodless periphery.

The immediate cause of death was pulmonary hemorrhage; the re-
mote cause, the broncho-pneumonia caused by the inoculation. The
lung worms aggravated the lesions already present. What is most in-
teresting in this connection is the fact that hog cholera bacteria were
still present in the Jung tissue, as the following will show:

Three roll cultures made from bits of lung tissue; the developing
colonies all alike and resembling those of hog cholera bacteria; no
liquefying colonies in any tube. Beef infusion cultures from the indi-
vidual colonies demonstrate the identity of the bacteria with those of
hog cholera. A rabbit inoculated with sterile beef infusion, in which a
bit of lung tissue had been torn up, remained alive, while another rab-
bit, inoculated from the pure culture made of the colonies of the roll
culture, died in six days with enlarged spleen, coagulation necrosis in
liver, extravasation in lower large intestine, and many hog cholera bac-
teria in spleen. Cultures from blood and spleen pure.

The lung disease in this animal could not have been more than three
months old, and was very likely due to the injury to lungs resulting
in adhesion to chest wall and the inflammation around the encysted
mass.

This experiment shows (1) that hog cholera bacteria, when intro-
duced into the lungs, donot produce a specific parenchymatous inflam-
mation of themselves; (2) that they may pass from the lungs by way
of the pharynx into the digestive tract and there produce their charac-
teristic effect.

Bacteriological observations.—The preceding experiments on rabbits
and the intrathoracic inoculation in case of the pigs are sufficient of
themselves to establish the fact that the bacteria described in the re-
ports of the Bureau for the years 1885 and 1886, and again found in this
epizootic, are the cause of hog cholera. It may be added, however,
that out of fifty-six cases (here reported) hog cholera bacteria were
found in the spleen of all but six. Even in these the cultures made
were too few to make the negative evidence of any value.

In many cases the hog cholera bacteria were associated with a rather
large bacillus, which, for the sake uf convenience, we will call butyric
bacillus.* This organism was only detected when a bit of spleen was
dropped into beef infusion, with or without peptone. The culture, kept
at about 35° C., contained on the second and third days a cloudy mass
limited to the bottom of the tube. The cloud was made up of bacilli,
rather large, with a spore in one extremity of the rod strongly refract-
ing the Hae The rod was not enlarged at this end in the fresh state.
When dried and stained, the shrunken protoplasm gave the spore. bear-
ing end a swollen appearance, reminding one of the tailed bacteria of
older writers. In the few tubes in which this bacillus alone was pres-
ent the liquid itself remained perfectly clear; when hog cholera bae-
teria were present, it became uniformly but faintly clouded. In liquid
cultures, without the bit of spleen, the bacilli did not develop. This
was evidently necessary as food material. In gelatine-tute and roll
cultures the bacilli did not grow. They are very likely anaérobie or-
ganisms, abundant in the alimentary tract, and absorbed from ulcers
or lesions of blood-vessels into the circulation before death, in the spore
state, and their development kept in check until that occurs. It is also
probable that they are important factors in the rapid changes which
may take place after death. They are quite constantly found in the
liver of different animals when post mortem changes have begun to de-
velop.

In some half dozen cases decomposition was so far advanced that no
thorough examination was made. At first it was thought that the ani-
mals had been dead several days, but the person in charge of the herd
asserted that they had died during the night. Although the tempera-
ture had fallen below 30° Fahrenheit (1° ©.), decomposition was far
advanced. It may be that the live animals crowded upon the dead
and thus kept the bodies warm. Yet this supposition is not capable
of accounting for the rapid changes. The hemorrhagic lesions may have
enabled various bacteria to become distributed throughout the body.
The heat disengaged by them during multiplication, aided by the body
heat of the animals still alive, may have been sufficient to keep up the
process of decomposition. This post mortem growth may also account
for the large number of hog cholera bacteria found in many spleens,

= “Whether ‘this bacillus is identical with the ‘bacillus of malignant. cedema, as has
been asserted by some, I do not know, as no experiments were made to test its path-
ogenic power.

59

although the temperature of the air was far below the point where mul-
tiplication may take place.

In the foregoing epizootic, as well as in those studied in 1885, and
1886, there was no difficulty whatever in demonstrating the presence
of the hog cholera bacillus in the spleen. The herd referred to in the
preceding pages was swill-fed, and the animals were very likely crowd.
ing each other more or less, not being compelled to hunt tor food.
Hence each one was exposed to a large quantity of virus. The same
may be said of the penned pigs at the Experiment Station. The dis-
eased animals found in different localities were brought to the station
and penned with healthy ones. A severe epizootic was quite invariably
the result, owing to the unusually good opportunity for infection in the
pens and the saturation of the floors and soil of the pens with virus.

When swine roam over a considerable extent of territory in search
of food, the virus is more widely distributed but less concentrated,
Less virus is therefore taken up by individual animals, and although
the disease is equally fatal in the end, the course may be somewhat
different and the lesions less extensive. At the same time the bacte-
ria may elude observation. They may remain more or less localized,
owing to the reactive power of the organism, which destroys those that
have entered the internal organs. To those who would give up the
search for hog cholera bacilli after a few unsuccessful attempts to find
them, we would reccommend the perusal of the following three cases,
after having reviewed the epizootic just described:

Hog cholera prevailed more or less in Montgomery County, Mary-
land, during the latter weeks of September and the early part of Oc-
tober, 1888. October 17 Mr. H.- lost about 22 out of a herd of 55
to 60 swine during the past four weeks. Of those now scattered in a
large field 2 appear ill; 1, a small black shoat, is killed by cutting its
throat and examined. The superficial inguinal glands are very much
enlarged, the surface mottled, dark red. The spleen large, but pale
and rather firm. The liver shows signs of invasion of the sclerostoma
pinguicola. The lymphatic glands at lesser curvature of stomach are
very large; cortex completely hemorrhagic.

The left lung normal; the principal lobe of the right lung has in it
a mass of tissue involved in broncho pneumonia, extending obliquely
from the free border to near the dorsal region, about 1 inch thick;
the lymphatics along the dorsal aorta are likewise hemorrhagic; the
stomach filled with food ; small intestines contain a number of attached
echinorhynchi; the large intestines distended with semi-solid fecal mat-
ter; the mucosa in general is normal, but in the cecum are two ulcers
about three-eighths inch across, round, slightly elevated, with center
blacx and periphery yellow; beneath the superficial slough is a
whitish, firm, new growth, extending to the muscular coat in the center
of the ulcer.

The spleen and the right lung were taken to the laboratory. From
the former cultures were made on agar, in gelatine and beef infusion,
by adding bits of spleen tissue as large as peas. Inno tube did any
development take place. A rabbit inoculated by tearing up a piece of
hepatized lung tissue in sterile beef infusion and injecting the turbid
liquid subcutaneously remained well.

Several miles from the first farm we came upon a herd of young pigs
which were just Showing signs of disease, although none had been lost.
One of them, with unsteady gait, which bid in the litter under a shed
and returned to it when driven away, was killed by bleeding from the
vessels of the neck. The lungs were without a sign of disease. Spleen
enormously enlarged and gorged with blood. The lymphatic glands of
groin and about stomach very large but rather pale, and cedematous
on section. Stomach filled with food. Large intestines overdistended
with very dry, hard feces, somewhat softer near cecum; in the latter
only one ulcer and this on the valve, about one-fourth inch across and
of the same nature as the one found in the preceding ease.

A portion of the spleen of this animal was taken to the laboratory
and cultures made, as in the previous case, with bits of spleen. All
cultures remained permanently sterile.

Several miles from the latter place we found the disease on a farm
situated on a hill. The swine were allowed to go a considerable dis-
tance down the slope toa marshy stream. The owner had lost 6 or 8
out of a herd of 20 to25 within six weeks. <A few were evidently ill,
but none were killed, as a dead one was found. It had probably died
during the night. The buzzards had consumed nearly all the intes-
tines through a small hole near the pubis. Putrefaction had already
set in. Spleen enlarged, slightly congested. In the small portion of
the large intestine, which still remained, an uleer was found three-
eighths inch across. The glands of lesser omentum with hemorrhagie
cortex. The stomach contains a small quantity of bile stained fluid.
Both lungs glued to chest wall by coagulated fibrin from blood extra-
vasation. Left lung contains about ten to fifteen hemorrhagic foci,
visible under pleura, one-fourth to one-half inch across. ‘Che principal
lobe of right lung solid, granular, involved in broneho-pneumonia. The
hepatized lobe was discolored by recent and extensive blood extravasa-
tion. <A gelatinous deposit under sternum resting on pericardium.
The semi-decomposed condition of the animal prevented a mor: careful
examination. Portions of the spleen and hepatized lung tissue were
taken for examination.

While the spleen of the two preceding cases showed no indieations
of bacterial life on cover-glass preparations, the spleen of this case con-
tained a considerable number of bacteria resembling hog cholera bacilli
very closely. On gelatine they grew differently from the latter, and
the cultures emitted a slightly offensive odor. In liquids they were
actively motile. ‘They were putrefactive bacteria, without effect upon
two rabbits inoculated with large quantities of the cultures. <A rabbit
inoculated with the diseased lung tissue remained well. The latter on
closer examination had a texture as granular as the roe of fishes, the
granules being inspissated cell masses in the alveoli and air tubes. At
least four different kinds of bacteria were present in large numbers.

The absence of bacteria from the spleens of Nos. 1 and 2 is in har-
mony with the results obtained in other infectious maladies when ani-
mals are killed in the early stages or during the height of the disease.
It is only in the last stages that the bacteria become most numerous and
appear in sufficient numbers in the internal organs to be easily detected.
In the third case, death was very likely brought on by pulmonary hemor-
rhage not infrequently found in hog cholera. The specific bacilli pro-
duced at first the ulcers, and were either working their way slowly
into the internal organs or else were being destroyed in the ulcer itself.

61

The latter termination would signify recovery; the former death. These
ulcers might be aptly compared to the malignant pustule in man, in
which the virus remains at first localized but may spread throughout
the system after atime. The presence of numerous ulcers in swine in
the first epizootic is to be regarded as a multiple infection, while in the
three cases just cited the infection was limited to a few foci or but one.
The ulcers would no doubt have revealed the virus, but our previous
experience with spleens of diseased swine made it seem unnecessary to
study the ulcer itself. As regards the lung disease of the third case,
nothing positive can be said. It resembles most closely chronic swine
plague. The germ of this disease was not present, however, as shown
by the rabbit inoculation.

Buzzards may carry the disease from one place to another. When
the dead animals are at all exposed to view they are immediately at-
tacked. Whether hog cholera bacteria are entirely destroyed in the
digestive tract of the birds can not be said, but there is nothing in the
range of our knowledge of bacteria which will exclude the probability
that the bacteria are not all destroyed during the process of digestion,
and that they may be distributed by these birds from place to place in
the discharges, .

THE CAUSATION OR ETIOLOGY OF HOG CHOLERA.

The suspicion entertajned by those engaged iu the study of diseases of
man and the lower animals that infectious or communicable diseases
are due to living organisms of the lowest order, capable of rapid multi-
plication by the process of fission and spore-formation, has been trans-
formed into conviction during the past ten years. A considerable num-
ber of the most common, most dreaded diseases have been proved to
be caused by exceedingly minute, plant-like organisms known under
the general name of bacteria. Among animals the micro-organisms
causing anthrax, black quarter, tuberculosis, glanders, strangles, infec-
tious pneumonia in horses and swine, and rouget in swine have been
very thoroughly demonstrated. The opinion has been steadily gaining
ground that in order to control infectious diseases we must learn their
causes and the life history of the pathogenic bacterium found in each
disease. These will suggest to us the measures that are most likely to
prove successful in combating such maladies. Moreover, it is: pretty
well accepted to-day that the prevention of infectious diseases is the
main thing to be arrived at in our studies, and that their treatment
when they have once obtained a foothold is at best tentative and rarely
successful. This is especially true of the lower animals. They cannot
be treated with the same care which is accorded to human beings at-
tacked by infectious diseases. They are (in some diseases at least)
always scattering the living virus and thereby endangering those still
free from disease.

In the investigation of swine epizootics these facts have been care-
fully borne in mind, so that most attention has been paid, first, to the
life history or biology of the micro-organism; second, to disinfectants
as destroyers of the specific bacteria; and third, to the various methods
of preventive inoculation.

THE BACILLUS* OF HOG CHOLERA.

During the past three years the number of swine affected with this
disease which have been examined is about 500. About three-fourths

*The term bacterium, implying a form genus between micrococcus and bacillus, has
been almost wholly given up by bacteriologists, and all those forms classed under
bacteria have been thrown together under the genus bacillus. This change is un-
fortunate for several reasons, inasmuch as many species were best classed under the
genus bacterium. This latter term, which was applied to hog cholera microbes in the
reports of 1885—c6-’87, is now reluctantly given up for the sake of uniformity.

63

64

of this number died at the experimental station of the bureau. The
remainder came from outbreaks of the disease within 2 or 3 miles of the
Station. Besides these, a small number of animals were examined in
some of the Western States. From perhaps 400 the same microbe was
obtained, there being practically no difference between the pathogenic ©
microbes obtained from all the outbreaks thus far investigated.

Of the internal organs the spleen contains the largest number of
bacteria, and in acute hemorrhagic cases they are sufficiently numerous
to be detected on cover-glass preparations. A ininute bit of spleen
pulp is rubbed on a cover-glass, dried and heated according to the ae-
cepted methods, and then stained for a few minutes in an aqueous so-
lution of inethyl violet. The bacteria then appear as elongated ovals
or short rods with rounded ends, chiefly in pairs. When the staining
has been very brief only the periphery of the rod is deeply stained, the
central portion being pale and simulating the appearance of an endo-
spore. When the period of staining is prolonged to half hour or more,
the rod may become uniformly stained.

Bacteria thus dried on a coverglass and mounted in balsam measure
from 1.2 to 1.5, occasionally 1.8 micro-imillimeters (.00005-.00006 inch) in
length, and about .6 micro-millimeter (.000024 inch) in breadth.

In sections of the spleen from acute lbemorrhagie cases the bacilli
may be found in considerable numbers. Sections were hardened in al-
cohol, cut dry, and subsequently stained with aniline water methyl
violet. They were in some cases decolorized in 1 per cent. acetic acid.
The bacilli then appear as short, plump rods, with ends rounded off;
sometimes they are short enough to deserve the name of ovals. Tie
periphery is more deeply stained than the central body of the rod.
They measure on the average 1.5 micro-millimeters. In such sections
the bacteria appear in small masses in the capillary spaces of the
spleen-pulp, rarely among the cells of the malpighian corpuscles
(Plate X, fig. 2). The masses appear more or less star-shaped. The
bacilli are crowded together in the center; from this, linear groups ra-
‘diate into the capillary network. Such masses may be 8 to 10 micro-
millimeters in diameter. They are fairly numerous in spleens from
acute cases. That the size of these colonies is not due to post-mortem
multiplication is shown by the fact that the largest and most numerous
colonies were found in the spleen of an acute case which was examined
within two hours after death, in the month of November.

In sections of ulcers hog cholera bacilli have been searched for, but
the examination of a large number of ulcers showed that no positive
results could be obtained. Different ulcers showed different bacteria,
sometimes large colonies of micrococci, sometimes groups of large ba-
cilli, following the course of the blood-vessels in the embryonic tissue
under the slough. These no doubt found their way in from the super-
ficial slough which seemed to be made up almost entirely of bacteria.
Moreover, hog cholera bacilli closely resemble many putrefactive forms,

65

so that even if they could be readily seen nothing but a good differ-
ential stain would enable us to recognize them. That they are present,
however, may be demonstrated by inoculating mice or rabbits with bits
of the ulcer. A small numberof mice may succumb to malignant edema.
The rest will die of hog cholera. In rabbits the local effect of such
inoculation is usually quite severe, owing to the putrefactive bacteria
introduced at the same time.

Staining of hog cholera bacteria.—On cover-glass preparations they are
easily brought into view by a few minutes’ contact with watery solu-
tions of the ordinary aniline colors, such as methyl violet, fuchsin and
methylene blue. Decolorizing agents, such as acetic acid, one-half to
1 per cent. must be used carefully lest the color disappear from the
bacillialso. When stronger dyes, such as alkaline methylene blue orani-
line water fuchsin, are employed, the bacilli are decolorized with greater
difficulty. Watery solutions should therefore be employed only for
cover-glass preparations where decolorizing is unnecessary. Forsections
it is well to harden tissues in alcohol. The sections may be stained
with Loffler’s alkaline methylene blue or with aniline water methyl
violet or fuchsin for from one-half to one hour. After aa few seconds’
contact with a 1 per cent. solution of acetic acid they are washed in
water, then passed through alcohol, turpentine, or xylol or cedar oil, and
mounted in xylol balsam. No stain which differentiates these kacilli
very sharply from others has been found. They are decolorized when
the method of Gram is employed.

Distribution of bacteria in the body.—This can be best determined by
the delicate method of cultivation. In acute cases the spleen contains
the largest number. In coverglass preparations of spleen pulp there may
be.four or five in every field of the microscope. In general, the liver
contains almost as many bacteria as the spleen. The lungs, lymphatic
glauds, and kidneys may also contain them in moderate number. They
are fewest in blood from the heart (right ventricle). In slow, chronic
cases, characterized by slight ulceration of the large intestine, the
number of bacteria in the internal organs is very small. From the
spleen of such cases cultures are made fertile only by using bits of tissue
as large as split peas.

When it is of importance to make a diagnosis from a chronic case it
might be well to adopt the method suggested by Frankel and Simmonds
for typhoid fever. They wrapped the spleen in cloths wet with a solu-
tion of mercuric chloride and placed it in a warm room for twenty-four
hours. The bacilli of typhoid, capable of multiplying in the organs
after death when the temperature is not too low, became sufficiently
numerous to be readily detected in sections. The same may be said of
hog cholera bacilli. It must, however, be borne in mind that in chronic
cases other bacteria may have gained entrance into the body and appear
in the spleen. These, multiplying at the same time, may give rise to
erroneous interpretations.

15612 6 C——5

66

When the destruction of the mucous membrane in the large intestine
is extensive, bacteria of various kinds may be found in the peritoneal
cavity. The serum collected often contains several varieties of organ-
isins, and when sections are made of the walls of the peritoneal cavity
micrococci and bacilli are seen resting in a thin layer upon the perito-
neum. Sometimes the pleural fluid, and still more rarely the pericar-
dial fluid, may give rise to cultures of micrococci. These resemble the
micrococci, causing suppuration in man (staphylococci) in their appear-
ance and mode of growth in gelatine. The presence of anaérobie bacilli
in spleen and liver has already been dwelt upon. The presence of bae-
teria in the peritoneal cavity is easily explained by their passage through
the ulcers in the intestines. It is a fact worthy of note that only very
rarely bacteria other than those causing the disease were encountered
in the spleen and the circulation. Perhaps those causes or agents which
destroy bacteria are less active in the serous cavities than in the blood
and spleen. The various complications of chronic ulceration already
mentioned, such as peritonitis, pleuritis, and pericarditis, are without
doubt due to this secondary invasion of bacteria, which have the power
to produce inflammation of serous membranes. It need not be said
that in the earlier investigations, when little was known of bacterial
diseases, the explanation of the presence of these microbes was very
perplexing and misleading.

Biology of the hog cholera bacillus.—The cultivation of bacteria in nu-
trient media outside of the animal body serves two distinct purposes:
(1) The diagnosis of specific forms so that they may be easily recognized,
and (2) the study of their biology or life history.

a, Diagnostic characters.—Hog cholera bacilli are not readily dis-
tinguished from a large number of other bacteria found in surface
waters and in the superficial layers of the soil, either in their form or
in their manner of growth in culture tubes. The more minor differen-
tial characters we can therefore obtain, the more certain our diagnosis
will be. For this end the hog cholera bacillus was cultivated in as
many media as were available.

If a bit of spleen pulp from swine which have succumbed to hog
cholera be thoroughly shaken up in a 10 per cent. beef infusion peptone
gelatine, liquefied by a gentle heat, and the whole poured upon a sterile
glass plate protected from the dust by a bell-glass and allowed to con-
geal, colonies of hog cholera bacilli will appear within forty-eight hours
as mere specks to the naked eye. Examined under a low power they
are spherical, with sharply defined border. The disk of the sphere is
homogeneous without any concentric markings, and of a brownish
color. This description applies to colonies beneath the surface of the
gelatine layer. Colonies which grow on the surface soon spread out
into thin pearly layers several times the size of the deep colonies, and
roundish or irregularly polygonal in outline.

Besides the deep spherical and the flat surface colonies there is oc-
casionally a third form present. This is a very faint cloud like colony

OE EE EEE

67

growing between the glass plate and the gelatine, spreading as a very
thin layer Jaterally and attaining the dimensions of a surface colony.
Many such colonies have spherical prolongations upwards into the gela-
tine layer so as to assume the form of a lid with a knob-like handle at-
tached to its center. It is very probable that the colony begins as a
sphere in the gelatine layer near its lower surface. AS soon as it
touches the glass, by virtue of its enlargement, spherically, it spreads
out into the attenuated, cloud-like layer. Such colonies are rare, ex-
cepting in so-called line cultures made by drawing a platinum wire across
the gelatine layer before it has congealed.

Perhaps the best device for studying the growth of such colonies is
the Esmarch roll culture.* The gelatine, coating the inside of the test
tube, is protected from contamination and desiccation for a long time.
The colonies have thus the opportunity of expanding to their utmost
capacity. Ina roll culture ten days old, for example, the deep colonies
were about one half millimeter in diameter, perfectly spherical, the disk
homogeneous, yellowish white, when viewed with a hand Jens. Under
a 1-inch objective it appeared reddish brown, with no markings. The
surface colonies in the same tube were about eight times as large, 7. e.,
4 millimeters across. They presented centrally an opaque white patch
or nucleus, outside of this a more translucent zone, beyond this another
opaque zone, and lastly a limiting translucent border. The colonies
were irregularly polygonal in outline. The alternation of thin and thick
zones was very likely due to the variation in.temperature to which
gelatine cultures were exposed in a badly heatvd laboratory, for they
are by no means always present. (Plate XI, fig. 2.)

Tube cultures, made by piercing the gelatine in a test tube with a
platinum wire previously forced into the spleen, show minute yellowish-
white spheres in the track of the wire in forty-eight hours. These rarely
exceed one half millimeter even after several weeks. The surface
growth spreads trom the place of inoculation as a thin pearly layer of
variable thickness, eventually becoming 4 to 6 millimeters in diameter ;
under especially favorable conditions of temperature, etc., it may be-
come still larger. When the inoculated bacteria are very numerous the
growth beneath the surface appears as a solid yellowish-white track, in
which the colonies have become fused together. The gelatine is at no
time liquefied. The bacilli grow somewhat larger in gelatine than in the
body of diseased animals. Occasionally filaments of considerable
length are met with, and in general irregular, involution forms are not

* These roll cultures are made as follows: The gelatine, liqnefied by gentle heat in
the tube in which it was sterilized, is inoculated with the tissue, blood, urine, or any
liquid containing bacteria, and carefully stirred up. A second culture may be made
from the first by transferring from it with a platinum loop some of the liquid gela-
tine. This is done when the number of bacteria in the first tabe may be too numer-
ous, A rubber cap is fitted over the mouth of the tube after replacing and trimming
the cotton-wool plug, and the tube placed horizontally in ice water and rolled about
its long axis until the inside of the tube is coated with a uniform layer of congealed
gelatine. The tube may also be rolled ona smooth block of ice, a method which I
first saw inthe Pathological Laboratory of Johns Hopkins University, and which is
very useful wher rubber caps are wanting, or when it is desirable to keep the plug
free from gelatine. ; AV?

68

uncommon. When a bit of spleen tissue is rubbed upon an inclined
surface of agar agar in a culture tube, isolated colonies make their ap-
pearance within twenty-four hours as circular, grayish-white, semi-
translucent, very flat cones 1 to 2 millimeters across. When the ba-
cilli are very numerous a slight prick of the spleen pulp with a platinum
wire is sufficient. Otherwise the too numerous colonies will coalesce
into a grayish, shining, semi-opaque layer of scarcely perceptible thick-
ness. Its appearance on agar can not be distinguished from the growth
of typhoid bacilli and a number of saprophytic bacteria. On blood
serum the growth appears asa very thin, grayish, translucent laver. In
bouillon, either with or without peptone, the bacilli grow rapidly enough
at 80° to 95° F. to produce a slight opalescence within twenty-four hours.
This does not increase in density subsequently. There is no membrane
formed on the surface of the liquid. When standing undisturbed for
one or two weeks, a white ring-like deposit of bacteria frequently forms
around the tube at the surface of the culture liquid. There is only a
very slight deposit formed, showing that multiplication in liquid media
comes to an end within a few days.

The length of the bacilli in bouillon is about .9 micromillimeter, their
width .4 to .5 micromillimeter, therefore somewhat smaller than in
the spleen. When examined in a drop of bouillon suspended from the
under surface of a cover-glass in a * cell,” the bacteria are seen to be
motile. Taken from cultures one or two days old they execute very ac-
tive spontaneous movements. Their movement is one of rotation as
well as translation. They quite invariably occur in pairs, and the
movement of rotation is about their point of union as anaxis. The pairs
of bacilli as they shoot across the field have thus an oscillating motion
at the same time. The bacilli do not come to rest at all, but swarm
about very rapidly until the liquid is dried up.

Though this motility is most marked in recent cultures, it may still
be seen at the end of one or two weeks in most liquid cultures.

The same active motion is observed in bacilli taken directly from the
animal, such as the spleen of rabbits, which have snecumbed to inocu-
lation. If a bit of spleen tissue be rubbed in a drop of sterile water
on a cover-glass and the whole examined as ahanging drop, in one or
two minutes the bacilli become as active as in cultures.

Growth on boiled potato, when at 95° F., appears as a faint straw-
colored deposit within twenty-four hours after inoclution. At 20° to
25° C., it appears one or two days later. It slowly spreads in all direc-
tions as a layer of perceptible thickness. The color changes to a dark
brick red, or may remain whitish. In general the growth is darker the
more rapidly the potato dries up.

The growth is also restricted by drying. In some sultures it has
covered almost the entire cut surface of the potato. In others it re-
mnained as a broad band over the line of inoculation. The bacilli multi-
ply very abundantly in milk without producing any alteration visible
to the naked eye. :

69

The diagnosis of hog cholera bacilli may therefore be made by taking
together the following morphological and biological characters: (i)
Short bacilli with rounded ends, or ovals, readily stained in aqueous
solutions of anilinedyes. (2) Growth at 65° to 80° F., on gelatine, with-
out producing liquefaction. (3) A rather feeble growth in beef infusion
coupled with active spontaneous movements. (4) Growth on the cut
surface of boiled potato at ordinary temperature as well as in the incu-
bator. (5) Active multiplication in milk without any macroscopic
changes. (6) Growth in vacuo. (7) Absence of any odor arising from
the cultures. (8) Fatal effect on rabbits, guinea-pigs, and mice when
inoculated. This will be discussed later on.

These characters are emphasized, since we have several times found
bacteria in the internal organs of swine which may have many points
in common with hog cholera bacilli; especially as regards their form,
motility, and growth in gelatine. In fact in was quite impossible to
decide until inoculations upon animals were made. The absence of
pathogenic power was thus made the chief criterion.

(b) Other physiological characters. —Though alkaline mediaare as arule
most favorable for bacterial multiplication, yet there is a slight devel-
opment in media containing a small amount of acid, such as Liebig’s
meat extract.

A feeble development was observed in sterilized hay infusion,

The temperature range of the active multiplication of hog cholera
bacteria lies between 60° and 104° F., being most favorable between
85° and 100° F.

Hog cholera bacilli, though they seem to develop best in presence of
oxygen, are capable of growing in what is practically a vacuum, 7%. é.,
they are facultative anaérobic organisms. Comparative experiments
made with such obligatory aérobie organisms as bacillus subtilis deter-
mined that while the latter shows no trace of growth in tubes from
which the air has been removed, hog cholera bacilli grow quite as freely
as in presence of air. When the latter are shaken up in liquid gelatine
in test tubes and the gelatine rapidly congealed the colonies that appear
throughout the gelatine sliow no difference in size, whether near the
surface where air can penetrate or near the bottom of the tube.

THE DIAGNOSIS OF HOG CHOLERA BY MEANS OF INOCULATION.

The inoculation of small animals in the study of infectious diseases
has been of the utmost importance from a diagnostic stand-point. Tre-
quently bacteria which are nearly identical in form, size, and many
biological characters, can only be distinguished from one another by
their effect upon smaller animals. This is especially true of hog chol-
era, since the specific bacillus closely resembles nany forms found in
decomposing liquids. In the following pages, therefore, a careful ex-
position of hog cholera as manifested in small animals will be made to
facilitate the diagnosis of this disease. During the course of these in-

70

vestigations rabbits have been found best for this purpose, although
ordinary house mice and guinea-pigs will answer almost as well.

If a bit of spleen tissue from acase of hog cholera be inserted under
the skin of the thigh, or simply rubbed upon a slight abrasion made
on the inner surface of the ear, or if the bacilli from pure cultures be
used, the disease will be induced. The rabbit will succumb within a
period after inoculation varying from five to fourteen days (very
rarely longer), depending upon the number of bacteria introduced.
The period of incubation, during which the animal shows no symptoms,
varies from three to five days before death. At this time the tempera-
ture rises from the normal (102.5°-103.5° F., according to the age of
the animal), to 107° or 108° F., and remains at that point unt‘l shortly
before death, when, if examined in time, a fall is observed. The height
of the fever is accompanied by loss of appetite and a tendency to sit
perfectly quiet.

The disease thus induces in the rabbit a typical continuous fever in-
variably ending in death. By way of illustration, the temperatures of
a few cases are here reproduced :

Rabbit inoculated June 18, with $ cubie centimeter culture liquid;
weight, 24 pounds; temperature, 102.5° F.; at end of first day, 102.7;
of second day, 104.6; of third day, 105; of fourth day, 108; of fifth
day, 106.4; dead on sixth day.

Rabbit inoculated June 20, with infeeted soil, one and one-half
months old; temperature on fifth day, 103.4; on seventh day, 103.8;
on eighth day, 103.8; on tenth day, 107.6; on eleventh day, 107.4; dead
on twelfth day.

Rabbit inoculated June 28, with $ cubic centimeter of culture liquid ;
weight, 2,3, pounds; temperature, 103.79 F'.; end of first day, 103.3;
of second day, 105.5; of fourth day, 107.8; found dead on seventh
day.

The lesions produced are very constant and characteristic. At the
point of inoculation there is a slight infiltration of the subentis and
fascia, and occasionally a slight superficial necrosis of the muscular tis-
sue. Thespleen is very large, perhaps three to five times its normal size.
The liver presents on its surface yellowish white patches which corre-
spond to one or more lobules which have undergone coagulation necro-
sis. These patches vary greatly in number but are rarely absent, pro-
vided the animal lived long enough to permit their formation, 7. e., not
less than seven to eight days after inoculation.

This necrosis appears chiefly in lobules near the surface, although
oceasionally the entire tissue is involved. In some livers the necrosis
is complete so far as the lobule is concerned. In others it is restricted
to the peripheral or portal zone of the lobule, in which case a large
patch of lobules usually undergo the same change. There can be no
doubt that they represent different stages in the process which seems

to begin in the portal area. When sections are examined under the mi-
croscope the liver-cells show as unstained masses without nuclei. There

71

is a remarkable absence of leucocyte infiltration around the necrosed
tissue. The bacilli are very well brought out in such tissues after thor-
ough hardening in alcohol, by staining over night in aniline water
methyl violet (tubercle stain), and decolorizing slightly in $ to 1 per
eent. of acetic acid. The deep blue bacilli appear in dense masses,
chiefly in the capillaries along the edge of the necrosed area. The ne-
crosis is most probably due to the plugging of the different vessels,
thus cutting off the blood supply.

The enlargement of the spleen and the necrosis in the liver are the
two important characters of the inoculation disease. In a moderate
number the intestinal tract is found diseased. The submucosa of the
duodenum near the pylorus is dotted with ecchymoses, which may fuse
into a single hemorrhagic patch. Besides this the submucosa of the
large intestine 2 to 3 inches from the rectum, é.¢., the straight portion
merging into the rectum, may be in the same condition. Sometimes the
mucosa is beset with minute bulging hamatomata. These intestinal
lesions are due to the discharge of bacilli from the necrotic foci in the
liver into the bile ducts and thence into the duodenum. The lesions in
the large intestines may be influenced by the more or less prolonged
stay of the feces before final discharge.

In some cases when the disease has lasted from ten to thirteen days
there is a peculiar exudate in the large intestine, which may be drawn
out of the anus in the form of bands or cylindrical masses 1 or 2 feet
long, consisting of a translucent, elastic, whitish material, finely fibril-
lated when examined under a high power. The duodenum may be dis-
tended with a straw-colored semi-gelatinous mass. Hemorrhagic lesious
may also be present. It seems very probable that the exudate is the
result of a fibrinous or croupous inflammation of the large intestine due
to the presence of hog cholera bacilli.

The lungs are occasionally the seat of hemorrhages. The kidneys
contain more blood than usual, but hemorrhages are absent. Hog chol
era bacilli are obtained by cultivation from nearly all the internal organs.
They are usually so abundant in spleen and liver as to be detected
readily in cover-glass preparations.

The following experiment shows how few bacteria are required to pro-
duce the disease :

.

: Inoculated with =
Rabbit No. culture liquid. Remarks.
Tie cass ema an nooiee Cleeeae= Dead on sixth day.
EtG here eae ee CNG et ee Dead on ninth day. |
[IQ ees se ~-s-e! agasooo GC: © obese: Dead on eighteenth day.
1E20). See eee cag hganCn Gree ss | Dead on eighth day.

The beef-infusion culture was diluted so that one-quarter of a cubic
centimeter of the liquid contained the equivalent given in the table. It
Ss probable that No. 19 took the disease from No. 20, penned with it.
The latter had ecchymoses in the duodenum, indicating that the bacilli

(2

had escaped into the intestinal canal and were being discharged with
the feces. The time of death of No. 19 suggests this view.

A very small number of bacilli, therefore, are sufficient to produce in
rabbits an infectious fever, or septicemia.

The characteristic action of hog cholera bacteria on the mucous mem-
brane is well illustrated by feeding cultures to rabbits:

September 11, 1888.-—Two rabbits were starved for one day and then
fed hog cholera bacilli from an agar culture on clover. This was readily
consumed.

One rabbit was found dead on the sixth day. Ageglutination of blad-
der to cecum; serosa of stomach reddened. Ileum about 6 inches from

valve invaginated for 2 to 3 inches. Spleen congested, slightly en-
larged. Liv er and kidneys engorged. Large numbers of hog cholera
bacilli in spleea, as tested by the microscope and cultivation on gela-
tine. The other rabbit died in thirteen days. Spleen very large, con-
gested; coagulation necrosis in liver. Lungs contained several dark-
red hepatized areas. Severe lesions were found in the large intestine.
The mucous membrane of lower colon and rectum were dotted with
small bulging hemorrhages, and the tube contained a cylindrical mass
of a material resembling colorless gelatine, partially softened in water
and very elastic (fibrin?). The duodenum was distended with a pale
yellowish translucent semi-gelatinous mass. Hog cholera bacilli as
above.

At the same time two other rabbits were starved for a day and then
5 cubic centimeters of a liquid culture was added to 20 cubic centime-
ters watcr and given them to drink. One rabbit died in ten days. The
lesions were the same as those in the rabbit just described, with this
exception, that there was no coagulation necrosis in the liver. The
other rabbit did not take the disease. It is quite likely that it may
not have taken much of the water.

When rabbits are not easily procurable the ordinary house mice may
be used. They usually appear quite well and active after inoculation
until some morning they are found dead. The period of the disease is
the same as that for rabbits. The spleen is very large; the liver con-
tains many centers of necrosis. Mice have been frequently fed both
with pure liquid cultures and with spleen pulp containing hog cholera
bacilli. They invariably take the disease and die within seven or eight
days after the first feeding, with lesions the same as those observed in
mice inoculated subcutaneously. Two mice were peculiarly affected the
day after eating some spleen pulp. They were scarcely abie to move.
Their limbs sprawled, and on being taken out of the jars they remained
in this position unable to escape. They died subsequently of true in-
fection. The symtoms recorded were due very likely to the absorption
of the ptomaine produced by the bacteria in the digestive tract.

There is a remarkable regularity in the length of the disease in inice.
Those inoculated at the same time and with approximately the same
dose usually die not more than a half a day apart; they appear lively up
to the night during which they die. In one case four mice, inoculated

at the same time, all died in the night of the seventh day, though they
appeared well the day previous.

(63)

The following experiment is worthy of record as indicating the effect
of hog cholera virus on mice that survived infection:

October 28, 1888.—Two mice were fed with bits of liver and kidney
tissue from mice which had succumbed to inoculation with hog cholera
cultures. The material fed had been kept in the refrigerator for nearly
four weeks in salt solution. Before feeding it was thoroughly mixed
with bread crumbs and placed in the mouse-cage. Both mice survived
the feeding and were active December 1, over one month after feeding.
One was thereupon killed with chloroform and examined. The spleen
was very much enlarged, not congested abnormally. On the ventral
aspect of the liver a whitish patch where diaphragm was adherent.
Under the patch a large abscess. This was without doubt the site of
extensive coagulation necrosis, which was now broken down.

The secoud mouse was killed December 19, over seven weeks after
being fed. The spleen was likewise very large, the liver intact, but
there were five abscesses in the left kidney, with adhesions to surround-
ing structures. On section one abscess was wedge-shaped, the apex
being at the pelvis; the whole only partly softened. These also were
the result of coagulation necrosis. We have here a striking illustration
of the mainly mechanical injury done by hog cholera bacilli.

The effect of hog cholera bacilli on guinea-pigs differs but little from
that exerted on rabbits and mice. The duration of the disease and the
lesions are the same. There seems to be a somewhat greater tolerance
in guinea-pigs, although the small number used does not justify any
decided statement.

Pigeons are also susceptible to this disease, but by no means to the
degree witnessed in the animals just mentioned. It requires about
three-fourths of a cubic centimeter of an ordinary beef infusion pep-
tone culture to produce a fatal resuit (/. e., about 150,009 to 3,000,000
times the dose necessary to destroy rabbits). The birds frequently
died within twenty-four hours after the injection, which was usually
made under the skin over the pectorals on one or both sides. The
pectoral after death is partly or wholly discolored, and has a par-
boiled appearance. The injected bacteria are present in the heart’s
blood and in other organs, notably the liver. If the dose is smaller
than three-fourths of a cubic centimeter, the bird may survive after
a week or two of pronounced illness. A large sequestrum forms in
the pectoral muscle, which is gradually absorbed. Occasionally the
birds will die after a week of illness manifested by diarrhea, ruffling
of the feathers, and a quiet, somnolent attitude in a corner of the
cage. Hog cholera bacilli are also present in the internal organs in
such cases. Feeding cultures has no effect.

Fowls have been frequently inoculated and fed with cultures without
showing any signs of susceptibility. Among other animals inoculated
were several white rats, one gray rat, one sheep, and a calf. In none
did the disease appear, In the sheep and calf a small abscess was
found at the place of inoculation.

VITALITY OF HOG CHOLERA BACILLI, AND THETR RESISTANCE
TO VARIOUS DESTRUCTIVE AGENTS,

The vitality of hog cholera bacilli in cultures remains for months un-
changed. The following is perhaps an extreme illustration :

A tube of beef’s blood serum, coagulated by heat, was inoculated with
hog cholera bacilli November 28, 1885. The platinum wire penetrated
the blood serum and the bacteria grew as aslender plug in the needle-
track and as a thin film on the surface. In July, 1887, more than one
and one-half years later, a tube of beef infusion inoculated from the blood
serum culture became promptly turbid, and contained the hog cholera
bacilli only. Two mice inoculated subcutaneously with a few drops
August 2, died August 8 and 9, respectively, with lesions characteris-
tic of the disease and with the bacilli present in spleen and liver. The
germs had not therefore lost their virulence. The blood serum had con-
tracted but slightly from loss of water, there being very little evapo-
ration from the culture tubes used.

Resistance of hog cholera bacteria to heat in liquids.—A knowledge of
the degree of heat necessary to destroy hog cholera bacteria is of con-
siderable importance, not only in its bearing upon the application of
heat as a disinfectant, but also upon the various processes that are used
in the preparation of pork for consumption.

Culture tubes containing about 10 cubie centimeters of beef infusion
were inoculated from a culture of a certain age and then placed ina
water-bath kept at the desired temperature. They were exposed tor
different periods of time and then removed to an incubator at 95° F.
When the tubes remained clear it was inferred that the bacteria had
been destroyed. A control tube was inoculated in every experiment
to make sure of the vitality of the culture used.

A momentary exposure to boiling water will destroy them. When
the temperature of the surrounding water is 158° F. (70° C.), the in-
oculated tubes remain sterile after an exposure of four to five minutes.
As it takes about four minutes for the temperature of the culture liquid
to reach 70° C., itis probable that a two minutes’ exposure to 70° C.
would be sufficient.

An exposure to 136° to 138° F. (589-59° C.), is sufficient to destroy
hog cholera bacteria in fifteen minutes. The same is true for bacteria
taken directly from the spleen. An exposure to 130° F, (54.5° C.) will
destroy them in one hour. Tubes exposed for one-quarter of an hour
become turbid within twenty-four hours. Those exposed for one-half

dad

fo

16

and three-quarters of an hour become turbid within forty-eight hours.
This shows that most of the bacteria have been destroyed by such pro-
longed exposure. ‘Tubes heated for one hour remain clear.

When the temperature is still more reduced, to 120° F, (49° C.), ex-
posure for a period as long as two hours is insufficient to destroy them,
although their growth may be slightly retarded.

It must be remembered that these results mean that the bacteria
must be actually exposed to these temperatures for the length of time
indicated. In the culture tubes employed it takes about five minutes
to bring the temperature of the liquid up to 70° C., and less for lower
temperatures. If, therefore, it takes longer than this for the heat to
penetrate into meat or lard containing these bacteria, their destruction
can not be regarded as certain within the time indicated above, and
the exposure to the required temperature must be correspondingly
lengthened.

|
Time in which

Hog cholera bacteria in 10 eubie centimeters bouillon placed in a water-bath at-—— _ destroyed.
TOME 2199 By) cease fe cae tana eo awe ee obs eae aio Bone Moat as octane Seen eyse te ieee | Immediately.
OCS: (SSOP MY foes fers di dae teas ce toma abate we ete che ciclcteleae x eicia areietanateta ee tens ete eriaiavotene | 4 minutes.
OSOVS PLS BS TAY) cee cits aie ate wistaleralet ere tc ole Metele atecnya re scterate ge of Speratc ae Site mc tstatareta rat ola tay ay earn 15 minutes.
§4359! Cs (1300. ) = nck ose cdce nig te seee case ed bsp as a ceteioaia eAejaaeie Se cieerae oot tee ae areas | 1 hour.

ADOC MAORI.) so ati tetes Sasa ierartors sare a ole aia SG tine seca cee es = cameos Ce ae eer aie | Not in 2 hours.

Bacteria do not so readily succumb to heat when dried and then ex-
posed to dry hot air. It was found that dry heat at 80° C. (176° F.) is
sufficient to destroy the bacteria when exposed in a dry state for fifteen
minutes.

In these experiments bacteria from cultures were rubbed on the inner
side of plugged and sterilized test-tubes. Gelatine was added after they
had been exposed to the heat and roll cultures made. Absence of growth
indicated the death of the contained bacteria.

Resistance to freezing is well illustrated in the experiments reported
in the section on the vitality of hog cholera bacilli in the soil during
winter.

Vitality of hog cholera bacteria in ordinary water.—The hardiness of
this microbe is well illustrated by its capacity for multiplication in or-
dinary drinking water. To determine this, the following experiment
was made:

September 8, a culture tube containing very clear Potomac drinking
water* which had been sterilized several weeks previous by a tem-
perature above 110° C., was inoculated with a platinum loop from a
pure liquid culture of the bacillus. By mixing a given quantity of this

water immediately after inoculation with gelatine, and making a plate
culture of the same, it was found that the water contained about 26,240

* When drawn this water did not contain more than 100 to 200 bacteria to the cu-
bic centimeter.

17

bacteria in 1 cubic centimeter. The water was kept in the laboratory,
in which the temperature corresponded closely with that prevailing out-
doors. It was examined from time to time on gelatine plates, and the
number calculated for 1 cubic centimeter. The following figures give
the results obtained:

September 8, 26,240 in 1 cubic centimeter (immediately after inocula-
tion).

September 9, 201,600 in 1 cubie centimeter.

September 10, 1,296,000 in 1 cubic centimeter.

September 11, aly numerous on plate to be counted.

September 13, 2,608,200 in 1 cubic centimeter.

September 15, 1519, 560 in 1 cubic centimeter.

September 17, 1,306,308 in 1 cubic centimeter.

September 29, 83,700 in 1 cubie centimeter.

October 12, 19,125 in 1 cubic centimeter.

October 21, 10, jee in 1 cubie centimeter.

November 18, 225 in 1 cubie centimeter.

December 6, a ‘few bacteria still present, as determined by liquid cult-
ures.

January 4, 17 in 1 cubic centimeter.

January 11, no growth on plates.

According to another experiment the vitality lasted about two
months.

June 13, 1888, 10 cubie centimeters, Potomac drinking water, sterilized
in a Salmon culture tube, was inoculated with a platinum wire to which
a minute bit from the surface growth of an agar-agar culture adhered.
Plate cultures prepared immediately after thoroughly shaking the tube,
indicated that each cubic centimeter of the water contained from
1,000,000 to 2,000,000 germs.

Plate culture of June 14 shows in ,!, cubie centimeter of water a very
large number of colonies. Roll cultures made June 22, July 3, and July
16 contain a smaller number.

A roll culture of August 4 contains about 200 colonies (7. e., about
6,000 in 1 cubic centimeter).

A roll culture of August 25 remains sterile. A tube of beef infusion
to which about 1 cubic centimeter of the water had been added Sep-
tember 15 contained a large coccus five days later; no hog cholera
germs.

These cultures show that the bacilli perished in about two months.
The difference in the results obtained in this and the last experiment
may have been due to the season of the year.

That the bacilli can be kept alive in clear river water for from two to
four months and perhaps longer is a fact very significant in itself. When
we consider, moreover, that the added bacteria in the first experiment
multiplied so that each individual was represented by ten at the end of
five days, the hardiness of the bacillus is very evident. The danger
from infected streams into which feces from sick animals find their way
is thus proved beyond a doubt. Stagnant streams and pools are more
dangerous, since the water is but slowly renewed, while in rapidly flow-
ing streams the bacteria are speedily carried away. On the other hand,
the latter may spread an epidemic from one place to another,

78

Resistance to continuous drying at ordinary temperature (60° to 80° F.—
A number of experiments were made to determine this point. Some of
them are reported in full in preceding Annual Reports of the Bureau,
and are therefore simply summarized in this place.

(1) A series of cover-glasses, upon each of which a drop from a liquid
culture had been dried, were placed in bouillon at different times. No
growth in bouillon after they had been dvied from seven to pine days.

(2) Minute bits of spieen tissue from a pig which had succumbed to
hog cholera were dried on cover-glasses. ‘These were capable of infect:
ing bouillon up to the twenty-third day.

(3) Spleen tissue dried. on four cover-glasses gave rise to pure cult-
ures of hog cholera bacilli after forty-nine days.

(4) Hog cholera bacteria from a liquid culture one week old, dried on
silk threads, were placed on a gelatine plate from time to time to ob-
serve any growth. They were stilPcapable of development after twenty-
one days, when the stock of threads was exhausted.

\5) Threads steeped in a liquid culture one day old and dried were
placed on gelatine plates, as described in series 4. No colonies ap-
peared on the twenty-seventh and twenty-eighth days. A few appeared
later on, Showing that even after thirty days a few still survived.

In these series of experiments the vitality of the bacilli was not ex-
hausted after forty-nine days in one series; in another it was destroyed
in less than ten days.

The following series of experiments, made during the present year,
show how very varied is the length of time during which the bacilli
remain alive when dried:

June 15.—Minute bits of spleen tissue, from a rabbit which had died of
hog cholera after inoculation with a pure culture, were rubbed on sterile
cover-glasses and kept under a flamed funnel, plugged with cotton-
wool.

On July 3, 6, and 9 two cultures were made by dropping into each
tube of beef infusion a cover-glass. All six tubes remained clear. The
bacilli had thus perished within three weeks.

In the following experiment hog cholera bacilli remained alive for
more than four months:

June 8.—From an agar-agar culture, three days old, some of the
abundant surface growth was placed upon sterile cover-glasses, each
receiving about as much as the point of a platinum wire could hold.
These were placed on a flamed glass support under a flamed and plugged
glass funnel, and kept in the laboratory, the air of which was moderately
dry.

Two cover-glasses dropped into beef infusion peptone June 25, One
culturerémains clear, the other clouded in one day ; contained only mo-
tile hog cholera bacilli.

Two covers were added to beef infusion June 29, July 9, and July
16. All six cultures became clouded and contained only hog cholera
bacilli.

Of two cultures made July 23 only ene becomes clouded, and is a
pure culture of hog cholera bacilli. Of two cultures made August 2,
both become clouded with Log cholera bacilli only.

79

Four cultures, made on August 9, 22, 50, and September 14, became
clouded with the same microbes, and these alone. A tubeinto which a
cover-glass had been dropped September 21 remained sterile. A tube
inoculated in the same way September 26, became turbid on the second
day, and contained hog cholera bacilli only. A tube inoculated on Oc-
tober 8 was still fertile. The stock of cover-glasses had become ex-
hausted. —

It will be seen from the above results that some of the germs were
dead in one and a half and three and a half months; all the rest were
capable of multiplication for four months. The prolonged vitality was
no doubt due to the massing together of the germs from the agar cul-
ture, for on those cover-glasses which failed to inoculate cultures, or in
which the appearance of growth was retarded, the quantity of growth
was smallest. The interesting question here arises whether it is the
oxygen of the air which gradually destroys the bacilli, since this is more
or less kept away when they are massed together, and since all pre-
vious experiments with bacilli suspended in liquids have shown that
the period of their vitality may average not more than two months
when in a dry condition.

On August 30, after having been dried for two months and twenty-
two days, two mice were inoculated with a liquid culture obtained from
one of the cover-glasses. Both died of hog cholera on September 14
and 15, respectively.

The vitality of hog cholera bacilli during continuous desiccation may
thus last from two weeks to more than four months.

In the soil, and in nature generally , bacteria are rarely subjected to
continuous drying, but to alternate wetting and drying. In order to
observe the effect of such alternation, some of the same agar-agar culture
used in the preceding experiment was placed in the bottom of a sterile
watch-glass under a funnel June 8.

June 15.—About one-third cubic centimeter of sterilized distilled
water added to the’ watch-glass, so as to cover the dried film completely.
The water was evaporated entirely next day.

June 22.—Sterile water added again; dried up next day.

July 3.—Water added again and two cultures made; both remain
sterile.

July 6.—A liquid culture made by adding some sterile water to the
dried culture mass, stirring it up and transferring the water with a sterile
pipette to a tube of beef infusion. This also remained clear.

Thus bacilli from the same culture which resisted continuous drying
for at least four months were destroyed in less than a month when a
moist and a dry state alternated. This fact, so striking and important,
needed confirmation.

September 15.—A considerable quantity of the surface growth from
an agar-agar culture two days old was rubbed on the bottom of a sterile
watch-glass covered by a plagged funnel as before. Thoroughly dry
next day.

September 18.—A small quantity of sterile distilled water added. This
was dried up next day; the germs had spread out into a thin layer,

80

September 21.—Sterile water added again and a tube of beef infusion
peptone inoculated with a loop from the liquid stirred up. Tube turbid
with hog cholera bacilli next day.

September 26.—Sterile water added again. The tube of beef infusion
peptone inoculated at the same time. Pure culture next day.

October 1.—The same process repeated ; culture contains hog cholera
bacteria.

October 8.—Dried bacilli wetted again with sterile water. The cul-
ture made from them becomes turbid; only hog cholera bacilli present.

October 15.—The same process repeated; the inoculated tube be-
comes turbid after forty-eight hours.

October 22.—After wetting the dried growth again, it was thoroughly
stirred up and several drops added to a liquid culture. This tube re-
mained permanently clear.

This experiment therefore confirms the other in showing that hog
cholera virus is far more quickly destroyed when it is alternately mois-
tened and dried than when it remains continuously dry. In both tests
the germs died in one-third the time required to destroy dried virus.

SOME EXPERIMENTS ON THE LENGTH OF TIME DURING WHICH HOG
CHOLERA VIRUS REMAINS ALIVE IN THE SOIL.

The virus of hog cholera is quite tenacious of life in spite of the fact
that no spores are formed. During the past year some preliminary
experiments were made concerning the vitality of hog cholera bacteria

in the soil. This becomes infected during epizootics of this disease by |

the discharges of the sick perhaps more thoroughly than anything else
in the surroundings of the animals. Moreoyer, it is the most difficult
to disinfect, as we have no knowledge of the depths to which the living
virus may be carried by water. If it can be shown that the life of such
virus in the soil is speedily destroyed, the precautions to be taken would
be quite different from those needed if it exists for a long period of
time.

Experiment 1.—A small flower-pot containing soil was sterilized by
moist heat at 110° to 118° ©., and protected from drying and dust by a
large bell jar. On its surface about 100 cubic centimeters of a bouillon
peptone culture of hog cholera bacteria was poured and the whole main-
tained moist and at thelaboratory temperature. The soil used was a very
fine loam from the grounds of the Department of Agriculture. The bulk
of the soil consisted of grains not larger than ;3, millimeter (,255 inch).
Roll cultures from the soil after a few days demonstrated the presence
of immense numbers of bacteria. From this soil rabbits were inocu-
lated from time to time by stirring up a little soil in some sterile beef
infusion and injecting the clear supernatant liquid hypodermically. The
soil was infected September 17, 1887. The appended table gives
the inoculations into rabbits to test the virulence of the soil. The rab-
bits which succumbed died of hog cholera, as indicated by the lesions
and the bacteriological examination,

81

No. wagon Ae ea Died. Remarks.
lation.
Mos. Days. : ee
Lt) Oct. 10 23 Oct lien starts ...--| Enlargement of spleen; coaguiation-necrosis in
liver; hemorrhagic lesions in duodenum and
rectum, in lungs and heart; numerous hog
cholera bacteria in spleen and liver.
=| Oct. 18 31 Oct. 24 ........-- | Spleen and liver and lungs as in No. 1.
3| Nov. 4 | 46 INGVaallolise sete cer Spleen, liver, duodenum, and rectum as in No. 1.
4 | Dec. 12 2 29 Deen 2aissoccncres Spleen large, pale; coagulation-necrosis in liver
slight; noother lesions; hog cholera bacteria
as in No, 1,
Jan. 9} Seog Remains well..-.-.
6 | Jan. 23 | 8) 623 ssiew ik) Cepesee dace oe

The infectious quality of this soil when a month old was tested on
two pigs, by feeding each directly with a tablespoonful of the soil. One
showed no disease; the second, a young pig, became very sick and was
killed on the eighteenth day, being unable to rise.

Autopsy.—Animal about eight weeks old, very thin. No skin lesions.
Lungs normal, excepting the cephalic and ventral lobes of left lung, the
ventral and the root of principal lobe of right lung. These are airless,
bright red, mottled with yellowish points, indicating broncho-pneu-
monia. The spleen wassmall. The lymphatic glands of large intestine
very large, tough, whitish. The walls of cecum and colon over one-
eighth inch thick; do not collapse when slit open. The mucosa is
everywhere covered by a firmly adherent yellowish-white slough, ex-
tending as far as rectum. The ileum for about 2 feet from lower end
has the mucosa likewise involved in superficial necrosis, but only on
the summit of the longitudinal folds. In the stomach a portion of the
fundus is covered by a friable deposit made up chiefly of large granular
cells with single nucleus. Gelatine and liquid cultures from heart’s
blood and spleen contain only hog cholera bacteria. The gelatine cult-
ures indicate only a moderate number of colonies. The bacteria had
also penetrated into the diseased lung tissue. They were obtained on
plate cultures, and a rabbit inoculated subcutaneously with some beef
infusion in which a bit of lung tissue had been torn up died in eleven
days with coagulation necrosis in livcr, enlarged spleen, and numerous
hog cholera bacteria in both organs. The broncho-pneumonia may
have been due to the aspiration of some of the soil during the forced
feeding.

It has thus been shown that moist soil, not allowed to dry out and
kept in a summer temperature ranging from 60° to 95° F., retained its
virulence for rabbits from two to three months. At the end of this
time fungi and other bacteria had found their way into the pot of soil,
as shown in roll cultures. This and other reasons drawn from observa-
tions of this germ lead to the conclusion that its life becomes extin-
gushed with its pathogenic effect on rabbits. This phase of the ques-
tion is not to be overlooked, for even if a germ shorld no longer prove
pathogenic, but remain alive, it is not improbable that it may regain its
original virulence under certain unknown circumstances.

15612 H c——6

82

The severe disease caused in the young pig with soil which had been
infected one month ago shows the great susceptibility of young animals
to this disease. Since rabbits are most susceptible of any animals to
hog cholera virus, if was not thought necessary to experiment on pigs
after the former failed to take the disease.

It may be argued that the conditions of this experiment were abnor-
mal, in that the bacteria were not exposed to the various meteorological
conditions, such as rain and drought, freezing and thawing, and the
competition with other bacteria in the soil. This is true. The con-
ditions just enumerated are opposed to such a long life in the soil. A
condition favoring it, on the other hand, is the low temperature in winter,
which may act as a means of preserving the life of bacteria.

These objections were partially removed by the following experi-
ments:

Experiment 2.—A small pot, about 5 inches across the top, filled with
soil, is placed in another pot of twice the diameter, also filled with soil
in such way that the rims of both are on the same level. In this posi-
tion they were sterilized for three and one-half hours, at a temperature
of about 110° C.,in a steam sterilizer. The outer pot was to protect
the inner one to some extent from coming in direct contact with the
garden soil in which it was subsequently placed. About 200 cubic cen-
timeters of a beef infusion culture of hog cholera bacteria three days
old was ultimately mixed with the soil of the inner pot by removing the
upper layers and pouring the culture liquid upon the deep layers and
then upon the surface, after replacing the superficial layers. The pots
were then placed in the grounds of the Agricultural Department so that
the top was level with the surrounding soil. Nothing was placed over
the surface to protect them from contamination with ordinary bacteria.

The infected soil was placed in the grounds December 16, 1887.
During the remainder of December the out-door temperature oscillated
slightly above and below the freezing point, remaining for several days
below this point at the end of the month. The soil in the pot was
saturated with water during part of the winter and the surface covered
with it. It had probably become tightly packed, and hence impervious
after the culture liquid had been poured upon it.

The appended table indicates the persisteuce in virulence of the in-
fected soil as tested upon rabbits. The soil was taken from the surface
of the pot, or from near the bottom as indicated, and the inoculations
made as in the preceding experiments :

83

[Soil infected December 16, 1887. ]

Date of Number of days |

No.| inocula- Sole after infection | Rabbit dies— Remarks.
; | tion. of soil. :
1/| Jan. 5 | Surface.....| 20 days .:.........| January 16....} One lobe of liver involved in coag-

| ulation-necrosis; bacilli of hog
cholera present. :

Cal eHeD el |. kdO a voc-: 1 month 13 days --| February 18 ..| Spleen very large, dark; coayula-

tion-necrosis in liver; numerous

| hog cholera bacill: in both organs.
Hebi fale Wepth 2s. 7. LT monthy 19 days: .2). 02. <2 --55-2s. Killed February 27; not discased.
Feb. 23 | Surface..... 2 months 7 days ..| March 5 ...-.. Spleen and liver as in No. 2; hem-
orrhagie lesions in duodenum
and rectum; hog cholera bzaeilli
present.
5 | Mar. 5 do. .....| 2 months 18 days .| Remains well
Gear ols tee O). scm =< SIMONGES D0 ays) s4|22-000 225-4,- 25.

Rabbit No. 3 was inoculated with soil from beneath the surface. This
was obtained by removing the inner pot, thrusting a small metallic
cork-borer previously flamed through the hole in the bottom of the pot
upwards, about half-way tothe surface. The soil brought down in the
inside of the borer was used for inoculation. In this way it was ob-
tained unmixed with soil from the superficial layer. The rabbit re
mained well for twenty days after inoculation. This is longer thau any
period of incubation which we have thus far observed. Owing to ex-
tensive disease of the external ear caused by psoroptes (lice), it was
killed on the twentieth day. Thereavere no indications of hog cholera.
The deeper layers of the soil had thus rid theinselves of the infectious
material sooner than the surface. Roll eultures showed the presence
of a large number of pearly colonies spreading rapidly and made up of
non-motile bacilli.

Rabbit No. 2 lived seventeen days after inoculation. Was this long
period of incubation due to an attenuation of the virus, or to the sear-
city of the surviving bacteria? The lesions were practically identical
with those usually found. In order to learn whether attenuation had
actually taken place, a.rabbit was inoculated subcutaneously with three
to four drops of a beef infusion culture prepared from the blood of No.
2. It died in five days with extensive coagulation-necrosis in liver;
spleen very much tumefied and petecchiz in rectum. There was no at-
tenuation, therefore, so far as the second rabbit is concerned. There
still remains the possibility that the bacteria, attenuated when inoca-
lated into the first rabbit, grew in virulence during the long period of
incubation until they had attained their original pathogenic power,
when the rabbit died.

Experiment 3.—February 20, two pots of soil, one within the other,
were Sterilized as in the preceding experiments. The soil of the inner
pot was saturated from below up with 100 cubic centimeters of a beef
infusion culture one day old, of hog cholera bacteria. The whole was
buried in the garden on a. level with the soil and not protected in

any way. Rabbits were inoculated with the soil as previously indicated.

84

[Soil infected February 20.]

) |
Date of : a Number of
No. | inocula- ep eaken daysatter | Remarks.

tion. inoculation. |

1 | Mar. 10 | Surface ..-.| 18 days -..-. | Rabbit dies on eleventh day. Spleen very large; coagula-
tion necrosis in liver; hog cholera bacilli present.

2 | Mar. 29 | Depth -....- 38 days ..--. Rabbit died on eighth day ; lesions as in No. 1.
3 52-00). - a SUTlace- 2s. Ado eee Rabbit remains alive.

Soon after the last inoculation the pot of soil was accidentally re-
moved by laborers working in the garden, so that the experiment came
toa premature close. It shows, however, that the bacteria in the depths
of the soil were alive thirty-eight days after inoculation, while at this
same time they were dead in the surface layers,

Haperiment 4.—Soil prepared, sterilized, and infected precisely as in
the preceding experiment, was buried in the garden April 4, 1888. The
soil soon became packed hard and dry on the surface to a depth of one-
half to l inch. The following table gives the inoculations:

{Soil infected April 4.]

No. | eines After soil infection. Boils baleen Remarks.
tion.
1) Apr. 25 | 21 days -...--. =j-=j[ SURIAC Sinner Divs April 30; enlarged spleen. Slight necrosis in
iver.
2 |---do.-..}....d0~..-....-.--- leDepthieseees Dies May 2. Same lesions as in No. 1.
3 | May 12 | 1 month 8days....; Surface ...-.. | Remains alive.
fe pet O Sica ncie <0! a oeactaesrae = | Depthy-eee=- Dies May 21. Same as No. 1, besides hemorrhagic
lesions in rectum.
5 | May 29 | 1 month 25 days -.| Surface .....| Remains alive.
OR 28d Olas 26i| ne 20 Oy os oe eeeee ser | Depth ...... | Dies June 6. Same lesions as in No. 1.
7 | June 15 |} 2 months 11 days..|..-.do -...=.- | Dies June 29; spleen and liver lesions as in No. 4,
Bi, a= LO; zen dl aad Oneea c ane Sateee |....do Bere Remains well. :
9 | July 14 | 3 months 10days..|.-.. d04 52. Do.
100 Peele die eo ede eooers Do.

The presence of hog cholera bacteria was demonstrated by cultiva-
tion from spleen and heart’s blood in all the animals that died.

Hexperiment 5.—Soil sterilized and infected with hog cholera bacteria
as in preceding experiments. Placed in the department grounds May
18. June 20, surface layer dry and very hard ; boring necessary to get
some of if out. Two rabbits inoculated from surface and deep soil.
The result of these and subsequent inoculations is given in the follow-
ing table:

85

[Soil infected May 18. |

}
o i Ph |
No. seine aS al ‘afoe: Se taken Remarks.
lation. tion. |

1 | eoMNeg20) | hS3:0aYS oss .5 26.2). Surface ..... Dead July 4 (hog cholera).
2 be BOO re een las a stlO ws seat santo aye 1, Depth 22... Remains well.
3} July 20 | 2 months 2days...| Surface..... Do
4 --do ....|...-do d seRere o teeort Depthie----- Do. |

Experiment 6.—July 14 a pot of soil was sterilized and infected through-
out with 100 cubic centimeters of a culture of hog cholera bacilli as
before and placed in the Department grounds.

|
|
Date of | Length of time : :
No. | inocula- after soil infec- Aoi taken | Remarks.
tion. tion.

AS eA 105) 27 days'-2..2..--.- Surface..... Dies August 23; spleen very large. Necrosis in
liver; hog cholera bacilli in spleen; intestines
diseased.

De OMe On) en OOh> bere att = PeVeptn soe Died August 14; spleen and liver as in No. 1.

3 | Aug. 24 | 1 month 10 days ../ Surface.....}| Remains well.

PALO sod GO) < conan sense Depth ...- Do.

These various experiments extended over the coldest as well as the hot-
test period of the year, and may therefore lay claim to more or less com-
pleteness. They may all be brought together in the following table:

Rabbits failed to take the disease when inoculated—
Date of :

No.| soilin- | = bee
| fection. |

With surface soil after— With deeper soil after—

Li) Sepiie Lye] SSE DERE BIG Eh ye GS ee See ee

2} Dec. 16 | 2 months 7 days....--...----. Jeeiteeieteiealore ae wine te mtaye ane erate | 1 month 19 days.
3 | Feb. 20 Pelemomihhy days ss. sstees awa ase. OP tek te LIS Fae | Not completed.
AAC aera a amon th 25 Cay Si aaa u sate sticte we -tals te wcowtecee eau eee bas 3 months 10 days.
DUNC Lo alamo n nS) ACA Syd se cae siteisismnibie csc anleet aneesee aes ee | 33 days.

Ce Renvnlcea il ormOntheLON ay Sic os - cies ceccacn ane robinieeisew ice erein cS eiaie sim ces | 1month 10 days.

It may be said in general that hog-cholera gerins will perish in the
soil in from two to four months, depending on the season, moisture, and
depth from the surface. In what direction these three factors influence
their vitality the experiments are not complete enough to show. We
may, however, safely assume that frost has no rapidly destructive effect
upon them, while drying (experiments 5 and 6) seems much more de-
structive. Attention has already been called to the destructive effect
of alternate wetting and drying. So far as the above results go, a pe-
riod of at least four months should be allowed for the natural destruc-
tion of hog cholera virus in the superficial layer of the soil, @. e., in
a layer extending about 2 or 3 inches below the surface.

86

A FEW ADDITIONAL OBSERVATIONS AS TO THE VITALITY OF HOG
CHOLERA VIRUS IN THE SOIL AT THE EXPERIMENTAL STATION.

(1) A pen has a concrete floor, with a gentle slope towards the back.
From January to December, 1886, at least 70 pigs died in this pen from
hog cholera. During this time all the liquid in the pen drained into
the field back of it. During February and March of 1887 a number of
pigs in this pen died of swine plague. Two survivors from the disease
were removed September 15, leaving the pen empty. Jn December,
1887, the infected ground behind the pen was inclosed, making a yard
6 feet deep and 16 feet long and communicating with the pen. Decem-
ber 15, 1887, 3 pigs about two months old were placed in the concrete
pen and allowed to run in the yard behind it. All three continued
well. To make sure that there were no ulcerations escaping observa-
tion one of the pigs was killed one and a half months after their trans-
fer to this pen. There were no lesions indicative of hog cholera; cult-
ures from the spleen remained sterile. The two remaining pigs were
well three and a half months later.

These observations show that ground thoroughly infected for more
than a year was free from infectious properties eight months after the
death of the last case.

(2) Upon a plot of ground of one-fourth to one-third acre about 100
Pigs which had died of cholera during 1886 were buried, being covered
with 14 to 2 feet of soil. During 1887 no animals were buried here, but
many had been interred within 3 to 8 rods of this plot during the latter
half of the present year. A triangular yard 16 fect on each side was
fenced off upon the old ground, with a movable pen in.one corner for
shelter.

December 15, 1887, 3 pigs were penned in this yard. They remained
well; one and a half months later 1 was killed and found healthy.
The two remaining ones were Well after three and a half months.

This experiment shows that ground containing the bodies of numer-
ous animals which had died of hog cholera was not infectious after one
year.

(3) The following notes are valuable in illustrating how rapidly the
eround may be freed of infectious matter :

A yard 6 by 10 feet was enclosed by a fence and made to communicate
with a double pen having concrete floors. This pen had been infected
by pigs from the outbreak described on page 37. The soil of the yard
is a clay loam.

November 27.—Nos. 434, 435 now occupy the pen and Nos. 436, 437
added to-day.

November 28.—Nos. 434, 435 both die of hog cholera, These had been
infected by feeding (see p. 50 for notes on these and cther animals in
this pen).

December 10.—Viscera from No. 42 fed to Nos. 436, 437. .

December 12.—Viscera from No. 43 scattered over the soil of the yard,

87

readily eaten by Nos. 436, 437; later in the day Nos, 439, 440, and 443
added.

December 17.—Viscera from No. 47 and No. 48 scattered over the
ground, and Nos. 448 to 453 inclusive placed in the yard.

December 27.—No. 445 dies of cholera.

December 28.—No. 448 dies of acute cholera.

December 29. —Nos. 436, 439, 440, 449, and 452 all die of acute cholera.
The pen may now be said to be thoroughly infected.

January 1, 1888.—No. 437 found dead.

January 3.—Nos. 450, 451, and 453 removed.

January 10.—After the yard and pen have been vacant for a week
and simply brushed out but not disinfected nor cleaned thoroughly
two healthy pigs (Nos. 479, 480) are placed in it to determine whether
the ground is still capable of giving the disease.

During the greater part of January the ground was frozen over, but
during February and March there are frequent, prolonged tbaws.

March 29.—Nos. 479, 480 have remained well since January 10. They
are now removed. The yard itself is now converted into a genuine
mud-bole.

March 50.—Two fresh pigs are transferred to this yard.

July 24.—They have remained well for nearly four months.

This virus was in the first place either destroyed or made harmless
by the prolonged frosts in January, so that the pen and yard were
thoroughly disinfected by natural agencies and perfectly safe two months
later. The disease did not re-appear in the following midsummer. It
may also be seen from the notes that the two pigs placed in the in-
fected pen but one week after the removal of diseased and infected ant-
mals did not take the disease, perhaps because the infectious matter
was frozen up and slowly killed in this condition before they could get
at it.

THE EFFECT OF SOME DISINFECTANTS ON ‘THE VIRUS OF HOG
CHOLERA.

In the report for 1826 there are given in extenso a series of experiments
to test the destructive power of the more reliable disinfectants on hog
cholera bacilli from liquid cultures usually from one totwo days old. The
results, owing to their practical importance, are also summarized here.

The method employed needs afew comments. <A few drops of cult-
ure liquid were added to the disinfectant solution in a sterilized wateh
glass under a bell glass. After certain regular intervals of time plati-
num loops holding about 23, cubic centimeter were used to transfer
this liquid to tubes of beef infusion. These were placed into a ther-
mostat and watched for a number of days. The loop of disinfectant
carried over into 10 cubie centimeters of sterile beef infusion is diluted
to such an extent (about 1,000 times) as to be practically of no account
whatever. This method is more sensitive than the method originally
employed by Koch. He used bits of silk thread impregnated with the

specific organism to be tested and placed them upon plates of gelatine
to develop.

88

It has been suggested that hog cholera bacteria may survive in the
brine from salted meats long enough to be exported to other countries
and communicate the disease. It need not be said that this is impos.
sible, for the attenuating action of a concentrated salt solution would be
in itself sufficient to speedily destroy the pathogenic power of the bacilli,
even if their life were not destroyed. The following experiment shows,
however, that they are absolutely killed within four weeks:

Ten cubic centimeters of a saturated solution of common salt was
added to each of three culture tubes. These were then sterilized and
1 cubie centimeter of a fresh bouillon culture of hog cholera bacilli
mixed with the contents of each tube. Small quantities of liquid from
one of these tubes were introduced into sterile bouillon every two or
three days. Up to the twenty-first day the bouillon became clouded,
indicating that the bacilli were still alive in the brine. After the
twenty-ninth day the bouillon remained clear. The two remaining
tubes of brine hitherto untouched were also found sterile when exam-
ined by means of cultivation a day or two later.

Mercuric chloride was found destructive to the bacilius when diluted
in the proportion of 1: 75000 (.0014 per cent.).

Several drops of a culture were mixed with about 1 cubic centimeter
of a .1 per cent. solution, and tubes inoculated from this at the end of
two, four, six, eight, and ten minutes. Tubes remain sterile. To show
that the antiseptic effect of the liquid transferred with the platinum
joop was nil, one of these tubes was inoculated again from another cul-
ture. This tube was turbid on the following day.

Five tubes treated in the same way with .05 per cent. solution. All
remain Sterile.

ive tubes inoculated with bacteria exposed for the same periods of
time to a .01 per cent. solution. All remain clear.

Five tubes treated as before, using a .005 percent. solution. Perma-
nently clear.

Tive tubes treated as before, using a .002 per cent. solution. All
tubes clear, excepting the one inoculated after six minutes’ exposure.

Five tubes inoculated atthe end of five, ten, fifteen, twenty, twenty-
five, and thirty minutes after exposure to a .001 per cent. (1: 100000).
Tubes inoculated after five and ten minutes turbid next day. On the
second day all but the one inoculated after thirty minutes turbid and
containing pure cultures of the bacterium.

The limit of disinfection for this period of time must therefore lie
between 1: 500000 and 1: 100000; hence five tubes were inoculated as
above, using a solution of 1: 75000 at the end of seven, ten, fifteen,
twenty, twenty-five, and thirty minutes. All tubes remained clear.

Carbolic acid destroys the bacillus in solutions containing from 1 to 14
per cent. of the acid by weight.

Five tubes inoculated after treating bacilli from a liquid culture with
ai per cent. solution for five, ten, fifteen, twenty, and twenty-five min-
utes. All turbid on the following day. The two last tubes were also
examined on gelatine plates and the cultures found pure.

With a2 per cent. solution five tubes inoculated after ten, fifteen,
twenty, twenty-five, and thirty minutes remained sterile. The same
result with a 1$ per cent. solution. With a14 per cent., tubes inocu-
lated at the end of seven, ten, fifteen, twenty, twenty-five, and thirty
minutes remained clear, excepting the first, which contained bacillus
subtilis.

89

Passing to a one-half per cent. solution, tubes inoculated at the same
intervals became turbid with the bacterium sown. With athree-fourths
per cent. solution the result was the same.

Passing back to a 1 per cent. solution, tubes inoculated at the same
intervals remained sterile.

There seems to be an incompatibility between the first and last series.
If we examine the others, however, we must conclude that the limit of
disinfection lies between 1 and 14 per cent.

Iodine water was prepared by shaking up some iodine in distilled
water, which assumed an amber tint. This solution destroyed the ba.
cillus in fifteen minutes, as the following experiment shows:

Six tubes were inoculated with bacilli after they had been exposed
to the action of the iodine water for seven, ten, fifteen, twenty, twenty-
six, and thirty-one minutes. On the following day the first tube became
turbid; on the second the ten-minute tube was turbid and found to be
a pure culture of the bacilli sown. The other tubes remained sterile.
One of the tubes, inoculated later, showed its capacity for sustaining
growth by becoming promptly turbid.

Permanganate of potash. —A series of experiments with this substance,
conducted in the manner described above, showed that the bacillus is
killed by fifteen minutes’ exposure to .02 per cent. solution (1: 5000).

In order to obtain this result a 5 per cent. solution was tried first.
Tubes inoculated after an exposure of the virus for seven, ten, fifteen,
twenty, twenty-five, and thirty-one minutes remained permanently clear.
One of these tubes, subsequently inoculated with the unaffected virus,
was turbid next day. Two and a half per cent., 1 per cent., one-half
per cent., one-fourth per cent., one-tenth per cent., and one-twentieth
per cent. solutions were tried in the same way. The six tubes used for
each solution remained sterile. Finally, a one-fiftieth per cent. (1:5000)
was used. Tubes were inoculated after an exposure of the virus for
two, four, six, ten, fifteen, twenty, twenty-five, and thirty minutes. On
the following day the four first tubes were turbid; the fifth and seventh
remained sterile; the sixth and eighth contained a fine bacillus. These
two tubes, as was found later, belonged to a lot which, through some
carelessness, had not been properly sterilized, and the majority became
turbid before use.

Mercurie iodide was found to destroy the bacillus in solution of
1:1000000 in ten minutes.

Two grams of potassium iodide and 1 gram of mercuric iodide were
dissolved in 100 cubic centimeters of distilled water, making a 1 per cent.
solution of the disinfectant in a 2 per cent solution of potassium iodide.

This solution, diluted with sterile distilled water so as to make .1 per
eent., killed the bacilius of hog cholera taken from liquid cultures in
less than five minutes; .01 per cent. (1: 10000), .002 per cent. (2: 100000),
OL per cent. (1: 100000), and .0005 per cent. (5: 1000000) destroyed the
germ within two minutes.

When the solution was diluted so as to make .0002 per cent. (2 : 1000000)
and .0001 per cent. (1: 1000000), it was found that with both solutions
tubes inoculated with bacilli, after an exposure of two and five min-
utes, were opalescent, the bacilli introduced having multiplied, while
the remaining tubes (ten to thirty minutes) were sterile. These two
solutions, therefore, were still powerful enough to kill the germ in ten

90

minutes. The dilution had been carried so far as to make them prac-
tically equivalent in disinfecting power.

Sulphate of copper.—This disinfectant, which seems to be more effect-
ive than most other mctallie salts, was ‘tried j in solutions containing 2
per cent., one-half per cent., one-tenth per cent. Poth the 2 per cent.
and the one-half per cent. solutions destroyed the germ within five
minutes. Tubes inoculated with bacilli after an exposure to the one-
tenth per cent. solution for five, ten, and fifteen minutes, became tur-
bid; those inoculated after an exposure of twenty, twenty-five, and
thirty minutes remained clear.

The disinfectant power for short periods of time may be said to lie
between one-halfand one-tenth per cent. In this, as in other tests, one
or two drops of the culture were added to 5 cubie centimeters of the dis-
infectant. A slight floceulent precipitate formed each time.

Of hydrochloric acid a 2 per cent. solution of the acid, made by adding
4.2 cubic centimeters of chemically pure acid (containing abont 40 per
cent. HCl) to 95.8 cubic centimeters of water, destroyed the germ in
less than five minutes.

Chloride of zinc.—A 10 per cent. solution of this salt failed to destroy
the vitality of the bacilliin ten minutes; 20cubic centimeters of (Squibbs)
chloride of zine, containing 50 per cent. of the salt, were added to 80 cubic
centimeters of sterile distilled water, to make a 10 per cent. solution. A
drop from a culture five days old was mixed with 6 cubic centimeters of
this solution, from which mixture tubes were inoculated at the end of »
five, ten, fifteen, twenty-five, and thirty minutes. The two first tubes
became clouded.

Sulphuric acid.—A .05 per cent. solution (1: 2000) was fatal to the ba-
cilli of hog cholera in less than ten minutes.

Without going into detail, it is sufficient to say that the results were
reached as indicated above. Tubes containing sterile beef broth were
inoculated at the end of five, ten, fifteen, tw enty, twenty-five, and thirty
minutes with bacteria exposed to one-half per cent. and one fourth per
cent. No development. Those inoculated with one-fortieth per cent.
became clouded, each being a pure culture of the bacillus inoculated.
When one- twentieth per cent. was tried only the five-minute tube be-
came clouded. The solution (by weight) was made from sulphuric acid
containing 96 per cent. of the acid (specific gravity 1.838).

It must be remembered that the foregoing tests were made upon bae-
tevia in an active, vegetative state. It is probable that in the dried con-
dition it wonld have taken solutions of the same strength somewhat
longer time to destroy their vitality. To briefly summarize the results,
placing the least-effective substance first, we obtain the following table :

Chloride of zine in a 10 per cent. solution destroyed the bacilli in’
liquid cultures in fifteen minutes.

Carbolic acid, 1 to 14 per cent. (1:100), in five minutes.

Iodine water, in fifteen minutes.

Hydr fochlorie acid, one-fifth per cent. (1:500), in less than five minutes.
(Only a .2 per cent. solution of this acid tried. ) .

Sulphate of copper, one-tenth per cent. (1:1000), in fifteen to twenty
minutes.
Sulphuric acid, one-twentieth per cent. (1:2000), in less than ten min,
utes.

Permanganate of potash, one-fiftieth per cent. (1:5000), in fifteen
minutes.

31

Mercuric chloride, one seven hundred and fiftieth per cent. (1:75000),
less than five minutes.

Mercurie iodide in one ten-thousandth per cent. (1:1000000), in ten
minutes.

The above table would without doubt be very materially altered if the
test had been made with virus mixed with considerable organic matter.
This is very well illustrated by the experiments on lime, crude carbolie
acid, and additional experiments on sulphuric acid, given in full in the
following pages. Mercurie chloride, for instance, often fails completely
in albuminous liquids, although it is one of the best destructive agents
of bacteria suspended in water. So permanganate of potash, which
would have little or no disinfectant power in liquids highly charged with
organic matter, has a very high power in this direction in the experi-
ments detailed above.

The only substances in the above list, which, in our estimation, would
be useful for purposes of disinfection, are mercuric chloride and car:
bolic acid. Of the former, more will be said in discussing the subject of
prevention. Carbolic acid as it usually appears in the market is too ex-
pensive tabe used on a large scale.

CRUDE CARBOLIC ACID.

Laplace (Deutshe Med. Wochenschrift, 1888, 121), found that the so-
called crude carbolic acid, which will not dissolve in water, is capa-
ble of solution when mixed with an equal volume of commercial sul-
phurie acid. A 4 per cent. solution in water of this mixture was suffi-
cient to kill anthrax spores within forty-eight hours, and a 2 per cent.
solution destroyed them within seventy-two hours. Pure carbolic acid
in a 2 per cent. solution has no effect on anthrax spores. The crude
material contains about 25 per cent. of carbolie acid. Experiments were
made to test the germicide effect on hog cholera bacilli. The crude car-
bolic acid used was a very dark, reddish, thick liquid, smelling strongly
of tar, and not translucent even in a layer one-half inch deep. Whena
drop of this liquid was added to water it broke up into a few globules,
which settled to the bottom without undergoing solution. When an
equal volume of commercial sulphuric acid was added and the mixture
thoroughly shaken, a few drops added to water caused a faint turbidity,
but none remained in a globular condition. When more was added the
water assumed a grayish, opalescent appearance. similar to water in
which a small quantity of soap is dissolved.

To test this mixture, a culture liquid was prepared like that used in ~
testing the disinfecting power of slaked and unslaked lime. (See p.
96.) Beef infusion (to which the white of an egg was added in the pro-
portion of one egg to 600 cubic centimeters of the infusion) was neutral-
ized and sterilized without previcus filtration at 110° C. in Erlenmeyer
flasks, containing cach about 150 cubie centimeters. This turbid liquid,
with its large quantity of flocculent material, was inoculated with hog

92

cholera bacilli and allowed to stand for a week. Each flask then re-
ceived a certain quantity of the mixture and was thoroughly shaken up.
After certain intervals of time a platinum loop of liquid was withdrawn
from each flask, mixed with gelatine, and a roll culture made to indi-
cate the number of surviving bacilli. To make sure of the vitality of
the bacilli in the culture a control culture was made from one of the
flasks before adding the disinfectant.

Number of colonies in roll
cultures at the end of—
Flasks with 150 cubic centimeters culture-liquid, to which was added of | bape ae

the mixture of carbolic and sulphuric acids—

One hour. | Four hours.

2 cubic centimeters per Cents (V0) ooo cecciee atic ein =) aleielalmislaiaaiel neal None .....-.| None.
IMeubic Centimeters— Peri OMG ae ae ae ae stealer late melee alate olelalarele fermi aial= alae tia 25-6 dO) meaner Do.
ZHCUpICICENtIMELELS— lapel COMbiar sae ee alain lem oie ellels clsiw'e ai alere = \sielp so atsl=t seg CON mn smenee Do.
Bicuple Cenhi nl oteLs—cip Ol COM bya emisaetie ei ne = sie oniasia ieee lates tela eee ais lac Ol- ease Do.
(OGY LN Neh Becca Buses cd Baers cease ces Se OEBCGS Sd SE Ssbnicos dasaEcaobRe oe Countless. --

The table skows that a one-half per cent. solution by volume is suffi-
cient to destroy the bacilli within one hour. What share the’sulphuric
acid has in determining this result can not be inferred unless tried by
itself under precisely the same conditions. This is what has been done
in the following experiment:

Five Erlenmeyer flasks, containing each about 150 cubic centimeters
of a culture fluid prepared precisely like that in the preceding experi-
nent, were inoculated with hog cholera bacilli and allowed to stand at
a temperature of 70° to 80° F., for four days. At the end of this period
each drop of the culture medium, as ascertained by roll cultures, con-
tained countless bacteria. Commercial sulphuric acid was added from
a sterilized burette to the flasks in definite proportions by volume and
roli-cultures made at the end of one, two and a half, twenty-four hours,
and four days by transferring a minute quantity of the agitated culture
on a platinum loop.

The accompanying table indicates the result obtained, the specifie
gravity of the acid being 1.8+.

|
|
|

| Number of colonies in roll cultures at the end of—

ae
Boas
Son Bs pape | Cheek.» | “238 pete oe eee
aHo ws Eo rela aa | Twoand | : 4
BaSos weight. | | One hour. one-half Frente Four days.
oma oe | | hours. IWAUIS
> | isa
Cure, | | |
ae .24 | Countless --| Countless. -.| Countless -.| 100 | None.
4 ARTs Sedov caeeses | 30 10°} None’s:2-.<2 | Do.
95 1.14 | None ....... | Sila ido | ae
17, DW0de |: 5). qe ee dort oes | None s.22--- dor eee | Doe se
3 BAe peor. Stset dos ssace pace) ee do} 24 <3 { Do

93

One half per cent. of sulphuric acid (by weight) is thus sufficient to
sterilize a richly albumiuous liquid in three to four hours. Remember-
ing that in the crude carbolic acid mixture the per cent. of sulphuric
acid (by weight) contained in the one-half per cent. solution (which was
capable of sterilizing a similar liquid in one hour) was .36, we must
conclude that there can be no great difference between the crude ecar-
bolic acid mixture and the sulphuric acid in regard to disinfecting
power. Weshall, however, recommend the former in disinfection, since
it may last longer in the soil in which sulphuric acid soon forms sulphates
and thereby loses its germicide properties. According to experiments
given on page 90, .05 per cent. sulphuric acid was sufficient to destroy
hog cholera bacilli in ten minutes when no organic matter was present.
In the above experiment, in which the liquid contained much organic
matter, about ten times as much was necessary.

ORDINARY LIME AS A DISINFECTANT FOR HOG CHOLERA.

Recent experiments made with ordinary lime (CaO) by Liborius
(Zeitschrift f. Hygiene 11, 1887, p. 15) have shown that water containing
but .0074 per cent. of lime is capable of destroying typhoid bacilli in the
course of a few hours. Cholera spirilla are destroyed by a solution con-
taining .0246 per cent. of lime. These two diseases resemble hog chol-
era in the mode of dissemination of the virus. In all, the stools are the
chief vehicle of the bacteria. Disinfection, therefore, becomes a most
important aid in the prevention of the disease.

Lime has many advantages over other disinfectants. It is, first of all,
not poisonous. It may be used almost anywhere with impunity where
mercuric chloride or strong acids are inapplicable. The soil, when
containing the germs of the disease, is not injured by being covered
with a small quantity of powdered or slaked lime. ‘The material is ex-
ceedingly cheap and can always be obtained without difficulty. The
experiments given in the following pages show that lime is a very effi-
cient disinfectant with reference to hog cholera virus, and therefore with
reference to the bacteria of swine plague, which are far less resistant
than the former.

The method is, in the main, based upon that used by Liborius, with
some modifications, which it is pot necessary to point out here.

(1) It was desirable to observe what percentage of lime in solution
was necessary to destroy hog cholera bacteria not mixed with any ap-
preciable quantity of organic matter. For this purpose water contain-
ing different quantities of lime in solution received about two drops from
a beef-infusion culture, each drop containing approximately 500,000 bac-
bacteria. Attheendof one-half hour about one-thirtieth cubic centimeter
of the fluid (usually 8 to 10 cubic centimeters) was removed with a flamed
platinum spiral and transferred to liquefied gelatine in atest tube. The
same was done at the end of three hours. This tube was then placed in
ice water and twirled between the fingers while in a horizontal position.

94

The gelatine, as it congealed, uniformly coated the inside of the test tube,
which was immediately transferred to a box in connection with a refrig-
€rator, where it was kept at atemperature of 75°F .* The temperature of
the laboratory during these experiments was frequently as high as 95° F.,
‘scarcely ever below 80° F., (July). Any bacteria not killed by the disin-
fectant would show as minute yellowish-white points in the layer of gel-
atine within forty-eight hours. The number of points corresponded to
the number of living bacteria introduced into the gelatine. These cul-
tures will be denominated roll cultures in the succeeding pages. By this
method it was found that lime-water diluted with three times the quan-
tity of distilled water was sufficient to destroy hog cholera bacteria im
one-half hour. A dilution containing six times the quantity of water
destroyed the bacteria in three hours, while a dilution containing twelve
times the quantity of water was not capable of destroying them in
twenty-four hours.

If we take .12 per cent. as the quantity of lime in lime-water, .03 per
cent. of lime will destroy all bacteria in one-half hour, .019 per cent. in
three hours.

| Number of coloniesin _,
| roll cultures prepared Liquid cultures
| at the end of— inoculated at

Lime-water diluted so as to contain of CaO. ) Piscean es the end of

| is | | twenty-four
One-halfhour. Four nae hours.
: cad : : |
OL) 3° EIN ao chassecase sone essa co emSssencecsasee S60 306 | INONO Ee seee None -.....| Sterile.
ORO Gi Grey COME eee nets see aaa ates era stel= etal clearer aistee oletate etette ante |tet OW sees oul) sec5 Do.
WOES FXO OLEC elie in AGce dase SHs cOcormonnaSacnoaDaSEuacmasHan- (®) see OnE ee Do.
OX03 peu Gent: Arar 1 paeeee a cetera se seein esate None ..---.-).-- dove. Do.
(Olngelle Mee eee Sae dspnodoosacoseeé 9509 Js 2oeesea bso apO snes | Countless.
II.

Of03) per. Cont wee cs sey..- aes )so eee ee eee oe alee oer | IN ONG - 534-e None k=s-2- | Sterile.
OS) othe (etal joes no saatincoducnasaosar socsenoseoacad Res aeeenr Very many..|..-- (OP a gcie= Do.
010098 emeont.vos eee: Sees eee See Mose Neene | |

Poon ON are ee Very many; Turbid.
Che elostwbor. aa5 <e soeelire oerce ae ce ea ae See ee cee eee | Countless. |
|

* Contains hay bacilli.

The quantity of the disinfectant used must be increased, with many.
disinfectants, with the quantity of organic matter present in the mate-
rial to be disinfected. The preceding experiment gives us therefore
only the minimum quantity that is necessary to destroy hog cholera
bacilli when organic matter is practically absent.

A second series of experiments was therefore made by mixing beef
infusion cultures with varying proportions of lime-water, and observing

“A description of this method is given by its author, K. Esmarch, in the Zeitschrift,
fiir Hygiene, i (1886), p. 293, ;

95

the quantity necessary to destroy all bacteria present. A preliminary ex-
periment was made by adding lime water in varying proportions to cult-
ure tubes containing about 10 cubic centimeters each of beef infusion
which had been inoculated the day before and were now opalescent. A
flocculent precipitate formed after the addition of the lime-water, which
soon settled to the bottom, the quantity of this precipitate varying di-
rectly with the amount of lime water added. The following table shows
that in all the cultures made by transferring a loop of the mixture of cult-
ure liquid and lime-water in the proportions there given at the end of
thirty minutes, four hours, and twenty-seven hours, no destruction or
retardation of bacterial growth could be detected. In the first tube con-
taining beef infusion and lime-water in the ratio of 2 to 1 the precipitate
left at first a perfectly clear supernatant liquid. This did not, however,
mean complete disinfection, as the roll cultures proved. Moreover, at
the end of three or four days this liquid became opalescent again, owing
to the rapid unchecked multiplication of the contained bacteria.

A quantity of lime amounting to .64 per cent. was not sufficient to
destroy the vitality of beef infusion cultures.

100%

5 Number of colonies in roll cultures prepared at
a7) | the end of—

Ae Lime : is PS a3} e 2

a water.| Lime. jl

a5 One-half | Four | Twenty-seven |...

2 hour. hours. hours. \Sev en days.
Gace Cue Per cent. |

10 5 | .04 Countless|Countless| Countless.... | Countless.
10 2 RO See sleet d Osa. Ha Oiets aps od Ome cee eee | Do.
10 1 | OL RUOL sacs COs ac | = oe do |
10 4 O0b7 22 Cotes e-dorasen|- <== Gh cocseer
it EEO) oe See [eictetee esta ate emit (aye Sel te See | RU CHENS ESRI
| |
*Check.

This experiment was therefore continued with relatively larger quan-
tities of lime. Tour portions of 40 cubic centimeters each of beef infu-
sion in culture flasks, in which hog cholera bacteria had multiplied for
twenty-four hours, were mixed respectively with one-half, one, one and
one-half, and two volumes of lime-water, and thoroughly shaken. It
was found by testing with roll cultures at the end of thirty minutes, four,
and twenty-seven hours that for every 40 cubic centimeters of culture
liquid it required 60 cubic centimeters of lime-water to destroy all bae-
teria within twenty-seven hours, while a large number were destroyed
within four hours. It required 80 cubie centimeters to completely ster-
ilize the culture fluid: in four hours, although nearly all bacteria were
destroyed within the first half hour. In the flask to which 40 cubic
centimeters had been added there was a partial destruction of bacteria
at the end of twenty-seven hours, At the end of six days the bacteria

J6

were aS numerous as in the flask containing 20 cubic centimeters of
lime-water, in which no destruction of bacteria or retardation of growth
could be observed. The percentage of lime in these cultures is given
in the following table:

IV.

: | Nunber of colonies in roll cultures prepared
& at the end of—

a Lime- Tana : ar =

A water. : Twent

& | ; y-

bs Cneslall Fourhours.| seven Six days.

our.
2 hours.
fq
att | ‘ =

exe: Cnc Per cent. |

40 20 .04 | Countless .| Countless -| Countless -

40 40 SWS, (aan doe. pen O eee! Very many.| Countless.

|
40 | 60 | SUP Sneath) Agece EAS TOW) sei +e NONG leer None.
40 e0| .08 | Afew....) None..... dana

When the lime-water was added to the beef infusion a light floceulent
precipitate was formed immediately as in the preceding experiment,
the quantity depending on the amount of lime-water added. This set-
tled to the bottom in a very short time, leaving a perfectly clear, slightly
yellowish layer of liquid above. In those flasks, however, in which dis-
infection was not accomplished, this layer of liquid remained turbid, or
else became clear at first, with the partial destruction or precipitation
of bacteria, and then became clouded again as the remaining bacteria
multiplied in it.

The quantity of organic matter which is present in substances to be
disinfected is ordinarily quite large. This is true of bowel discharges
which contain the specific hog cholera bacteria, and which should there-
fore be thoroughly disinfected. To prepare a solution containing a con-
siderable amount of insoluble albuminous matter, the method of Liborius
was adopted. Beef was chopped finely and allowed to soak over night
in the refrigerator in twice its weight of water, as in the preparation
of beef infusion. After the meat had been removed from the liquid
in a press the latter was neutralized and the white of an egg was
added in the ratio of one egg to every 600 cubic centimeters of liquid,
The whole was boiled and the coagulated masses allowed to remain in
the liquid. The amount of solid particles and lumps, when deposited
on the bottom, formed a layer nearly as deep as that of the liquid above
it.

This mass of liquid and solid matter was placed in Erlenmeyer flasks,
each receiving 150 cubic centimeters. The whole was sterilized for sev-
eral hours at a steam pressure of 12 pounds and subsequently inoculated
with hog cholera bacteria. At the end of three days, when each drop of
the culture liquid contained nearly a million of bacteria, milk of lime,
made by adding lime in the ratio of one gram to 9 cubic centimeters of

97

water, or, in other words, milk of lime containing 10 per cent. of lime,
was added in various quantities as shown by the following table;

Vv.
- Number of colonies in roll cultures made
a at the end of—
7) Milk
No. é of Lime.
a) | uime, Twenty -
| One-half Three Seem here
ce : four Six days.
Y hour. hours. hen:
joa)
C.c. | cc. Per cent.
a 150 | 40 2s les NONE aeere= None*.. -= | None... -
2 150 | 20 si2e 3 S500 =a 5 see COna se cy= leew GLO} =o.
3 150 10 AWE Veecntlily eastllbemeli sae lea Oya |
4 150 | 5 soo esned ates «| paced O yee |....do ...| None. |
| | | |
Boleet50| 2 | .18 |Very many. Very many.| 50 | Very many.
WS Nia | Gosche eee ate e's Countless. | |
* About 12 fungi. t About 100 fungi. § Check (beef infusion).

In all the experiments the cultures containing tne precipitated mat-
ter were shaken up before testing so that the quantity taken for the
roll cultures (about 51; to 35 cubic centimeter on a spiral of platinum)
consisted of solid particles as well as liquid.

Within thirty minutes after the addition of the milk of lime the pre-
cipitate had settled so as to leave the supernatant liquid perfectly
clear in flasks 1, 2, and 3; in flasks 4 and Sit was still turbid as be-
fore the addition of the lime. It cleared up in No. 4 soon after, but re-
mained permanently turbid in No. 5. In none of the other flasks did
this layer become turbid even after seven days. In these the bacteria
were permanently destroyed, as the table shows. That the lime trans-
ferred to the roll cultures could have had no retarding effect on the
growth of any bacilli present was proved by adding at least four times
the quantity of lime to a gelatine tube which had been inoculated with
a drop of culture fluid. Countless colonies appeared in the gelatine
layer in due time. The check tubes were tested oaly at the beginning
of every experiment to test the vitality of the cultures used. Since hog
cholera bacteria will remain alive in the beef infusion employed for
weeks and months, there was nothing to be gained in making roll cult-
ures from these check tubes more than once.

The table shows that 5 cubic centimeters of a 10 per cent. milk of
lime was sufficient to sterilize within one-half hour 150 cubie centime-
ters beef infusion containing much suspended albuminous matter. This
would be equivalent to about one-half gram of ordinary unslaked lime,

or about .0032 gram for every cubic centimeter of liquid, ¢. e., 32 per

cent. We may assume, therefore, that for every twenty pounds of

fecal matter or discharges from diseased pigs only one ounce of lime

in the form of milk cf lime is needed, provided the two are thoroughly
15612 HC 7

98

mixed. The less complete this mixing can be the more lime must be
added to make the disinfection thorough. By comparing the amount
of lime necessary when there is little or no albuminous or other organic
matter present and when there is a large quantity of it, we are im-
pressed with the importance of always taking into consideration the
circumstances under which disinfection is to take place. Thus the
bacteria of hog cholera are destroyed in one-half hour when placed
in water containing only .03 per cent. of lime. When there is present
beef infusion diluted to one-third the original strength it requires .08
per cent. of lime. When the suspended albuminous matter is consid-
erable it requires .32 per cent.

It may be more convenient to use unslaked lime either in small lumps
or powdered shortly before application to the mass to be disinfected.
That this may be done the following experiments are sufficient proof:

Erlenmeyer flasks, containing each from 100 to 200 cubie centimeters
of beef infusion in which there was a large amount of suspended mat-
ter, as in the preceding experiment, were used for this purpose. After
inoculating each with hog cholera bacteria they were allowed to stand
for forty-eight hours. At the end of this time the flasks contained many
millions of germs in each cubic centimeter. Unslaked lime was broken
up into lumps as large as peas or beans, and thoroughly heated over a
Bunsen flame to destroy any adherent spores and drive away any moist-

ure. After cooliug, this was thrown into the culture-flasks in the pro-

portion, by weight, of 2, 1, 3, and 4 per cent., respectively. The flasks
became very slightly warmer. After thorough shaking the suspended
matter soon began to settle down, leaving a clear, supernatant liquid,
which remained clear after ten days’ observation. The liquid in the last
flask (4 per cent. lime) cleared up most tardily. The attached table shows
that even as little lime as $ gram in 100 cubic centimeters was sufficient
to permanently destroy all bacteria in a liquid very rich in albuminous
substances. Even at the end of eight days the flasks containing the
smallest amounts of lime were sterile. ,

Vale

Number of colonies developed in roll culture pre-
pared with ,5 cubic centimeter of infusion at the

: : | end of—
Beef infusion. Per cent.
ODAC OT ae
By | ees Twenty- | j; ;
One hotr. | Four hours. | ¢ 47 hours. | Eight days.

100 cubic centimeters plus 2 grams CaO. 2 heNone!ssss-e | INoné)-- =. None .....
120 cubic centimeters plus 1.2 grams CaO 1 Jetset LOU serie A fow..--.- ado aaa
200 cubic centimeters plus 1 gram CaO. .5 | Very any -.| None’. ---- |nstto LOM ees None.

200 cubic centimeters plus .5 gram CaO. 2bi| sesd0ysed sae lose doers | =u Ole es OOS

The table shows that in the flasks containing one-half and one-fourth
per cent. of lime there were still a considerable number of living bacteria

99

at the end of the first hour, although destroyed at the end of four hours.
The presence of bacteria in the flask containing 1 per cent. of lime at
the end of four hours, although none were detected at the end of the
first hour, shows that all bacteria are not necessarily destroyed simul-
tancously.

A second experiment, conducted precisely as the preceding, confirmed
the latter in every respect. The quantities were chosen somewhat dif-
ferently, as the appended table shows, in order to find out the lowest
percentage of lime that will destroy all bacteria within a given period
of time.

; VI.

Number of colonies in roll cultures made with 35
cubie centimeter of the beef infusion at the
end of—

Beef infusion. He a BEET z
Lime. Twenty- ats
One hour. | Three hours. four abe
hours. NS:
Per cent.
100 cubic centimeters plus 1 gram CaO .... I | Wery many -| None is--..-- None ...} None.
200 cubic centimeters plus 1 gram CaO. .. IPNONGI. oenst= Hered Wnepeeene =e GOmas- meas
200 cubic centimeters plus .5 gram CaO... 2 | Very many . 50) |22.d0)---.| Wor
200 cubic centimeters plus .3 gram CaO... .15 | Countless...) Very many.. 50 | Do.
Check tube ...... Dect ees octane folate oe eels Cre ee Ce ese QOleneeue |

The lime was powdered, and heated in a platinum evaporator to de-
stroy all adherent spores. There was scarcely any perceptible rise of
temperature when the lime was added to the liquid. The first flask con-
tained a culture eight days old, the remainder contained cultures four
days old. From the table it will be seen that one-half per cent. of un-
slaked lime is sufficient to sterilize a very turbid albuminous liquid in
four hours, one-fourth per cent. in twenty-four hours. Fifteen-hun-
dredths percent. was almost enough to destroy all the germs in one day
while at the end of five days all were dead.

DISINFECTION OF THE SOIL WITH LIME.

The same fine loam used in the experiments to determine the vitality
of hog cholera bacteria in the soil was used here. The method pur-
sued was briefly as follows:

Into small beakers, plugged with cotton wool and sterilized at 150°
C. for several hours, about 50 grams of slightly moist soil was intro-
duced, and the whole sterilized under steam pressure at 110° C. About
10 eubic centimeters of a beef-infusion culture of hog cholera bacteria
was then stirred up with it. After a certain length of time milk of
lime was added and thoroughly mixed with the soil. The destruction
of the bacteria was noted at certain intervals of time by taking small
bits of the soil on a platinum loop and making roll cultures therefrom.

100

The table appended gives the results of a series of experiments carried
out according to this plan:

Sane a cdlomesi in roll BS eared from a small
| bit of soil after—
Number and date of Queen Check re i, =
experiments. | in soil. | culture Sora al One | Two) Three | Five| Six | Seven
Ginseng day. days. days. |days.|/days.| days.
1888. | Per cent. |
I.—Jan.18...... 1 te) (2) 0 0 OF) «2's emia teers ol ee
II.—Jan. 20 ...... | 2 | 0 100 O ese ec] ee cdl ns cine ce oll esters | Sea el
IIT.—Jan. 23. ..... ales ne 40 0 | 34] 0 10 |c-- <3] 22. 0a) eee
IV.—Jan, 24 ...... 4 | 00 (2) 250 | 1000 GO | ene catiell bs cio inet Cee
Weston Sie ee un es Rf oer 20 (| oe ee a () @)
Vi.—Jane3l =. 33 3 | ~ 0 (2) 6" eee 00) | Oeeeee 0 oo
NAO Gis el eee | 4 Cyr, Meact sees 0 Oalteease Ose 0
VIII.—Feb.10 ...... a (?) 0 0 (UM aaaooe O4)szenen 0
IX.—Feb. 235 ...- Re lltp ico lee) one o tes (). }iceers ee
K.—Feb. 235. ....! aR feo Ka lleena( 8) fel as ete Hhcoa sO eer (©) |sce-se|.c8 eee
KieJnne 772.2 | ac ties @ 2) se I> ao Bal tees 0 0
XIL.—June77. -...| ik | on 0 0! 0 Ovieetoe ee 0
1 Countless colonies. 5 Rabbit ana of hog cholera ‘aifte® inoeneee
2 Less than o, but still too numeroustoo beesti- with soil on nine teenth « day.
mated. e Te microccus multiplies in the soil. ;
3 Fungi present. Rabbit inoculated with soil on eleventh day
4 A few fungi present. remains alive.

The following may serve to explain more fully the tabulated experi-
ments and results obtained:

I. Fifty grams sterile moist soil, infected with 10 cubic centimeters
of a beet-infusion culture January 5. January 18: 5 cubic centimeters
ofa 10 per cent. milk of lime (9 cubic centimeters water and 1 gram
ordinary unslaked lime) was stirred up with it. This is equivalent to
1 per cent. of lime. <A roll culture from the infected soil was made in
all experiments before the lime was added, to make sure of the pres-
ence of living germs.- Roll cultures, to which three loops of milk of lime
were added, showed no diminution in the growth of colonies, proving
that the small amount of lime (fraction of a loop) added with the soil had
no retarding effect. In this experiment 1 per cent. lime was sufficient
to remove from the soil countless bacteria (as shown by check-roll) in
three to four hours.

Il. January ale To another beaker of soil, prepared and inteeted with
the preceding, 2 per cent. milk of lime was added and stirred up. The
result identical with Experiment I.

Ill. January 23: 24 eubie centimeters of 10 per cent. milk of lime
added (= 4 percent.). The check-tube contains so many colonies as to
have an opalescent appearance. Disinfection is nearly completed after
one hour. A few eclonies develop in the one day and three day tube.

Ly January 24: 1} cubic centimeters of 10 per cent. milk of lime
(= 4 per cone no disinfection i is brought about. During the first
twenty-four hours there is a decided diminution in the number of colo-
nies, but a decided increase thereafter.

V, VI. January 31: The sterile soil in two beakers was infected yes-
terday with a beef-infusion peptone culture three days old, 10 cubic
centimeters being added to each beaker. To-day enough milk of lime

4
SE

Oe ee ee

101

(5 per cent.) is added to two beakers to make one-half per cent. and
one-quarter per cent., respectively. The check-tubes show subsequently
countless colonies. The table shows a slight diminution in the number
of colonies for the first twenty-four hours, then an increase. No disin-
fection. For the one-half per cent. beaker there is apparently a complete
destruction during the first two days, but subsequently the few remain-
ing multiplied again. No disinfection here. This result seems to disa-
gree with the third experiment. The discrepancy was, however, caused
by the fact that the milk of lime was not thoroughly shaken up when
used.

VII, VIII. In these experiments the lime was thoroughly stirred up
before use, and in both beakers disinfection has taken place. The
germs in the soil before adding the lime were not so numerous, because
the soil had been infected from a liquid culture only fifteen minutes
previous and no multiplication could have taken place. ,

IX, X. The conditions of the experiment are the same as before.
The soil is infected with a liquid culture two days old. Seven days
later check-tubes are prepared from each beaker of soil. One receives
one-half per cent. lime, the other three-quarters per cent. (7. ¢., 5 eubie
centimeters and 7.5 cubic centimeters of a5 per cent. milk of lime to 50
grams soil). The table shows that the beakers were invaded by a mi-
crococeus after the first day, which multiplied enormously in the soil,
so that hog cholera colonies could not be detected. After nineteen days
two rabbits, inoculated with a little infusion made from the soil, sue-
cumbed to hog cholera.

March 13: Rabbit inoculated subcutaneously with sterile beef infusion,
in which a little of the one-half per cent. lime soil had been stirred up.
Rabbit dead March 19. Spleen enlarged, congested; kidneys, lungs,
and duodenum with hemorrhagic foci. Beginning necrosis in liver.

A second rabbit inoculated from the three-quarters per cent. lime soil
in the same way and at the sametime. Rabbit dead March 21. Lesions
the same, in addition to a hemorrhagic condition of the lower portion of
large intestine. In both hog cholera bacteria present.

XI, XII. Experiments carried out as the preceding ones. The bac-
teria were permanently destroyed, as shown by the roll cultures made
up to the seventh day, and unsuccessful inoculation of rabbits later on
the eleventh day.

From these experiments we may conclude that three-quarters to one
per cent. of lime will destroy hog cholera bacilli in the soil. Itis highly
probable that a smaller per cent. of lime (one-quarter to one-half per
cent.) will be amply sufficient when simply scattered in a thin layer
over the surface where the great majority of the disease germs will
remain until destroyed by natural agencies.

IS THERE ANY RESISTANT SPORE STATE IN THE LIFE HISTORY OF
THE BACILLUS OF HOG CHOLERA?

This question can now be answered with the help of the foregoing
experiments.

Stained in dilute aqueous solutions of aniline colors the bacilli from
the tissues of animals which have succumbed to the disease stain in
such a way as to leave the impression that each bacillus contains an
endospore. A narrow band of stained substance bounds an oval pale

102

body, which is but slightly tinged. It appears that a rather resistant
envelope prevents the voloring matter from passing readily into the in-
terior of the bacilli.

Ifa drop from a recent liquid culture be suspended from the lower
surface of a cover-glass and examined in a glass cell with a homogene-
ous immersion objective and.small diaphragm, the following appear-
ances are worthy of record: The bacteria in the center of the drop of
culture fluid are in very active motion. Ifthe periphery of the drop be
examined there will be found a dense layer of bacteria caught there by
the slow desiccation and consequent contraction of the drop. These,
some of which are still moving slowly, appear slightly larger than the
forms in the center of the drop. Asthe drying proceeds and the film
of water becomes thin, the bacteria appear to be made up of a distinet
dark berder surrounding an almost transparent body. In most forms
there is a slightly thicker border at the ends than at the sides of the
short, rod-like bodies. When stained slightly this border takes the
stain well, while the body of the rod remains pale. The fact that the
structural and color pictures correspond is strong evidence that the
microbe possesses a rather dense membrane, which in optical section is
seen as a narrow dark border.

Involution forms may occasionally simulate endogenous spore forma-
tion. When hog cholera bacilli are placed upon the surface of gelatine
with a drop or two of blood, a few days are sufficient for the formation
of a large number of filaments from two to many times the length of
the bacilli as they are found in the tissues of animais. The ends are
rounded or irregularly pointed ; the width of the bacilli varies; in gen-
eral, they have the physiognomy of abnormal forms. In each bacillus
there may be from one to four oval, square, or oblong, clear spaces.
When stained they remain without color, thus simulating spores. When
carefully examined in a fresh condition, there is no refrangibility—they
are mere holes or spaces left by the irregular breaking up and retrac-
tion of the protoplasm.

Microscopical characters, however, are now and then misleading, un-
less we interpret them by physiological experiments. Judging from
what have hitherto been considered properties of bacterial spores, the
microbe of hog cholera can not lay any claim to the production of true
endogenous spores. Their absence is determined by results of experi-
ments recorded in the preceding pages:

(1) The thermal death-point of the bacilli at 58° C. An exposure to
this temperature for fifteen to twenty minutes destroys not only the vi-
tality of cultures of all ages, but also the germ in the tissues of the in-
fected animal. A momentary exposure to boiling water is equally effi-

cacious. :
(2) The bacteria are destroyed by disinfectants in solutions which are

incapable of destroying spores.

103

(3) They are killed by simple drying far more quickly than are spores;
at the same time their resistance to drying is much greater than might
be expected under the circumstances. In the experiments recorded
some dried bacteria in spleen pulp were killed in less than a month;
others resisted forty-nine days. For cultures we may put the limit, ac-
cording to experimental data, between one and four months. It is this
continued vitality in the dried state that suggests the existence of a
membrane which is more resistant than that possessed by the great
majority of bacteria in their vegetative state.

(4) Subjected to various conditions of moisture and dryness, of freez-
ing and thawing in the superficial layers of the soil, they are destroyed
after an exposure of between two and four months.

The facts brought out by the study of the bacillus lead to the con-
clusion that a distinct spore state, so called, does not appear either
within the animal body or in nature.

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WAYS IN WHICH SWINE BECOME INFECTED.
BY WAY OF THE DIGESTIVE TRACT.

(a) Feeding diseased viscera.—In at least 90 per cent. of swine, hog
cholera may be induced by feeding to them the viscera of animals which
have died of the disease. The lesions produced are exceedingly severe.
The mucous membrane of the large intestine is extensively ulcerated
or completely necrosed. In animals which have contracted the disease
in the ordinary way in. infected pens the ulceration of the large intes-
tine, at times very severe, usually stops abruptly at the ileo-cecal valve.
When this is slit up, the mucosa belonging to the small intestine up to
the free border of the valve is in the great majority of cases normal,
while the mucosa of that surface of the valve facing the cecum may be
extensively ulcerated. In many animals fed with infectious matter the
ulceration involves the entire ileum. ‘This is well illustrated by the
following cases:

January 8, 1886.—Pig No. 165 was fed with the viscera of two pigs
which had died of hog cholera. It was found dead January 26, after
manifesting no marked symptoms of disease except a tendency to lie
quietly in its pen. On examination the subcutaneous fat was found
diffusely reddened. There was a slight peritonitis, indicated by a con-
siderable quantity of straw-colored effusion and some fibrinous stringy
deposits. here were also a few local excrescences on the small intes-
tine, due to the irritation ot echinorhynchi. Spleensomewhat enlarged ;
on its surface a few bright red punctiform elevations. Right heart dis-
tended with a clot. Local hepatizations in lungs, probably caused by
lung worms,which were very numerous. Stomach but slightly reddened.
A numberof ulcers in the duodenum, the mucosaof which was reddened.
The mucosa of the ileum for 1$ feet from valve was completely ne-
crosed, the walls thickened, and the serosa of this portion dotted with
ecchymoses. On the upper portion of the ileum there were scattered
ulcerations on a deeply congested membrane for 6 or 7 feet. The entire
length of the large intestine was covered with dirty, yellowish ulcera-
tions varying in diameter from a pin’s head to nearly an inch. The
mucosa itself was very deeply congested in the czcum and colon, and
the walls much thickened. Ascarides and echinorhynchi numerous in
small intestines. The liver attached to diaphragm in several places by
a whitish exudate.

A tube of meat infusion with peptone inoculated from the spleen of
this animal was found to be a pure culture of the motile bacillus of hog
cholera. Line cultures on gelatine plates confirmed the microscopic
examination. <A tube of nutritive gelatine inoculated from the spleen
at the same time contained in each needle-track, several days later,
from ten to fifteen colonies of the same organism. ‘Two cover-glass pre-
parations revealed no bacteria. This fact, combined With the small
number of colonies in the tube culture, gave evidence of the small num-

105

106

ber of germs in the spleen tissue. Inoculations on mice and guinea-
pigs gave substantially the same results as those obtained hitherto.

No. 159 was fed with viscera of No. 165 on January 28. TFebru-
ary 5, its eyes were sore and nearly closed ; it was quite weak. It died
the following day, only eight days after infection. The skin on ab-
domen was reddened in patches; the subcutaneous tissue diffusely.
The superficial inguinals, as well as the, glands in the abdomen, were
deeply congested, the cortex more especially. Those of the thorax
were nearly pale. The spleen was dotted with a few punctiform blood-
red elevations. Beneath the epicardium and endocardium of both auri-
cles and the endocardium of the left ventricle were extensive patches
of extravasated blood. Kidneys enlarged and congested throughout. ~
The lesions of the ileum, caecum, and colon in this animal were quite
as extensive as those of the case just described ; there were no ulcers
in the rectum, however. Those of the colon had black centers, point-
ing to a recent origin from blood extravasations on the surface of the
mucous membrane.

In the spleen of this case the characteristic bacteria of hog cholera
were exceedingly numerous, as determined by cover-glass preparations.
Two liquid cultures proved pure when tested on gelatine plates. In the
needle tracks of a tube culture in gelatine innumerable colonies ap-
peared in afew days. Inoculations into animals from subsequent eult-
ures proved equally positive.

Pig No. 156 was fed with the viscera of No. 159 February 18, and
after manifesting the usual symptoms of hog cholera, died “ebruary
25, seven days after feeding. Among the marked lesions produced by
the disease was a complete necrosis of the upper two thirds of the colon,
with scattered ulcers along the lower third. Eight feet of the lower
portion of the small intestine, beginning at the valve, was necrosed.
In the spleen there were numerous small grayish spots, probably cen-
ters of necrosis, as they showed no longer cell structure when crushed
on a slide and stained. The fundus of the stomach was also deeply
congested.

The spleen, to which organ the microscopic examination was limited,
contained the characteristic bacteria, asshown by cover-glass prepara-
tions. Three liquid cultures made from the same organ were found to be
pure cultures of the same microbe when tested by line cultures. <A tube
culture in gelatine developed in each needle-track numerous non-lique-
fying colonies.

In these animals the mode of introduction of the virus determined the
seat of the severest lesions. It is probable that the food passes quite
rapidly through the small intestine; that in the stomach the action of
the bacteria is more or less limited, because they have not sufficient
time to*multiply, and probably because hindered by the acid condition
of the organ, though they will multiply with considerable vigor in
slightly acid solutions. The prolonged stay of the food in the large in-
testine permits multiplication, and thereby causes the first and severest
lesions to-appear here. When these have become very extensive, soas
to paralyze the action of the large intestine, the ileum becomes involved
in a similar manner, possibly by a partial stoppage of the infectious
matter in this portion of the intestine.

It may therefore be said, in general, that the feeding of hog cholera
viscera produces lesions like those found in natural infection, only more

107

severe and more extensive. The duration of the malady is also much
shortened. The notes given above are quoted from one of the reports
of the Bureau. Since they were written numerous other pigs have been
fed in this way in the course of vaccination and other experiments with
precisely the same result. We must therefore emphatically deny the
truth of statements made now and then in agricultural journals that hog
cholera can not be communicated to healthy swine feeding upon the vis-
cera of those dead from this disease. Such statements are pernicious
in tendency, and aggravate the evil which this malady carries with it. *

(b) Feeding pure cultures of hog cholera bacilliimThe successful re-
production of this disease by feeding pure cultures of hog cholera bac-
teria proves not only that the bacteria fed are the true cause of the
disease, but also that infection may and does take place in this way.
We again quote from the report for 1886 some experiments which
demonstrate that swine may take the disease and die by simply swal-
lowing somewhat more than halfa pint of beef broth in which hog cholera
bacteria were growing.

December 13, 1886.—Three pigs were fed with 300 cubic centimeters

each (three. fifths of a pint) of a beef-infusion culture of hog cholera ba-
cilli kept in the thermostat, at 95° I., for three days. The culture was
contained in two flasks. When examined both were found pure. The
pigs were prepared for the feeding as follows: No. 348 received no food
for over twenty-four hours. A 2 per cent. solution of sodium carbonate
in beef infusion was then given to increase the alkalinity of the stomach.
Of this about 1 liter was consumed. It was then fed with 300 cubic cen-
timeters of culture liquid mixed with beef broth to make 1 liter. No.
350 was starved in the same way, but received no alkali before consum-
ing the culture. No. 342 was not deprived of food before eating the cult-
ure.

The result confirmed our anticipations. No. 348 showed signs of
disease in two days. On the third it was unable to rise, and died on
the same day. The post-mortem examination showed a considerable
congestion of the mucous membrane of the duodenum and jejunum, as
well as of the large intestine. The fundus of stomach affected in the
same way. The liver was gorged with blood, as well as the portal
system. There were no marked lesions of the other viscera. That hog
cholera bacilli had also entered the blood was shown by two pure cult-
ures in beef infusion obtained from the spleen. <A gelatine culture
from the liver contained about six or seven colonies.

No. 350 was a more typical case, and demonstrated the severe local
effects of the bacillus much better, since the animal lived longer. It
ate fairly well until the feurth day, when its appetite gave way and
diarrhea set in. From this time it grew weak and thin, being scarcely
able to walk. It died on the tenth day after feeding. The lesions of
the alimentary tract were exceedingly grave. Beginning with the
stomach, the mucous membrane was * dotted with closely set elevated
masses as large as split peas, and larger patches of a whitish viscid sub-
stance, made up entirely of cellular elements (diphtheritic ?). When
removed, a raw, depressed surface was exposed. ‘he membrane itself

*Tt may be possible that those who make this claim were confronted with swine
plague. This dise ase, although resembling hog cholera very closely in many features,
we have not been able to reproduce by feeding.

108

was pale. Besides a general injection of the ileum, Peyer’s patches were
more deeply con vested, and the uppermost covered witha thin, yellow-
ish film, not removable, and most likely dead epithelium. In the cx-
cum and colon the mucosa was superficially necrosed, and converted

into a continuous layer of a dirty whitish mass about 1™™ thick. The
walls of the intestine were greatly thickened and very friable.

Microscopic sections showed an extensive cellular infiltration of the
submucous connective tissue which had separated the masses of fat
cells, concealed the connective tissue fibers, and caused a great thick-
ening of the entire layer. The mucosa itself was greatly altered. The
surface was necrosed and converted into an amorphous mass. In some
places the necrosis involved the entire depth of the crypts of Lieber-
kiihn, a series of striae indicating their former existence. Those whose
epithelium still remained were plugged with a cylindrical mass, inclos-
ine broken-down nuclei. The bacteria had exerted their poisonous
effects from the surface of the mucosa towards the depths, destroying
the surface epithelium and glandular structures and involving second-
arily the submucous layer. Near the rectum this continuous mass of
dead tissue was replaced by isolated ulcers embedded in an intensely
reddened mucosa. The ileo-ceecal valve was much swollen, but the
necrosis did not extend into the ileum, although there were a few ulcers
near the valve, and the epithelium had a pale, Iusterless aspect, as if
dead. The liver was filled with blood, which readily clotted as 1t owed
from the cut surface. Spleen con gested and but slightly enlarged.
Lungs hypostatic. The lypmphatic g elands in general not much affected.
Two. liquid cultures from the blood were turbid next day, and contained
hog cholera bacillionly. In a gelatine tube culture from the liver about
a dozen colonies developed in each needle-track.

No. 342, which was fed with the same quantity of culture liquid, but
was not deprived of food previously, wassomewhatill on the following day.
It recovered, however, and continued apparently well for several weeks.
It began thereupon to grow thin and weak. On January 26 it was no
longer able to rise, and was therefore killed for examination, in order to
conclude the experiment. On opening the abdominal cavity it was at
once perceived that the animal had been suffering from a very intense
disease of the large intestine, a portion of which was firmly attached to
the bladder. When dissected out and slit open, the mucous membrane
of the ceeum and colon was found replaced by a brownish friable layer
of necrosed tissue. The wall of the intestine was infiltrated to such an
extent that it was nearly one-fourth inch thick, and socegenerated that
the forceps easily tore through it. The thickness of the walls pre-
vented the intestine from collapsing after it was opened. Its only con-
tents was a brownish liquid mass. The glands of the meso-colon were
very large, some like horse-chestnuts. On section the entire tissue was
very pale, almost white. Thespleen was somewhat enlarged ; the Mal-
pighian corpuscles unusually large and prominent on section. Lungs
and heart normal; kidneys deeply reddened throughout.

This case is very interesting in completing the information gained by
this feeding experiment. No. 348, which had been fed with sodium car-
bonate, besides being deprived of food, died three days after the ingest-
ion of the culture. No. 350, which was simply starved, died ten days
thereafter, while No. 42, which ate the culture without being previ-
ously starved, was dying on the thirty-fourth day.

These results show that infection may occur by way of the digestive
system, provided the destructive action of gastric digestion be pre-

109

vented, as was done by starving and by the use of an alkaline car-
bonate. )

They also indicate how purely local this destructive action may be.
Gelatine cultures from these animals showed that the internal organs
contained but very few bacteria. So few were they in fact that the
microscope alone could not have demonstrated their presence in the
spleen.

In addition to the cases given, equally positive results were obtained
at four different times by the feeding of pure cultures. Someof these
results have been mentioned in other places (see page 207 of the Report of
Bureau of Animal Industry for 1885). It was also found that small
quantities up to 100 cubic centimeters (2 pint) may be fed to most pigs
without obtaining any fatal results. Sometimes the fed animal becomes
very sick, but recovers; sometimes no disturbance whatever is pro-
duced. :

These ‘experiments prove conclusively the causal relation between
the bacilli of hog cholera and the disease so called. They show that
pigs fed with nothing but sterile beef infusion, to which the minutest
speck of growth from a hog cholera culture was added and in which the
bacilli thus introduced were allowed to multiply for one or more days,
were destroyed by a disease identical with hog cholera, but far more
rapid in its course and more severe in its manifestations.

SUBCUTANEOUS INOCULATION.

Subcutaneous inoculation with hog cholera bacilli from cultures is
successful in only a smail percentage of cases, except when these germs
are unusually virulent. In the report for 1885 several cases of success-
ful inoculation are given, among which the following deserve to be
briefly quoted:

November 27, 1885.—Two pigs (Nos. 112, 114) were inoculated sub-
cutaneously into the thigh with 5 cubic centimeters each of a pure liquid
culture. No. 114 died nine days after inoculation. The superficial ingui-
nal glands were swollen, with hemorrhagic points in medulla. Spleen en-
larged, dark. Extravasations on auricular appendages of heart. Lungs
edematous; bronehial glands enlarged, dark red throughout (hemor-
rhagic). Glands of abdomen in general hemorrhagic, except those of
mesentery ; petecchize under serosa of cecum. Kidneys with glomeruli
appearing as blood-red points, the entire organ congested. Mucosa of
fundus of stemach, lowest portion of ileum, and of the cecum and colon
deeply reddened with slight extravasation. Cover-glass preparations as
well as cultivations in gelatine and beef infusion revealed hog cholera
bacilli, and these only.

No. 112 died on the 15th day. Diarrhea appeared two days before
death. The lesions in this animal resembled those of No. 114, with the
following differences: Spleen very large, dark, friable. Kidneys less
congested. Lungs with minute hemorrhages throughout the paren-
chyma. Eechymoses beneath the endocardium of left ventricle. Lym.
Lage and digestive tract even more congested and hemorrhagic than
in No. 114.

110

The success of these inoculations among numerous failures in subse-
quent trials must be ascribed to the exceptionally virulent disease of
that year, for no cases have been observed since which died so sud-
denly and presented such severe hemorrhagic lesions of the various
vital organs.

The following experiments, made with blood taken from the heart of
swine affected with hog cholera and killed for the purpose, are taken
from the report for 1886:

September 10.—A pig dying with the disease was killed, the heart care-
fully exposed, and the blood drawn with a disinfected hypodermic
syringe. Nos. 329 and 333 received subcutaneously 5 cubic centimeters
each, one-half in each thigh. No. 329 ina few days lost its appetite, be-
came weak and stupid. Found dead October 5. Slight local swelling at
the points of inoculation; superficial inguinals greatly enlarged; hypo-
static congestion of lungs; complete necrosis of mucous membrane in
cecum; large scattered ulcers in colon, showing as whitish patches on
serous surface and encircled by a crown of enlarged blood vessels; bac-
teria in spleen.

No. 333. Slightly ill for a time; fully recovered; died December 2,
with no other lesions than engorgement of liver; no signs of former ul-
ceration.

A second experiment was made in the same way.

October 13.—Nos. 324 and 325 inoculated as in the preceding experi-
ment, 10 cubic centimeters of blood being used for each animal. No. 324
was found dead November 1, after being off feed for a time; deeply red-
dened skin over caudal half of abdomen; superficial lymphatics ex-
tremely large and serously infiltrated; on section, hemorrhagic points ;
at point of inoculation the connective tissue is infiltrated ; 50 to 75 eubie
centimeters clear amber serum in abdominal cavity ; papille of kidneys
deeply reddened; slight congestion, but no ulceration in large intestine;
lymphaties in general moderately tumefied and congested.

No. 325 found dead October 29; reddening of skin as in 324; ex-
travasation in connective tissue; spleen greatly enlarged, purplish ; _
lymphatics of thorax and abdomen purplish—enlarged; petecchia on—
section of kidney and pelvis, also over entire surface of epicardium ;
lung tissue mottled both on surface and on section with purple spots,
due to blood extravasation into alveoli, so that it scarcely floats ; mucous
and serous surface of small intestine dotted with petecchiz ; small hem-
orrhages on the surface of the mucous membrane and into the submu-
cous tissue of the eacum and upper colon; ulceration beginning.

On first thought we might be inclined to attribute these successful
results to a greater virulence of the germs in the injected blood. This
view needs further confirmation, however. The injected blood coagu-
lating in the connective tissue contains in it the bacteria, which are not
only protected from the aggression of cellular elements, but have actu-
ally a store of nourishment upon which they may live and multiply.
No such advantages are presented to bacteria suspended in liquids
which are readily absorbed, leaving them to the mercy of the tissues
surrounding them. ‘The local reaction in the above animals was very
insignificant compared with that produced by liquid cultures. In order

111

to come to any conclusion it would be desirable to add a few bacteria
from cultures to fresh blood, and observe the relative virulence by sub-
cutaneous inoculation. ,

Elsewhere in this volume will pe found a small number of successful
inoculations with pure liquid cultures among a large number of unsuc-
cessful ones. The inoculations were made for the purpose of determin-
ing whether they would confer immunity. In reading over these ex-
periments it will also be seen that such injections produce swellings
varying from the size of a pea to a hen’s egg. The tumor is developed
in the subeutis and consists of a yellowish white, tough tissue, breaking
down in the center into a grumous mass after a period of one or more
montks.

In view of these facts we can not consider wounds or bites anes
on the surface of the body a means of infection, excepting, perhaps,
epizootics of extreme virulence. Nor can we ascribe much Tee :
the stings of insects in inoculating the virus from one animal to another,
as this would correspond to subcutaneous inoculations on a minute
scale. Flies may, however, infect food in various ways, to be dwelt
upon in subsequent pages.

INTRA-VENOUS INOCULATION.

The injection of hog-cholera virus (from the spleen of a pig examined
near the city of Baltimore, Md.) into the circulation was tried but once,
and this trial was successful in producing a hemorrhagic septicemia
such as we frequently encounter in outbreaks of the disease, and which.
proved fatal in less than three days.

November 12, 1888.—Pig No. 90, black and white, about five months old.
The right er ural vein was exposed by raising a triangular flap of skin
over it after thoroughly disinfecting the latter with a one- fifth per cent.
solution of mercuric chloride. Five cubic centimeters of a beef infusion
peptone culture inoculated from an agar culture about a week old was
injected into the exposed vein with a hypodermic syringe thoroughly dis-
infected with 5 per cent. carbolic acid. The liquid culture was two days
old when used. Two hours after the inoculation the temperature had
risen from 1033 F. to 107°.. November 13 there was no swelling, but a
slight serous oozing at the place of inoculation. The appetite was good.
November 14, at 3) p.m., the temperature was 1073. The animal was

disinclined to move, although it came to eat in the. morning and even-
ing. November 15 it lay on its side quietly, with occasional kicking.
Found dead at 4 p.m. Autopsy held immediately.

General blush on skin of ventral aspect, snout, and lips. No swell-
ing at the point of inoculation; slight blood extravasation. Spleen en-
ormously enlarged, 14 inches long, 2 to 3 inches wide, and one-half
to 1 inch thick, 2 eorged with dark blood, and friable. Superficial in-
guinals enlar ced, edematous; on section diffuse pale red spots; cortex
congested, Bronchial and renal glands enlarged, partly hemorrhagic,
gastric elands hemorrhagic throughout substance. The blood is thick,
dark colored, coagulation slight, even after several hours’ exposure to
the air. Several ‘petecchie on epicardium of right auricle. Right side
of heart distended with blood; in it a small “white clot. Left side

112

contracted, empty. Lungs normal, excepting one-third of left ventral
lobe, which is collapsed. Kidneys enlarged, deeply congestcd through-
out. The surface is thickly dotted with minute deep red points. The
papille, so deeply reddened that any extravasations would be unrecog-
nizable. <A few petecchia in pelvis. Bladder contains about 30 grams
of urine tinged with blood. The whole mucosa of stomach is deeply
congested. In fandus it is hemorrhagic with numerous patches of nee-
rosed epithelium one-fourth to one-half inch across.

The upper 8 inches of duodenum in the same condition as the fundus
of stomach. Numerous red points scattered over mucosa of entire small
intestine. In lower ileum a few hemorrhagic points. The mucosa of
cecum and upper colon very slightly congested, but the remaining two-
thirds intensely so. Hemorrhage here and there sufficient to stain the
feces with blood which were otherwise normal. The mesenteric and
meso-coli¢ glands all deeply congested throughout their substance.

Cover-glass preparations from spleen pulp showed a large number of
hog cholera bacteria. Cultures from the same revealed the presence cf
the same organisms only.

INFECTION BY WAY OF THE LUNGS.

It has been maintained by some observers that infection may take
place through the lungs. Bacteria dried and carried about with the
dust are supposed to be deposited in the lung tissue by the inspired
air. It is of considerable importance to determine whether germs car-
ried by currents of wind can in this way produce an outbreak at a dis-
tanee. There are two questions involved which must be dealt with
separately in order to get as clear an idea as possible of this rather
perplexing subject. (1) Do bacteria of hog choleza when inhaled pro-
duce a disease which is similar to the disease described in these pages,
i. e., Without extensive lung lesions; and (2) do hog cholera bacteria pro-
duce a specific disease of the lungs when there deposited just as they
produce intestinal disease whenswallowed? The first question, whether
the lungs may be considered an entrance of the virus when in the dried
condition, is one for which not sufficient proof is at present forthcom.
ing. Several experiments have been made at the experiment station
to produce the disease by spraying pigs ina tight box with liquids con-
taining hog cholera bacteria and by injecting them suspended in liquids
into the trachea. In no instance was the disease produced. Several
times bacteria were injected through the walls of the thorax into the
pleural cavity and Jung tissue without any result, excepting in two in-
stances given on page 55. In one animal there was some pleuritis but no
pneumonia. On the other hand the large intestine in this animal was
severely diseased as in natural infection. In the other animal death
occurred seven menths after inoculation. The lung disease was most
likely the comb‘ned effect of lung worms and the mechanical injury re-
sulting from the inoculation.

If we must conclude, therefore, that animals are but rarely infected
through healthy lungs, it is still less likely that these bacilli produce
quite uniformly disease of the lungs, as has teen assumed by other ob-

113

servers without adequate proof. In the notes of the outbreak given on
page 54, this subject has been pretty thoroughly discussed in the light
of evidence furnished by bacteriological tests. The results there reached
inay be briefly summarized that lung disease or pneumonia of a severe
character is not often found in hog cholera. The slight broncho-pneu-
inonia frequently met with is most probably due to.catarrhal conditions
and to the aspiration of foreign bodies. There is, however, this very dts-
eased condition of the lungs which may favor infection through them.
When there are present foci of broncho-pneumonia, hog cholera bacteria
inhaled may lodge there, multiply in the secretion of the smaller bronchi,
and cause an extension of the disease not possible in healthy lungs.
From there they may be coughed up and swallowed, carried into the
large intestine, where they exert their most destructive activity. In
this sense the lungs may become the entrance of the virus, but only
when previously diseased. In the examination of such diseased lobules
of the lungs, in the outbreak referred to, hog cholera bacteria were found
in almost every case. In these cases it is difficult to decide whether
they entered the diseased lobule from without by way of the bronchi—
i. €., With the air inspired—or whetber they were deposited there by the
circulating blood.

The question of the relation of lung disease to hog cholera has been
complicated by the existence of an infectious pneumonia in swine, which
we have called swine plague. This disease, which will be treated of
in a special publication, appears over a large part of our country at
times in virulent epizootics. It is caused by a widely distributed septic
organism, and appears occasionally in swine suffering from hog cholera.
In a number of such cases both disease germs have been obtained from
the same animal.

We do not exclude infection through the lungs as improbable in hog
cholera, especially in epizootics characterized by more than usual viru-
lence. At the same time long experience at the experiment station has
shown that swine do not become infected in pens only a few hundred
feet away from pens full of sick and dying animals. Currents of air
can thus have but little power in distributing germs capable of inducing
the disease.

SOME OBSERVATIONS GN THE PATHOLOGICAL ACTION OF HOG-
CHOLERA BACTERIA.

We have frequently recurred to the fact that the intestinal tract seems
to suffer more or less exclusively in hog cholera. The changes there
produced belong chiefly to the necrotic and ulcerative type, combined
with a variable amount of neoplastic growth in the bottom of the ulcer.
In connection with this work it has been impossible to make any ex-
tended observations on the genesis of these ulcers owing to the exactions
of other work. Whatever may be suggested here must be regarded
simply in the light of inferences fron lesions as they were observid
post mortem.

15612 7 e——S8

114

The ulcers are produced in most cases by a process beginning at the
surface of the mucosa. This is shown very well by sections of ulcers
in which only a portion of the tubular glands have been necrosed.
What this process is must be left an open question. It seems very
probable that the bacilii invade the tubules and blood-vessels of the
mucosa, by their rapid multiplication plug the latter, and cause a coagu-
lation necrosis of the most superficial portion of the membrane. The
various bacteria present in the intestine then complete the breaking
down of the nembrane, and an ulcer is formed. Ulcers may, however,
be formed by bacteria carried thither by the blood, for ulcers are pres.
entin those animals upon which subcutaneous inoculation has been
practiced (p. 110). In these cases the plugs or infectious emboli are
situated probably in the submucosa. The resulting ulcer is deeper and
more extensive.

The formation of plugs or thrombi is coniirmed by inoculations in
rabbits (p. 69). The process of coagulation necrosis, as the result of
plugs in the capillaries of the liver, may be seen in almost every case,
Microscopic examination likewise reveals their growth in masses in the
internal organs.

The nature of the hemorrhagic lesions so frequently observed in hog
cholera demands some attention. The rupture of minute and some-
times larger blood vessels is no doubt due to the same process of throm-
bosis and embolism in which the thrombi and emboli may be made up
more or less entirely of bacteria, Whether these plugs have a directly
destructive action (necrosis) upon the delicate vascular wall so as to
produce rupture and extravasation, as has been suggested in former
reports, or whether the action is merely mechanical, or whether both
causes are at work, it would be impossible to say. At all events these
hemorrhages are frequently the precursors of ulcers in the intestine,
and in some cases the only lesions which were observed were hemor-
rhages from large and small vessels. We may picture to ourselves the
process, beginning, in most cases, with local ulceration in the large in-
testine (cecum). The bacilli may be carried thence through injured
vessels into other parts of the body, and to other portions of the in-
testine, where fresh ulcers may appear; or the bacilli may be carried
onward from the first uleers to portions of the intestine lower down,
where they again attack the mucous membrane.

In many cases the quantity of virus introduced into the digestive
tract is so great—as when pure cultures of hog cholera bacilli are fed—
that destruction of the mucous membrane goes on at the same time
throughout the cecum and colon, becoming less severe as the rectum is
approached. The paralysis of the large intestine may cause extensive
necrosis of the ileum. In these eases the action of the bacilli is purely
superficial at first, penetrating deeper and finally reducing the entire
wall to a friable mass, greatly swollen by the infiltration of leucocytes.
fn such feeding experiments we may also observe grades of lesions ag

115

we go away from the valve in the ileum and in the colon, Instead of
the conversion of the mucosa into a thickened, discolored, and roughened
membrane, ab amorphous, dirty grayish exudate may be found on it.
The destruction, going on very slowly, causes a reactive inflammation,
manifested by the exudate.

The genesis of the intestinal lesions in the rabbit i is somewhat differ-
ent. They appear quite late in the disease as a result of the discharge
of bacilli from the necrotic foci of the liver tissue into the bile duct.
They are limited to the duodenum and large intestine, and are especially
severe in the latter, forming there peculiar hwematomata or blood tu-
mors, accompanied with a fibrinous exudate. The same lesions are
obtained by feeding cultures. In view of this localization in the rabbit
and pig we must admit that hog-cholera bacilli exert their primary
action where they are retained for a considerable time by the feces.
and thus have an opportunity of multiplying before they attack the
mucous membrane.

The size of the spleen, sometimes enormous, seems to stand in no
direct relation to the number of bacilli present. Sometimes a very
highly corgested spleen harbors only the average number of germs.

The presence of hog cholera bacilli in the lung lesions met with in a
small percentage of cases has already been dwelt upon (p. 54). The
lesions themselves show nothing characteristic. They are usually re
stricted to the most dependent lobe, the ventral on one or both sides,
and to the writer they simply indicate a proneness of catarrhal inflaum-
mation in young pigs, due, no doubt, to the aspiration of food and dirt,
consequent occlusion of bronchi, atelectasis, and broncho pneumonia.
The hog cholera bacilli which may be found here in most cases are present
for the same reason that they are found in the spleen. Circulating in
the blood, they find the contents of the diseased and plugged air tubes
and alveoli a very suitable inedium for multiplication. In this way they
may add to the irritation and cause extension of the disease.

Itseems pretty certain that the chief damage done by hog cholera bacilli
lies in their power to grow in plugs in the small vessels. The simple
reason why we have such severe lesions in the intestinal tract, although
the bacilli are present in small numbers in the internal organs also, lies
in the anatomical nature of mucous membranes in general and their
exposed situation with reference to putrefactive processes.

If the obscure action of these bacilli on cells and cell-life could be
formulated at all, in the present state of our knowledge the writer
would assume: 1. That they exercise a more mechanical influence by
thrombosis, which leads, in the mucous membranes, to circumscribed
necrosis. Death occurs not by the direct poisonous action of ptomaines,
but from secondary causes, such as changes in the liver, septic infec.
tion. 2. Inacnte cases the bacilli possess a greater power of invading
the circulation. There they multiply rapidly enough to cause rupture
of blood vessels in all the vital organs. Death may occur in these cases

116

by a ptomaine poisoning of the nerve centers due to the large number
of bacilli in the blood, or the loss of so much blood drawn from the
circulation, or, what is more probable, by hemorrhages in the substance
of the central nervoussystem. Whether this greater ability to invade
the vital organs depends upon the production of a more poisonous: pto-
maine, which paralyzes opposing forces, or to other physiological prop-
erties, belongs to the future for solution.

Concerning the variation in the destructive nature of hog cholera
bacilli little that is positive can be said. We have observed, for instance,
that the disease dies out after a time in a herd, very frequently because
there are no more animals left, or because the few that have survived
have been exposed in such a way as to acquire immunity. But it has
also been observed at the experiment station that the disease may dis-
appear, even when fresh animals are exposed to it from time to time.

The decline in virulence may be <lue to the particular season with its

frosts or droughts, and other meteorological changes, or it may be due

to a gradual weakening of the virus as it passes through the system of

the exposed swine. We have observed several times that when a series
of animals are fed with infected viscera, each from the one preceding it,
the earlier ones of the series will develop the most severe disease. The
later ones are affected by a more chronic malady, and finally a pointis
reached when no disease is produced. In such ar experiment self-inoe-
ulation or vaccination must be eliminated, as the animals are not exposed
previous to the feeding. But aside from this gradual dying out of par-
ticular epizootics, we have noticed a difference in the outbreaks them-
selves from year to year. In some the acute, hemorrhagic type would
prevail, in others a more chronic ulcerative type. Such differences are
most likely due to modifications of the disease germ itself, although here
also it is difficult to eliminate differences in the animals due to race,
feeding, cleanliness, ete., and differences due to the time of the year.
As regards the manifestation of differences in the bacteria themselves
none can be formulated.

BACTERIOLOGICAL INVESTIGATIONS OF HOG CHOLERA IN NEBRASKA,
ILLINOIS, AND MARYLAND.

The facts which have been gathered concerning the bacillus of hog
cholera were obtained chiefly from epizootics occurring in the District
of Columbia. The advantages of a bacteriological laboratory con-
nected with the Bureau made investigations possible which could not
be made in the field. It. was, however, necessary to confirm the results
already obtained by investigations elsewhere. These have led to the
discovery of the same bacillus in Nebraska and subsequently in Ili-
nois, thus identifying the disease in widely-separated localities.

Nebraska.—In March, 1886, the bacillus of hog cholera was isolated
from one of ten spleens sent from Kansas and Nebraska. Though care-
fully removed by the inspector and placed in sterilized bottles plugged

ee

117

with cotton wool, none came in good condition, owing to the long delay
on the road. Small bits of spleen were placed under the skin of a num-
ber of mice. Two which had been inoculated from the same spleen
died of hog cholera. These experiments are reported in full in the Third
Annual Report of the Bureau, and therefore need only to be summarized
in this place. The bacillus obtained in a pure condition from these mice
was carefully tested upon other mice, upon rabbits, and upon pigeons.
The pathogenic effect was the same as that of the bacillus from eastern
outbreaks. It was, however, readily observed that the Nebraska ba-
cillus was less virulent, as it did not kill guinea pigs. A number of
inoculation and feeding experiments were made upon pigs in order to
produce the disease. All but two failed to show any disease. These
two, fed with liquid cultures, were made ill, and one very sick was killed
on the ninth day after feeding. The large intestine showed intense
congestion, vith a few patches of adiptheritic membrane in the cecum.
No bacteria were obtained in cultures from the internal organs. This
experiment, which was not very satisfactory, was repeated by feeding
a larger quantity of culture liquid. The result was entirely satisfactory,
as the following description of the experiment will show. Moreover,
the feeding took place nearly nine months after the microbe had been
obtained originally from the spleen. During this time it had been cul-
tivated in various media, passed through mice and rabbits, so that no
trace of any spleen substance or foreign material could have been pres-
ent in the culture liquid which was fed. The result also indicates that
the pathogenic power of the bacillus was in great part retained during
this time.

A flask containing between 500 and 600 cubic centimeters of sterile
beef infusion was inoculated from a culture (rabbit), and after standing
six days in the incubator the entire amount was given to a pig which
had not been fed for thirty six hours. The culture liquid was covered
with a thin membrane, and on microscopic examination contained only
the motile bacillus. The animal became dull and weak, eating little.
The bowels were loose on the fourth day. On the fifth it was unable
to rise, and on the sixth it was found dead. The autopsy notes are
briefly as follows:

In the abdominal cavity several hundred cubic centimeters of a red-
dish serum, a thin translucent exudate covering the peritoneum of the
intestine, which is diffusely reddened. Between the layers of the mesen-
tery, along the line of attachment to small intestine, an abundant trans-
lucent gelatinous exudate. Spleen very dark on section; the surface
dotted with elevated points of extravasated blood. Liver congested.
Lungs normal, with exception of a few lobules, which are simply col-
lapsed.

Almost the entire digestive tract was found involved. Around the
cardiac orifice of the stomach a zone of mucous membrane about 2
inches in width was covered with whitish diphtheritic patches. Isolated

118

ulcers in duodenum. Abont 6 or 7 feet of the lower portion of the
small intestine very much thickened, the mucous membrane covered
with a thin sheet of necrosed tissue, whitish, brittle. The caecum and
portion of the colon greatly thickened and covered with a thick layer
of necrosed tissue very rough and brownish. Near rectum necrosis
gives way to closely set, isolated, roundish diphtheritic elevations of a
whitish color, which leave a raw surface when scraped away.

These lesions were, therefore, as intense as any produced by feeding
pure cultures of hog cholera bacteria obtained from the East. The spe-
cific identity of the two bacteria from Nebraska and the East was thus
completely established.

In the liver and spleen the bacteria were few, for a cover-glass prep-
aration from eachorgan did not show any after some searching. Liquid
cultures from the blood (heart), spleen, and liver were turbid on the
following day, and all contained the motile bacillus. Within four days
complete membranes had formed on the surface. That the bacteria
were very few in blood from the heart was indicated by a gelatine tube
which had been inoculated several times with a platinum wire dipped in
blood; no colonies were visible on the fourth day. Of three liquid
cultures, each inoculated with a loop of blood, tworemained sterile. It
was presumed that the liver would contain the largest number, inas-
much as the portal circulation received its blood from the seat of the
disease. This assumption was confirmed by the very abundant colonies
surrounding a piece of liver tissue which had been dropped into a tube
of nutrient gelatine.

In order to make certain of the pathogenic powers of he cultures
obtained from this case of feeding the tube culture from the liver was
used to infect two rabbits. The skin on the inner aspect of one thigh
was carefully shorn and disinfected with .1 per cent. corrosive sublimate.
An incision was made through the skin, and witha loop dipped in the
surface growth of the culture a minute quantity was introduced into this
pocket. The larger of the two rabbits was found dead on the fifth
day. The lesions were briefly as follows:

Slight amount of pus at the place of inoculation. Neighboring ingui-
nal glands enlarged and infiltrated with blood. Surrounding vessels
much injected and very tortuous. Liver very friable, spleen dark and
enlarged; both dotted with points and stellate spots of coagulation
necrosis, especially numerous on the caudal surface of the liver. Both
organs contained the bacteria of hog cholerain large numbers. Lungs
hypostatic. A small number of ecchymoses beneath pleura; very few
bacteria in kidneys and heart’s blood.

The second rabbit was found dead on the sixth day. The lesions
were the same, if we except the more pronounced coagulation-necro-
sis in the liver and its absence in the spleen. The bacteria of hog
cholera were distributed as above; very abundant in spleen and liver ;
lungs normal.

Gelatine tube cultures from spleen and liver of these rabbits confirmed
the microscopic examination. Liquid cultures from the blood contained

119

the motile bacteria, which had formed a brittle surface membrane on
the second day.

Differential characters of the hog cholera bacillus from Nebraska.—The
bacillus when stained on cover-glass preparations from the spleen and
other viscera, closely resembles the one found in the disease prevalent
in the East, so that it is impossible to distinguish them in this way.

A few minor differences revealed in the various culture media indi-
cated, however, that the two microbes were not alike in every way, and
brought up the very interesting question of the variation of species
of bacteria and the influence of such variation on the severity of epi-
demics.

The most noteworthy difference was observed in liquid cultures.
Within twenty-four hours after inoculation from the spleen or blood the
culture liquid became turbid, and upon its surface a complete membrane
was present in nearly every case. This whitish membrane is not homo-
geneous, but made up of patches of varying thickness, and when shaken
slowly settles to the bottom in Jumps and floceuli. The microbe of
Eastern outbreaks does not form a membrane within several days after
inoculation, and then only when the tube remains perfectly quiet. It
appears as a whitish ring attached to the glass.

In other respects the two microbes differed so little that no mention
need be made of these differences here. We have, therefore, only the
membrane ‘on liquid cultures and a slightly diminished virulence, by
which the bacilli from Nebraska were distinguishable from those ob-
tained from Eastern epizootics. Both of these characters are variable
ones. The membrane can be produced in part by cultivating the East-
ern germ for a long time at a high temperature. The variation in vir-
ulence is observable during the course of alinost every epizootic.

Illinois.—From the spleen of an animal affected with hog cholera the
specific bacillus was obtained during some investigations conducted in
this State in the summer of 1886. The bacillus presented no differnces
whatever from the one obtained in Eastern outbreaks. Its effect upon
rabbits asd mice was precisely the same. Its fatal effects when fed to
a pig is well illustrated by the following experiment:

A pig was kept without food for over twenty-four hours. A 24 per
cent. solution of sodium carbonate in meat broth was then given to
it. Ofthis itconsumed about one liter, taking thus about25 grams of the
salt. It was then fed with about50 cubic centimeters of gelatinecultures
and 100 cubic centimeters of liquid cultures of the hog cholera bacillus
obtained from rabbits which had succumbed to inoculation and from the
original gelatine culture of the spleen made in Champaign County,
Ill. The animal was found dead December 4, scarcely three days af-
ter feeding. This was the briefest period of illness thus far observed.
The lesions were very pronounced. Pyramids of kidneys deep red
throughout; glomeruli visible as dark points. Lungs pale, not fully
collapsed. Right heart filled with semi-coagulated blood. Liver gorged
with blood. Mucosa of stomach intensely reddened, especially along

fundus, and covered with a thick layer of tenacious mucus. Mucous
membrane of ileum similarly affected. Peyev’s patches exceedingly

120

dark red, showing through serous coat. When viewed from the mu-
cous surface the elevated border gives each a slightly concave boat-
shaped appearance. The colon also deeply congested, almost hemor-
rhagic in patches, filled with a small quantity of semi-liquid feces. The
rectum still filled with consistent masses. The mesenteric glands con-
gested.

The feeding had thus produced a very severe inflammation of the
digestive tract. The diagnosis was further confirmed by obtaining pure
liquid cultures from the spleen, the liver, and blood from the heart. The
bacteria were not sufficiently numerous in these organs to be detected
by the microscope. To make sure that the carbonate of soda had no
corrosive effect, another animal was treated precisely in the same way
by starving and feeding a solution of the salt. No ill effects whatever
- were manifested.

Inorder to test the specific pathogenic character ofthe bacillus obtained
from thisanimal a largerabbit was inoculated subcutaneously with about
one-eight cubic centimeters of a liquid culture from the blood. On the
sixth day the rabbit was lying on its side; abdominal breathing very
jabored. It-was found dead on the next day. Slight thickening of the
subcutaneous tissue and fascia covering the thigh muscles at the point
of inoculation. The muscular tissue covered with minute eechymoses
around the infiltrated patch. Small quantity of serum in the peritoneal
cavity. Spleen very large, blackish, exceedingly friable, and crowded
with bacteria. Liver enlarged; interlobular tissue pale;-the entire
parenchyma very soft and brittle. Dotting both surfaces of all the
lobes are small, grayish-white patches, involving one, two, or three,
rarely more, acini, and bounded very sharply by the acini themselves.
Peculiar figures are thus formed, three contiguous ones giving the
patch a clover: leaf appearance. On section they are found to extend
to the depth of one or several acini into the parenchyma. The great ma-
jority of these masses of coagulation-necrosis involve lobules on or near
the surface. Only a few are in the depths of the organ. When sucha
whitish mags is spread on a cover- glass and stained innumerable bac-
teria of hog cholera make their appearance. The rest of the tissue is
likewise crowded with them. Beneath the pulmonary pleura are large
purplish patches of extravasation, which on section extend deeply into
the parenchyma. The lung tissue isin general congested. Blood from
the beart contained very few bacteria. No cultures were made.

Maryland.—During September and October, 1888, an epizootic of hog
cholera was started at the experiment station by a sick pig brought
from near the city of Baltimore, Md. The hog cholera bacillus had been
previously obtained from the spleens of two animals killed at Balti-
more. At least twenty, which had been either simply exposed in pens
or fed with the viscera of dead animals, succumbed to the disease. In
all cases pure cultures of the specific bacillus were obtained directly
from the spleen. Its effect upon rabbits and mice, its appearance and
mode of growth, did not differ from the bacillus as described in the fore-
going pages.

RELATION OF HOG CHOLERA TO THE PUBLIC HEALTH.

The importance of knowing whether or not certain infectious animal
diseases have any deleterious influence upon human health, or are.the

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121

direct cause of human disease, is not even second to the economic im-
portance attaching to animal diseases. ‘There are some animal diseases,
such as glanders, tuberculosis, anthrax, and rabies, which are directly
communicable to man. This transmissibility was known before the
specific bacterial organisms of these diseases had been discovered.
There are other animal diseases not proved to be transmissible to man,
whose causes have only been definitely recognized within the past few
years. As regards these it is quite pertinent to ask, in the light of
present knowledge, whether they have any relation to human diseases.
Animal diseases when communicated to man may become so changed in
character as to be unrecognizable. Hence we must determine whether
the specific micro organisms of animal diseases are found in human dis-
eases or not; in other words, whether the causes are identical. During
the course of these investigations this problem has been constantly
borne in mind. The question to be settled first has reference to the
presence of hog cholera bacilli in human diseases. There are two mala-
dies of mankind which resemble hog cholera in many respects—typhoid
fever and dysentery.

Typhoid fever is an infectious disease of man, prevalent throughout
the civilized world, while hog cholera is known to exist only in North
America and the British Isles, and during last year it has been identi-
fied on the continent of Rurope. Hence there could be no clese relation-
ship between the two diseases, for they would naturally occur together
if they were identical. But there is another reason for their non-iden-
tity; the micro-organisms which produce them are different. Tbus the
typhoid fever bacillus is a longer rod than the hog cholera bacillus, its
movement in liquids is more sluggish and of a somewhat different char.
acter. Its growth on boiled potato is almost peculiar to itself. More-
over, it has no pathogenic effect upon any animal thus far tried, and
we know that the hog cholera bacillus is fatal to mice, rabbits, guinea.
pigs, and pigeons after subcutaneous inoculation, and to pigs when fed
to them. Hence there remains not the shadow of a doubt that genuine
typhoid fever and hog cholera are distinct diseases.

They do, however, belong to the same general class of infectious
diseases. In both, infection very likely occurs chiefly through the food
and drink. In both the lesions are ulcerative in character, located in
the pig in the upper portion of the large intestine, in man in the lower
portion of the small intestine. It is true the ulceration may be the
secondary stage of processes primarily different anatomically speaking,
but we know as yet too little of the relative effect of irritants of the
same kind, but of different intensity, to venture any positive statement.
In both diseases the invasion of internal organs by the specific micro-or-
ganisms takes place, so that they are readily obtained from the spleen.
In both they appear in clumps or colonies in the capillaries. There is
also a general resemblance of the two organisms, both as regards their
appearance, motility and growth in various media when we compare

122

them with the bacteria of other infectious diseases in man and animals.
We may therefore conclude that although these two diseases are en-
tirely distinct there exists a close relationship between them as to the
cause, the manner of infection, and the type of disease.

Hog cholera is allied to the disease or group of diseases known as
dysentery even more closely than to typhoid fever. It resembles, per-
haps, most nearly that form called epidemic dysentery. Of the causes of
this disease very little is known. That the epidemic type is caused by
micro-organisms of some kind is now generally accepted, and it is also
believed that there may be several distinct species of micro-organisms
which are capable of producing diphtheritic and ulcerative lesions of
the large intestine.* Anatomically hog cholera and diphtheritie dys-
entery are very much alike. The question whether hog cholera virus
can ever produce a dysenteric affection in man is not answered until we
have learnt more of the causes of tie latter disease.

The danger, if any there be, of causing disease in man would only oc-
eur upon farms where the opportunity is afforded for infection of food
and water by the discharge of diseased pigs. The preparation of pork
by cooking is sufficient to destroy the bacilli if by any chance the flesh
of diseased animals should get into the market. Experiments have
shown that a temperature of 140° I. is sufficient for their certain de-
struction. The temperature reached in boiling, roasting, etc., is of
course much higher than this.

In addition. to these conclusions, which follow from the facts devel-
oped by our experiments, it may be said that with the thousands of
post-mortem examinations made by ourselves and other investigators,
there has not been a single case where the operator became infected.
In several instances it has been recorded that fresh wounds upon the
hands have been covered with virulent material during the examinations
without producing any appreciable effect. And through all the years
that this disease has prevailed so extensively in the United States there
has not been a case reported where it has been shown on good evidence
to have been transmitted to the human species.

Notwithstanding these facts, however, we should expect, with the
prevailing carelessness in disposing of the carcasses of swine in many
sections during such outbreaks, that there would be a more or less
deleterious effect upon human health, not from the specific nature of
the disease, but from the decomposing organic matter. ‘Too often these
careasses are left to putrety near dwellings, or are thrown into streams
to contaminate them with decomposition products. Such practices are
dangerous to the health of the community and should be prevented by
the local sanitary officers.

* Investigations of the Egyptian dysentery by Koch and Kartulis have shown that
the cause is an organism belonging not to the class of bacteria, but to the protozoa,
and assuming the form of anameba. This is found in large numbers in the ulcerated
walls of the intestine.

PREVENTION OF HOG CHOLERA.

ISOLATION, DISINFECTION, AND CLEANLINESS AS PREVENTIVE MEAS-
URES.

It is frequently necessary to apply preventive measures before intec-
tious diseases have actually appeared in a herd. The disease may have
appeared on a neighboring farm, and the problem then arises: How can
the infection be prevented from spreading to other farms? How can
the surrounding farms keep the malady from their premises ?

The sources and channels of infection are as follows, the most common
and important being placed first :

(a) Pigs purchased from infected herds, or coming in contact with those
Srom infected farms, or running over grounds occupied by diseased sicine
within two or three months.

(b) Infected streams may communicate the disease to herds below the
source of infection.

(c) Virus may be carried in feed, implements, and on the feet and cloth-
ing of persons from infected herds and premises.

(d) Winds, insects, birds (particularly buzzards), and various animals
may transport hog cholera virus.

(a) In regard to a, it may be said that no pigs should be purchased
from any locality until one year after the death of the last case of chol-
era. There are frequently near the end of an epizootic chronic cases
which may live for three or four months without showing any distine-
tive signs of disease until they suddenly die. The post-mortem exam-
ination usually reveals extensive ulceration of the large intestine.
The disease may thus linger in a herd long after all danger has appar-
ently subsided. By bringing any chronic cases in contact with hitherto
unexposed healthy swine the disease may spring up anew, as a dying fire
would when supplied with fresh fuel. Although our experiments have
shown that the disease germs may all disappear from the soil in three or
four months, the uncertainty of knowing whether there are any chronic
cases continually adding fresh virus to the soil makes the period of one
year not too long to avoid the introduction of unexposed pigs. It is
advisable, in districts where hog cholera is very prevalent and is rarely
absent for any length of time, for farmers to raise their own pigs and
not trust to any animals from outside. In this way infection may
be at least in part kept under control. When animals have been ob-
tained from places which are not above suspicion they should not be
brought in contact with swine already on the place, but quarantined as

123

124

far as possible from them and kept under careful observation for at
least one mouth.

(b) Perhaps the most potent agents in the distribution of hog cholera
are streams. They may become infected with the specific germs when
sick animals are permitted to go into them or when dead animals or
any part of them are thrown into the water. They may even multiply
when the water is contaminated with fecal discharges or other organic
matter. LExperiments in the laboratory (p. 76) have demonstrated that
hog cholera bacilli may remain alive in water for four months. Making
all due allowance for external influences and competition with other
bacteria in natural waters, we are forced to assume that they may live
at least a month in streams. This would be time enough to infect every
herd along its course.

(c) Hog cholera germs are not immediately destroyed by drying.
Laboratory experiments show that they may retain their vitality from
two to four months. Hence it is not difficult to see how a person walk-
ing on infected ground and among infected animals may earry on his
shoes and clothing dried germs of the disease to any neighboring herd.
For the same reason hog cholera germs may be carried from infected
grounds to others by feed, and by farming implements which have come
in contact with infected ground.

(a) There is no reason to suppose that currents of air have much in-
fluence in spreading the disease. Observations at the experiment sta-
tion of the Bureau have left no doubt that healthy pigs may be kept on
the same farm with diseased ones without becoming infected, provided
the infection is not carried in feed and implements, or on the shoes and
clothing of persons from the sick to the heatthy. Moreover the disease
is an intestinal malady, and all evidence points to infection through
the food rather than through the air inspired.

The agency of flies and other insects is perhaps equally limited when
infection is to be carried from one place to another. Our experiments
show very well that the sting or bite of an insect is not sufficient to pro-
duce the disease. It is possible, however, that they may carry the
virus from one place to another in the same yard. This will be dis-
cussed more fully under another head.

The agency of buzzards in distributing the disease in the Southern
States seems probable, although there is no positive proof. These birds
will readily consume carcasses of dead swine. If the hog cholera germs
are not destroyed by digestion it is reasonable to assume that the feces
contain the living germs, which may cause the disease to break out at
some distant place. Of course, the remedy would be to immediately
destroy or bury dead animals.

There is some reason to believe that rats, dogs, and perhaps other
small animals may carry the germs upon their feet or in their hair and
thus infect premises. It is probable that the contagion is only rarely
transported in this manner, but there are outbreaks the origin of which

125

it is difficult to explain otherwise. We may readily conceive, bear-
ing in mind the facts enumerated above, how such animals: might be-
come contaminated with moist, semi-liquid, or liquid matters containing
the germs, and that these substances drying upon the feet or hair would
adhere for a considerable time. If an animal thus infected should go
into uninfected lots occupied by swine and deposit there the smallest
particle of the germ-containing material, either in liquids standing in
the feeding troughs or in moist organic matters suitable for the multi-
plication of the microbes, an outbreak of the greatest virulence might
be setup. The number of conditions which must coincide for the spread
of the disease in this way probably accounts for the comparative rare-
ness of this kind of infection.

Granted, then, no communication between infected and uninfected
farms, there still remains the danger of infected water-courses, upon
which it is impossible to lay too much emphasis. In facet, if the disease
exists anywhere along a stream all farms below that point are liable to
infection unless use of the waterin any form whatever is given up dur-
ing the season.

By paying particular attention to these points, there is no doubt that
the disease can be warded off, even when in the immediate neighbor-
hood. Hog cholera is analogous to typhoid fever, dysentery, and Asiatic
cholera in man in many particulars, and there is a quite unanimous
opinion that these diseases are most ccmmonly transmitted through
drinking water. The same may be predicated of hog cholera, and the
mysterious spreadof this plague will no doubt frequently be understood
by examining the water courses.

When the disease is in the neighborhood it has been customary with
some to feed swine on some so-called ‘‘ preventive” medicine. These
are frequently prepared or invented by individuals who have little, if
any, knowledge of the action of medicines. The outcome is that the
animals fed with these unknown compounds are not only not benefited,
but their vitality is actually reduced, and when the disease appears it
destroys the weakened animals much more easily. The writer has made
post-mortem examinations of several animals in the West where such
preliminary treatment was going on, and the peculiar changes of the
internal organs, not like any known disease, could only be referred to
the action of such preparations. It must be remembered that there are
few medicines which are not injurious or poisonous in large doses:
They should not be used thus excepting under special conditions, and
only given as recommended by those who have been trained to know
the peculiar value and effect of drugs.

The condition of the animals themselves is of great importance in
favoring ur preventing infection. When pigs are fed with liquids in
which the specific bacilli only are present, those that have been de-
prived of food for some time previous take the disease, while those
hose stomachs contain food that is undergoing digestion do not take it

126

readily. If, besides starving the animals, they are fed with some alka-
line solution, by which the alkalinity of the stomach is inereased, the pa-
thogenic effect is still more pronounced. Any disorder of digestion by
which the secretion of gastric juice is diminished or checked and the
mucus is increased in quantity will increase the susceptibility of the
animal to infection, because the alkalinity of the mucus will favor
rather than destroy the virus. Any mode of feeding which produces
constipation and over-distension of the large intestine is likely to favor
the disease, as the virus is retained fora longer time. During epizootics,
therefore, besides the preventive measures suggested, the animals
should be carefully fed upon food which tends to keep the bowels open
and the feces soft, and which does not interfere with normal digestion.

When there is a suspicion that a herd has been infected, although
the disease has not yet appeared, disinfection, and all the rules laid
down below (p. 130) should be carried out with great care, as if the dis-
ease were actually present.

When hog cholera has appeared in a herd or on a farm, precautions
should be taken for two reasons: (1) To prevent the virus from being
carried to other farms and infect other herds. (2) To prevent’ the loss
of the entire herd, or, if this is not possible, to stamp out the disease in
such a way that the ground shall not infect healthy animals subse-
quently.

The rules under the first head should be prescribed by law to protect
property from the consequences of the carelessness or the willfulness
of those who refuse to take proper precautions. They may be summar-
ized as follows:

(a) The dead animals should be immediately disposed of, either by burial
or by burning, or if they are taken to some rendering establishment their
transportation should be governed by well-defined rules which will prevent
the dissemination of virus on roads, in wagons, ears, etc.

(b) Streams should be curefully protected from pollution.

(c) No animals should be removed from any infeeted herd or locality to
another free from the disease for at least six months after the last case of
disease.

(a) The proper disposal of dead animals is a matter of great impor-
tance, for the bodies not only contain the germs of the disease, but the
latter will multiply enormously during summer heat in the internal or-
gans after life has been extinguished. Each dead body must therefore
be regarded as a focus of the disease unless properly disposed of. It
may be buried. In such case it must be so deep that no animal can get
at it. Itshould be covered by a layer of powdered or slaked lime sev-
eral inches thick, and the ground over the body likewise sprinkled with
a thin layer of the same. If the carcasses are burnt, care should be
taken that any parts not consumed are buried as directed. If they are
earried away some distance to rendering establishments, at best a dan-
gerous pocedure, employés of such establishinents should be compelled

127

to wrap around the carcasses impervious cloths wetted with a 2 per cent.
solution of earbolic acid, so as to protect the roads from the virnlent
drippings.

(b) The danger from infected streams has already been mentioned at
length. These must be protected by law in sucha way that no sick ani.
mals should be allowed to go near them, and that no careasses be thrown
into them or deposited where drainage may carry the virus from tbe
body into the water. Nor should the drainage from pens be permitted
to flow into them,

(c) Hogs are frequently affected with cholera of a mild form, which
lasts for several months before some form of septic infection or degen-
erative changes in the internal organs produce death; hence it is im-
portant to insist upon knowing when the last case of disease occurred.
Since it has been demonstrated that hog cholera germs may remain
alive in the soil from three to four months, this rule will not appear un-
reasonable as a safeguard.

These rules will be sufficient, if properly executed, to confine the
disease within narrow limits. There is no doubt that hog cholera virus
dies out over the greater part of our country after epizootics have swept
over it. We have no reason to believe that it ean survive in the soil
from one end of the year to the other. It is, in fact, highly probable
that it is transported and distributed from afew places where, for some
reason, cases have occurred throughout the year and have thus kept
the virus alive. There are no experiments on record which show that
the hog cholera germ may be found in the soil and water independent
of the disease. It has been looked for, but has never been found, ex-
cepting in the body or discharges of diseased swine.

In view of the fact that the disease can be kept under control, the
legislatures of those States which suffer most severely from this plague
should take steps to enact rules similar to those formulated above.
The States of Kansas and Nebraska have on their statute-books laws
of this character, which read as follows:

AN ACT to prevent the spread of disease among swine.

Be it enacted by the legislature of the State of Kansas, It is hereby made the duty of
every person who owns or who has the control of any hog that has died of any dis-
ease to bury or burn the same within twenty-four hours after such hog has died, and
any person who knowingly fails or refuses to comply with the provisions of this sec-
tion shall be deemed guilty of a misdemeanor, and upon conviction thereof shall be
fined not exceeding one hundred dollars.

Src. 2. Whoever shall knowingly barter or sell any hog afflicted with any disease
without giving full information concerning said disease shall be deemed guilty of a
misdemeanor, and upon conviction thereof shall be fined not exceeding one hundred
dollars.

Sec. 3. Whoever shall knowingly barter or sell any hog which has died of any dis-
ease shall be deemed guilty of a misdemeanor, and upon conviction thereof shall be
fined not exceeding one hundred dollars.

Src. 4. Whoever shall throw or deposit a dead hog in any river, stream, creek, or
ravine shall be deemed guilty of a misdemeanor, and upon conviction thereof shall
de fined not exceeding one hundred dollars.

128

AN ACT to prevent the spread of hog cholera and other kindred diseases, and prevent traffic in an-
imals dying from infectious or other diseases.

Be it enacted by the legislature of the Slate of Nebraska, That it shall be the duty of
the owners of swine or other domestic animals dying from cholera or other diseases,
within twenty-four hours after their death, to cause the carcasses of such animals to
be suitably buried or burned up on the premises owned or occupied by such person.

Src. 2. If the owner of any swine or other domestic animals dying from cholera or
other disease, or any other person, shall sell or dispose of the carcass of such swine or
other domestic animals, to any person for the purpose of manufacturing the same into
soap or rendering the same into lard, or for other purposes, or if any person shall buy
or otherwise obtain the carcass of any swine or other domestic animals, dying from
cholera or other disease, for manufacturing purposes as aforesaid, or any other pur-
pose except that of burial or burning, as provided in the preceding section, every
such person shall upon conviction be fined in any sum not less than twenty-five dol-
lars nor more than one hundred dollars, or be imprisoned not exceeding six months.

Sec. 3. Whereas an emereeney. exists, this act shall be in ace and take effect from
and eared its passage.

Approved, March 4, 1885

These laws, although not sufficiently explicit, touch upon the most
important points, and are important movements in the right direction,
We would suggest laws embodying the three heads in their entirety as
given above under a, b, and ¢, together with directions for their proper
execution. The disease, spreading so easily and rapidly, requires great
promptness of action and quite different rules from those which must be
adopted in the suppression of glanders or tuberculosis, for example.
The difference is due to the nature of the specific microbe, so unlike
those causing the two diseases mentioned.

It is not strange that so little attention has been paid to the restric-
tion of this disease in the past, since legislators and boards of bealth
and State veterinarians have had no scientific basis upon wuich to
frame laws. Even now efforts are being made in various quarters to
coutrovert or openly deny the accuracy of the investigations and re-
sults obtained by the Bureau, and throw the whole subject back into
the chaos in which it was but a few years ago. This must have any
thing but a salutary effect upon those intrusted with the framing and
execution of specific laws for the protection of domesticated animals.

Having thus far dwelt upon the means which must be adopted to
prevent the spread of the disease from one place to another, it becomes
necessary to consider some of the measures that should be employed in
checking it after it has once taken foothold ina herd. But how are

e to recognize the disease? To answer this question it may be well
to recapitulate briefly some of the more important features of the mal-
ady in as simple language as possible:

It is quite common for the disease to announce itself by a few sudden
deaths. The stricken animals may seem well a day, perhaps only a few
hours, before death. In order to remove any doubts as to the precise
nature of the disease, it is best to examine one or more of the animals
before burying or burning them, This should be done ina secluded

a

a

129

place which pigs can not reach, and the ground thoroughly disinfected,
as will be deseribed later. The disease in the sudden cases can be
easily recognized. The spleen is, as a rule, very black and enlarged.
Spots of blood from the size of a pin’s head to a quarter inch or more
will be seen in the fat under the skin, on the intestinés, lungs, heart,
aud kidneys. The lymphatic giands are purplish instead of a pale pink.
When the large intestines are opened they are found covered with these
dark spots of blood more or less uniformly and entirely. Often the
contents are covered with clotted blood. Any or all of these may be
considered as signs of the disease in its most virulent form. In many
outbreaks the early cases do not succumb sorapidly. They grow weaker,
lie down much of the time, eat but little, and usually have diarrhea.
Most of such cases may linger for weeks, meanwhile scattering the
poison in the discharges. The disease may be recognized in these cases
as soon as they are observed to act suspiciously, and there should be
no delay in determining at once the nature of the disease. When the
animal has been opened the large intestine should be carefully slit up
and examined, beginning with the blind or upper end. There will be
seen roundish, yellow or blackish spots, having an irregular, depressed,
sometimes elevated surface. These spots correspond to dead portions
of the mucous membrane, and they are frequently seen from the out-
side aS soon as the animal is opened. Sometimes the membrane has
been entirely destroyed. (See also pp. 39-52.)

In order to comprehend fully the reasons for the preventive measures -
suggested, let us briefly trace the various ways in which hog cholera
bacteria may pass from a diseased or dead animal to a healthy one.

Pigs may become directly infected by feeding on the carcasses of such
as have died of the disease, or by eating food contaminated with the
feces and urine of sick animals, or they may become indirectly infected
by feeding upon materialin which hog cholera bacteria are accidentally
present, and in which they have multiplied. This would include milk,
water, and perhaps most vegetables in a boiled condition. It has been
pointed out in preceding pages that hog cholera bacteria multiply very
abundantly in milk, especially in warm weather, that they remain alive
in water for months, and that they multiply upon boiled potato. It
has also been shown by an extended series of experiments (p. 8&0) that
they may remain alive in the soil for from one to four months. The
sources of infection are thus numerous esough. Tt has likewise been
demonstrated that these disease germs will resist drying. Hence, dried
discharges of the sick or the dried body of dead animals are still in-
fectious.

The channel of infection is in most cases the food and drink. This
has been frequently demonstrated and emphasized in these pages.

The food, after leaving the stomach, passes in a liquid condition
through the small intestine, so that this never seems filled; in facet, its
only contents are a coating of semi-liquid matter over the mucous mem-

15612 HC 9

130

brane. It passes through the small intestine quite rapidly, but on
reaching the large intestine the undigested remains become more con-
sistent, because the liquid is re-absorbed, and are kept here for some
time. The bacteria, if not destroyed by the gastric juice, pass quickly
through the small intestine, but in the large intestine they begin to
multiply and attack the mucous membrane, which they destroy. Thus
the feces or discharges of diseased pigs, wherever deposited, scatter
larger or smaller quantities of the virus in this way, completing the
circle of infection.

In order to prevent the remaining healthy animals in an infected
herd from taking the disease the following measures are suggested as of
importance, some or all of which may be carried out according to cir-
cumstances:

(a) Removal of still healthy animals to inclosed uninfected ground or
pens, as far as possible from infected localities.

(b) Destruction of all diseased animals.

(c) Careful burial or burning of carcasses.

(d) Repeated thorough disinfection of the infected premises.

(c) Great cleanliness, both as to surroundings and as regards the food,
to prevent its becoming infected.

(a) The importance of this measure need not be insisted upon, after
what has been stated of the various ways in which pigs may be infected.
The distance to which they may be removed will, of course, depend on
cireamstanees. They should be kept so far away that there can be no
means of communication, either by direct contact, by drainage of the
surface of the soil, or by gusts of wind. They should not be kept too
closely confined, for if the disease should have attacked one or more
and not manifested itself before removal, the infection would become
general. Even after this precaution is taken, latent disease among such
as are apparently healthy may infect the new grounds and the remain-
ing healthy animals. This danger is increased by the fact that not un-
frequently a number of animals become infected from the same source
at the same time. Some will show symptoms very speedily ; in others
the disease will remain latent for a longer time. Under such cireum-
stances it is impossible to properly isolate the well from the sick, Then
there is the difficulty of preventing the well animals from carrying the
virus on the skin and feet into their new quarters. These drawbacks
may be in part overcome by very prompt action when the first signs of
disease appear in a herd, before the virus has had an opportunity of
being scattered about. The bodies of those to be removed may be
fairly well disinfected by pouring over them a 2 per cent. solution of
carbolie acid, and forcing them to walk through such a solution.

(b) This measure is recommended to prevent the further spread of
the virus by the diseased animals. In view of the fact that few re-
cover, that even these few are stunted and of little value, that there is
no reliable means of treatment which will eventually cure, destruction of

131

all sick animals is the simplest and most economical procedure in the
end.

(c) The disposal of carcasses has already been discussed (p. 128).
This very important measure should never be lost sight of.

(d) Among the various disinfectants which can be recommended are
the following:

No. 1. Slaked or unslaked lime, used both as a powder and as slaked
lime, containing about 5 to 10 per cent. of dry lime (from $ to 1 pound
of lime to a gallon of water).

No. 2. Crude carbolic acid, prepared by adding to the crude carbolie¢
acid obtainable from druggists at about 90 cents a gallon an equal
quantity of ordinary sulphuric acid. This mixture is to be carefully
added to water in the proportion of 2 ounces to1 gallon of water, about
14 per cent. volume (see p. 91).

No. 3. A 1 per cent. solution (volume) of ordinary sulphuric acid (14
ounces of the acid to 1 gallon of water).

No. 4. A 2 per cent. solution of pure carbolic acid. This is prepared
by heating the crystals slightly until they melt and adding the resulting
liquid to hot water, in the proportion of 14 ounces to half a gallon of
water. (A pound of carbolic acid, crystallized, retails at 55 cents.)

No. 5. Boiling water.

The careful laboratory experiments with these disinfectants, upon
which their practical application is based, are given on p. 87. Weshall
confine ourselves in this place to a description of their employment.

Disinfectants are substances which, in solutions of a certain strength,
are capable of destroying disease germs. Consequently they should be
applied wherever the disease germs are supposed to be. In ease of hog
cholera they are attached to the sides and floorings of pens and to the
various utensils used in cleaning them. ‘hey are mixed with the earth
over which the diseased animals have run, or in the water which they
have frequented. In the report of the Department for 1886 the use of
mercuric chloride (corrosive sublimate) was recommended, as it is a pow-
erful disinfectant. Since that time other disinfectants have been tested
which are equally cheap and easily procurable. The main objection to
mercuric chloride is its extremely poisonous character, which makes it
undesirable to deal with. This substance has, therefore, in spite of its
powerful germicide properties, been thrown out of our list of available
disinfectants.

The wood-work of pens, fences, flooring, ete, is best disinfected by
using upon it, with a broom, solution No. 2 until thoroughly wet. In
preparing this solution it should be stated that the mixing must be
done in a glass bottle or jar and the mixture poured slowly into the
proper amount of water in a wooden pail. This should be rinsed out
after using to prevent the acid from slowly destroying the iron hoops.

Whenever No. 2 is not obtainable No. 3, which seems to be equally
efficient, may be used in its place.

132

Lime is a very efficicnt disinfectant for hog cholera. Experiments
have shown (p. 93) that a solution containing only .02 per cent. will de-
stroy the bacteria. When much organic matter is present, as much as
.O per cent. to 1 per cent. may be necessary. We recommend the pro-
portions given under No. 1, which give from 10 to 20 times the strength
required. The resulting liquid is not too thick to be easily manipulated
It may be used on wood-work as a whitewash, and it may be eSDraae as
a thin layer over the soil which has been infected.

The 2 per cent. solution of pure carbolic acid should be used when-
ever No. 2 may act injuriously by virtue of the sulphuric acid which it

contains.

In general we recommend the use of No. 2 or No.3 as often as it may
seem necessary. I should be dashed upon the infected pens, troughs,
tools, and over the infected soil. When there is no objection te lime
this may be used on the soil, as it is equally efficient. The discharges
should be covered with powdered or slaked lime, and this should be
thrown in abundance into pools or wherever water stagnates. In the
case of troughs for feed, iron tools, etc., which are liable to injury, the
disinfectant should be washed away with boiling water if this is at hand.
Boiling water will destroy hog cholera germs by simple contact, and
the disinfection wili thus be made more complete. Shoes may be dis-
infected by rubbing them with solution No. 4.

It must be carefully borne in mind that no manure from sick pigs
should be removed until it has been treated with disinfectants. The
cleaning must be done after disinfection and not before, to prevent the
dissemination of living virus.

The ageney of mice and rats in transporting virus will depend upon
the promptness and thoroughness with which disinfection and cleanli-
ness are practiced. Mice are more dangerous than rats, in so far as
they may take the disease by feeding (p. 72). Flies can cnly carry
such small quantities of the virus that they are not likely to prove dan-
gerous if disinfection and cleaning of feed troughs are attended to.

If these measures are carefully carried out, the disease may either be
checked or else mild cases only will appear, owing to the small quantity
of poison which the animals are likely to consume with the food.

The epizootic may be terminated by the destruction of most of the—

herd. This unfortunately is usually the case. What precautions must
be taken to prevent subsequent outbreaks ?

If only a few animals remain, it is best to slaughter them; they are
likely to suffer with the disease in a mild form and continue to infect
the premises. If no more animals remain, there should be a final
thorough disinfection and subsequent cleaning of the whole exposed
territory, including every nook or corner where the disease has existed.
This should be done with solution No. 2 or No. 3 as directed, used as
freely as possible. After one or two days the ground may be covered
with a thin layer, one-eighth inch or more, of slaked lime in the strength

133

above given and left undisturbed. If there is no objection to whitewash,
this may be applied to infected wood-work as an additional safeguard.
Even after this thorough treatment, it is best not to place any fresh pigs
on the premises for at least four months after the final disinfection.
When animals still remain that have been exposed and have not taken
the disease, no fresh animals should be introduced for at least six months
after the termination of the outbreak. The disinfection must have been
equally thorough.

After all this trouble has been taken there is stil] remaining the dan-
ger of a fresh introduction of the disease, and we would therefore again
call attention to the rules iaid down in the beginning of this chapter.
These, after all, must be considered as mostimportant. It is much easier
to keep the disease away than to eradicate it after it has been intro-
duced, without great loss of time and money, We would also suggest
that in those regions where the danger from hog cholera epizootics is
always present, the methods of keeping hogs be simplified in such a
way that disinfection may be practiced without too much labor and un-
certainty as to the results. It is only necessary to visita few farms to .
be convinced of the difficulty that may be met with in endeavcring to
eradicate the disease. The hogs are allowed to stray into the most
out-of-the-way places when sick instead of being kept in inclosures of
definite form and size, which are readily accessible. The poison is thus
scattered in such a way as to make disinfection impossible. It is cer-
tainly not necessary in raising pigs to allow them to stray into arbors,
behind hedges, hide themselves under barns and outhouses. In some
farms which we have visited, and which were said to have hog diseases
most of the year, there seemed to be no places about the house or gar-
den where pigs did not go. Under such circumstances disinfection is
is quite impossible. The pens aud other wooden structures, fences, ete.,
are also apt to be in a very dilapidated condition, so that cleaning is
very much complicated. Even under such circumstances the germs will
finally perish without disinfection if enough time be given, since they
gradually die in the soil and water, as our experiments have shown. A
period of from six to nine months after all animals have been removed
will be, in general, sufficient to purify the soil of these disease germs.
In fact the natural disinfection is very probably accomplished in many
cases in from three to four months, but it would not be safe to rely upon
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TREATMENT OF HOG CHOLERA.

Upon this subject very little should be said, for the reason that dis.
eased animals are a source of poison and a menace to healthy animals,
and should be destroyed. Moreover treatment is exceedingly unsatis-
factory, as the disease cither terminates fatally, whatever remedies are
used, or generally makes the animal useless if it should recover. We
therefore urgently recommend slaughter of the sick and thorough dis-
infection as the safest and most economical treatment in the end.

Treatment, however, is resorted to by a large number of owners of
swine. The number of specifics, so-called, which are being advertised
is legion. We have tried some of the best recommended and found them
of no avail. Nor is there any ‘“‘ specific” known in the range of veter-
inary or human medicine that will cure diphtheritie and ulcerative dis-
ease of the large bowels except time, combined with: careful dieting,
rest, and a few palliatives to relieve pain. It isimpossible to carry out
this treatment on swine. The success frequently reported with spe-
cifics in hog cholera are very probably due to the fact that the treat-
ment is usually adopted in mild forms of disease of a different nature
which is mistaken for cholera, or when the acute outbreak is over and
the plague has assumed a chronic character. The affected swine linger
for a time with very slight symptoms of disease, and this change is
credited to the ‘‘ specific” employed. Remembering that the severest
injury is done to the walls of the large intestines in this disease, we
regarded it important to determine what medicine would give a prompt
and copious evacuation of the bowels in the very beginning of the dis-
ease. Various medicines were tried by Dr. Kilborne, at the Experiment
Station, among others the following: ;

(1) Calomel and jalap.—February 20, 1888. To No. 463, 30 grains
calome!; to No. 467, 23 grains jalap; to No. 468, 30 grains each of eal-
omel and jalap. February 21. Same dose given again to Nos. 463
and 468; no result.

(2) Calomel.—March 7. To Nos. 441 and 442, each one dram of dry
calomel. March 8. To 441 same dose mixed with castor-oil; to 442
about 1$ drams with castor-oil. No. 441 was freely purged after second
dose, continuing for twenty to thirty-six hours. Noz 442 was freely
purged after sixteen hours, continuing sixteen to twenty hours, when
it died. At autopsy were found intense inflammation of stomach, super-
ficial necrosis of the mucosa of large intestine with deep reddening
resembling hog cholera. No bacteria found in cultures from spleen.
These changes were no doubt due to the calomel.

135

136

(3) Calomel.—March 8. Nos. 463 and 468 received each one dram
éolomel in 2 drams castor-oil. No. 468 was purged freely in twenty
hours, continuing thirty-six hours. No. 463 was purged in sixteen
‘hours and made ill for several days. :

(4) Epsom salts.—Nos. 403 and 405 (weight 50 pounds) received each
1 ounce. Bowels slightly relaxed for one or two passages. Nos. 339
and 377 (weight 50 pounds) received each 2 ounces in water. No. 339
was purged and made slightly ill. No effect on 377.

(5) s. 402 and 404 (weight 50 pounds) received
one-half dram each ; ; no effect. Nos. 372 and 380 (weight 65 pounds)
received each 2 drams, mixed in molasses; no effect. The same ani-
mals, five days later, received each 4 drams with molasses; no effect,
except aeeoloeiitn of feces.

(6) Castor-oil and turpentine. 387 and 388 (weight 50 to 60
Seas received each 14 ounces castor-oil and one-sixth ounce turpen-
tine; noeffect. No 387 received, five days later, 25 ounces oil and one-
sixth ounce turpentine. No. 388 received, five dayclatcn 25 ounces oil”
and one-third ounce turpentine; no effect.

(7) Linseed-oil and turpentine. ’_Nos. 083 and 399 (weight 50 to 60
pounds) received each 24 ounces oil and one-sixth ounce turpentine ;
no effect. No. 383 receiv ed, five days later, 4 ounces oil and one- sixth
ounce turpentine. No. 399 received ‘five days later, 4 ounces oil and one-
third ounce turpentine. Both were made sick for a day or two. No
catharsis.

These trials show how difficult it is to cause movement of the large
bowels in swine, and they also suggest that this very sluggishness may
make them susceptible to inflammations and ulcerations such as we
find in nog cholera and frequently in swine plague.

It was our intention to obtain a eathartie which would freely purge
without causing any inflammation or irritation of the large intestine.
Of those tried, calomel is the only available one. This must be carefully
given, as it may produce the very inflammations which it is designed to
check, and destroy life, as was actually done in experiment 2.

Concerning calomel Hllenberger* says:

Calomel (in combination with castor-oil) is especially serviceable with swine; with

larger animals when the contents of the intestinal canal are to be disinfected, and in
inflammatory fevers. It should be given to ruminants with the greatest caution.

It was our purpose to try calomel after having made these trials upon
healthy animals, when the disease died out at the Experiment Station,
and further investigations had to be postponed.

If the large intestine has been promptly evacuated the next important
step is to give only that food which leaves but little irritating waste to
pass into the large bowel, such as milk and gruels. In short, it is best
to use only boiled or scalded food so as to help the process of digestion
as much as possible. It may be necessary to repeat the dose of calo-
mel after afew days. As to this mode of treatment our experience is
not sufficient to warrant any positive statements, and it is simply sug-
gested to those who wish to run the risk of treating this disease.

137

There is another line of preventive and curative treatment which may
prove valuable in the future, namely, the feeding of substances with the
daily food which, while not injurious to the animal itself, may keep in
check the multiplication of the virus in the intestine -by an antiseptic

-action. It is very important, however, to bear in mind that a large
number of those medicines which act as disinfectants and antiseptics
are likewise injurious or even poisonous to the animal itself. A too
abundant feeding of such material, while it may reduce the mortality
and lessen the severity of the disease in the sick, is liable to cause in-
jury to liver, kidneys, and other vital organs, whereby the nutrition of
the animal may be permanently injured. Such medicines, when care-
lessly given to healthy animals as preventives, may irritate the large
bowel sufficiently to reduce its vitality and power of resistance when the
disease actually appears. The proper medicine to feed must therefore
be selected with care, and we trust that experiments to this effect may
be carried on at the Experiment Station at an early date.

There is still another line of treatment which demands attention,
namely, the introduction of a sufficient amount of some disinfectant
into the body to be absorbed and thus to make the whole body oppose
the multiplication of bacteria. Koch tried this method by injecting
mereuric chloride into guinea-pigs and afterwards inoculating them
with anthrax bacilli. The animals all took the disease and died.

At the laboratory of the Bureau mercuric iodide, a still more power-
ful disinfectant, was tried upon rabbits.

A solution was prepared containing .0OL gram mercuric iodide and
.002 gram potassic iodide in a cubic centimeter. Of this .5 cubie centi-
Se was injected beneath the skin of the back of four rabbits (Nos.

1, 2, 3, 4) for eight successive days. On the third day Nos. 1,2 2, 3, and
a fresh rabbit (cheek), No. 5, receiv ed hy podermically into the inner sur-
face of the thigh 4 cubic centimeter of liquid containing one-millionth
cubie centimeter of a beef infusion culture of hog cholera bacteria about
one day old.

All the inoculated rabbits died, the dates being given in the appended
table. Rabbit No. 4, which had received the iodide only, to observe
any poisonous effeet, remained well. The ‘lesions were those of hog

cholera, and the specific bacteria were present in oie spleen. The total
amount of the iodide given was .004 gram, about ;5 grain.

.5 cubic centimeter of | Inoe ulated with one- mile
ry 7 al SS eh lionth cubic centimeter a
No. yo per cent. mercuric.| Giiture hoe cholera bac Remarks.
icdide daily. sera cna bh |
teria.

L | dianei22 torosinelusive. Pune 2h. fce..0. se ade ccs cen Died June 30. |
Qe 2a = MOUS eeitcceiae aerinaters)| rte. CODE tees eae 3 ene Died July 3.
Sh les Orn gemma eemeeee eee SATO ON then accra ee aresicsees Died July 6.
4 600) ls ftex. 2s ease eee leehens aeons eM pbc das
ye (SpA CNAs a noes om Sra ot Prone Dae hoo ie wre aris eee Died July 3.

* Weighing each about 2 pounds.

138

At the same time healthy pigs were fed with the same substance in
minute doses, to observe any toxic effect that might appear. These exper-
iments were likewise interrupted in their application by the disappear-
ance of the disease at the beginning of the year. While we therefore
recommend in general the use of a purgative, such as calomel, in the
beginning of the disease, and careful feeding subsequently, we have as
yet no actual experimental evidence that such treatment will be of any
avail, owing to the frequent interruptions of the work.

EXPERIMENTS ON THE PREVENTION OF HOG CHOLERA BY
INOCULATION.

During the past six or seven years the attention of the world has
been centered upon the brilliant experiments of Pasteur in the line of
preventive inoculation for animal diseases. Many others lave since
then followed his footsteps with variable success. Among those dis-
eases for which preventive inoculation is more or less in vogue in some
European countries, especially in France, are anthrax among cattle and
sheep, charbon symptomatique, affecting the same animals and perhaps
identical with the disease known as black quarter or black leg in this
country. This is not the place for discussing the absolute value of vae-
cination in these diseases, nor to point out the reasons why they are
not regarded of much value by scientists of Germany and other States.
Suffice it to say that the Bureau has devoted a large amount of time in
testing all the available methods of attenuating hog cholera virus for
raceinal use, to determine whether any vaccine could be placed at the
disposal of the publie that might prevent the enormous losses entailed
each year by this dreaded germ disease. In the following pages most
of the work done (chiefly during the winter and spring of 1886) is briefly
reproduced,

Inoeulations of small doses of strong virus tin the form of liquid cultures
was first resorted to, because it had been observed that pigs rarely take
the disease when culture liquid in such quantities is injected directly
under the skin. We reasoned that if injections of small doses do not
cause the disease, why may they not prove effective in preventing natu-
ral infection? The cultures were not therefore attenuated, as Pasteur
has done, with anthrax, because the step was deemed unnecessary.

A lot of animals were at first inoculated twice with very small quan-
tities, the period between the two inoculations being about two weeks.
This time was sufficient to reveal any disease which might have been
induced by the inoculations. Two weeks after the secoud inoculation
the animal was infected either by allowing it to feed upon the internal
organs of pigs which had died of the disease or by exposing it to the
sick and dying in an infected pen. It was soon found that the inocu-
lations were by no means prot ctive, in whatever way the virus entered

130

{40

the system, for subsequent feeding usually produced cases of the most
acute character and with the most severe and extensive lesions. The
doses of inoculated cultures were gradually increased in quantity with-
out yielding any better results. Of a large number of animais sub-
jected to inoculation only five took the disease unmistakably as a con-
sequence of the operation. The experiments, including tables and
post-mortem notes, are given in extenso as they were made.

In reading them over it will be noticed that the virus was cultivated
chiefly in liquid media, and the solid media, more particularly nutritive
gelatine, were only employed to test the purity of the cultures. When-
ever these cultures were used for inoculations they were previously
tested on gelatine plates by drawing a platinum wire, dipped into the
culture, through the gelatine layer two or three times before the gela-
tine had become solid. Among the hundreds of cultures thus tested in
the space of several months not one was found impure. Series of eult-
ures extending up to the tenth generation were usually carried on by
inoculating fresh tubes each day. The last culture tested as described
above gave precisely the same colonies as the first in all the series thus
far prepared. The culture-tube, described in the First Annual Report
of the Bureau, was used almost exclusively for these cultures in liquid
media. The advantages and accessibility of cultures in liquids for
purposes of inoculation, the readiness and ease with which quantities
or doses may be determined, finally, certain characteristics of growth
in liquids, place this method on a level with, if not above, that of solid
cultures for experimental purposes. For diagnostic purposes, solid
media are to-day a sine qua non of bacteriological work.

Experiment 1.—Pigs Nos, 152, 167,168, and 175 were inoculated with
pure cultures in beef-infusion peptone as follows: On January 23, one
drop of the seventh culture, derived from the spleen of pig No. 114;
on February 8, with one eighth cubic centimeter from a culture derived
froma guinea pig. Both cultures were diluted in sterile normal salt solu-
tion in such a way that 1 cubic centimeter of fluid was injected each time.
Theinneraspectof the thigh near Poupart’s ligament was chosen, and the
liquid was introduced beneath theskin into the subcutaneous tissue with
au hypodermie syringe. There was no perceptible swelling at the site of
either inoculation, excepting in No. 175, in which there were two tumors,
each the size of a walnut, at the seat of the firstinoculation. In order to
test the extent of the immunity which these inoculations might have
conferred, feeding the viscera of pigs which had suecumbed to hog
cholera was resorted to, the animals being transferred to the large in- -
fected pen for this purpose. Nos. 168 and 175 were fed in this way
March 5,and two animals not inoculated (Nos. 158 and 189) were fed
with them. All four died; the two vaccinated animals in about twenty
days, the others in about fifteen days after feeding. March 13, Nos. 152.
and 167 were fed with two check animals, Nos. 176 and 190. These four
also died of hog cholera; the two vaccinated ones averaging twenty
days, the others eleven days after feeding. The inoculation may be
said to have simply retarded death from five to nine days. <A table

141

giving a summary of these facts is appended, together with a brief
description of the post mortem appearances :

|
: | Fed with hog- Number of
No. | January 23. | ®ebruary 8. | cholera vis- Died. days after

| cera. | feeding,
|
Drops. ce. ¢.

152 1 4 | Mar. 18 Ie BiAssese 21 |
167 1 % | Mar. 13-.-.. SA Tegal realare aki
168 il H.C REAL WO. a= 3s | Mar. 28 4] 2
175 1 4-|° Marl 5)=. =< Mar. 22 17
1BYs) ee cee edgesa Senccebodneee | Mar. 5.-...- Mar. 21 16 |
S91 PPeessaane telat soradtewa tone. | Mats Dees | Mar. 19 14 |
TRON | oeee ies epee ee come marlon see peMfarey Leer 2 Mar. 23 10 |}
To Joes aR een ncon||eeos so seneece Mar, 13.. Mar. 25 12 |

Autopsy notes.—No, 162. Skin of limbs and abdomen dotted with purple
spots; on abdomen, general reddening. Points of extravasation and
ecchymosed spots throughout the subcutaneous connective and fatty
tissue and on gastro-splenic omentum. Superficial inguinal glands
greatly enlarged and congested. Spleen enlarged, filled with blood,
and very soft. Petecchiz on epicardium. Numerous lobules of the lungs
collapsed. Glomeruli of kidneys appear as deep red peteechiz. In
cecum and upper portion of colon extensive and deep ulcers. A few in
the ileum near the valve. The mucosa of the stomach, small and large
intestine, thickly covered with dark red points or petecchiz.

No. 167. Dying, and hence killed by a blow on the head. Spleen swol-
len, friable; epicardium dotted with points and spots of extravasation.
In lungs a few collapsed lobules. Lymphatic glands generally very
deeply congested, similarly the mucous membrane of fundus of stomach
and the kidneys. Large ulcers in cecum and upper portion of colon.

No. 168. Subcutaneous and sub-peritoneal tissue contains numerous
ecchymoses from one-eighth to three-fourths inch in diameter. Spleen
enlarged, gorged with blood, friable. Petecchiz on epicardium. Lungs
not collapsed; its parenchyma contains numerous deeply-congested
areas from one-eighth to one-half inch in diameter. Kidneys enlarged,
with extravasations on surface and in parenchyma. Cortex of lym-
phaties in general deeply congested. Extensive, almost continuous,
ulceration of cecum, and upper portion of colon, in part blackish, the
remainder of the large intestine being the seat of severe inflammation
and extravasation. Mucous membrane of stomach similarly involved.

No. 175. Subcutaneous tissue dotted with pale red spots. Tumor at
the place of the first inoculation firm throughout, pale yellowish. Su-
perficial inguinal glands, as well of those of thorax and abdomen, with
purplish cortex. Spleen tissue still firm, dotted with numerous bright
red points, but slightly enlarged. Beneath the entire epicardium and
endocardium many extravasations. Ccum and upper portion of colon
extensively ulcerated. Serous surface of large intestine dotted with
extravasations.

No. 176. Slight reddening of skin and subcutaneous fatty tissue.
Cortex of Jymphatic glands in general deeply congested. Spleen much
enlarged and surface dotted with numerous bright red elevated points.
A tew peteechiz on endocardium and epicardium. Lungs deeply con-
gested throughout; kidneys likewise inflamed. Stomach slightly red-
dened at fundus; small intestine also slightly congested. Serosa of large

142

intestine dotted with extravasations. The mucosa of cecum and small
portion of colon one mass of necrosed tissue. Walls thickened.

No. 189. Ixtensive and deep reddening of skin of abdomen, throat,
and limbs. Subcutaneous tissue only slightly reddened; spleen eu-
larged, gorged with blood, friable. Besides the general congestion of
the lungs there are small darkerareas, representing hemorrhagic lobuies.

sronehial glands and those along lesser curvature of stomach swollen

and gorged with blood; the other lymphaties only moderately congested.
Besides a small number of ulcers throughout the large intestine, the
mucous membrane is deeply congested and dotted with occasional
hemorrhagic points. Kidneys extensively inflamed; on section the cor-
tex shows extravasations.

No. 190. Considerable reddening of the skin of abdomen and ventral
aspect of limbs; very sligbt in subeutaneous tissue. Spleen greatly
enlarged, dark purple ; blood flows freely on cutting into its very soft.
Lungs contain regions of congestion and hepatizations, possibly due
to the presence of a few lung worms. Lymphatic glands near stomach,
the bronchial and superficial inguinal glands, deeply congested. Mu-
cous membrane of stomach extensively congested; a large patch of
extravasation in fundus; large intestine severely inflamed, with occa-
sional extravasations; no ulcerations.

The diagnosis of hog cholera was confirmed in every case by finding
the specific bacillus in cover-glass preparations of splenic tissue and
obtaining therefrom pure cultures in liquid media and in gelatine.

Experiment 2.—In conjunction with the first series of inoculations, two
pigs (Nos. 149 and 161) were inoculated at the same time, as follows:
January 23, with 1 cubic centimeter of the seventh culture in beef-infu-
siou peptone. No reaction at the place of inoculation in No. 149; a
tumor as large as a marble in No. 161. On February 8 both received a
second injection of 1 cubic centimeter. Two swellings as large asa
chestnut at the place of the second inoculation in No. 149; in No. 161
also a considerable thickening was present. No. 149 was fed Mareh
5 with four of the preceding series; No. 161 on March 13 with the
remainder of the preceding series and some to be subsequently spoken
of. Both died of hog cholera. The accompanying table and brief
autopsy notes explain themselves :

Inoculation. | |
3 | Days
IN@) | Sas pe Fed. | Died | after
| | Peedins
| Jan. 23. | Hebs3: | feedine:
-- | 7 4 eS. | od
WR ECRICH PEE) SCE | |
| |
149 | 1 1 | Mar. 5! Mar. 24 | 19
| 161 | th 1 | Mar. 13 | Apr. 14 | 32

No. 149. Slight reddening of the skin and subeutaneous connective
tissue; the tumors produced by inoculation firm, pale yellowish, only
one showing softening within; spleen considerably enlarged and full of
blood ; ascarides in gall bladder, which is ulcerated ; mucous membrane
along fundus of stomach intensely congested; the mucous membrane
of cecum and upper portion of colon one mass of ulcers; in the remain-
der of colon they are isolated; kidnevs congested.

145

No. 161. Great emaciation; spleen enlarged and gorged with blood,
very soft; all excepting the posterior region of each lung hepatized
and the bronchi filled with a thick creamy mass, which consists almost
entirely of pus corpuscles; lymphaties but slightly congested ; adhesions
between adjacent coil of large intestine and bladder ; cecum and colon
studded with large deep ulcers; valve greatly enlarged ; intense con-
gestion of mucous membrane of ‘fandus of stomach.

Cover-glass preparations from the spleen of both contain the charac-
teristic bacilli. Gelatine and liquid cultures from the same organ were
pure.

The comparatively large dose of strong virus used for vaccination was
not capable of protecting these animals from the disease communicated
by feeding. There was no suspicion of disease caused by the vaccination
when they were fed, and the time intervening between the two injec.
tions was sufficient for any development of disease from the injected
virus.

Heperiment 5.—Pigs Nos. 151, 169, 170, and 178 were inoculated as
in the preceding experiments on F ayia 8 and 23 with 2 cubic centi-
meter of a beef infusion peptone culture derived from a guinea pig and
the seventh culture from the spleen of a pig in the same medium. The
dose was diluted in salt solution so as to make 1 cubic centimeter of
liquid. In No, 151 the second inoculation produced a tumor about 1
inch long and one third inch thick. The first was scarcely noticeable.
In No, 169 the first inoculation resulted in a bean like nodule; the see-
ond produced several of the same size. In No. 170 neither inoculation
showed more thana very slight swelling. In No. 178 both inoculations
produced rather extensive swellings.

On being fed with the viscera of pigs known to have died of the dis-
ease all took the disease and died; two on March 13 and the remain-
ing two on March 19, ¢. e., one in eliineeen: ove in eighteen, and two in
twenty-two days after feeding. A table summarizing these facts and
brief post-mortem notes are appended :

Inoculation. | | Die
——— = Fed. | Died. Ale
| Feb. 8. | Feb. 23. feeding.
|
| c.c¢ | ce. ¢
151 3 | 4; Mar. 13 | Mar. 26 13
169 4 4 | Mar. 19} Apr. 10 | PP]
170 | k 4 | Mar. 13| Apr. 4 | 22 |
178 k 3 Mar. 19 Apr. 6 | 18 |
|

Autopsy notes.—No. 151. Purplish spots on skin of abdomen and paler
ones in subcutaneous tissue. Inoculation tumor cuts like cheese; yel-
lowish-white. Extravasations under endocardium and_ pericardium ;
left lung mottled from hemorrhagic areas ; cortex of lymphatic glands
infiltrated with blood; these of meso colon and lesser curvature of
stomach dark purple throughout; kidneys pale; hemorrhage into pel-
vis of left kidney ; extravasations into mucosa of stomach 3 moderate

144

number of ulcers in cecum and colon; large quantity of blood in the
lower 6 or 8 feet of ileum and in the large intestine, clotted in the
former tube, where the mucous membrane is deeply congested.

No. 169. Small tumor on the left side, the place of the second inocu-
lation ; spleen enlarged and congested, with large hemorrhagic infarcts ;

consider able effusion in the large serous cavities. Besides the eeneral

congestion of lungs, there are scattered throughout its parenchyma
hemorrhagic foci. Hemorrhagic inflammation of kidneys manifested
by bright red glomeruli throughout its cortex; lymphatics in general
deeply reddened; numerous petecchize in stomach, small and large intes-
tine. In cecum and colon, large, deep ulcers.

No. 170. Redness of skin in abdomen; nothing at places of inoculation ;
spleen enlarged, friable, full of blood; abdomen, thorax, and pericardial
cavity contain much yellow serum; congestion of the jun gs with darker
hemorrhagic foci throughout; anterior lobes collapsed; } kidneys enlarged,
with a few extravasations on surface and in parenchyma; mucous mem-
brane of stomach and intestines covered with many hemorrhagic points
aud spots. In large intestine, including rectum, numerous old ulcers,
some 1 inch across. Lymphaties in veneral hemorrhagic.

No. 178. Died quite unexpectedly. At the place of first inocula-
tion two firm whitish masses; spleen enlarged, friable; its substance
contains hemorrhagic infarets; extravasations beneath both serous sur-
faces of the heart; congestion of lungs, with numerous darker hemor-
rhagic foci; ly mphatie glands of abdominal cavity very dark and gor oe
with blood; extensive ulceration about the ileo-cecal valve, in the e
cum, and colon; in the lower portion of colon and in the reetum mane
ous small extravasations. Hemorrhage into pelvis of both kidneys.

The post-mortem determination of a severe type of hog cholera in
these four cases was confirmed by finding in the spleen of each animal,
by means of cover-glass preparations, numerous specific bacteria of this
disease. Cultures in liquid media made from every spleen were found
pure when examined microscopically as well as on gelatine plates. This
experiment likewise proved the inefficiency of small quantities of non-
attenuated virus introduced beneath the skin in preventing an invasion
of the micro-organism from the alimentary canal.

Haperiment 4.—A third lot of four pigs (Nos. 117, 171, 172, and ek
between three and five months old, were inoculated as before with .2
cubie centimeter each from the second beef infusion peptone culture
derived from a pig’s spleen. On March 1 they were inoculated with
.2 cubie centimeter from the second culture derived from a pig’s spleen.
In No. i17 there was a slight swelling after the first, and one as large
as a chestnut after the second inoculation. In No. 171 a mass 1$ to 2
inches long and three-fourths inch in diameter was found at site of the
first inoculation. There was but a small nodule at the place of the
second inoculation. In No. 172 two lumps, like smail marbles, formed
after the first inoculation; after the second only a small nodule formed.
In No. 174 the reaction after the second inoculation was manifested by
an irregular tumor about 2 inches long and one third of an inch in diam-
eter, the reaction at the place of the first inoculation being less marked,

Of these four, two (Nos. 117 and 172) were fed with the viscera of
pigs dead from hog cholera, together with two control animals (Nos.

145

192 and 193), on March 19. The rest (Nos. 171 and 174) were simply
placed in the large infected pen March 22, with those that had been fed
with infectious matter. Below the result is given in a tabulated form.
It shows that all the animals succumbed to the disease, those simply.
exposed by contact with the sick as well as those fed. Of the inoeu-
lated animals, those fed died in twenty-one and eighteen days after
feeding; those exposed, in twenty-two and twenty-five days, respect-
ively. Those not inoculated died twelve and nine days, respectively,
after feeding. Here, likewise, we notice the prolongation of life in the
inoculated pigs.

No. | Feb. 13. | Mar. 1.| Tale of Tecding |. Died. eee.

é and feeding.

CBG Cnc
117 22 .2 | Fed Mar. 19....... Apr. § 21
171 .2 -2 | Exposed Mar. 22..| Apr. 13 22
172 2 2 | Fed Mar.19....... Apr. 6 18
174 2 .2 | Exposed Mar. 22..) Apr. 16 25
a ol Ee See | eee Fed Mar. 19....... | Mar. 31 12
LOBF | asocesser|| Seis ccs se esecle do ..-----.-:.| Mar. 28
* Checks.

The lesions found at the autopsies of these pigs are briefly as follows:

No. 117. Extensive reddening of the skin of abdomen; great enlarge-
ment of spleen, which is gorged with blood, very soft; petecchial dis-
colorations on surface of lungs and on section; large intestine studded
with broad, deep ulcers as far as the rectum; a few in Meum.

No. 171. Skin over ventral aspect of body deeply reddened ; hemor-
rhagic spots under peritoneal covering of diaphragm and large intestine
and under capsule of kidneys; lungs congested, containing numerous
dark hemorrhagic lobules; part of anterior lobes collapsed. The spleen
very large, dark colored; nodes slightly raised above surface, shown on
section to be hemorrhagic infarcts; lymphatic glands generally highly
congested ; petecchial spots on surface and in cortex of kidneys; hemor-
rhagic foci throughout mucosa of stomach and intestines. About four
large ulcers in czecum and colon.

No. 172. Reddening of skin of ventral aspect of body and of subeu-
taneous tissue generally; firm, pale yellow, cheesy masses, surrounded
by a thin membrane at place of inoculation; engorgement of spleen
and lymphatic glands; extravasations in parenchyma of kidneys. In
cecum and colon numerous deep ulcers, some coalesced. Mucosa of
stomach generally congested, and that of intestines thickly dotted with
petecchiz.

No. 174. Deep reddening of skin of abdomen; encysted cheesy mass
at site of first inoculation; great enlargement of spleen; prominent red
points on surface; effusion into abdominal cavity; anterior lobes of
lungs collapsed, remainder normal; lymphatics highly congested ; three
large ulcersin cecum ; valve thickened and ulcerated ; petecchiz numer-
ous throughout mucosa of stomach and intestines.

No. 192. Control animal ; reddening of skin of ventral aspect of body
and of subcutaneous tissue; spleen swollen ; full of blood ; friable ; at-

15d12-o C———10

146 :

electasis of the small anterior lobe of each lung; ulcers on the mucous
surface of gall bladder; cortex of lymphatic glands infiltrated with
blood ; mucosa of large intestines congested; numerous ulcers in caecum
and upper colon.

No. 193. Subeutaneous connective tissue considerably reddened ;
spleen but slightly enlarged; not much softened ; mucous membrane
of stomach, of large and small intestines, deeply congested ; contents
of large intestine fluid, chocolate colored.

in cover-glass preparations from the spleen pulp of these animals,
numerous bacteria of hog cholera were found in each preparation. Both
gelatine and liquid cultures from every spleen proved to be pure ecult-
ures of the bacillus of hog cholera.

The diagnosis made on post mortem was thus confirmed by micro-
scopic examination and culture.

Experiment 5.—To determine the effect of a single inoculation, on
February 13 two pigs (Nos. 115 and 160) received subcutaneously each
1 cubic centimeter of the second beef infusion peptone culture obtained
from the spleen of a pig. In No. 115 a tumor as large as a marble was
found at the seat of inoculation March 9. In No. 160 the tumor was
elongated, about 2 inches long and three-eighths of aninch thick. No.
115 was fed with viscera taken from cases of hog cholera March 19,
No. 160 was simply exposed to the disease by being transferred to the
large infected pen. No. 115 died April 8. No. 160 recovered and was
well May 6. The detailed account of this experiment is appended;

- 5 Date of feeding and , Days after
is Feb. 13. exposure. Effect. feeding.

Cc. c.
115 1 eedeviar.s1 Ope aa Died Apr. 8 - 29

160 1 | Exposed Mar, 22....| Recovered ..

Post-mortem notes.—No. 115. Firm, pale yellow tumor at seat of in-
oculation, encysted; center undergoing softening. Spleen tumefied,
very dark and friable. A few extravasations beneath serous coverings
of heart. In cortex of kidneys numerous hemorrhagic points; cystic
degeneration of right kidney; advanced ulceration of ca#eum and
colon ; scattered petecchiz in mucosa of stomach and small intestine.

No. 160. Was very low for a time, beginning with April 1. It was
barely able to stand and its appetite was poor. It rapidly recovered,
however, and was gaining flesh in May. Whether the animal was suffer-
ing from hog cholera or from the Sclerostoma pinguicola (kidney worm),
with which some of this lot were found affected, can not be said.

In order to determine whether a single injection of a comparatively
large quantity of culture liquid, while not inducing the disease, would
protect against the disease itself, the following experiment was per-
formed:

Experiment 6.—Four pigs (Nos. 202, 204, 205, and 212) were inoculated
April 2 with 14 cubic centimeters of a seventh culture in beef infusion with
1 percent. peptone one dayold. Four additional pigs (Nos. 206, 207, 208,

147

and 209) received but one cubic centimeter of the same culture. The re-
maining four of thesame lot (Nos. 203,210,211, and 213) were reserved as
checksupontheexperiment. Of these Nos.203 and 213 had atemperature
of 106° F’., and hence weresuspected of disease. This suspicion was soon
confirmed after they had been placed in a pen alone. Both had asevere
diarrhea, one dying April 11, the other April 13. The lesions were con-
fined to the mucous membrane of the large intestine, which was dotted
withnumerous elevated lemon. yellow tough masses a few lines across, sim-
ulating ulcers. On close examination, however, this impression was dis-
pelled. These tough masses were easily removed in toto from the mu-
cosa, Which presented a slight depression without any loss of substance.
They were evidently exudates from the mucosa (croupous?). There were
no bacteria in the blood or in a bit of spleen dropped into a culture tube.
No development took place in either tube.

Of those inoculated with 14 cubic centimeters two died from the imme-
diate effects of inoculation. No. 204 died in eleven days and No. 212 in
seven days. In No.204 atough tumor had formed atthe point of inocula-
tion on each side. The mucous membrane of the large intestine was com-
pletely necrosed and the spleen enlarged. In No. 212 local swelling was
present on one side. The stomach and large intestine were deeply con-
gested, with points of commencing ulceration in the latter. In both ani-
mals the bacillus of hog cholera was presentin cover-glass preparations of
the spleen. Nos. 202 and 205 seemed to remain unaffected by the inoc-
ulation. One month and a half later both were exposed to the disease
in the large infected pen. A month later they were removed with oth-
ers to a clean pen, after having apparently resisted infection. No. 202
was gradually wasting away, and died July 24, more than two months
after exposure. In the large intestine were cicatrices of healed ulcers
and such as were healing. The severest lesions were in thelungs. Both
were adherent by means of bands to the costal pleura, and were exten-
sively hepatized. No. 205 was alive and well August 15.

Of the second lot, which had received 1 cubic centimeter of the same
culture the results were nearly the same. Twosuccumbed to theinocula-
tion, one died of infection, and a fourth survived. No. 208 died fifteen
days after inoculation. Besides the inoculation swellings, enlarged and
congested spleen, the mucous membrane of the largeintestine was covered
with extensive deep ulcers, and the walls much thickened and softened.
The corresponding lymphatics in the meso colon deep purple. No. 209
died in six days after inoculation. There was general congestion and
extravasation of blood in the internal organs, involving the entire mu-
cous membrane of the alimentary tract, especially the large intestine,
the lymphatics and serous membranes, the spleen, and kidneys. Ulcera-
tion had not yet begun. In both animals the spleen was crowded with
bacteria and furnished pure cultures of the specific germ.

Nos. 206 and 207 were not affected by the inoculation. They were
exposed with the preceding lot, as indicated in the table. No, 207, after

pints 148

apparently resisting infection in the infected pen for a month, died July
18, after having been in a clean pen since June 21. The extensive ne-
crosis of the mucous membrane of thececum and upper portion of colon,
with the absence of any acute inflammation elsewhere, gave evidence of
a chronic case of hog cholera. No. 206, though still alive, is emaciated.

The two remaining check pigs, which were exposed with the preced-
ing animals in the same infected pen, both died of hog cholera; No.
211 found dead June 21. The most marked changes were a small num-
ber of ulcers on a pale mucous membrane scattered over the cecum and
colon. No. 210 lived a month longer than its mate. The existence of
hog cholera was demonstrated by a general necrosis of the mucous
membrane of the cecum and an extensive pigmentation in the remain-
der of the iarge intestine. The lungs were adherent in places and much
congested.

When we gather together the facts presented by this experiment we
shall find a certain number of interesting ¢ ductions springing there-
from. In the first place, we note the peculiarity of the intestinal lesions
of the two animals which died from some unknown cause, presumably
not hog cholera. We next point to an additional demonstration of the
specific nature of the bacillus of hog cholera, for out of eight inoculated
four died, and the age of the lesions corresponded well with the length
of time elapsing between inoculation and death.

Those animals which resisted the inoculation were in part protected,
as two among four were still alive on August 17, and the remaining two
died, probably from effects of the ulceration, months after exposure.

| Died from = *Pesure Removed
No. | Inoculated April 2. pacen safeat aa iesutna. Remarks.
; : pens. pens.
ie | — =
*202 | 1% ¢. c. culture liquid :|:-.2..---- | May 18 | June 21 | Died July 4.
204 hectare Oh Benpasnisacoes te eX ors Li Be aera aeacs se oats soe
200i tema (MSS ns paseaostisslseacsocesc |----do ...| June 21 | Alive August 17.
D2 ere stern « 00: 3-en5> essen | -Acprilet) |e saeee eee Meee rears
206 | 1c. c. culturo liquid..|...... -....| May 18 | June 21 | Alive August 11, but unthrifty.
OG NS eke Oe Se 2 Sebo ste: | aaa ce Eee ee Reger | area en ie Died July 18.
20Ba| face: 6M os52 hese \eArrrrala Rie | Pee tae eee Pe aaessoan’ |
209 se eed UKs SSaneepperbe | April 8 Gee ea Foe, ee
1208) eae. 5 few sway anes ac Ears each on hae SSeeral Sere pee ete Died April 11, from some unknown dis-
| ease.
W2NOF|\ Ss saree caches woe wee Soetewte meee sae | May 18 | June 21 | Died July 21, of hog cholera. —
POU pe nk ee see eh ee eee {is Aven aegis Bale dO alee Died June 21, of hog cholera.
P2138") Sonsas coos sees Sooo nese es | name eee | Le ee eles See eee Died April 13, from same disease as No.
| 203.
* These animals were one and a half months old at date of inoculation. | Checks.

Experiment 7.—Having determined that even large doses of liquid
cultures of the bacillus of hog cholera can be borne without produe-
ing the disease in most cases, it was thought advisable to make two in-
oculations of strong virus, a first one with a small quantity and a second
with a large quantity.

149 .

First inoculation, April 21: Nos. 214, 227, 223, and 222 received 4
cubic centimeter of a third culture in becf infusion containing 1 per
cent. each of peptone and glucose. The liquid was diluted with sterile
salt solution, so as to make } cubic centimeter. It was injected, one-
half beneath the skin of each thigh. After waiting two weeks, in order
to determine whether the inoculation had not produced disease, a second
injection was practiced May 6, the thirteenth and fourteenth cultures
of the same series being used for this purpose. The animals received
1,14, 2, and 24 cubie centimeters of the culture liquid, respectively.
No untoward results following the injection of these large doses, they
were transferred to the large infected pen May 25.

A second lot (Nos. 226, 228, 215, and 229) were treated in precisely the
same way and at the same time, excepting in receiving $ cubic centi-
meter for the first dose instead of + cubic centimeter.

|
2 | Expos- | e
First Second | HI ; 5 Days
No. inoculation, inoculation, | Laraeient | ees after first
Apr. 21. ay 6. | Sere “"~* | exposure.
| pen. |
3 = aa wea r 2 ae Ee a
Cc. ¢. c.¢.
214 4 1 | May 25| July 1 37
227 4 tp |. .2do...22'| Junes27 33
223 4 DI ela adorn =| hly + 2)/P 38
232 4 | OM. dole. dale «1 | 37
226 | 1 |.-.do....| July 3 | 39
228 Z| 14 |..-do....| July 13 | 49
215 4 | Qe \e-2do eee dtily, 10) 46
229 4) 24 |...do ....| June 27 | 33
ER Nee ar yea.5 90) nec Eee .|---do saan, A | lee
S54 eit aes oe SSE See Sees |---do ... | June 27 | 33 |
* Checks.

No. 214, being in a dying condition July 1, was killed. Jn the cecum
and colon were found very large, deep, blackish ulcers upon a pale mu-
cosa. The case was evidently one of chronic hog cholera. A pure
liquid culture of the hog cholera bacillus was obtained from the spleen.

No. 227 died June 27. Thelymphatic glands were deeply congested ;
the mucosa of large intestine was generally pigmented and covered
with large blackish ulcers. Small yellowish ulcers were also found in the
ileum. The points of injection were occupied by encysted, partly lique-
fied masses.

No. 223 was found dead July 2. At the points of injection encysted
masses were found, the contents of one of which were discharging through
an opening in the skin. The mucosa of the entire large intestine deeply
congested. Scattered ulcers of varying age and size in the cecum and
colon. SBacilli in spleen.

No, 232, after a period of unthriftiness, was found dead July 1. The
autopsy revealed a chronic broncho-pneumonia, with pleuritic adhesions
of right lung. The mucous membrane of the cecum and colon, besides
being studded with a large number of shallow ulcers, was deeply and
uniformly congested, the congestion involving also the lower portion of
the ileum. On both thighs an encysted semi-liquid mass indicated the
seat of the inoculation.

150

Of the second lot, which had received 4 cubic centimeter of the first
inoculation, all succumbed to the infection.

No. 226 died July 3. The characteristic lesion was extensive ulcera-
tion, together with deep congestion of the mucosa of large intestine.
Encysted masses at the points of inoculation. A considerable number
of hog cholera bacilli in the spleen.

No. 228 died July 13. In this animal the mucosa of czcum and colon
presented a continuous mass of necrosed blackish tissue, the ileo-cecal
valve being enlarged to twice the normal size. <A few scattered yellow-
ish ulcers in the lower portion of the colon.

No. 215 died July 10, probably affected in the same way, though no
post-mortem examination was made.

No. 229 died July 27. In this case the lymphatic glands were in
general deeply congested; ecchymosis beneath the serous membranes.
Pigmentation of the mucous membrane of the stomach, duodenum, ileum,
and large intestine from former extravasations. Several large ulcers
on the valve and some others in colon. Ulcers in the cardiac portion
of the stomach. Encysted masses at the point of inoculation.

Nos. 224 and 225 were penyed with the above eight animals as checks.
No. 225, after being sick for a few days, was found dead June 27. The
mucosa of the cecum and upper half of the colon was extensively pig-
mented and ulcerated, the lower half deeply congested. The ileum ul-
cerated for 5 or 6 feet from the valve. Many of the ulcers were so deep
as to have produced inflammation of the serous membrane and thickening
of the intestinal walls. The othercheck (No. 224) lived over two months
after exposure, being unthrifty during this period. On post-mortem ex-
amination the mucosa of large intestine was considerably pigmented,
and sears of healed ulcers were present. A large suppurating wound
of the lower jaw, involving the bone, may have contributed towards
the fatal issue.

Experiment 8.—These inoculations having failed to produce immunity
from natural infection, another experiment was tried by augmenting
the dose of strong virus used for the second inoculation. Thus Nos.
239, 242, 244, and 245 received each 4 cubic centimeter for the first in-
oculation May 27, No. 243 being retained in the same pen as a check.
Of these No. 239 died of hog cholera as the result of the inoculation.
The remaining three, received two weeks later, on June 10, 2 cubic cen-
timeters each of strong virus. The cultures were prepared in beef in-
fusion with 1 per cent. peptone. They were usually the third or fourth
culture, not more than one day old. A second lot (Nos. 240, 254, 255,
and 256) were inoculated at the same time and in the same way, with
this exception, that the second dose was increased to 3 cubie centime-
ters. On June 24 all were placed in the large infected pen.

No. 239 died June 2, within six days after receiving 3 cubic centime-
ter of the culture, and as a result of the inoculation. ‘The lesions were
those of a very acute case, engorged spleen and lymphatics, intense con-
gestion of the mucosa of the large intestine and of the intestinal tract
in general. The lungs were likewise engorged and dotted with extrava-
sations. This animal was eating and apparently well on the morning
of death. The spleen was crowded with bacilli of hog cholera, and pure
cultures were obtained from it.

No. 242 died July 17. The characteristic lesions of hog cholera were
found in it; extensive ulceration of the cecum and colon; engorgement

151

of spleen and lymphatic glands with blood. Eneysted masses at the
point of inoculation. No, 224 succumbed July 9 with practically the
same lesions, besides the presence of a considerable quantity of serum
in the abdominal cavity.

The check to this lot died July 13. The depth of the ulcerations in
the czecum and colon had implicated the serous covering, so that adhe-
sions had formed between the cecum and abdominal walls. Punetiform
ecchymosis on serosa of ileum; the mucosa not affected. The mucosa
of cecum was found completely ulcerated, the necrosis stopping ab-
ruptly at the edge of the valve; in the colon the necrosis resolved itself
into large isolated ulcers.

Of the second lot, No. 240 died July 10. At the place of inoculation
a firm pale yellowish mass, about linch long, was found. The lower
portion of ileum, the cecum, the upper portion of colon, contained ul-
cers of different sizes. The duodenum was occluded by a clot of blood.
No. 254 died the same day, with lesions of a similar character. No, 255
died July 20. The spleen in this case was greatly augmented in size
and gorged with blood. The right lung was congested and adherent to
wall of thorax; considerable effusion in this pleural sac. The cecum
and upper portion of colon covered with deep blackish ulcers. A few
small ulcers in ileum.

e Expos:
Wo. {inoculation insceiaion | ,™2%, | Time, | aetor hrst
May 27. June 10. oS | of death. exposure.
C.c. c.¢
239 We Gacbaadcsodl haepogsngs June 2t|... -
242 3 2 | June 24 | July 17 23
244 3 2 do....| July 9 15
245 $ 2 Wea Ol) ee clloeeamoeeide Jodagde sconce
S240 eeatentn slg Ra's) |e areteiate apo [sick do ....| July 18 19
240 3 3 do July 10 16
254 3 3 Ci Kopel eeac Oyisee 16
255 | 4 3) |e--d0 July 20 | 26
256 4 CT Mosely Are eae meee lal ane aes
WEY I Aiieocerindal|sosoc6 465ei0| ssn esas sepeecoaee (eGasoccacde
* Check. t From inoculation.

The foregoing experiments demonstrate the important fact that pigs
can not be made insusceptible to hog cholera by subcutaneous injec-
tions of pure cultures of hog cholera bacteria, according to the method
used by Pateur in anthrax vaccination. They show how injudicious it
is to draw conclusions extending to infectious diseases in general from
experiments made upon one disease only.

THE £FFECT OF FEEDING SMALL QUANTITIES OF CULTURES.

It has been already demonstrated (p. 107) that hog cholera can be pro:
duced in pigs by feeding such as had been starved for a day with con-
siderable quantities of cultures of the specific bacteria. From 200 to
400 eubic centimeters of a beef-infusion culture were necessary to de-
stroy the animal.

152

Assuming that small doses may produce a mild form of the disease,
it seemed worth while to determine whether animals which had been
fed with small quantities of culture material would resist infection when
placed with sick animals in thoroughly infected pens. The following
experiment shows that even after this treatment pigs are still suscepti-
ble to the disease: d

Nos. 379, 380, 381, 382, and 370 were starved for thirty-six hours and
then fed pure cultures of hog cholera bacteria in simple beef infusion,
The quantities given are tabulated below. They were diluted with
eef broth to facilitate feeding.

: at : a5) a No.
wo, | Agestan- | Quantity, [Placed in} Died tn | of days
“™ | liquid fed. pen. pen. posure.
x ————— —s
CAL
380 | 5 months . 10 | Apr. 15 | June 20 66
SHO ed OO (52h 20) "5-00-22 2. |s May? 24 39
BP hdl e ese yes Sac 40) 32400) 2) Nay oO 25
381 doeea! 60 sd0 4] Mlayaok 46
S103 |PsecdOnse a - LOORN Sedo se) Apr 20%
feeoul ee MOnthss| eee ee see | Apr. 19 | May.11 |} 22
Le toi al ike (epee | eee eg edoreta|/eAupIn 230 11 ®
(ee ona O) oa 2b bee taseacric Apr. 30.| May 17 | 17
UCL Boon l)eesae Ra oReeas do ....) Beets | ee eet
* From injury. t Checks.

All appeared to be affected by the feeding on the following day by
refusing food more or less. Slight improvement on.the second day, with
the exception of 381. On the third day 381 still very i!]. On the fourth
day 382 seems more affected than 381. Within the next few days 382
refuses food, the rest eat. In the second week they had recovered.
The growth of 382 was materially checked by the feeding, so that it
had not gained any weight even after several months.

April 15 they were transferred to a pen infected with hog cholera, in
which acute cases had lately appeared. A number of check animals
were transferred to the same pen soon after. . The result may be briefly
summed up as follows:

No. 379 began to fail from May 10 and died May 24. Lymphatic
glands generally enlarged and congested; those of meso-colon very
much so. Spleen very much enlarged; quite firm. Large number of
yellowish coagula in abdominal cavity. Adhesions between cecum
and adjacent organs. Liver very much cirrhosed; gives a gritty sen-
sation when cut. Several deep, extensive ulcers from 1 to 2 inches
across in cecum, involving the serous membrane. In lower colon and
rectum considerable congestion and hemorrhage. Lungs normal, with
exception of a few subpleural ecchymoses. Both sides of heart filled
with white thrombi. This animal, therefore, had chronic hog cholera,
which, no doubt, caused the fatal peritonitis.

No. 382, the stunted pig, showed signs of the disease May 1 and died
May 10. Very emaciated; connective tissue of body stained deep yel-
low. Spleen very large and full of blood. Lymphatics but slightly
enlarged and reddened. Considerable yellow serum in abdominal

~

153

cavity. Right heart filled with dark and washed clot. Lungs normal,
excepting a few subpleural ecchymoses. Extreme cirrhosis of liver.
Mucosa of great curvature of stomach deeply congested, mucosa of large
large intestine in patches.

No. 381 took sick soon after its removal to the infected pen, but the
disease seemed to be mild until it was found dead May 31. Animal
with a fair quantity of fat: Skin of ears, pubis, and throat deeply red-
dened. Lymphatic glands generally enlarged and infiltrated with blood.
Spleen very much enlarged, but tissue quite firm. Lungs hypostatic ;
no hepatization. Epicardium covered with pale spots of extravasation.
Liver partially sclerosed; hepatic ducts filled with viscid yellow bile.
Medulla of kidneys dotted with petecchiz. Mucosa of large intestine
apparently normal. In the lower colon the feces are blood-stained, and
oecasional small clots are loosely attached to mucosa.

No. 370 was injured by fighting after being transferred to the infected
pen so as to be searcely able to stand, and died April 20. On both
hind limbs there was extensive extravasation in the subeutis. The super-
ficial inguinal glands were deeply congested. Spleen enlarged and

“<gongested. A moderate number of bacteria present, which are not hog

cholera bacteria as shown in cultures. Left lung collapsed, reddened
in part and adherent to chest’wall by a plastic exudate. Centers of
acini of liver deep red, tissue soft. Kidneys congested. Stomach con-
gested along fundus; digestive tract otherwise normal. This animal
died from injury to limbs and lung, and there may have been septic
infection as indicated by bacteria in the spleen.

No. 380 became ill May 6, died June 20. Decomposition advanced.
Lungsand glands normal. Liver small, sclerosed. Superficial necrosis
in cecum and upper colon with cicatrices of healing ulcers.

Gelatine tube cultures from the spleens of 382, 3883, and 397 showed
innumerable colonies of hog cholera bacteria. Cultures from the spleen
of 381 remained sterile. A larger number of cultures would probably
have shown their presence.

As to the fate of the check pigs exposed with the preceding lot very
little need be said.

No. 383 had been fed with 250 eubie centimeters of a beef-infusion
culture of the hog cholera bacteria from Nebraska as far back as De-
cember 19. It recovered, however, after an illness of three or four days.
March 16 it received a tracheal injection of swine plague bacteria, with-
out any untoward result. It was exposed to hog cholera as a check
April 19, and died very suddenly May 11. It had hemorrhage in sub-
cutis, lungs, lymphatic glands, in stomach, small and large intestine.
In the cecum there was an ulcerated patch about 2 inches across. Its
base was very firm and nearly one-third inch thick. Was the ulcer the
result of the feeding five months ago?

No. 387 became very dull and off feed one week after its removal to
the infected pen, and died April 30. Skin of abdomen reddened. Lym-
phatics generally hemorrhagic. Ecchymoses on lungs. Extravasations
in medulla of kidneys. Beginning ulceration in large intestine. Con-
gestion and sliglt hemorrhage in fundus of stomach.

No. 394 died May 17 after a few days of dullness. Hemorrhagic con-
dition of spleen and lymphatie glands. Inflammation and extravasa-
tion in stomach. Ulceration and intense congestion of large intestine.
Eechymoses beneath pleura of lungs.

No. 399 was alive and apparently well June 15. Hog cholera bacteria
were found in the spleen of 387 and 394, especially numerous in the
latter. They were not looked for in 383. |

154

There was no protection from the feeding of cultures even in those
animals which were most severely affected thereby. There was, how-
ever, a marked difference between this lot and the check animals, in
that the latter died of the most severe septicemic or hemorrhagic type
of the disease, while the former succumbed to a chronic infection. If
we take the average duration of the disease in the pigs fed with cult-
ures and those not fed, the ratio will be approximately as 19 to 8 or as
24 tol. These figures indicate a considerable retardation of the fatal
issue, which is equivalent to a partial immunity. Another fact of im-
portance needs to be considered in connection with these figures. Three
Of the pigs fed with cultures were affected with a more or less advanced
cirrhosis of the liver and the post-mortem notes will show that this liver
disease largely contributed to the death of the animals. An important
question arises in this connection as to the origin of the cirrhosis. It
may have been due to the feeding of the cultures. If so, the remedy
would be as bad as the disease. But even setting aside this possibility,
the method of feeding living bacteria gan only have a theoretical im-
portance in leading to other methods. It not only scatters the living
virus, but it may induce ulceration in the large intestine which, while
not recognizable, may be slowly destroying the animal.

INJECTIONS OF STERILIZED CULTURE LIQUID TO PRODUCE IMMUNITY.

Bacteriological investigations of the past few years have shown pretty
conclusively that during the multiplication of pathogenic bacteria there
are formed chemical substances or ptomaines which are poisonous to the
animal economy. The researches of Brieger have done more than any
others to confirm this theory. It is now generally believed that it is
these poisons which produce such grave symptoms in infectious diseases
rather than any other vital manifestation of bacterial growth. In the
spring and summer of 1886 Sirotinin made some experiments (Zeit-
schrift fiir Hygiene, I, 463) with the bacillus of typhoid fever, in which
he endeavors to show that the smaller experimental animals can not be
infected by this bacillus, but that death caused by injection, subcuta-
neously or otherwise, must be attributed to an intoxication caused by the
presence of a pitomaine in the cultures. The results actually proved
that the injection of sterilized cultures may produce death accompanied
by lesions resembling those produced by living bacilli. Beumer and
Peiper (Zeitschrift fiir Hygiene, II, p. 110), after a long series of experi-
ments, are brought to the same conclusion, that the typhoid-fever or-
ganism does not multiply in the body of smaller experimental animals,
that there is, indeed, no true infection, and that the severity of the symp-
toms depends entirely upon the quantity of culture material iniected ;
in other words, upon the quantity of the poison or ptomaine therein
contained. They also point out the important fact to which. we wish
to call attention, that death does not follow the injection of large doses
if small non-lethal doses have been given previously, and from this
fact they argue that perhaps immunity may finally be brought about

155

by the injection of sterile cultures in successively larger doses. That
the chemical products of bacterial growth may produce immunity is no
new theory, but it seems to have gained ground but recently among in-
vestigators.

TESTS WITH STERILIZED CULTURES ON PIGEONS.

In our experiments pigeons were selected at first, because more easily
obtainable and manageable. They proved, however, a very good choice,
since they do not take the disease readily and thus are made insuscepti-
ble by small doses of culture liquid. A culture in beef infusion, con-
taining 1 per cent. peptone, in which active multiplication of bacteria
ceases in a few days, is fatal to adult pigeons, as a rule, when three-
fourths of a cubic centimeter is injected subcutaneously over the pec-
toral muscle or superficially into the muscle itself. The intra-muscular
injection is more rapidly fatal. The effect of these inoculations has
already been dwelt upon, but it is restated here on account of the im-
portant principle involved.

The pigeon, after such an injection, may be dead within twenty-four
hours. The inoculated pectoral muscle is more or less discolored
throughout its depth. There may be a regurgitation of food from the
crop, a8 grains are found mixed with mucus in the mouth and cesoph-
agus. The injected bacteria are present in small number in heart’s
blood, liver, and spleen.

About one-half of the pigeons do not die so soon. The bird stands
quietly in a corner of the coop, with feathers ruffled, wings slightly
separated, and tail feathers drooping. The discharges are usually ab-
normally liquid, at times mixed with considerable mucus. The bird
usually dies within a week. The pectoral muscle will then be found
extensively necrosed, the surrounding tissue very hyperemic. The in-
jected bacteria are found, sometimes in considerable number, in the
liver and heart’s blood.

The rapidly fatal cases might be regarded as the result of simple
intoxication or ptomaine poisoning. There is, however, some bacterial
multiplication. In the more chronic cases there is an undoubted infec-
tion, characterized by multiplication of bacteria in the internal organs.
Pigeons are far more susceptible in winter than in summer, conse-
quently in the heat of midsummer the control animals occasionally
resist and thus impair the value of the experiments.

The experiments were carried out as follows:

Culture tubes containing about 10 cubic centimeters of beef infusion
with 1 per cent. peptone were incculated with hog cholera bacteria and
placed in the incubator at 349-369 C. After a certain number of days,
varying from three to ten, the tubes were exposed to a temperature of
58°-60° C. for about one hour. Inoculation of fresh tubes showed that
bacteria had been destroyed. This test was always resorted to to make
sure that no living bacteria were injected.

156

From 1 to 1.5 cubic centimeters of this culture liquid were injected with
a hypodermic syringe beneath the skin of one pectoral muscle. This in-
jection was repeated once or twice. Some days after the last injection
the bird was inoculated with living bacteria. About # cubic centimeter
of a beef infusion peptone culture was injected beneath the skin of the
other pectoral or into the saperficial layer of muscular fibers. The vac-
cinated pigeons remained alive and well; the control pigeons nearly all
died. These statements are best illustrated by the tabulated results of
a few experiments.

The first one, made in January, 1886, is given below. The control
bird and tke one which had received avery small quantity of sterile
culture liquid died within two days after the test inoculation; the rest
were well more than a week later.

I.—1885--'86.

Injection of—

| Culture

liquid con- |
No. Sterilized culture liquid. taining =| Remarks.
living
bacteria.
| |
Dec. 24. Jan. 21. Jan. 29.| Feb.6. | Total.| Feb. 13.
ee oes i | —|—— ==)
Cac. PG | c.c cc. | Ce | c.e
10 Se des tends eGo IN Seaeon 3 Well February 20.
100 SLebeaseos yD 1.5 1.5 4.5 a Do.
ED epee ee 1.5 | 1.5 1.5 4.5 | 3 Do.
13's [esto He. ee Ac ries Gd 3 Do.
8 Hee eh eae- a4 lencoeees 8 8 | Diedin forty-eight hours.
1b Ue eee eee Ol es Be ele lea te tec 2 | Died in twenty-four hours.

A second series of injections, made to confirm these rather remarkable
results, was equally unequivocal in its answer:

I1.—1886.
Subcutaneous injection of—
No. Sterilized culture liquid. ae Remarks.
Feb.19. | Feb.24. | Mar. 2. Total. Mar. 8.
c.c cc CNC: c.¢ c.¢.
16 il ili; 3 | 23 | 3 Well after several weeks.
17 1 1 1 3 3 Do:
18 1 1 1 3 2 Do.
19 tel ees berid 1 2 3 Do.
20 if eae 1 2 g Do.
21 cig Ea a 1 2 3 Do.
pple EEA a oye eee Behl ose. .oSaH nooHnesaselscaontodtcaor Dead March 9.
OP ills. hte Agiesa el hdieeaate te etal eat ae baterd [eles eltei are 3 Do.
DA & |Sce eee |etacpectaeilbee ae settee eee 3 | Remained well.

157

The third control bird (No. 24) was of a different race of pigeons. A
good authority consulted at the time regarded it as having some of the
characters of the carrier pigeon. Leaving this aside, the result is suf-

ficiently convincing.

In aseries of experiments made more recently, cultures were used
which had been concentrated by evaporation in vacuo. About 100 eubie
centimeters of beef infusion, containing 2 per cent. peptone and one-half
per cent. sodium chloride, was inoculated and kept in the incubator for
five days. It was then reduced to 20 cubic centimeters by evaporation
at 40° C., and sterilized at 60° C., for three-quarters of an hour. Sub-
sequent inoculation of fresh tubes showed that the liquid was free from
living bacteria. The injections were made as usual, the needle entering
the pectoral muscle very superficially.

ITI.—1887.
Sterilized concentrated culture Fete
liquid. liquid.
35a ee eal iit hea, Remarks.

Equivalent

‘ of ordi-
Apv.19. | Apr. 22. a ult. | ABT 25:
ure fluid.

cc. c,¢, c.c, Cc. C.

1 4 3 24 | 2 | Well May 31.

2 } 4 22 | 3 Do.

3 4 4 24 | % | Slightly ill April 26; well May 31.
4 Uy escheat oss < 5 2 | Well May 31.

5 Me Weceecninas: 5 ne] Do.

6 Dh eters wis sree 5 8 Do,

Tt, dlpeedeecaed eeencrecrd lsemecurcrent | Died April 26, 9 a.m.

BP lt eneeceseel Soecocnted||>cemoe heen 2 | Died April 26, 1 p.m.

Dera aatarosimc alll aptala ccna} |eetaaiss aeioee $ | Died April 30.

Jn order to determine whether the introduction of sterilized culture
liquid into the digestive tract of pigeons would be equally efficient in
giving them immunity, three pigeons were fed on three days (Septem-
ber 8, 10, 13), each receiving about 30 cubic centimetersin all. ‘The cult-
ure liquid consisted of beef infusion, to which 1 per cent. peptone had
been added. The feeding was carried out by introducing a catheter into
the pigeon’s crop and injecting through this by means of a syringe. On
September 16, three days after the last feeding, these three pigeons and
two checks were inoculated with # cubic centimeter of unattenuated
culture liquid. The three fed pizeons and one check died from the ef-
fects of the inoculation, the second check was well September 29. The
blood and liver of No. 1 were examined by adding a few loops of heart’s
blood and a minute piece of liver tissue to two roll-cultures. In each
about 50 colonies developed. In the liver of No. 2 bacteria were very
numerous. The feeding therefore had no effect whatever in conferiing
immunity.

158

Vi.

Fed with sterilized cultures five .
days and nine days old. Tnoculation of
ss a ES 4 unheated R k
culture liquid DEES

16

No. | Sept.8 | Sept. 10 | Sept. 13. Sept. 16.

Cone; ee: Cue: BO
1 10 10 16 3 | Dead September 17.
2 10 10 10 3 | Dead September 23.
3 10 10 10 3 | Dead September 24.
70) 55 herd pecogseuag boSatoaso5 3 | Died September 19.
Bil eee qae= sel em eterine eet eae 3 | Well September 29.

tate a. arm ~

The protected pigeons very rarely show any signs of illness. They
are as active and as eager for food as before the final inoculation. In
all a small sequestrum is formed in the pectoral muscle, where the
injection has been made, and this, at the end of a few weeks, is sur-
rounded by a dense membrane which seems to act as an absorbing
surface for the sequestrum. No indication of any reaction is found on
the side into which the sterile cultures are injected. The three tables
may be summarized as follows: Of twenty-four pigeons sixteen received
sterilized cultures, eight being reserved as checks. Of the former none
succumbed to the final inoculation ; of the latter seven, or 87.5 per cent.

The conclusion to be drawn from these experiments is obvious. The
birds are protected by the injéction of sterilized cultures so as to resist
a fatal dose of living bacteria. The sterilized cultures contain only the
products of bacterial growth. Among these the ptomaine-like bodies—
some of which we now know, owing to the researches of Brieger—are
very likely the agents that produce immunity.

In the pigeon the mode of infection before and after vaccination is
probably as follows: The injected bacteria multiply very actively in the
muscular tissue; the ptomaine there produced may enter the circula-
tion in quantities large enough to produce speedy death. If the animal
resists for a time, the absorbed ptomaine reduces the vitality of the
tissues to such a degree that bacteria, entering the circulation, begin
to multiply in the internal organs. The additional quantity of ptomaine
thus produced finally kills the bird.

When ptomaines in culture liquids have been previously introduced
the first shock caused by the local production of ptomaines in the mus-
cular tissue is overcome. ‘The bird resists successfully general infec-
tion until the bacteria have been destroyed locally. The process is then
checked, and the sequestrum in the muscular tissue becomes encysted.

It has already been stated (p.69) that rabbits, mice, and guinea-pigs are
very susceptible to the inoculation disease, a millionth of a cubic centime-
ter of culture liquid being sufficient to cause a fatal issue. Experiments
like those on pigeons were made upon rabbits with slightly larger doses,
but no immunity was gained thereby. The rabbits succumbed invariably
after inoculation. (See report of Department Agriculture for 1886, p.

159

637.) In the light of later experiments* made in Pasteur’s laboratory,
the failure of the metaod in case of rabbits must simply be ascribed to
the small quantity of culture liquid used. In the experiments there re-
corded from 80 to 120 cubic centimeters of culture liquid were required
to protect guinea-pigs from malignant cedema, while in our rabbit ex-
periments only 5 to 6 cubic centimeters were used in all. We did not
delay, however, with the further demonstration of this principle upon
small animals, and applied it experimentally to pigs. The quantities
injected were not sufficient, however, and the animals took the disease,
as the following experiments show:

TESTS WITH STERILIZED CULTURES ON PIGS.

Experiment 9.—In order to test the effect of heated cultures upon
pigs, the following experiments were made March 1: Two animals (Nos.
162 and 173) received hypodermically each 9 cubic centimeters of a sec-
ond and third culture, twelve and thirteen days old, respectively, which
had been devitalized by heat. March 9 a second dose of 9 cubic centi-
meters was given in the same way, using a fifth and eighth culture
eighteen and fourteen days old, respectively. These cultures were
made in beef infusion containing 1 per cent. peptone, excepting one,
which contained about 2 per cent. of blood serum in place of the pep-
tone. After the second inoculation of No. 162 a swelling appeared on
one side. Both were fed with viscera infected with hog cholera, and
placed with sick and dying pigs in a large infected pen. No. 162 was
found dead March 29, and No. 173 April 5. The appended table and
notes give a summary of the experiment:

No. of days
Died. after feed-

ing.

No. Mar. 1. Mar. 9. Total. Fed.

162 9 yg "18 | Mar.19
173 9 9 18 | Mar. 19

Mar. 29
Apr. 5

10
17

No. 162. Subeutaneous fatty tissue much reddened. Mucous mem-
brane of stomach considerably ulcerated; mucous membrane of small
intestine deeply congested. For 8 or 10 feet above the ileo-czcal valve
the mucous membrane of ileum is completely necrosed. Large ulcers
in cecum and upper portion of colon.

No. 173. Subcutaneous fatty tissue slightly reddened. Petecchis un-
-der pulmonary pleura. Extravasations under serosa of czcum and
colon. Inflammatory adhesions of large intestine with walls of abdo-
men. A patch of extravasation beneath peritoneal layer of dorsal ab-
dominal wall nearly 2 inches across. Spleen very much enlarged and
softened. The mucous membrane of large intestine and several feet of
ileum necrosed and breaking down. Fundus of stomach deeply con-
gested.

This experiment clearly showed that this method was no protection
to the animal when the latter was infected by feeding.

* Annales de V Institut Pasteur, December, 1887, January, 1888.

160

It now became necessary to determine whether this method would
confer immunity upon animals simply exposed to the disease by cohab-
iting with diseased animals in infected pens.. Observations made upon
other diseases by investigators, and by us upon this disease, seem to
lead to the inference that it frequently depends on the quantity of virus
introduced into the system whether the disease will make its appear-
ance or not. In feeding, this quantity is considerable; in simple ex-
posure in infected pens to diseased pigs, the amount of virus taken into
the body with the food and drink is necessarily in small and repeated
doses. ‘The following was therefore planned :

Experiment 10.—Four pigs (Nos. 163,164, 177, and 196) were inocu.
lated March 13 with heated virus, each receiving 44 cubic centimeters
beneath the skin of each thigh. The cultures in beef infusion with 1
per cent. peptone were about fifteen days old when heated. The second
inoculation was made March 16 from a culture in an Erlenmeyer flask
about eleven days old, and containing about 50 cubic centimeters of
culture liquid. Each animal received 10 cubic centimeters as before.

March 51 these animals, together with two check pigs (Nos. 195 and.
201), were placed in a large infected pen. Within a period of three
weeks from this date at least fifteen pigs died of hog cholera in this
pen. The two check animals died on the 14th and 19th of April, re-
spectively. Of four vaccinated animals only No. 163 showed signs of
the disease and gradually developed into a chronic case, dying of general
debility on May 1. The three other vaccinated animals remained ap-
parentiy well for months after, although constantly exposed to the dis-
ease in the infected pen.

Vaccination.

No, |——_________| Exposure.) Died. Number days after exposure.
Mar. 13 | Mar. 16 |
Cc. C. €: C.
163 9 | 10 | Mar. 31 | May 1/ Thirty-one days.
164 SI UO peaoscemode |eoceaascen
177 9 10 Mar. 31 | July 23 | Three months and twenty-three days.
196 9 10 |.-.do....| July 7) Three months and seven days,
LOG is a natretes< Sell nce ae ---d0....| Apr. 19 | Nineteen days.
QOD | soc cise sQhlllmiesteeiziecte -.-do....| Apr. 14 | Fourteen days.

Autopsy notes.—No. 163. Spleen not much enlarged; texture firm ;
effusion into pericardial and thoracic cavity ; lymphatic glands enlarged,
but pale; two ulcers in stomach; small intestine normal; mucosa of
cecum and colon studded with many extensive and deep, yellowish
ulcerations. On cover-glass preparations of the spleen only a few bac-
teria could be seen. Two liquid cultures inoculated from the same organ
remained sterile. No colonies appeared in the gelatine tube inoculated
with blood from the heart. A few developed in the eelauiae tube inoc-
ulated from the spleen.

No. 195. Spleen greatly enlarged; gorged with blood; very friable ;
shreds of a fibrinous exudate on serosa of intestines ; much serum in
abdominal cavity ; petecchiz on epicardium of auricles; small ventral
lobes of lungs hepatized ; mucous membrane of gall bladder ulcerated ;

161

extensive ulceration and inflammation of mucous membrane of caecum
and colon. Hemorrhagic inflammation of kidneys.

No. 201. Spleen but slightly enlarged ; lungs extensively hepatized ;
intense congestion and commencing ulceration of the mucosa of large
intestine; stomach and portion of ileum similarly congested. Though
no bacteria were found on a cover-glass preparation, a pure culture was
obtained by carefully dropping a piece of spleen tissue into a culture
tube. This was tested on gelatine.

After apparently resisting the infection for several months, the remain-
ing pigs (Nos. 164, 177, and 196) were transferred to aclean pen. No.
177, not very thrifty, began to decline, and finally died July 23. Among
the most prominent lesions were a plastic exudate on the epicardium
and numerous large old ulcers in the large intestine. The mucosa itself
was extensively pigmented. No. 196,o0n removal from the infected pen,
seemed in good condition, but it died July 7, after some days of
unthrifty condition. In this case, the mucous membrane of the large
intestine was pigmented and there were what appeared to be cicatrices
of old ulcerations. In all of the large serous cavities there was con-
siderable effusion. In cover-glass preparations of the spleen there were
no hog cholera bacteria to be seen, but numerous bacilli resembling
those of malignant cedema.

Haperiment 11 was made in the same way upon Nos. 197 to 200, in-
clusive, and No. 157. March 24 each animal received in the thigh about
10 cubic centimeters of a mixture of heated cultures in beef infusion with
1 per cent, peptone about fourteen days old. March 29 an equal amount
was injected, one-half into each axilla, these cultures being about fifteen
days old. These animals were kept until April 29, when all but No. 157
were placed in the large infected pen. From that date on pigs died almost
every day of the disease, so that the infection must have been quite
thorough. Unfortunately no check animal was exposed at the same
time. In these animals the slight swelling at the seat of inoculation
disappeared in a few weeks.

They remained well, with the exception of No. 199, which became
emaciated and was found dead May 19, about one month after exposure.
The three remaining animals were apparently unaffected nearly two
months after exposure. At this time No. 197, which appeared rather
thin, was killed, to determine if any ulcerations were present. But the
mucous membrane of the intestine was entirely normal, with no indi-
cations of former ulcerations.

Injection of heated
virus. ! ;
No Time of |
fs exposure. |

Mar. 24 | Mar. 29

Remarks.

Haha
a C.e. | Cue. peril
197 10 | 10 | Apr. 20 Killed June 10;
| healthy.

198 10 10 |...do... Well June 10.
199 | 1) 10 |. do wes: Died May 19.
200 | 10 10 |...do....| Died July 12.
157 | 10 10 | May 25 | Died June 28.

15612 Hw c——11

162

Autopsy.—No. 199. Slight extravasation in subcutaneous connective
tissue. Spleen somewhat enlarged, filled with blood, friable; consider-
able effusion in peritoneal cavity. Right lung in part hepatized; pleu-
ritic adhesions to chest-wall; hemorrhage in and about pelvis of kid-
neys; lymphatic glands purplish; extensive and deep ulceration of the
mucosa of large intestine.

Pig 197, killed for examination, was very auemic. There was some
pale serum in abdominal cavity. The kidneys and lymphatic glands
showed evidence of chronic inflammation. The lungs were exceedingly
pale. No evidence of inflammation or ulceration in any portion of the
intestinal tract.

It must be borne in mind that these animals were constantly exposed
for a period of several months to the virus of the disease, and that a
continual struggle between the organism and the invading parasites
must have been going on, which naturally would tend to lower the vi-
tality. Such severe conditions as these are probably never realized
among herds. ;

The later history of No. 200 does not, however, bear out the first
supposition that complete immunity was attained. After being contin--
ually exposed in the infected pen from April 20 to June 21 it was re-
moved to a clean pen, where it continued to grow very weak. It died
July 12. The autopsy revealed a plastic pleurisy over the right lung
and a fibrinous exudate upon the epicardium. The mucosa of the cecum
was extensively necrosed ; in the colon the ulcers were isolated ; the
solitary follicles were very prominent. A small bit from the epicardial
exudate was placed beneath the skin of two mice. One of them dicd
ontheeighteenthday. Thespleenwas greatly enlarged. Numerous hog
cholera bacteria were present in this organ and the liver. The epicard-
ial exudate of the pig must have contained but very few, for they could
not be demonstrated in cover-glass preparations. The long period of
time from the inoculation of the mouse to its death is also evidence of
a very small quantity of virus.

No. 157, inoculated with the rest, became quite lame in the hind limbs,
so that it was thought best not to expose it to the disease in the infected
pen for the time being. It soon recovered its power of locomotion, and
was transferred to the infected pen May 25 and removed therefrom
June 28. In the new pen it grew rapidly weaker, and died June 28.
On post-mortem examination the right lung was found entirely hepatized
and adherent to the chest-wall. The mucosa of cxecum and colon was
studded with large and deep ulcers; that of the fundus of stomach was
deeply congested.

Yxperiment 12.—It became desirable to determine whether repeated
subcutaneous injections of heated cultures, until a large amount had
been introduced into the system, would be more efficacious in produc-
ing immunity. For this purpose the culiure liquids were concentrated,
by using a 2 per cent. solution of meat extract with 2 per cent. peptone
for some of the injections; for the remainder a 2 per cent. solution of

163

peptone in beef infusion. The cultures were made in Erlenmeyer flasks,
plugged with cotton wool.

The table given below gives the date of the injection and the quan-
tity used each time. It will be noted that Nos. 191 and 194 received
two, Nos. 216 and 218 three, and Nos, 217 and 221 four doses eac ot
the heated culture liquid. The injections were made two days apart,
the exposure in the infected pen and among diseased animals about one
week after the last inoculation. Nos. 220, 232, and 235 were placed in the
infected pen at the same time, to determine the virulence of the infee-
tion upon pigs which had not received any injection.

| Heated virus. | ne a
No. j SS SSS : Total. gas temarks.
| Apr.20. | Apr.22. | Apr. 24. | Apr. 26. | en 5
ae n aPYiad = ra eee (is ¥
| c.c. cc. | C.c. c. C. Cc. | eee
216 | 9 8 Fee a ees 242 | May 4...| Died May 17.
217 | 9 8 ae 8 324 |...do....) Died May 19.
218 9 8 7 Te D4 tel madoe en! Do.
| 221 9 8 ik 8 324 |...do....| Died May 23.
Sy a a ed 10 | 8 qe eadoys. 3 Dia:
|} 194 | io Stee. Soy Soeaaeeee 10 8 18 |...do....| Died May 19.
| -*220 cane ect Sea et | Me. anti Neo dts Als eS ot ...do ....| Died May 17.
| *232 | spactasog) coseé<cdPocsodecsciastosence fsoosanena. ---do ....| Died May 23,
| CPEB) |) SececeSoc|tnececaoad|cosda, ase ae ae do | Died June 12. |

* Checks.

All of the inoculated and control animals died with periods ranging
from thirteen to nineteen days, only one living thirty-nine days, aud
this one a control animal. Of those that had received two doses, No.
191 died May 23 (nineteen days after exposure) with considerable ul-
ceration in czeecum and colon. No. 194 died May 19, with extensive and
deep congestion of the lymphatic glands in general, of the kidneys,
stomach, and large intestine. In the latter, ulceration was not yet be-
gun. No. 216, which had received three doses, died very unexpectedly
thirteen days after exposure. The lesions were of the hemorrhagic
type, involving extravasations and ecchymoses of the intestinal tract,
more especially of the large intestine, heart, lungs, lymphatic and sub-
cutaneous fatty tissue. Ulceration in large intestine very slight, the
congestion being intense. No. 218, treated like the former, died fifteen
days after exposure. The lesions were like those of No. 216, but not so
severe. Ulceration as yet very slight.

Nos. 217 and 221, which had received four injections, died fifteen and
nineteen days after exposure, respectively. The lesions in No. 217,
which died very suddenly, were hemorrhagic in character, the ulcera-
tion in the cecum and colon being quite superficial. In No. 221 the
nlceration was more pronounced, the general congestion and extrava-
sation much less so.

164

Of the control animals the lesions of No. 220 were of the hemorrhagie
type, resembling those of No. 194 very closely. In No. 232 there was
extensive ulceration of the mucous membrane of the large intestine.
In No, 255, which lived for thirty-nine days after exposure, the mucosa
of tye cecum and upper portion of the colon was involved in complete
necrosis nearly 5 millimeters thick. Beyond this the necrosis took the
form of isolated ulcers. Owing to the depth of the ulceration inflamma-
tory adhesions had formed between the cecum and adjacent organs.
There was no reactionary swelling of the inoculated animals at the
point of injection.

Those animals in which the disease took the hemorrhagic type sue-
cumbed very suddenly, as if the invasion had taken place ina single
day. In those animals in which symptoms of weakness and loss of ap-
petite appeared some days before death the well-defined lesions were
as a rule limited to the large intestine in the form of ulcerations. The
former cases represent a class in which the bacilli invade the entire
vascular system; in the latter the absence of a general congestion and
extravasation scems to indicate a more local multiplication of the spe-
cific disease germs in the intestinal tract.

This mode of vaccination, as shown by the results recorded, did not
prove to be any protection to the animals, as they died, most of them,
within a brief period after exposure from avery acute attack of the dis-
ease.

The spleen examined in about one-half of these cases contained the
bacillus of hog cholera, usuaily in large numbers. T'rom a few cultures
were made which were found pure.

Huperiment 13.—A final experiment was tried in which each animal
received hypodermically 40 cubic centimeters of heated culture liquid
jn two doses. The cultures were made in beef infusion with L per cent,
peptone, the growth being killed by a temperature of 58° C. the third
day after inoculation. The flasks used were shaped like Erlenmeyer
flasks, a glass cap being fitted over the flask by means of a ground-glass
joint. which contracted into a straight narrow tube plugged with glass
wool. The removal of a cotton-wool plug was thus avoided, the ‘cap
being removed for inoculation. This culture flask affords better venti-
lation and a more rapid evaporation of the culture liquid than does the
culture tube with the bent ventilating tube.

165

The following table gives ail the facts necessary for an understand-
ing of the experiment and its results:

| |
|

Heated virus. | Expos: | eh Siegen) |
Le SSS SS Se oteatal Remarks. first ex-
June 14.) June 17. pens. PESunes
ee c.¢, cc
231 20 | 20 40 June 21 | Died July 7.. | 16
233 13 | 20 33 |.. do....| Died July 9.. 18
266 20 | 20 AOR Si do ttc Wando ssi2sh=% | 18
CPE | are eee fetes S53 ee oe ee Ove OIG dulvasee 17
267 20 | 20 40 |...do....| Died July G . 15
268 20 20 40 |..-do....| Died July 10 i)
| 269 20 Boil: siaugeanistag ty Mime ages eo 19
| Bit On| kaos eters. eps Riche tec POL sie ctty PSS do Died July 9 18
pee ee wera riree ye ee Bae ska a wl,
* Checks.

It will be seen that all the experimental animals died, inoculated as
well as check animals, within a few days of one another, death taking
place about sixteen to eighteen days after the first day of exposure. A
brief synopsis of the post mortem appearances will not be amiss in this
connection.

In No. 231 the spleen was very much enlarged and gorged with blood.
The intensely congested mucous membrane of the eecum and colon was
dotted with small. superficial uleerations. In No. 255 the congestion of
spleen, and ulceration with congestion of the large intestine, were also
marked. No 266 presented the saine lesions. The ulcers in the caecum
were fron one-quarter to one-half inch across No. 250 (check) differed
from the preceding cases in presenting severer lesions, greatly enlarged
and congested spleen and lymphatic glands, superficial necrosis of ‘the
entire colon and great thickening of the walls, extensive extravass
tion of blood beneath the mucosa of duodenum.

Of the second lot of four, treated in the same way, No. 267 presented
very severe lesions _ consisting of intense congestion ‘and extravasation,
involving the spleen, ly mphatie ¢ glands, lungs, ‘and kidney. The left lang
was adherent to costal pleura. There was considerable hemorrha ge in
the pelvis of both kidneys. The large intestine was least changed, the
mucosa being slightly uleerated and containing some hemorrhagic spots
and points. This animal was first to die out of this lot of eight. In No.
268 the congestion involved the lymphatic glands gene) rally and the
mucosa of the large intestine, which was extensiv ely necrosed in its
upper portion. . No. 269 resembled No. 267 in the severity of the lesions.
The lungs were noteaffected, however, while the ulceration of caecum
and upper colon was very extensive and deep. No. 270 (check) pre
sented extensive ulceration of the large intestine and a greatly enlarged
spleen. In five cases the spleen contained the bacteria of hog cholera
more or less abundantly. In two none could be seen on one or two
cover-glasses. No local swelling had developed at the points of injec-
tion in any of the inoculated animals.

The quantity of culture liquid in these cases was likewise too small to
have any beneficiai effect. Experiments are now being prosecuted in

166°

the same direction by injecting very large quantities. These are, how:
ever, not completed.

The experiments on the use of sterilized cultures have thus not be-
come practically applicable as yet. The great importance of this prin-
ciple, however, has been duly appreciated within the past year in foreign
countries, notably in France, where experimentation of this kind has
been carried on by pupils and assistants of Pasteur. The principle is
destined to be serviceable in other infectious diseases, and may eventu-
ally take the place of the older methods of Pasteur wiich utilize attenn-
ated cultures of bacteria. These are often sufficiently virulent to destroy
sheep (anthrax), and in this way may themselves become the agents
that distribute the disease. For this reason anthrax vaccination is only
practiced in those regions where the disease is more or less endemie, and
where the losses exceed a certain percentage each year.

Chantemesse and Widal* have recently endeavored to set aside the
claim of the Bureau of having first demonstrated this principle, in favor
of the more recent researches made in Pastew’s laboratory. Hiippet
has, however, shown the absurdity of this claim in pointing to the ex-
periments of the Bureau as having been published nearly two years
prior to those of Chamberland and loux.

2 * Annales de U Institut Pasteur, February, 1888.
t Fortschritie der Medicin, 1888, 289.

EXPERIMENTS ON THE Se OF HOG CHOLERA BACILLI

Heat has been used by Pasteur in the attenuation of anthrax virus
by exposing cultures of anthrax bacilli to a temperature of 42°-43° C.,
continuously for a certain number of days. Cultures kept in a thermo-
stat at this temperature for about thirty-one days were so attenuated
that they were incapable of destroying animals larger than very young
mice. Kept in the same conditions for only twelve days inoculation
failed to destroy adult guinea-pigs.* The former culture was denomi-
nated the first, the latter the second vaccine. To make sheep immune
they were inoculated subcutaneously with the first vaccine, twelve days
later with the second vaccine. Subsequent inoculation with strong virus
had no effect upon the vaccinated animals, although it was quite inva-
riably fatal to those which had not been so treated.

Although Pasteur’s discovery must be considered a scientific event
of great importance, its practical application is by no means a perfect
success. Experiments conducted by Koch, Gaffky and Loffler, in Ber-
lin, have shown that the process of attenuation does not always go on
uniformly, and that the strength of the vaccine can not always be relied
upon. A few animals may die as a result of the first or second inocu-
lation. This fact induced the last International Congress of Hygiene
at Vienna to adopt the resolution that anthrax vaccination should not
be practiced upon sheep in any locality unless the disease causes a loss
of 2 to 3 per cent. annuailiy. It was also shown in the experiments at
Berlin that immunity after vaccination is not absolutely perfect when
the virus is introduced with the food. This is perhaps the most com-
mon way in which infection takes place.

The results obtained by Pasteur are sufficiently valuable to make it
at least desirable to try heat attenuation for other bacterial organisms,
although it does not follow by any means that the same process will
suffice for all or even a small number of disease germs, for these differ
among one another very widely.

Kitt* has tried heat in the attenuation of the virus of Black Quarter
in Germany by exposing the diseased muscular tissue, which had been
thoroughly dried in the air and ground to a fine powder, to the steam of
boiling water at 100° C. for four, five, and six hours continuously.
The spores of the bacilli of this disease were sufficiently attenuated after
a six-hours’ exposure that sheep inoculated with the powder in certain
doses remained well after inoculation with strong virus. The reaction

* Compt. rend. Acad. des Sciences March 21, 1881. _
*Centralbl. f. Bakteriologie und Parasitenkunde, 1888, ¢. 571.
167

168

after the vaccinal inoculation was very slight. Hog cholera virus is
destroyed by a fifteen to twenty minutes’ exposure in a water-bath at
58° C.; a momentary contact with boiling water is sufticient to destroy
it, so that Kitt’s method is not applicable to it, but only to baeteria
which form spores.

The following experiments were undertaken with a view to test the
method of Pasteur on hog cholera bacilli, and to obtain, if possible, a vae-
cine similar to that employed in the prevention of anthrax. Although
only a preliminary step has been taken in this matter, and the promise
of favorable results is not flattering, we consider it best to publish the
results thus far obtained.

The first step in the process was to obtain, if possible, a cultivation
which should prove harmless to rabbits. This was to be accomplished
by placing tubes in a thermostat, kept at a certain fixed temperature as
nearly as possible, and inoculating rabbits from time to time to deter-
mine any diminution in the pathogenic activity.

April 9, 1888.—Four Salmon tubes of beef infusion peptone were in-
oculated from an agar-agar culture of hog cholera bacilli two weeks old
and placed in a d’Arsonyal thermostat, the internal temperature of
which registered between 42° and 43° C. Two series of inoculations
were made on rabbits, one from one of the original liquid cultures at
different intervals, the other from a culture renewed at the end of every
five days by inoculating a fresh tube. The result is most easily under:
stood by examining the following table: ‘

Agar culture.

Apr. 9, | b.i. p. *(a).

Apr. 14, b.i. p. (a;).

Apr. 19, b. i. p. (ay).

Apr. 19, rabbit | inoculated | Apr. 19, rabbit inoculated.
Apr. 25, died. Apr. 24, died.
® Apr. 24, b.i. p. (a3)
| : = :
|
i}
Apr. 30, rabbit. Apr. 30, b. i. p. (a1). Apr. 30, vabbit. «
May 4, died. May 5, died,

May 4, b.i. p. (a5).

|

May 9, rabbit. May 9, b.i. p. (a6). May 9, rabbit.

May 18, died. May 16, died.

169

The first inoculations were made April 19, with culture a, which had
been in the thermostat ten days, ard eulture a,, which had been freshly
madeon April14. Both rabbits received about $ cubic centimeter of the
culture liquid hypodermically. Rabbit a, died in five days with extensive
coagulation necrosis in liver and enlarged spleen. Rabbit @ died on the
following day with the same lesions. In both hog cholera bacilli were
very numerous on cover-glass preparations of spleen, and obtained pure
in cultures. The same resuits were obtained in all subsequent cases,
so that no further mention need be made of this.

Two rabbits were inoculated in the same way April 30, one from the
original culture a, the other from a;. Both died May 4 and 5, respect-
ively. Lesions the same as with the first pair.

Two rabbits were inoculated May 9, one from the culture a, now thirty
days old; the other from a;, the fifth renewal of a. Both rabbits died
on the 7th and the 9th day, respectively. The lesions were practically
the same, with the addition of slight hemorrhagic lesions in the in-
testinal tract. The period of the disease was slightly prolonged.

The result was not very satisfactory. If any atfenuation was go-
ing on, its final attainment would demand too long a period of time,
The experiment was therefore stopped and another undertaken. The
temperature of the thermostat was raised to 45° C., to hasten the pro-
cess of attenuation.

Apr. 23, agar culture.

May 12, b.i. p. (b).

May 22, rabbit inoculated. May 17, b.i.p.(b!).

|

May 29, died.
May 22, b.i.p. (v?).

It was found that cultures inoculated from b failed to develop at the
assigned temperature, so that this experiment was not continued any
farther. It deserves to be mentioned, however, that a rabbit inocu-
Jated from the original culture, which had been kept at 45° C. for ten
days, died seven days after inoculation with enlarged spleen and co-
agulation necrosis in liver.

170
A temperature of 435-449 C. was next chosen and the experiment con-
ducted in the same manner, as the appended table will show:
(163 D.)

May 16, agar culture.

May 29, b.i. p. (a) (42.59-44° C.)

| June 4, b. i. p. (a.)

June 8, rabbit.
June 14, dead. = =

June 8, rabbit.
| June 15, dead. |

| June 8, b.i. p. (fails to
grow).

|

| |

|

| |
|

|

June 18, rabbit.

June 13, Di. p- (a2).
June 23, dead. L

June 18, rabbit.
June 24, dead. June 18, b. i. p. (a3).
| |

| | ie ho |

} |
{ } Hl

| j |
1
~ | | ;
|
| 2

| }

98 rallbl:{ ‘ :
Hea os | June 23, b. 1p. (a4).
yey r | (Supposed impure,
but found pure.)

June 28, rabbit.
(Remains alive.) |
(Culture dead.) |

June 28, guinea-pig. June 28, b. i. p. (a4).
July 10, dead.

ies |
July 10, rabbit. July 10, rabbit. July 10, b.i. p. (as).
(Remainsalive.) (Remains alive.) (Culture dead.)

May 16. agar culture.
May 29, b.i.p. (b) (48$9-4¢° C.)

July 14, placed at 369-359 C.

| |
P| it aa
July 25, rabbit. August 9, rabbit. August 4, b. i. p.
July 30, dead. (Remains well.) (Sterile.)

Pit

The rabbits inoculated from the original culture after remaining at
the temperature of 43.5°-44° C. for ten and twenty days died from
the inoculation disease, but those inoculated from the same tube, after
thirty and forty-three days, remained permanently well. This was not
due to an attenuation of the culture, but to its death. Turning to the
series of rabbits inoculated from the cultures renewed every five or
ten days, those receiving culture liquid ten, twenty, and thirty days
old died from the inoculation disease, while one inoculated after
forty-three days remained alive, because the culture was dead, 7. ¢., it
failed to fertilize fresh tubes after repeated inoculation. An adult
guinea pig, inoculated from the same culture material, thirty days
old, died in twelve days as a result of the injection. In this case
only a few drops had been injected. This experiment demonstrates
that in general the pathogenic power of hog cholera bacilli is only
destroyed by the death of the organisms themselves. This is a very
important fact. It will be remembered that in the attenuation of an-
thrax bacilli their virulence was gradually diminished, and a time was
reached when they failed to kill all but mice, while they still retained
the power of multiplying in intritive liquids. In the above experi-
ments even guinea-pigs, which are less susceptible to this disease than
rabbits, died twelve days before the culture was found dead. The
latter may have been dead some days before this, for no tests were made
meanwhile.

This fact has an important bearing upon the nature of the pathogenic
activity of hog cholera bacilli. It shows that there are two elements
involved, (1) the ptomaine action of the organisms; (2) their mechanical
effect. That there is a ptomaine action of these bacilli has been con-
clusively proved in the experiments of the Bureau made upon pigeons
several years ago. But this ptomaine action is evidently secondary to
the mechanical effect of the bacilli in forming plugs or thrombi in the
blood vessels and thus causing destruction of tissue by impeding the
circulation. This tendency to act mechanically is not lost as long as
the bacilli are alive, as shown by their fatal effect on rabbits and guinea-
pigs shortly before they themselves are destroyed.

At the temperature employed (43.59-44° C.), the original bouillon-
peptone culture a died between the twentieth and the thirtieth day
after the beginning of the exposure. The culture from this, renewed at
the end of every fifth or tenth day, died between the thirtieth and
forty-second day. Another culture b (see table), which had been re-
moved from the thermostat after the forty-sixth day and kept at the
temperature of the laboratory (about 30°-33° C., during July) was still
fatal to a rabbit on the fifty-seventh day. Another rabbit, inoculated
ten days later, remained well, and a fresh culture made at the same
time remained sterile, showing that theapparent immunity of the rabbit
was due to the death of the bacilli injected. This experiment also
shows pretty conclusively that the pathogenic power of these specific
organisms expires only with their life, and not long before.

172

It is evident from our own experiments, and more recent ones made
in France and Germany, conducted on the same lines, that the amount
of immunity which we may expect to gain from preveutive inocula-
tion will depend on the quantity of ptomaines produced by the specifie
microbes @. ¢., upon their poisonous nature. In other words, our sue-
cess will depend upon the relation borne by the ptomaine to the disease
process. If this factor is very great it is highly probable that prevent-
ive inoculation either with ptomaines or with attenuated cultures will
be successful. But if there is in addition a mechanical element, which
may or may not overshadow in importance the ptomaine element, the
problem is not only complicated, but may fail.

There are two other points in connection with these experiments which
demand attention. One is the variation in the length of life of the dif-
ferent cultures exposed to the same conditions. This would be a seri-
ous hindrance in obtaining vaccinal cultures of uniform strength, should
this method ever prove successful.

There was a noticeable change in the appearance of the serial cult-
ures after a sojourn in the thermostat. There was a tendency to mul-
tiply rather more abundantly, to grow in minute flakes and to rise to
the surface to form a thin, unbroken membrane. The motility was
somewhat impaired after atime. These changes gave rise to the sus-
picion of impurities, but tests on gelatine plates showed that the sus-
picion was unfounded. These experiments will be continued on pigs
under similiar conditions to determine whether any immunity can be
produced by this method.

HOG CHOLERA, OR DISEASES CLOSELY ALLIED TO IT, IN OTHER
COUNTRIES,

GREAT BRITAIN.

This disease was first detected in 1862, where it has been known under
various names, the most common of which is swine fever. Owing to
the fact that there are recognized at the present time three distinct in-
fectious diseases of swine in different parts of Europe and America, it
is impossible to state whether the disease known as swine fever in
England represents two distinct maladies, hog cholera and swine plague,
or hog cholera alone. This question can only be solved by a thorough
bacteriological investigation, such as has not been made there in very
recent years. There is enough evidence, however, to warrant the state-
ment that hog cholera is prevalent in Great Britain. There is, on the
other hand, no experimental basis for the statement that the other dis.
ease, Swine plague, also exists there. These two diseases produce le-
sions of the large intestine, so easily confounded with each other, that
great care must be taken in making a diagnosis. We must also con-
sider that the three well-marked swine diseases now known as hog
cholera, swine plague and rouget, were only a few years ago regarded
as one disease designated by a great variety of names; that even to-
day no clear idea exists among most pathologists as to what the precise
differences between these diseases are.

In a brief report on swine fever in Great Britain, by Professor Brown,
of the Agricultural Department, in 1886, we do not notice that any.
doubt exists in his mind as to the oneness of the disease in Great Brit-
ain and its identity with hog cholera. He even reproduces a plate from
the report of the United States Department of Agriculture for 1885,
in which the characteristic ulcers of hog cholera are showh as an illus-
tration for his text.

That there may be several diseases included under the term swine
fever is evident from the statements made in this report concerning tine
annual importations of diseased swine from other countries. Swine
fever is said to have aifected animals imported from Holland, Denmark,
Sweden, Norway, and the United States. Now, hog cholera appeared
in the North European countries for the first time in 1887. The swine
marked diseased may have been affected either with swine plague,
which exists on the Continent, or with lighter non-infectious forms of
lung disease not uncommon in pigs at any time in the year.

173

174

We quote from Professor Brown’s report those parts which may prove
interesting to American readers, using the language of the report itself
whenever possible:

Symptoms of swine fever.—-It is most important that the farmer
should be acquainted with the signs which indicate the existence of
swine fever at the earliest period of its development; but unfortunately
the disease is very difficult of detection in the early stage in the greater
number of cases, and the symptoms which are generally believed to be.
specially indicative of the affection, viz., redness of the skin on certain
portions of the body, and diarrhea of a peculiar kind, do not appear until
the disease is fully developed, and in numerous instances are not ob-
served atall. The animals feed fairly well, show no rise of temperature ;
they are vigorous, and for several days, and even for several weeks, be-
tray in no way the disease. It requires very careful and prolonged ob-
servation to notice that at one time or another—at any rate at rare in-
tervals—the swine have ashort cough. not an important departure from
the healthy state. Very few experts, to say nothing of the owner of the
pigs, would suspect swine fever because he happened to hear the ani-
mals cough at rare intervals; and there is in these mild cases, which
Dr. Klein considers constitute the majority, absolutely nothing else
which would be noticed; the skin remains quite free from any appear:
ance of disease. It is true that the inguinal glands are distinetly en-
larged, but unless the owner thinks of inspecting these small lymphatic
glands (kernels) under the skin of the pig’s groin, and knows what
their proper size isin health, he has no chance of recognizing the disease
in this obscure form. In the organs of these apparently healthy pigs
there are found on dissection very pronounced symptoms of disease, so
pronounced in faci, that it seems astonishing that during life the ani-
mals presented such slight signs of it. And these very slight signs, it
may be remarked, were only noted by the observer in the cases of pigs
which were under constant observation after they had purposely been
infected with the disease.

Swine which are affected with swine fever in the oceult form may
be moved about freely, sent to market, bought and sold over and over
again, distributing the infection wherev er they go, without exciting the
least suspicion in ‘the minds of those who buy or sell or keep them | that
they are infected with a deadly and highly contagious disease, and in
this way many outbreaks may occur without the origin of the infection
being discovered.

In the more pronounced forms of swine fever the symptoms which
are shown by the sick animal will not be very definite until the affection
is fairly advanced. Dullness and diminished appetite, with hot skin
and occasional shivering fits, with rise of internal temperature from the
normal 103° to 105° or 106° I*., are among the first signs of infection,
and should always be taken as justifying a strong suspicion of the ex-
istence of swine fever, especially if the disease is known to be in the
locality.

It has been remarked that pigs when suffering from swine fever in
the early stage often seek to hide themselves beneath the litter on the
Hoor of the sty; but this action is so common among swine that it
would hardly be likely to attract any attention, and even when noticed
it would not be looked upon as a symptom of any disease. There is,
however, to the practiced eye a great difference between a healthy pig,
which, in its desire for warmth, or quiet, or for some other reason, buries
itself under a lot of litter, and one which performs the same act. in obe-

LS

dience to the instinctive effort of a sick animal to get out of the way
of the light and its companions, and everything under the sun, and’
suffer in seclusion. The healthy pig when disturbed emerges from its
retreat alert and ready for action. The sick one objects to move, and
if compelled, crawls from his Jair, trembling and discontented.

Sometimes there are sigus of partial paralysis, and the pig moves in
an unsteady manner from side to side, frequently losing the use of one
cr both hind quarters, and dropping to one side, or dragging both hind
legs as it attempts to move forward. There is no loss of sensibility
with the defective motion, as the animal if touched will indicate pain
by a sharp cry.

Diarrhea may occur early in the disease, after a short period of con-
stipation; and the evacuations are generally light in color at first, be-
coming darker by and by, often from the mixture of effused blood. In
severe cases the intestinal discharge consists almost entirely of blood,
with masses of clot and loosened pieces of exuded lymph from the in-
flamed and ulcerated mucous membrane of the digestive canal.

A symptom which is considered to be characteristic of swine fever
may sometimes be detected early in the disease. Red patehes or
blotches appear behind the ears, inside the arms, and under the belly.
Professor Axe describes a distinet eruption in the form of red spots,
from one to three lines in diameter, slightly raised above the surface,
so that they may be felt by drawing the finger over the skin. The erup-
tion is not always present, and often there are not more than half a dozen
spots extending over a large surface; but in other cases they are very
numerous. After two or three days the spots subside, and are followed
by a second, third, or even a fourth crop, and after their final disap-
pearance the cuticle becomes ragged and scales off.

Small water bladders (vesicles) appear on the surface of the red spots
when the fever remains very high, and the fluid contained in them either
escapes or becomes dried up, forming a gray crust on the surface.

Discharges of thin fluid from the eyes and nose commonly takes place
early in the course of the disease, and, as it advances, the discharge
becomes thick and purulent, sticking about the eyelids and openings
of the nostrils. Diarrheais more constant as the disease goes on. The
voided matter is offensive and often streaked with blood ; prostration
occurs and is soon followed by complete collapse, and the animal dies
in a state of unconsciousness or in violent convulsions. Death may take
place at various periods from the commencement of the affection, some-
times after a few days’ illness, while in other cases tke animal may linger
for two or three weeks.

In reference to the change of the color of the skin in marked cases of
swine fever, it may be observed that there may be, independently of
the raised spots which Professor Axe describes, a diffused redness, or
regular patches of redness, or a purple tinge in different parts of the
surface ; but these signs are not to be expected in all or even in the
majority of cases of the disease; and it is well known that redness of
the skin is asymptom of some commen diseases of swine. It arises, for
example, from exposure to wet and coid; contact with sea-water, or
spray during a voyage, will also produce it; a journey in a railway
truck which has been lime washed is another cause; consumption of
wash with which salt liquor has been mixed is followed by severe, often
fatal, inflammation of the mucous membrane of the digestive canal and
sympathetic irritation of the skin; and the symptom has also been
noticed in acute indigestion which has resulted from eating freely of
mangolds. Redness of the skin, therefore, either in patches or gener-

176

ally, can not be accepted as sufficient evidence of the existence of the
swine fever.

In certain instances the symptoms of swine fever may be so well de-
fined during life that an opinion may be given promptly and without
much risk of error, but under ordinary conditions the conclusion must
be the result of the careful consideration of the history of the outbreak,
or of the evidence which can be obtained by dissection of the organs of
a diseased animal; and for this purpose it is better to kill a suspected
pig than to take the carcass of one which has died some time before the
commencement of the,inquiry, and has probably undergone post-mortem
changes which will render obscure the true morbid appearances.

Experience has placed beyond all doubt the fact that swine fever
when if once obtains a hold on a herd of swine does not spare them.
It is true that a proportion, and it may be a considerable one, of the
older animals particularly, will escape with a mild attack, and in some
of tliese mild cases there will be no characteristic symptoms to attract
attention. In fact, 1t will appear that animals have escaped the dis-
ease; but the critical observer will find some signs of the disease in the
majority of the swine which have been exposed to infection. Cases
which are often reported of swine fever attacking two or three swine of a
large herd and sparing the rest may safely be put down to the eredit of
any disease but swine fever. And the same thing may be said of those
cases which are traced to the consumption of indigestible food, or the
exposure of the animal. to hardship or unsanitary conditions of exist-
ence.

Post-mortem appearances in swine fever—Some of the changes which
are affected in the organs of the body by the ravages of swine fever
can only be appreciated by the pathologist; others, and those most
distinctive perhaps, are patent to the ordinary observer; and on this
point it is worth while to note the description which was given before
the members of the Royal Agricultural Society in 1865 by Dr. William
Budd, of Clifton, who was the first scientist in this country to investt-
gate the disease, which was at that time looked upon as anew one,
Dr. Budd’s attention was particularly attracted to the changes which
had occurred in the digestive organs, which he called a series of ulcer-
ations of peculiar character, variously distributed over the intestinal
tract, from the stomach to the rectum inclusive.

The first stage of the local affection appears to be the development
(amid all the phenomena of acute inflammatory disturbance) in the sub-
stance of the mucous membranee and in the submucous tissue of an
adventitious deposit (or cell growth) resembling in many of its charac.
teristics the well-known yellow matter of human typhoid. When Dr,
Budd gave this description, the outgrowth from or deposits on the mu-
cous membrane of the stomach and intestines were seen more frequently
than they have been of late years; in fact, in all well marked cases
they were the prominent objects in the post-mortem appearances—soft,
spongy masses, sometimes in very severe cases stained a dark red by
the blood, which was extravasated into the intestines, varying in size
from that of a large pea to a walnut, circular or oval in shape; some-
times several masses were joined together; but whether large or small,
separate or confluent, the deposits, from their color in contrast with the
membrane on which they were placed, were very striking objects.

A very curious appearance was sometimes seen in the intestines of
swine which had partially recovered from the fever and afterwards died
from exhaustion, or were killed for the purpose of examination. The
mucous membrane in these cases was spotted with the small masses of

~~ a

A

deposit which had lost the soft, spongy or fungoid character, and be-
come dense and, so to speak, leathery looking, not unlike yellow leather
buttons, marked with concentric rings, or, as Dr. Budd remarks, like
slices of columba root.*

The first simile will perhaps be more suggestive to the farmer than
the latter, as slices of columba root are not familiar objects. The mu-
cous membrane of the intestines, especially the large intestines, was
often covered with ulcers, and the masses of deposit which have been
referred to were generally found to be in connection with deep excaya-
tions, the result of the ulcerative process; but in all cases the edges of
the ulcers were elevated above the surface of the mucous membrane,
and presented a soft fungoid character.

In some cases the whole of the mucous membrane of the intestine
was covered with a croupous or diphtheritie deposit of a dirty white
color; and it was only after the deposit had been cleared away that
patches of inflamed, and perhaps ulcerated, structure could be seen.

In some instances the diphtheritic deposit was so abundant as to fill
the intestinal tube, and leave no canal for the passage of the feculent
matter, and rupture of some part of the intestine was the natural re-
sult of this blocking up of the passage.

The next illustration is copied from a report on swine plague in the
Report of the Bureau of Animal Industry, Washington, United States
(for 1885), and it may serve to indicate at the saine time the character-
istic appearances of the disease and the identity of the swine plague
(hog cholera) in the United States of America and the swine fever of
this country.

Besides the appearances which have been described as occurring in
the stomach and intestines, especially in the large intestine, there are
nearly always observed patches of congestion in the lungs, with here
and there condensation of the lung structure, which present a fleshy
character quite distinct from the healthy state. There are also changes,
easily distinguished by the pathologist, in the liver, kidneys, spleen,
lymphatic glands, and also in the cavities of the heart. In short, it
may be affirmed that the morbid changes in swine fever are so per-
fectly well defined that no error in opinion can occur when all the evi-
dence which a post mortem inspection affords is in possession of the
inquirer.

In this description we are led to infer that the writer has before him
genuine hog cholera. At the same time some of the features dwelt upon,
such as the croupous and diphtheritic deposits or exudates in the large
intestines, are more Jike those found in severe epizootics of swine
plague.t

There is another fact which proves that at least part of the swine
fever of England is the hog cholera of the American continent. This is
presented by the investigations of E. Klein. In his report upon swine

*These neoplasms we have also encountered chiefly in adults. They must be
looked upon as results of a greater resistance on the part of the mucous membrane,
such as we may expect in old animals,

tA plague like hog cholera may perhaps change its character under influences such
as climate and locality, or under influences found in race, breed, ete., of animals. This

may frequently account for modifications of diseases caused by the same micro-
organism.

Pore Hc —— 12

178

fever in the supplement to the Seventh Annual Report of the Local Gov-
ernment Board for 1877 Dr. Klein gives a very good account of the
pathological anatomy of this disease, together with some researches on
the nature of the cause and the mode of infection. Though calling the
disease pneumo-enteritis, his text, as well as the statements of Professor
Brown, quoted above, show that the accompanying lung disease is no
more severe than in hog cholera. The microbe which he described in
this report is a large spore-bearing bacillus. The methods which he
employed in his bacteriological work were those of the times, not con-
sidered now as capable of giving any trustworthy information. Conse-
quentiy, ata later date he regarded it as necessary to again go over the
ground, and published his results in Virchow’s Archiv, XCV, 468, in
1884. In this monograph he describes the inoculation disease in mice
and rabbits very much as we have found it, laying particular emphasis
upon the coagulation-necrosis found in the liver. His cultures con-
tained a motile bacillus from .002 to .003 millimeter in length. Wemay
therefore coneiude that a germ closely resembling or identical with the
hog cholera bacillus is found in cases of swine fever, and that hog
cholera actually exists in England.

The history of the struggle with swine fever in Great Britain since
1878 shows that it has been very severe. Numerous orders have been
issued, beginning with the contagious diseases act in 1875, to restrict the
extension of the disease, but all appear to have been without avail, since
the malady was as widespread and as virulent in 1885 as ever before.
This was without doubt due to the inefficient and incomplete execution
of the orders. By the order of December 17, 1878, the slaughter of
swine affected with the disease was made compulsory, and compensa-
tion was to be paid out of the local rates for all swine slaughtered by
order of the local authorities. The order also provided that no swine
should be moved out of a pig-sty or other place without a license, and
then only for slaughter. After this order had gone into effect weekly
returns were received from the inspectors of local authorities, which
showed that in 1879 the disease had prevailed, at some time during the
year, in forty-four counties in England, six in Wales, and three in Scot-
land.

The continued spreading of the disease gave rise to the swine fever
order of 1879. This contained provisions for the declaration of infected
places and for the slaughter of healthy swine which had been herded
with diseased ones, and also for regulating the exposure for sale of swine
in fairs and markets. This order was only partly carried out, for out
of 17,074 swine attacked 3,416 were allowed to die and 124 recovered.
In 1882 the disease was more prevalent than in 1879. Slaughter of
diseased and exposed animals was continued as before. Thus of 14,765
swine attacked 11,903 were slaughtered, 2,799 died and 18 recovered.
Anorder of council was passed in July, 1882, providing for the decla-

io

ration of swine fever intected areas by the privy council, and giving
power to local authorities in England and Wales to prohibit or regulate
the movement of swine into their districts from the district of any
other local authority in Great Britain. The order also empowered
local authorities in Scotiand to prohibit or regulate the movement into
{heir district of swine from the district of any other local authority in
Scotland; it did not appear, however, that the loeal authorities availed
themselves of these powers, except in very few cases.

In 1884 the area of the disease rather increased, while the number at-
tacked did not grow larger. [Further orders of council were passed
this year containing provisions relating to swine fever. The most im-
portant change made referred to the provision for slaughter of diseased
swine, which was objected to by some local authorities as a costly and
comparatively ineffectual measure. By an order passed in May the
compulsory provision was revoked, and the slaughter of diseased swine,
as well as those herded with them, was left to the discretion of the lo-
eal authority. Another order of council, passed in July, 1884, pro-
vided for the formation of aswine fever infected circle round an infected
place in any district to which the order might be applied by the privy
council at request of a local authority. The order was applied during
the year to five counties and ten boroughs.

In 1885 the disease grew to dangerous proportions, threatening the

- entire stock of pigs in the country. The extension was due to the pur-
chase of swine at fairs and markets, and it was therefore deemed ex.
pedient to impose restrictions on the saie of swine in all parts of Eng-
land. Accordingly an order of council was passed prohibiting the ex-
posure for sale of Swine except for slaughter within three days, and then
only with the license of the local authority of the district in which the
sale was to be held. Provision was also made for the exhibition of
swine at agricultural shows.

This so-called markets and fairs order did a great deal of good, but, as
it did not prohibit private sales, the disease even increased in some
counties, owing to the unrestricted sale and movement of swine.

** Tt was continued in operation until the end of November, and dur-
ing its operation the centers of disease were so far advanced in number
that it was deemed expedient to have recourse to slaughter of diseased
swine, and also of those which had been in the same pig-sty ov shed with
diseased swine. With this view the swine fever compulsory slaughter
order was passed, and came into operation on the Ist of December. The
order provided that local authorities should slaughter all swine that at
any time in the month of Deeember were affected with swine fever , and
all swine being or having been in contact, or in the same pig- sty or
shed, with swine affected with swine fever.

Ge Compensation was to be paid to the extent of half the value of a dis-
eased pig and the full value of a healthy pig, but the amount was not
to exceed 40s. for a diseased and £4 for a healthy pig. During the four
weeks to the end of 1885, the effects of the system of compulsory

180

slaughter were not altogether satisfactory. In fact, fresh outbreaks of
swine fever continued to occur in the same districts, and even in the
same premises, owing to the way in which the order was carried into
effect in regard to the slaughter of swine which had been exposed to
infection. For example, if a let of swine were inasty which was sepa-
rated a few feet from the sty in which disease existed, the animals were
not slaughtered, because they could not be said to be in contact, and

they were clearly not in the same sty, although it might fairly be pre--

sumed that the swine so situated were exposed to risk of infection

through the atmosphere, or by the agency of persons or things by which °

the virus of the disease could be conveyed to a considerable dis-
bamcess Ae pee

“Slaughter of diseased and infected swine was adopted in some dis-
tricts with satisfactory promptitude. In others a number of animals
were allowed to die before any action was taken. The disease, after
being stamped out in some districts by the energetic action of the au-
thorities, was reintroduced from other parts of the country where the
law was administered in a perfunctory manner. In short, nothing like a
serious and decided effort was made to get rid of the affection, and as a
natural consequence the good effects of restrictions were partial and
temporary.

“Imperfect cleansing and disinfection of premises may be reckoned
among the causes which have contributed to the continuance of swine
fever, notwithstanding the operations of regulations which might have
been expected to produce good results. Very frequently swine are
kept in places which can not be cleansed and disinfected effectually, so
as to make them safe for the next lot of pigs which will be brought i in
as soon as the place is declared free. Old, half-rotten styes with moldy
floors can not be cleared of infection by any known process. ‘The only
course in such cases is to remove the infection-saturated timber and soil
and submit them to the action of fire; but no power is vested in the
authorities to do this necessary work, and the only expedient which
they can employ is that of refusing to declare the infected premises free
until the necessary alterations and improvements are completed. In
this somewhat roundabout way they may attain the object—that of
keeping out fresh swine to become victims to the disease, but this kind
of pressure can only be applied under certain circumstances.

“Tree movement of infected and of actually, although not observably,
diseased swine, and their exposure in fairs and markets, has all aiong
been a fruitful cause of the spreading of swine fever. Many inquiries
have been made with the view of tracing the origin of different out.
breaks, and the conclusion has generally been that they were due to
introduction of swine recently purchased at public sales.

‘Under the system, which has obtained for years, of slaughtering dis-
eased swine, and allowing the apparently healthy to live, the extinction
of the disease could not possibly be secured. And it is only i in the com-
mon course of things that the malady has gradually extended all over
the country from the sale and movement of diseased and infected swine
which often showed no signs of disease, and would be passed as free
from swine fever by any one but an expert who is familiar with every
phase of the malady. “*. * ,*

‘In reference to the measures which should be adopted for the ex-
tinction of swine fever in this kingdom, it is not necessary to enter into
details. On three oceasions in the last twenty years the stamping-out
system was successfully applied to cattle plague. - Exactly the same

-

181

means would certainly succeed in ridding us of swine plague, and there
is no ground for the expectation that any less severe measures of re-
pression would be effective. It is, however, an essential condition of
success that the action taken should be uniform and general in applica-
tion. But it is impossible to suggest any means of securing the neces-
sary uniformity while the execution of the law is in the hands of some
hundreds of local authorities who entertain different views as to the
necessity for attempting to get rid of the disease by legislative meas-
ures, and are not agreed as to the proper means of effecting the object.”

SWEDEN AND DENMARK.

In the fall of 1887 a disease closely resembling hog cholera appeared
in Sweden among swine, which rapidly spread from place to place,
showing itself very fatal and causing alarm and consternation among
the agricultural population. The disease invaded the territory of Den-
mark, where stringent measures were adopted to prevent its further
spread. ‘The following communication, received by the Department of
State from our consul at Copenhagen, and kindly forwarded, may serve
to illustrate the measures employed by the authorities in checking the
epizootic. After giving briefly the symptoms of the disease, and the
lesions caused thereby, Mr. H. B. Ryder continues as follows:

The very prompt and stringent measures taken by the Danish Gov-
ernment, it is to be hoped, will be the means of localizing as well as of
effectually stamping out this malignant pest. For example, circulars
have been sent trom the home department to all the sheriffs through-
out the kingdom, instructing them to make publicly known that all
persons who within the last two months may have purchased hogs or
young pigs trom Copenhagen, or in its vicinity, should immediately give
notice thereof, so that their entire herds might be submitted to veter-
inary inspection. Furthermore, an ordinance has been issued strietly
prohibiting all transport of live hogs or young pigs from one district to
the other , and that no remove! of the animals shall be made from their
present dwellings, excepting by special permission for the purpose of
immediate slaughter; and, lastly, power has been given to all the police
authorities, on any suspicion of disease, to order the immediate slaugh-
ter of the animals, and a post-mortem examination of the careass to be
made by the veterinary officials; and on the appearance of the disease
in any locality under their jurisdiction to order the immediate slaughter
of a part or the entire herd as may be deemed necessary.

It is thus to be hoped that by these measures further spread of the
disease may be arrested. It is, however, much to be feared that, in
addition to the losses entailed upon the kingdom in the destruction of
animals in the course of the disease, the sorely tried farmers in these
days of agricultural depression will also be subjeted to material loss in
a diminished sale to foreign countries of their swine products. An
order has already been issued by-the German federai council prohibit-
ing all importation into the German Empire of swine, pork, and sau-
sages from Sweden, Norway, and Denmark, which will be most seriously
felt by the agricultural interests, as the exports of live hogs and young
pigs are almost entirely directed to Germany, whilst the exports of pork

182

and hams are mainly forwarded to Great Britain, as will be seen by the
following table, namely:

Counanes Average | 495,

Of l-ve hogs and pigs to— | lead. | TTead.
Germany sca noes anaes so cia Sees » remanence mein Stemi ae ett 276, 166 | 192, 27
EN OF WY cass Sotemtine seine ae ss see eee aneslesiaeaaen ee ae meee eee G6, Skt | 4, 704
Great eBritiatn 2 sce sce cee sent ere ee ene ee eee eee te eee tee 2, 895 128
Woltind Maeda ies oc SA Senda et coe a a ae ee | 1,243. | eee

Of pork and hams to— Pounds. Pounds.
Great Britainge = fee secu s eeke occa see eee nee ee arene | 12,550, 000 | 20, 240, G00 ”
COVA S Sees eon ee ek eS Oe oe OR CR noe Sera ee ee cera 2, 930, 000 7, 180, 000
Siedler 2 eo ia ciate acts ciara ah a ar aarti etic te Searels 38, 970, C00 8, 030, C00
INOTWiaiveece ace sane Sean RA 4 EE 2 OS ES RE DORIS ome UOCUa TS 1, £00, 009 700, 000

From the foregoing figures full evidence is afforded that whilst the ex-
ports of live stock have met with considerable decline in the latter years
a great increase has taken place in the exports of swine products, due
to the large number of slaughtering and salting establishments which
have been erected in this country for the development of the pork, ba-
con, and ham trade with England; and thus the loss to the agricultural
interests, it is to be hoped, will not be quite so severely felt as would
have been the ease in former years under similar unfortunate conditions,
and it is scarcely to be feared that England will likewise place obstacles
in the way of the free imports of the products into her ports; for inas-
much as the imports of swine into Great Britain from this country have
for some time only becn admitted in slaughtered condition, and set-
ting apart the facts that swine in mature stage for slaughter are farless
exposed to this disease than young pigs, there will be found at the same
time, under the close inspection which has been introduced throughout
the Kingdom, and the energetic steps taken by the authorities in all
eases of suspicion, an almost certain probability that no pork from a
diseased animal can possibly be exported. The sale of swine products
for home consumption plays likewise a very important part; and it is
here again to be feared that restricted sales will be sensibly felt until
the temporary scare iu partaking of swine flesh lias had time to sub-
side.

In order that the energetic measures taken by the Government for
the stamping out of the plague may be crowned with full success it will
be necessary that theagriculturists should give at the same time a loyal
support to the issued instructions‘and work hand in hand with the au-
thorities. He who may delay in reporting or may attempt to conceal
any disease or suspicion of disease that may show itself at his place
will simply be committing a crime against the class to which he be-
longs, and honesty in this as well as in other cases will be found the
best policy ; for whereas he who reports the breaking out of disease
amongst his stock will receive two-thirds of the valueof the slaughtered
diseased animals, and full compensation forthe slaughtered sound ones,
the dishonest party will incur not only risk of confiscation of the dis-
eased meat offered by him for sale, but’ will also render himself liable
to heavy fines. The closing of Germany to the importation of these
products undoubtedly can not fail to entail severe loss upon the agri-
cultural classes ; but if success can only attend the stringent measures

if

183

adopted for preventing thefurther spread of the disease it must be hoped
the prohibition will be of short duration, and that agricultural interests
will soon recover from the blow. But should the devastating plague,
on the other hand, spread over the whole Kingdom it will be nothing
short of a national calamity, the destructive effects of which will long
be felt, as will easily be understood from the following table of the num-
ber of hogs and young pigs to be found in the Kingdom under census
of 1881, viz:

Hogs. Young pigs.
Head. | Head.
| In the islands-.:......:- | 280, 317 392, 884
jf 2GonO held Eni ease pee oconcce 242, 100 | 334, 707
| ofall tees 527, 417 | 727, 591

Great responsibility will thus rest not only upon the veterinary and
police authorities but also upon the agriculturists in devoting all possi-
ble energy in their mutual exertions to prevent the further spread of
this dreaded evil.

The disease is supposed to have been introduced into Sweden by dis-
eased boars, imported from England for breeding purposes. Thence it
was carried to Denmark,* in which country it first appeared on the
dumping grounds near Copenhagen, on which numbers of swill-fed pigs
were kept.

Chiefly young pigs up to the age of four months were attacked, the
period of incubation lasting from five to twenty days. The infected
animals refused food and were at first constipated. Later on diarrhea
set in, characterized by the discharge of yeliow putrid masses, frequently
mixed with blood. The temperature often rose to 105°-107.5° I’. The
animals were indifferent to surroundings. Tail and head drooping.
Conjunctiva reddened, frequently glued together with dried-up mucus.
lkespiration in many cases quickened and labored. Occasionally a muco-
purulent discharge from the nose. Notinfrequently reddening in patches
was observed on the ears, snout, abdomen, about the anus, and inner
side of thighs. The animals became very weak; posterior part of body
Swayed in moving about. They concealed themselves in the bedding.
and finally were unable to rise. Death followed insensibility and con.
vulsions.

A characteristic sign of this plague were diphtheritic changes on the
apex, sides, and under surface of the tongue, as well as on the mucous.
membrane of the cheeks, hard and soft palate, and the tonsils. On these
parts grayish white or yellowish opaque patches appeared, which were
Sharply defined and were converted Jater into ulcers by removal of the
slough.

Ip one herd the teats of several sows were affected with dark gray,
sloughing sores, with inflammation of the udders. These were infected

*Schiitz: Die Schweinepest in Diinemark. Arch. f. wiss. 1. prakt. TLhierheilkunde, XIV,
1888, p. 376.

184

from the diphtheritic sores in the mouths of the sucking pigs. In Den-
mark the disease was first recognized in this way. The acute disease
lasted from five to eight days, but sometimes death occurred sooner
than this.

The disease appeared in Denmark in Sepiember. In December the
plague took on a more chronic character and became less infectious.
The infected animals frequently showed no indications of disease, only
they were smaller and thinner than others of the sameage. There was
occasionally coughing and diarrhea. Some recovered, others perished
by a gradual wasting away. The post-mortem appearances were very
characteristic. The large intestine was attacked in every animal, and
in acute cases the small intestine and stomach likewise were reddened
and swollen, and the surface in part covered with athin layer of a gray-
ish white or grayish yellow soft mass, which consisted of fibrin. This
same layer was very thick in the large intestine, easily lifted away in
toto in some places; in others the attachment was firmer (diphther
itic). In other acute cases there was simply reddening and svwell-
ing of the mucosa of stomach and small intestine, and diphtheritic
changes in the large intestine, the fibrinous exudate being absent.
Moreover, the follicles, Peyer’s patches, and mesenteric glands were al-
ways tumefied.

The seat of the diphtheritic process was the whole large intestine,
more especially the cecum. The follicles and Peyer’s patches were
nearly always affected. The ulcers appeared when the slough had come
away. Inthe place of the follicles button like sloughs were formed,
which gradually invaded the whole thickness of the wall, spread later-
ally, and ran together into larger patches. The wall thus converted
into a cheesy mass was frequently one-fifth to two-fifths inch thick, on
the surface irregular, colored yellow, brown, or green. Hemorrhage,
due to the ulceration, was observed in one case.

In many animals the lungs were healthy. In some a muco-purulent
eatarrh of the bronchi was present, which caused atelectasis in one or
more places with young and weak animals. Usually the ventral and
anterior lobes were affected. In the diseased lobes homogeneous,
cheesy masses appeared Jater, sometimes as large as walnuts. These
masses led subsequently to inflammation and adhesion of the pleura to
chest-wall, pericardium, ete. The spleen was not changed as a rule.
In a few cases only it was somewhat enlarged, soft, dark red.

When we compare these lesions with those found in our country, we ob-
serve the absence of hemorrhagic lesions and enlargement of the spleen,
and more marked exudative and diphtheritic changes if the large intes-
tine. In numerous sections of ulcerative changes we have not observed
any relation between these and the follicles. The lung lesions corre-
spond closely. Whether they are due to the disease or not must be left
undecided. We have frequently seen caseous changes in the lungs
of animals free from infection, and they are, perhaps, due to collapse,

185

broncho-pneumonia. and subsequent interference of the circulation,
rather than to the direct action of bacteria.

The specific bacteria which are the cause of the swine disease are
described briefly by Selander,* and according to his description they
closely resemble hog cholera bacteria in form, motility, growth in gela-
tine, and appearance in tissue. Their growth on potato is said to re-
semble that of the bacilli of typhoid fever in man, and thus to differ
from that of hog cholera bacilli. Their effect on the lower animals cor-
respond also, although the descriptiofis are too brief for careful com-
parison. There is no mention of the coagulation necrosis found con-
stantly in the liver of rabbits inoculated with American hog cholera,

In the beginning of the present year (1883), Dr. John Lundgren, pro-
fessor of veterinary medicine in the University of Stockholin, was sent
by the Swedish Government to study swine diseases in this country.
He spent several weeks in the laboratory of the Bureau studying the
bacilli of hog cholera. A culture of the swine pest bacilli from the
Swedish epizootic was at that time subjected to a careful examination.

In gelatine, the swine pest germs grow very much like hog cholera
bacilli. On the surface of the gelatine the growth is very thin, translu-
cent, of a pearly luster, and spreads more-rapidly than the hog cholera
growth. On agar-agar the growth is more abundant and more rapid.
Beef infusion, with or without peptone, is converted into a very turbid
liquid within twenty-four hours at 95° F., while hog cholera cultures are
barely opalescent at that time, and remain so. Two mice were inocu-
lated from an agar-agar culture of the Swedish germ under the skin of
the back. Both were slightly ill next day. On the second day one
was found dead. The cultures from it remained sterile. It probably
died from some other cause. The second mouse remained well. Ona
rabbit the effect was equally negative. No rabbit survives inoculation
with hog cholera bacteria.

The effect of both germs on pigs was next tried. Two Erlenmeyer
flasks, containing each about 300 cubic centimeters (two-fifths of a pint) of
sterile bonillon, were inoculated, one with the American, the other with
the Swedish germ, and placed in the thermostat at 95° F. On the follow-
ing day both flasks were clouded ; the Swedish culture was covered by
an iridescent, very thin membrane. A comparative microscopic exami-
nation showed the Swedish bacteria to be nearly twice as large as the
American; their movement was far less active than that of the latter.

On the same day two pigs, starved for about twenty four hours, were
fed with these cultures by drenching, 7. e., the liquid was poured into
the mouth, so that none was lost. The pig fed with the Swedish culture
showed no signs of disease at any time after. The other pig on the
fourth day had a very liquid diarrhea, and was found dead the next
morning. On examination the spleen was found gorged with blood,
but only slightly enlarged. Mesenteric glands enlarged and reddened.

* Centralblatt f. Bakteriologie, ete., 1828—i, 362.

186

Stomach and ileum intensely inflamed (enteritis); grayish masses (diph-
theritic) attached in patches. The ileum was invaginated and projected
for 25 inches into the cecum; mucosa of this portion necrosed; walls
infiltrated, thickened, and ecchymosed, In czecum the nucosa was cov-
ered by a very thin slough. In the colon the membrane was deeply
reddened, covered by a catarrhal exudate, and dotted with numerous
very minute ulcers. Heart and lungs normal. Roll cultures in gela-
tine as well as liquid cultures from the spleen contained only hog cholera
bacteria. The invagination wase very likely the result of the violent
inflammation.

These comparative experiments show that the two germs, though
very much alike in appearance, were quite different with reference to
their pathogenic effect. Professor Lundgren was inclined to the opin-
ion that he had taken the wrong culture on leaving his native country.
It may also not be improbable that this was the true germ attenuated
on the way hither. As no communication has been received from him
since his visit here, the question must remain an open one.

FRANCE.

During the summer of 1887 a disease was introduced into the vicinity
or Marseilles by swine from Africa, which developed into an epizootic
of a very fatal character. It caused great losses in the south of France,
and at the time scientific men were sent from Paris by the Government
to investigate the cause and suggest. a remedy, if possible. According
to Rietseh, Jobert, and Martinand * the disease is chiefly restricted to
the intestinal tract, lasting from ten to twelve days after the first symp
toms have appeared. Occasionally it may last but three or four days,
or be prolenged to several weeks, but itis quite invariably fatal. Some-
times there is diarrhea, sometimes constipation ; the fever is not con
stant, the cough very rarely heard. The hind limbs are weak, the walk
tottering. Appetite often persists to the end. The skin may become
reddened in spots, especially on the limbs and ears. Pigs over a year
old are much less susceptible.

At the autopsy the lungs, liver, kidneys, and spleen are usually found
unchanged, and the disease limited to the digestive tract. The stomach
and the small intestine near the valve are ulcerated. Ulcers are present
in the large intestine on the valve, in the cecum and colon. They may
measure 3 to 4 inches in diameter. In animals affected with a chronie
form of the disease, there may be ulcers on the inferior surface of the
tongue and on the inner aspect of the lips. The internal orgaus are
free from bacteria. But from the contents of the intestine and the ulcers
a motile bacillus was obtained. Mice are killed in ten days after sub-
cutaneous inoculation wich cultures of this organism. Of ten adult
mice fed with cultures two died in fifteen days. Of ten young mice al]

Compt rend, Acad. ‘Sciences, January 238, 1888,

187

died when fed, the first in thirty hours, the others in fifteen to twenty-
three days. Rabbits are but slightly susceptible. A young guinea-
pig, fed with cultures, died twenty-two days later. The intestine showed
characteristic ulcers.

Dr. Rietsch very kindly sent to the Bureau a culture of the germ
which he found. It was compared with the American hog cholera germ
and the following characters determined :

The motile bacilli of the same form as hog cholera bacilli, but larger,
grow far more abundantly and rapidly in beef infusion. A thin mem-
brane and a copious deposit are produced in a few days, and the liquid
becomes very turbid. On gelatine the colonies do not differ appreciably
from those of hog cholera. The surface colonies spread in thin irides-
cent patches from 2 to 5 millimeters in diameter. In tube cultures the
isolated deep colonies grow to about one-third of a millimeter in diameter.
On the surface the growth is rapid and spreads over the greater part of
that which is available. The patch produced is whitish, uniform in
thickness, very irregular in outline, inclosing round spaces of uncovered
gelatine. In the bottom of the tube a few air-bubbles appear. On po-
tato the growth forms a glistening, pale-yellow patch at the ordinary
temperature.

They thus resemble the Swedish germs very closely, differing by so
much from hog cholera bacilli. A rabbit and two mice inoculated with
the Marseilles germ remained well. Eaually soa pig fed with 400 eubie
centimeters (four-fifths of a pint) of a beef infusion peptone culture.

So far as our examination of the Swedish and Marseilles cultures
have gone, they have shown them identical both as regards their posi-
tive and negative characters. They differ from hog cholera bacteria
enough to constitute at least a variety. But the investigations of
French savants of this Marseilles epizootic differ somewhat as to the

ause,

Cornil and Chantemesse* described a disease discovered among swine
in the vicinity of Paris, which they consider identical with the German
Schiceineseuche and our swine plague. Subsequent experimentst to
determine the biological properties of the bacteria causing the disease
Show that they are not dealing with the true swine plague germ (cer
tainly not as we have observed it in this country), but with one reseni-
bling more nearly hog cholera. Their researches concerning vaccina-
tion are reported to have been successful on rabbits and guinea-pigs,
but since that time nothing has been published concerning experiments
on pigs.

While Rietsch and Jobertt come to the conclusion that the Mar-
seilles disease resembles hog cholera closely, Cornil and Chantemesse
regard it identical with swine ple vue, » although the germ they describe

cone Mid. Cou Sciences, 1887, Cy, p. 1281.
t Compt. rend. Acad. Sciences, 1888, CVI, p. 612.
pales) en LOQG:

188

is not identical with the swine plague germ as studied in Germany and
in the United States.*

It is interesting in this connection to trace the march of infection in
the south of France as reported to the French Academy by Fouquet as
an excellent illustration of the ways by which infectious diseases may be
scattered broadcast over a country:

‘The disease did not, as was supposed, appear in Marseilles toward
the end of June, but in the month of April, and [have been able to locate
three entirely distinct centers of the outbreak due to the same cause—
the introduction of African swine. . These three centers are: The village
of Caillols, midway between Aubagne and Marseilles; the village ‘of
St. Marthe, 6k", northeast of Marseilles, and the herds of the Mediter-

ranean distilleries.

(1) From the 10th to the 15th of April, a breeder of Caillols received
a drove of black swine from the province of Oran (Algiers). From the
first week some cases of pneumoniat showed themselves among the last
animals; the disease gained rapidly, causing many deaths. The surviy-
ors were sold on the 4th of May following.

On the 8th of June the same piggeries were restocked, partly with
African and partly with Russian swine. Towards the end of the month
there were cases of pneumonia. The Russian swine resisted less than
the others. August ‘16 the piggery was again emptied. Finally during
September the third attempt was made, exclusively with African swine.
This also proved a failure. The survivors were sold in October.

During this time the disease reached the neighboring piggeries stocked
with a mixed Marseilles breed. The breeders of Caillols, alarmed by
the ravages of an epizootic the nature and cause of which they did not
know, decided to sell out at any price. The neighboring localities, St.
Marcel, St. Loup, San Joan du Désert, ete., were successively infected.
Infection was spread by the sales and exchanges of sick and suspected
animals, by means of transportation (carts often used in common by sey-
eral establishments soiled by the dejections of the sick and afterwards
used to transport healthy animals and their feed), and also by the lat-
eral canal of Huveaune, which receives at certain points running water
coming from the erounds on which the piggeries are located.

At the beginning of September all the valley of Huveaune, from Au-
bagne as far as Marseilles, was infected. Diseased pigs from this re-
gion we meet again in the market of Aubagne, at the fair of September
21, and which be came later one of the most active agents In spreading
the disease in the departments.

(2) Toward the middle of the month of August the disease appeared
ina piggery in St. Marthe, stocked exclusively with African swine.
These animals came directly from Oran without coming in contact with
any other of their species. Several days later one of the largest breed-
ers in that vicinity, who for three months had not brought a rsingle pig
to his establishment, and whose piggery was at least 600 feet away from
the preceding one, sustained a considerable loss, especially among the
pigs of 130 to 175 pounds.

*In a recent review of the reports of the Bureau of Animal Industry by Duclaux
(Annales de 0 Institut Pasteur, July, 1888), the reviewer regards this disease as iden-
tical with hog cholera, and states that Cornil and Chantemesse had at first overlooked
the motility of the germ ‘they were studying.

Pies pe 670:

t The writer calls the disease infectious pneumonia for waut of a better term,
aliiougl Rietsch distinetly states the intestinal nature of the maiady. Fouque was
no doubt led ast ray by the early, misleading notices of Corril and Chantemesse,

189

(3) Finally, on the 25th of June, sick pigs came from Oran to the pig-
geries of the Mediterranean distilleries. There were very soon a num-
ber of victims of pneumonia, not only in the distilleries but also in the
neighborhood, where there were from 4,000 to 5,000 in a comparatively
small territory. A great many ofthe sick died ; the others were quickly
sent to different cities to be delivered to the butchers. I have traced
the history of six sows which were sold from the midst of infection to
Estaque; thence they passed through the conmune Rove and arrived
in August at Gignac, where they introduced the disease. By an odd
coincidence some sick pigs from the same locality were taken to the fair
at Aubagne and bought by a breeder of Gignac.

The fair at Aubagne, on September 21, marked the most important
phase in the progress of contagious pneumonia. During the first fort-
night in October there was a veritable explosion of the disease , Which,
up to this time, had been scarcely known.

The importation of the disease by animals bought at the fair of Au-
bagne can be traced with the great»st precision in the suburbs south
and north of Mi irseilles, also as far as Gardanne, in the communes of
Septemes, Vitrolles, Pennes, ete., to Gignac, as mentioned above, even
into the neighboring departments, which continued with the others to
receive consignments of Marseilles swine. It is aiso necessary to men-
tion Puget, Ville et Grasse, among the localities infected.

In the beginning of December 153 swine were shipped from Mar-
seilles to Nice; nearly all died in a few days. From that time cases
appeared among the native pigs.

On December 22 another lot of 133 pigs were shipped; 33 were des-
tined for Nice and 100 for Italy. These Jast were sold on the 24th, in the
market of Vintimille: nearly all died very soon.

For several years Marseilles annually exported to Spain, and espe-
cially to Barcelona, a great number of pigs. Contagious pneumonia
had been causing losses there. for several months, even, it is said, at
Majorka, in the Balearic Islands. The Spanish breeders, believing the
outbreak of the disease with them was attributable to the importation
of French pork, obtained from the authorities the permission to impose
a quarantine of six days, at Port Bouc, on swine from Marseilles, to be-
gin on the Ist of the following February. This measure has not been
enforced up to the present day.

From what has preceded I believe [ can conclude that the epizootic
of contagious pneumonia which has raged during the year 1887 in the
interior of France, and which at this time continues its ravages there,
is of African origin. It has been introduced by Algeriap swine which
came from the province of Oran, This disease has made 20,000 victims
in several months in the province of Bouches-du-Rhone.

Pigs, and especially those from three to nine months old, are oftenest
attacked; larger pigs appear less susceptible. The Mar seilles breed,
the English (Yorkshire and Berkshire), and the Russian swine are more
susceptibie than the African swine.

Two months ago about 50 pigs two to three months old, coming from
Cazcres and Le Fousseret, in the Puce ae opere ae Maret, were used to
Stock a farm in Gignac. These pigs, placed in the pens which had con
tained sick ones, and which had only been very imperfectly disinfected,
remained in good health, while more than a hundred. cases of conta.
gious pneumonia appeared around them in the same piggery. After-
wards more than 2,000 Gaseon swine were imported by the single com-
mune of Gignac. Up tothe present time the disease has not re -appeared.
Are we here confronted by a new example of natural immunity com-

190

parable to that noticed long ago by Chauveau in Algerian sheep in
regard to anthrax ?”

Taking into consideration what we know now of these epizooties and
enzootics of swine diseases in foreigu countries, we are forced to the
conclusion that the disease in Sweden, Denmark, and France is closely
related to if not identical with hog cholera as it is found in our own
country, while the minor differences in the disease as manifested in
these epizootics, and in the germs producing it, can be explained on
the principle of the variability of disease germs, a principle in favor of
which much evidence has already been obtained in recent bacteriologi-
cal researches.

DESCRIPTION OF PLATES.

PLATE I:

Cecum of a pig affected with hog cholera laid open to show the ulcers of the
mucous membrane. The ileo-cewecal valve is near the center of the page, and
the small intestine, with the cut end tied, is above. The smallest ulcers have
sloughs of a uniformly yellowish color; the larger ones have zones of differ-
ent color, while the largest are brown or blackish. It will be seen from the
plate that the slough or new growth in most ulcers projects slightly like a
small flat button.

IPE AGH OES

Cecum of a pig fed with viscera from a case of hog cholera, slit open to show
the mucous membrane thickened and quite uniformly necrosed, with isolated
deeper ulcerations. The ileo-czcal valve is very much thickened, its mucous
membrane ecchymosed and ulcerated. The lymphatic glands of the meso-
colon and those in the angle formed by the entrance of the ileum into the
cecum are purplish, with cortex engorged with extravasated blood. They
illustrate the condition of the lymphatics of both thorax and abdomen in
the acute hemorrhagic form of the disease.

PLATE III:

Ceeum of a pig inoculated with blood from a case of hog cholera. The entire
mucous membrane is necrosed. Jn the upper portion of the figure about the
valve there are groups of minute pigment spots. -The valve is open to show
the intact mucosa of the ileum. This figure also serves to illustrate the con-
dition of the mucous membrane of czcum and colon in pigs fed with cultures
of hog cholera bacilli.

PLATE LY :

Cecum of a pig, showing round and elongated cavities on and around the ileo-
cecal valve. These are ulcers from which the slough dropped away during
remoyal. The base of the ulcers-is formed by the muscular tissue of the in-
testinal wall. The ulcers appear as if the mucosa had been punched out with
a sharp instrument. The edge of tho ulcers in the upper portion of the colon
with the slough still adberent. The Jungs in this animal were normal, if we
except a few collapsed areas from one-half to three-fourths inch across.

PLATE VY:

Ulcers in the lower portion of the small intestine (ileum); not very frequent.
Note the large, deep ones with puckered, ragged border, and the very small
ones with a thin superficial slough, stained with bile.

PLATE VI:

Kidney from pig No. 7 (see p. 41), showing the hemorrhagic condition of cortex
and engorged glomeruli. In this animal the disease was marked by the
hemorrhagic condition of other organs.

191

192

PuaTE VII:

Right lung from a casv of hog cholera. The lung tissue is nowhere infiltrated
or hepatized, but studded with hemorrhagic spots which are found in the
parenchyma as well as under the pleura. This animal, placed in an infected
pen, died on the twenty-second day of exposure. There were hemorrhages in
the subcutaneous connective tissue; lymphatics in general hemorrhagic.
Petechix in stomach and large intestine. In the cecum and on the valye a
few ulcers with hemorrhagic base.

PuLaTE VIII:
Heart with subepicardial hemorrhages especially numerous on left auricle,
PLATE IX:

Fia. 1. Collapse of various groups of lobules in the pr‘acipal lobe of a pig’s lung. -
Frequently found in young pigs which have died of hog cholera, in those af-
fected with lung worms, and in a small percentage cf those slaughtered dur-
ing health.

Fig. 2. Broncho-pneumonia affecting animals under various conditions and not
infrequently found in animals which have succumbed to hog cholera. (See p.
54). The air cells and smallest air tubes are shown distended with a yellow-
ish material which is of a dry, caseous consistency, and may be teased out in
the form of minute branching cylinders.

PLATE X:

Fig. 1. From a cover-glass preparation of the spleen of a pig which died of hog
cholera. Stained in an aqueous solution of methyl violet and mounted in
balsam. Outlined with a camera lucida, using a 33 homog. immersion (Zeiss),
ocular 2 (x 800): a, distorted red blood corpuscele ; b, bacilli in pairs.

Fic. 2. Section from the enlarged and congested spleen of pig No. 94 (see Second
Annual Report Bureau of Animal Industry, p. 193), which died very suddenly
with extensive homorrhagic lesions of various organs. Spleen hardened in
alcohol two hours after death ; stained in aniline water methyl violet and
decolorized in 1 per cent. acetic acid; mounted in xylol balsam; outlined as
in Fig. 1. Note the large group of bacilli occupying the capillary meshes of
the spleen pulp, all extra-cellular.

PLATE XI:

Illustrative of the growth of hog-cholera bacilli on gelatine.

Fig. 1. Various colonies from gelatine plates: a, embedded in the gelatine layer
(deep colony), usually spherical or egg-shaped; ), flattened colony growing
on the surface of the gelatine layer; ‘c, ¢’, c’’, growing between the layer of
gelatine and the glass plate as very thin films; the knobs on c’, ec’ repre-
sent the part of the growth in the gelatine layer.

Fig. 2 represents both deep (a) and surface colonies (b) growing in a gelatine
layer coating the inner surface of a test tube. A tube of gelatine was inocu-
lated by stirring up in it, while liquid, a minute fragment of spleen tissue
from a case of hog cholera (No. 464, p. 51), transferring a drop from this to a
second tube, and then rolling out the latter in ice water. Culture seven days
old. The zones on the surface colonies are very likely due to changes of tem-
perature in the laboratory, alternately retarding and augmenting the growth.
This mode of growth is by no means common.

Figs. 3, 4, 5 represent the growth of hog cholera bacilli in tubes of nutrient gela-
tine, showing the isolated colonies in the depth of the gelatine and the con-
fluent growth on the surface. Fig. 3 represents a culture three days old
(epizootic near Washington City, 1885), inoculated from the spleen of a pig.

-Fig 4, fourteen days old, inoculated from a culture which was prepared di-
rectly from the spleen of a pig in Illinois, 1886. Fig. 5, inoculated from the
blood of a rabbit which died from inoculation with bacilli from Ilinois cult-
ure; ten days old. The difference in growth observed may be due to a
greater or less alkalinity of the culture medium or to a slight physiological
difference in the bacilli themselves.

193

PuaTE XII:

Fig. 1. Agar agar culture of hog cholera bacilli in thermostat, four days old.

Fig. 2. Potato culture under a bell glass, twelve days old.

Fig. 3. Potato culture in a test tube containing an abundance of moisture. The
plug was made impervious with sterile paraffine. The growth is whitish,
very glistening. The difference in color between Fig. 2 and Fig. 3 is caused
by the different conditions of moisture.

PuaTE XIII:

Fig. 1. Coagulation necrosis in the liver of arabbit which died six days after in-
oculation. The small, yellowish spots are groups of acini completely ne-
crosed. The larger patch to the left shows the necrosis in the form of a net-
work.

Fig. 2. Liver of a rabbit inoculated with one thirty-second cubic centimeter (by
dilution) of a beef infusion peptone culture one day old. Dead on the seventh
day. The coagulation necrosis on the left is more diffuse. On the right are
cysts of coccidium oviforme.

Fig. 3. Enlarged spleen from the same rabbit (natural size), Weight of rabbit,
1i pounds. The spleen of this rabbit was but moderately enlarged as com-
pared with the spleens of most rabbits which succumb to hog cholera.

Fig. 4. Spleen from a healthy rabbit weighing 2% pounds (i. e., one and a half
times the weight of the diseased rabbit.

PuLates XIV, XV, XVI:

Photomicrographs of hog cholera bacilli which developed in different media. All
were made at a uniform magnification of 1000 diameters, with the Zeiss apo-
chromatic objective of 3™™ and 1.30 numerical aperature, using projection
ocular No. 4 and Abbe condenser with largest diaphragm. Orthochromatic
plates and picric acid screen.

PLATE XIV:

Fig. 1. Coverglass preparation from spleen of rabbit inoculated with hog cholera
bacilli. Stained&two to three minutes in aqueous solution of fuchsin. Mounted
in xylol balsam. x 1000.

Fig. 2. Coverglass preparation from bouillon-peptone culture five days old.
Stained in aniline-water-fuchsin for five minutes, and decolorized in one per
cent. acetic acid for a few seconds. Mounted in xylol balsam. x 1000.

PLATE XV:

Fig. 1. Coverglass preparation from bouillon-peptone culture one day old.
Stained same as Fig. 1 of Plate XIV. Mounted in xylol balsam. x 1000.

Fig. 2. Coverglass preparation from gelatine culture two days old. Stained same
as Fig. 2, Plate XIV. x 1000.

PLaTE XVI: .

Fig. 1. Coverglass preparation from colony of hog cholera bacilli taken from an
Esmarch tube, made directly from spleen of pig, fifteen days old. Stained
same as Fig, 1, Plate XV. x 1000.

Fig. 2. Coverglass preparation of hog cholera bacilli from agar culture fifteen
days old. Stained same as Fig. 1, Plate XIV. x 1000.

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Plate TV.

A.Hoen & Co. Lithocaustic, Baltimore.

G.Marx fecit. :
Pe er re See Pee eorRS IN CARO UImE

——
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HEMORRHAGIC

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A.Hoen & Ca. lithocaustic, Baltimore.

Plate VI.

G.Mar~x fecit.

A.Hoen & Co. lithocaustic, Baltimore.

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Plate VIL.

G.Marx fecit.

A.Hoen& Co Baltimore

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G.Marx fecit. A.Hsen& Co. Lith

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G.Marx fecit, A F

A.Hoen & Co. lithocatstic, Baltimore.

COLLAPSE AND BRONCHO-PNEUMONIA.

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Plate X.

Fre. 2.

G.Marx fecit. A.Hoen & Co. Lithocaustic, Baltimore.

BOG SGHOLE RA DBACTLIUT,

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CULTIVATION OF HOG CHOLERA BACILLI.

Plate XI.

G. Marx fecit,

A.Hoen& Co. Lithocaustic, Sattimare.

CULTIVATION OF HOG GHOLERA BACILLI.

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DIAGNOSIS OF HOG CHOLERA BACILLI. ( ALS Bl

¥ Ca. Lit

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PHOTOMICROGRAPHS OF HoG CHOLERA BacILLus. :

Pile. 4 x OOO:

COVERGLASS PREPARATION FROM LIQUID CULTURE ONE DAY OLD.

Bae ovr we ale OF

COVERGLASS PREPARATION FROM GELATINE CULTURE TWO DAYS OLD.

PHOTO -GRAVURE CO. N.Y.

PLATE XVI
PHOTOMICROGRAPHS OF HoG CHOLERA BACILLUS.

“egne
gait,
re
im, So
S ais e
f Be em 4
Fic. 1. x 1000.
COVERGLASS PREPARATION FROM ROLL CULTURE (ESMARCH TUBE)
‘ FIFTEEN DAYS OLD.
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Pieces. x 2000,
*

COVERGLASS PREPARATION FROM AGAR CULTURE FIFTEEN DAYS OLD.

PHOTO-GRAVURE CO. N.Y

ih pl xX.

Agar-agar cultures ..... Renee wasn sine suk cals sil cinalsicmipelassielsiaceisielse sees 68
Attenuation of hog cholera virus by heat ..-.-.. inion st bo MoS tLe e SE Oc hOOOre 167
ingcnlosio® hopcholena, GescriptlOn Of a-rearics se e< sae sae or n= mainn rion 63
Bacteriological observations..........-...----.--..----- Spec BaOP ao HeCBe -- 98,58
ony ar hoe eholern, DAC eee aa an nen Seed aesaeg>sninbne = aataaiob ans 5
Binley VlusiliveOn sViNU Sele = ome aye semeetanaoeja~ = lac selaciclicem 4s cclalacine asi 88
Burial of carcasses....-..----..---- Se Cee REC UOIBE HEAT DOOKUnEe acre 126
PEO aACHIn in BOS CHOIOTA CASOS)) .6.- <nocao4 se eeen access pcacldnaeucdele 58
MA AAs CALTIOLS) Of GISGASO tse! ea =o)= aiocisieiieleenlocelsciec si necc iso cisactcce 61
Cr nirndlly Gia Ga Byala Sa So. 55846 DSOAaSe coed chenbo co UASaEd cose eos Hoeoe 136
Carbolic acid as a disinfectant .................-- Sere an Se leb cate ealseeeet as 88
ride. As) CIMMIBGhANG 5a ceo ee anon naese ss -<<5oneeeSa shee = 91
Manhaniies sOmOc o ONUSWING) soem sees 1s) o-oo oa pee eae seeioectece seals e matsne,= 135
PMTCT et reise t MINER ua Aetedet o Sina cin eae e em eia tcc on cu = Sey eo ese cincemees 63
Chloride of zinc as a disinfectan®. .:J2......-..---------- ieese- dost we sees 90
er LCAULONA MT HOC. CHOLORBe note < 5 aij -Glsseeaclee Soe- seeeenl ose saelaric nls 54
Contact with the sick producing-hop cholera, ..--...---5. ~~ 25-0 -2sc0s coceee dL
Mormosive suplimate (see Mercuric: chiorids)) 2.-- -<-.<- <---)eriseisiasiais eee - = 83
Siiivatvoniot hoo cholera Daciliy o--— cadences eq cigar siseicttecl a-\-locwleclc ssche 65
SaMcesupnave as)ar disintectamt.-4 o-<.-c/ceenes i -,-4ee< ce ceioe ss acne ence 90
PEMA TK SWAN CISGASO TN. So on < oaicnin,2 a a oe aaemiseel ans Seca escet Scieckeiicts 181, 183
Detmers, Dr. H. J., investigation of hog cholera ....- weed anata Mist ahaloahtas 23
iiaonostsot homicholerabacilli., 5. seesasiee wesc ciscckesicl st -ceiodectisenins 66, 69
Miceshveltract as a channel of infection: ..---..522--+-= esq. --ci' sees onln 105
Diseased viscera, feeding to swine. (See Feeding.)
Biswieetants, effect on hop cholera Viras,. 4-2... 2.0025 0e-e-s--0enacinn nse 37
WISE CMR i ES ne eae ee Ee ero aeearen ee ae 131
Distribution of hog cholera bacilli in the body ....-.. ate aes tte cya sheila Se 65
rye cuect on hom cholera bagulissiso= fitness sn~ Se~ ee osc 2 oo oe ones cece 73
Myepntery, relanon te hor. cholends25 Yo02), 26s). ods. eae se nic es scene ewes 122
Etiology of hog cholera. (See Causation.)
fod hos cholera. Pail tor AWwile.- ...<. soc iecks Subs.to coeds. 5. 2e%e- 107
viscera to produce the disease. -....--.-..---------+--- 50, 105
PEMA AMNOANA. GF INtEEhION, 2d.— 440520 ch o~enceecsa altos Guseebeatbediedes 105
HOwilsseneeh OlimoculatlOonvOlasacecm conse ctecc oo <me eee tate WSs site cieew lene ee
RECO ERMINE MINEO) Wet. chek. A eric an teat stale, wom et Se Rae eae oeiebee aoe 186
econ. Cheech on hom cholera, ViTuss. 2c... 0528s lo ected Jace. Bee ok Bese 76
Gelatine culiares of hoz cholera bacilli _... 2 c.2s obsess Wet os eleeee Sele ote 67
Seti bean WING TAVOR IM cocks coccwe etowtoacac cat cuales ituerb equa te 173
Guinea-pigs, inoculation disease in .......... Re aise Sees RE eee 73
Pear ebeci abor Cholars, VITUS; ..s<ccccqnss sat See Re Se Oh eveeeee Stes eees 75
eee ctne ME ORIONAY. o/2%-6 Ge ins ew ss Sk eis Soest De he on BSE 34, 52
mfistory, of lor cholera in, the United States.... ..-...ed2 ee 0252-0 eke. eee g
INVER AbLONSE een. So Heke Bob e Bete bs Sone d twee 14

Page.
Hop cholera, bacillus of =0s.- 2022-3 eee epee 63, 66, 75, 78, 80, 87
Causation Of. 22. %ccecs sheen a aoa gOS Oe eee eee eee 25
history of investigations concerning. .... .<.. ..--.s.cs0d= «sees 14
introduction and spread in the United States.................. 9
or allied. diseasesin, Prameeier j4- fan doec. 2 ane eee eee 186
Great Britain: 35.5-)---5- Sisided see os roe 173
Sweden and Denmarke.....2c.--2 7 seeee 181
PreventiOn-Of 2.220, isteestieeeSe ees Sa ee eee eee ee eee 26
produced by feeding teas... s5sesese eee coe eee 50, 105, 107
inoculating pure cultures of hog cholera bacilli... 55
treatmentio€y <cocc wvesaseh sncoun ears acts stacctcoeesk oot eee ree 25, 135
Hydrochloric acid asa disinfectant .-<-+-5-secte= snes e+e ee eee ae eee 91
Tihinois, investigations. in... 2. cic2cs.decc deckoe weet e en eeee eee eee 119
Infection.of swine, modes: Ofis. 66 .<.02s4 sos san s5aneceS Fosse ee eee eee 105
Inoculation experiments. (See Preventive inoculation.)
of small animals with hog cholera bacilli...........-..-..---<- 69
fodine as.a disinfectant: 6.454 sear edussa sae dso ssenesntsose oss asso eee THRES
Isolation im hos cholera <.5.c2ssa4seechaasee tnanaeee a ee eee nee eee 123
Wein, H., inivestigations.in swine diseases); =s255 25225-2502 er se eee eee eee 177
Law, Dr. J., investigations in. swine diseases-.s--s+.2s--.-.-.----+22+ eee 19
Haws withireterence to hom -cholera:ss15..-cas-1ss4-oe eee eee ee ee eee 127
Lime asa disinfectant. ..52cssansenssssoAcnacge soe se ese ees oe eee eee 93
Lundgren, Dr..J..,, Investigations) Of j55ss0 sasaae cases tases seen eee eee 185
Lungs, infection. by. way: Ofssas.-sse case au ssaass at 255 Sasso eee eee 112
Tung lesions in-hog. cholera... . 2.055 s<0¢ssee0sas6¢ Ply os0i 2k ee 54
Marseilles, spread of swine diseases from ....-.-....--------------= Ji See 1838
Maryland, hog: cholera-i.: aso2 cssncssace ce stee see ease eee Rae ees 59
Nebraska, investigations 5 co xsanes 7 «ocletel ease | eee eeese ep Spoohoe oo: 116
Pathological actioniof hog:choleraibacillussss2 ss22- 22-22 -ee oe eee eee 113
Pens, vitality. of. Virus An) sass sarreeas oasaaera senso scot shane ae oe ee ee &6
Permanganate.of potash as a disinfectant <5 72 jase. eto see ee eee 89
Piceons, Imocwlation :Ofives-1 so-so ese tees joi LO eee 73
vaccination of, with sterilized cultures....-...---- dls noteetise Rees 155
Plates, desetiption. Of | 2 ai<- acces dots qodarcainwin nt aoeele be eh a ae ane te ee 191
Post-mortem appearances inhoc cholerarcse-se--- -s esses ae tee 34, 39, 59, 106, 107
Potato cultures S25 2526 -12ss ss ecsais oe waree ates Bot aleides UO te Rat eS ee 68
-Préeventionsor hog .cholénaiy 5521s stom «(= sorts) -inial eosin era ease e eee 205 Leone
Preventive inoculation. of swine by feeding. 220-2). 2/2222 Joo eee eee ee 151
with small doses of strong virus .------.---- 139
with sterilized. cultures.-..-...-.-2+-.---e- 159
Prevention of: Swine fever sos so sesjaee ste eee meee bie) bo se ech ee 179
Public health, relation of. hog, cholera.to...-.. . 2s): sioner ee ones Reece 120
Rabbit, disease produced. by. feeding aas2 2052 22) focc ato = cee ee 72
Rabbit, inocmlation-disease Il! sacs 42 255424 s2soe 55 eee eee eee 70
Snow, Dr..E..M., investigations. Of. £2.22 9s.25s<s020 hice sees Se tere 17
soil, disinfection, of, . with lime wifes dose sees = eae e eee «Hs AUR aee eee 99
vitality of. hag cholera bacilli in.........-.2 2002 dapeee sae oeete eee ~ 80, 86
Spores, do. hog, cholera. bacilli produce .... ......ose8 oss 22). oo 2 101 ©
Staining.of. hog cholera. bacilli. .- 22... .2622. 40 ocsaesan= dan tae ee 65
Streams distributing. virus: .-— 2-02-42 -.-r-0 35 f0[= oe ee ee 126
Subcutaneous inoculation of Swine. .2-- 42 c--- 4-4 e = Se eee ee ee 109
Sulphate of copper. (See Cupric sulphate.)
Sulphurie acid asia disinfeetantmeo.-. «2-s2eeeee dase ose eee ee ee ae 90

Sutton, Dr. G., investigations of swine, diseases. 2-- .22- 6s. - 5.2.25 nee 12,14

197

Page.

SUVGE ON Si MerQUse ISESele Se mateoeisyer saae) accel a aicldveen Sis occscimecscs cssceepe 181

Swedish and American hog cholera, comparison of .-..-...--.-. ..-....----.- 185

WIN CMOvelae Tose MONT LeMPLESTONG Olas setae so atcyncleisi=\s\ elie wiels Soivie a eos cas cece 176

Sy) oe eS GF ATS ee 174

Symptoms and post-mortem appearance in hog cholera ......----.---.------- 33

Table of hog cholera epizootics in the United States.............0..-..----- 11

Tables showing vitality of hog cholera bacilli in the seil............---. 81, 83, 84, 85

eee ae onOm OU Olena Pose ets cm wets Ses. eccle Soda deoeds boa cne cece se 25, 135
Mypuciaweyver, relation to hog cholera. <2. <2... 2-66 see csle ween ceca e-ee- 121
WiIGerativer lesions: s<..2-s..5e-ce ce = Si ck Cio cea GO CO RE Oe ee oo, 00
RPI TN BCs oat Scrat a aa cice Gis ealelwigQ Mare an cide cw cele saeede vate ne as 69
Merms'of swine, Inoculation; into. --..-.-.-....----.4 Mra eae ane (aie apaibia = we 111
Minas of hos cholera bacilliim the: soil ... 2.0 22... .see <2 + coe cceacesse- 75, 80, 86
Sneak mua hOT Of, ON Naty oo me acacee aon = aie ose reson wees este dacs =~ 167
Didier bec Of ae CHOlTA DACUI Wie ene. acc caste eaeece seciee cette sestna cscs 76

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