4 ” Sett : eat : : Seay a Ie ; : ate “e eo ~ Say, oe oa ‘ é . ee (4 PaONS.S sree Sesh tee t COB pe Sa COPYRIGHT DEPOSIT: Ne f ly vib a ria 1 arma’ Bey, 3 j 4 a kK a ~ a Swi’, wr gh Cr chien Ge, THE MACMILLAN COMPANY NEW YORK - BOSTON - CHICAGO - DALLAS ATLANTA - SAN FRANCISCO MACMILLAN & CO., LIMITED LONDON - BOMBAY + CALCUTTA MELBOURNE THE MACMILLAN CO. OF CANADA, Lt. TORONTO i HOG CHOLERA ITS NATURE AND CONTROL BY RAYMOND R. BIRCH, B:S., D.V.M., Pu.D. PROFESSOR IN CHARGE OF THE NEW YORK STATE VETERINARY COLLEGE EXPERIMENT STATION AT CORNELL UNIVERSITY, ITHACA, NEW YORK jdew Pork THE MACMILLAN COMPANY 1922 All rights reserve d PRINTED IN THE UNITED STATES OF AMERICA CopryriIcHT, 1922, By THE MACMILLAN COMPANY. Set up and printed. Published September, 1922. ©ciA681947 Press of J. J. Little & Ives Company New York, U. S. A. SEP 27 1929 + | oe PREFACE My object in preparing this book has been to place in the hands of those who handle hog cholera definite and authoritative information regarding the disease. There are abundant publications dealing with hog cholera but for the most part they consist of technical papers covering certain restricted phases of the disease, or of attempts to circumscribe the entire subject in the scope of a few pages. Neither meets the needs of the man who must handle hog cholera in the field. More- over these publications appear as bulletins or as special papers in technical journals, and usually they are not at the veterinarian’s command at the time he needs them. We are rapidly discarding the old belief that any one who can use a hypodermic syringe can cope with hog cholera. Questions constantly arise regarding diagnosis, complications, when or whether to immunize, which method to use, the subsequent care of the herd, the handling of young pigs, slaughtering from infected herds under inspection, and many other individual prob- lems. The effective handling of hog cholera, like the handling of other diseases, is founded on exact knowledge of the malady itself, but hog cholera differs from other in- fectious diseases in that preventive vaccination against it has served to open the new field of swine practice. Vv Vi PREFACE The result is that there are many veterinarians who will not attempt to cope with the disease, or who, making the attempt, feel the need for guidance. This volume is in no sense a compilation. For the most part it reflects personal experiences gained during ten years of intimate contact with hog cholera in the capacity of practicing and consulting veterinarian, anti- hog-cholera serum producer and research worker, but acknowledgment is due many other members of the veterinary profession whose researches and observations have revealed many of the foundation facts on which the subject matter rests. For statistical and other data I have consulted other authors freely, relying for sta- tistics especially on the numerous and excellent publi- cations of the United States Bureau of Animal Industry. I am indebted to Dr. E. A. Cahill, Director of the Pit- man-Moore Biological Laboratories, Zionsville, Indiana, for some of the illustrations. Dr. V. A. Moore, Dean of the New York State Veteri- nary College at Cornell University, and Dr. J. W. Benner of the College Experiment Station Staff have read the manuscript, and each has offered many valuable sug- gestions which are deeply appreciated. Great care has been taken to make the book a conserva- tive and accurate guide for the practicing veterinarian who must accept farm conditions as he finds them and handle hog cholera so as to secure and retain the con- fidence of his clients. If among other imperfections there are departures from this ideal I trust that my readers will direct my attention to them. R. BR. G. CHAPTER I II VIL XI CONTENTS History AND Economic IMPORTANCE . 2. e« « NATURE AND CAUSE OF HoG CHOLERA. «2. e« e Mernops OF DISSEMINATION . . « © e« e CONIPLIGARIONS Co uk Se Oe a ow Oe ee SYMPTOMS AND UUMSIONS.. 9.6. 6. « «4! ot ss D1AGNOSIS, DIFFERENTIAL DIAGNOSIS, PROGNOSIS PREPARATION OF ANTI-HOG-CHOLERA SERUM AND PGC OLOLERA VIRUS 6s ie in “es A AGL. Meruops or Usina ANTI-HOG-CHOLERA SERUM . Hanpuing Hog CHOLERA IN THE FIELD... Hog CHouera, Meat INSPECTION AND GARBAGE VEG, ee th Oe Gnan bese Fa Rew orm tapne lane al ConTROL AND ERADICATION OF HoG CHOLERA . PAGE 118 158 Me 230 ILLUSTRATIONS Shoats affected with acute hog cholera . Lung of pig cae ere due to acute hog cholera . . Ra Cem a ates Left auricle of pig’s heart showing Dee due to acute hog cholera. . . sip Naas Spleens showing hemorrhages which are rather typ- ical of acute hog cholera . tt a), : Kidney of pig showing numerous petechiz due to acute hog cholera . DN gS tek NE a Ba Lymph glands of pig Sn onaHe) hemorrhages caused by acute hog cholera . ; Bleeding room in anti-hog-cholera serum laboratory. (Courtesy Pitman-Moore Biological Laboratories) Corner of anti-hog-cholera serum laboratory. New York State Veterinary ¢ College at Cornell Uni- versity sa ae - : ° Post-mortem room where aiid on virus pigs are held PEA RS ‘ la se A close view showing the hypering process Bleeding unit, and hog prepared for bleeding Bleeding for serum . Testing anti-hog-cholera serum Injecting anti-hog-cholera serum in the ham . 1X PAGE 37 46 48 49 51 54 a 79 88 on 99 101 107 119 ILLUSTRATIONS Method of holding shoat for injecting serum in axillary space . ‘ An improvised method of holding shoats for immun- izing’. Convenient hog holder made from 1% inch gas pipe, and flexible clothes wire . 5 oie ees Method of preparing snout rope for confining large hogs. ly aL Seed Be 2 Method of noosing the snout of hog Injecting serum behind the ear . . PAGE 120 121 123 124 125 129 HOG CHOLERA CHAPTER I HISTORY AND ECONOMIC IMPORTANCE Hoe cholera seems to have appeared first on American soil in 1833, at which time an outbreak of the disease was reported in the Ohio valley. It is not definitely known whether the malady orig- inated in this country or in Europe, but it is a rather significant fact that the wild hog has flourished in Eurasia, and not in North America, in spite of the fact that the fauna of the two continents are in most other respects very closely related. It is also of special significance that the earliest authentic report we have of the disease in this country was made at a time when railroads were first being put into operation. It is there- fore possible that it really existed in America prior to that time, and that lack of facilities for its rapid spread prevented it from assuming the proportions of an epizootie. It is true that as early as 1822 an epizootic dis- ease resembling hog cholera was reported in 1 2 HOG CHOLERA France, and there is evidence that prior to 1833 outbreaks of a similar nature occurred in other parts of continental Europe. But even with pres- ent-day knowledge hog cholera and other infec- tious swine diseases are sometimes difficult to differentiate, and we are thus in the dark relative to the true causes of all the earlier outbreaks. According to the most authentic records, hog cholera appeared in England in 1862, and from there, in 1887, it was carried to Sweden in a ship- ment of boars. In this same year the disease ap- peared in France and Denmark, and its spread was so rapid and persistent that all European countries have suffered severely from its ravages. To-day, no large area devoted extensively to swine raising is entirely free from hog cholera, and so far as we have been able to ascertain, no country, once invaded, has succeeded in freeing itself of the malady. The Scandinavian countries seem to have suffered least from its effects. Because of its rapid spread and high mor- tality hog cholera has caused and is causing enor- mous losses, the estimate being that in the United States it is responsible for ninety per cent of the deaths from all swine diseases. In this country the annual losses caused by it during the last four decades have ranged between $13,000,000 and $200,000,000, and in the two decades ending with the year 1914 the average annual loss per one HISTORY AND ECONOMIC IMPORTANCE 3 thousand hogs has been approximately 66. In 1897, the loss per thousand ran as high as 180. Since 1914, the losses due to the disease have been gradually diminishing, and it is believed that more effective sanitary measures and more extensive and judicious use of protective serum have been responsible for this decline. Naturally a disease of such great economic im- portance has been the object of close and pro- longed study. In 1875, Dr. James Law furnished the United States Department of Agriculture with a report setting forth accurately the symptoms and lesions of the disease, and speaking for its transmissibility. Three years later, as a member of a commission of nine men appointed by the De- partment to investigate the disease, he succeeded in transmitting it by inoculation experiments. Dr. Detmers, acting as a member of the same commis- sion, isolated an organism which he regarded as its cause, but his findings were not confirmed. In’ 1885, Dr. Daniel Elmer Salmon and Dr. Theo- bald Smith isolated an organism, now known as B. suipestifer, which they believed to be the true cause of hog cholera. Their work was confirmed by trained investigators in this country and Hu- rope, but all attempts to produce immunity to field outbreaks by using B. swpestifer as an im- munizing agent ended in failure. Thus during the late nineties considerable doubt had developed 4 HOG CHOLERA among some scientists relative to the true signifi- eance of this organism in its relation to epizootic hog cholera. This doubt was aroused because hogs that sickened as a result of injections of B. suipestifer cultures failed to transmit disease to checks, because those that survived injection with cultures of the organism were not immune when exposed in field outbreaks, and because these cul- tures did not always produce disease, while blood from hogs sick as a result of natural infection proved to be quite generally infectious. In 1903, de Schweinitz and Dorset of the United States Bureau of Animal Industry demonstrated that the true cause of epizootic hog cholera is a filterable virus, and this marked an epoch in the history of the disease. Proceeding in the light of this new knowledge, Dorset, Niles and McBryde succeeded, in 1908, in adapting to hog cholera the principles employed by Kolle and Turner, Nicolle and Adil-Bey in pro- ducing a protective serum against rinderpest, a disease of cattle caused by a filterable virus. The work of Dorset and his associates was con- firmed by numerous investigators, among whom were Uhlenhuth, Hutyra and Xylander, and the epochal field experiments conducted in this coun- try by Dr. Niles and described by him in the re- port of the United States Bureau of Animal In- dustry, 1908, fully established the great practical > HISTORY AND ECONOMIC IMPORTANCE 5) usefulness of anti-hog-cholera serum in checking the inroads of hog cholera in the field. Since 1908, rapid advances have been made in providing for an adequate supply of serum, in refining it, in working out methods for its use in the field, and in regulating its production so as to prevent sale of that which is contaminated or im- potent. All important hog-raising states in the Union have made provision to manufacture serum, and scores of private laboratories which have been established are being operated under super- vision of the Bureau of Animal Industry. In the refinement of the serum the aim has been to pro- duce, at low cost, a clear, sterile, potent product with good keeping qualities. This ideal is rapidly being attained, but there are still serious questions regarding uniform potency and keeping qualities of the clear serum, and the equipment required in making it is rather crude, and cannot be said to have passed the developmental stage. Finally, it should be related that with the knowledge that hog cholera can be controlled, there has appeared a quickened interest in all other maladies that affect swine, especially those frequently complicated with hog cholera. Undue importance has sometimes been attached to some of these diseases, and such extravagant claims have been made for certain biologics used as pro- phylactic or therapeutic agents that there has 6 HOG CHOLERA been a sharp reaction, and there are indications at present that the trend of opinion may even swing too far in the opposite direction. The dis- eases that complicate hog cholera present very real problems, and experimental work looking to- ward a deeper understanding of them is one of the immediate needs of the present day. CHAPTER IT NATURE AND CAUSE OF HOG CHOLERA Hoe cholera is an acute, communicable, febrile disease which attacks swine of all breeds and ages, but does not affect other domesticated animals, or man. It is a septicemia. Occasionally a per- acute form of the disease is recognized during the first days of an outbreak and chronic hog cholera is frequently observed among the stragglers that survive the more severe and rapidly terminating forms. In the individual, the disease is charac- terized by sudden onset, inappetence, chilling; very high fever, arched back, a disposition to hide in the litter, constipation followed by diarrhea, general weakness in the later stages, accompanied by purplish discolorations of the skin covering the belly, ears and snout. In the herd, the onset is relatively slow, the first death usually preceding subsequent ones several days, but after the first week the outbreak rapidly gains momentum, and in a comparatively short time all hogs become in- fected. The mortality ranges between 80 and 100 per cent with a strong tendency to approach the latter figure. a 8 HOG CHOLERA Young pigs, especially those farrowed and nursed by immune mothers, are often immune to cholera during the first few weeks of life, and a general impression that all pigs nursing immune sows are likewise immune seems to have gained ground. This impression is not in accord with the facts, for we have seen individual pigs born of immune mothers and suckled by them, dead of hog cholera on the seventh day following birth, and under like conditions of birth and sustenance we have frequently seen entire litters succumb to the disease before attaining an age of four weeks. Among older hogs raised in localities where hog cholera is not prevalent, the ‘‘natural immunes’’ so frequently mentioned are by no means common, and it is probable that in places where they are found in considerable numbers they owe their im- munity to the fact that they are exposed to cholera as young pigs, and suffering only a slight reac- tion, are rendered immune. As a general rule, young shoats, old hogs, and sucking pigs are most susceptible to cholera in the order named, and, as would be expected, recoveries from the disease are less frequent among young shoats, and more frequent among old sows and sucking pigs. The cause of hog cholera is a filterable virus, probably an organism too small to be visible with the highest magnification now obtainable, and pos- sibly possessed of characteristics which prevent it NATURE AND CAUSE OF HOG CHOLERA 9 from taking stains that render bacteria more plainly visible. The virus readily passes porce- lain and infusorial earth filters which retain all visible bacteria, but it is itself retained by the finest porcelain filters. It does not pass through colloid membranes. In the human subject, mea- sles, mumps, scarlet fever and smallpox are among the diseases caused by filterable viruses, while among animals rinderpest, foot-and-mouth dis- ease and rabies are some of the diseases that fall in the same group. The classification is a rather loose one, being based entirely on the fact that these viruses will pass filters that retain visible bacteria, rather than on morphological or cultural characteristics. There is no conclusive evidence that hog cholera virus has been propagated outside the bodies of infected swine. After a hog has been exposed to the disease and actually infected, the virus ap- pears in the blood stream in about four days, and thus all vascular organs harbor it during the at- tack. In the later stages of a few chronic cases, we have found the blood free of the virus, but we do not know whether this is the rule, nor is there definite knowledge of the part played by ‘‘car- riers’’ in harboring it. It is eliminated through the excretions. The urine is regularly infectious, the feces may or may not contain it, and the dis- charge from the eyes and skin ulcers is infectious 10 HOG CHOLERA at least in some instances. Just how any one of the filterable viruses operates to produce disease is quite unknown, but it is certain that hog cholera virus has a selective action for epithelial and en- dothelial cells. Virulence. Hog cholera virus produces speci- fic disease only in swine, and very small quantities of infected material are sufficient to cause death in susceptible animals. According to King, sub- cutaneous injections of 1/86 of a mil of virulent blood produced the disease, while lesser amounts produced only a mild reaction, or none at all. Natural infection usually occurs by way of the digestive system, but the disease is readily pro- duced by subcutaneous, intravenous or intra-abdo- minal injections of small quantities of virulent material. : Resistance. Most of the natural influences to which hog cholera virus is subjected do not oper- ate to destroy it rapidly. Drying, sunlight, and low temperatures seem to have no immediate at- tenuating effects, although it is a fact that most infected yards which remain uninhabited from three to six months do not endanger susceptible pigs placed in them. There is, though, a consid- erable tendency for hog cholera to recur on old infected farms, and this fact indicates that there are exceptional cases in which the span of life of the virus is greatly prolonged. NATURE AND CAUSE OF HOG CHOLERA se A Putrefaction is the only natural influence which operates to destroy the virus rapidly. Ac- cording to Uhlenhuth it will live in putrefying car- easses for about eight days, but undoubtedly the many influences which govern putrefactive proc- esses render data of this kind of value merely in establishing tendencies. It is certain that decom- posing carcasses do not harbor the virus regu- larly, and likewise it is true that virus kept in bot- tles in the laboratory often is killed when putre- faction develops. When sufficient preservative is added to prevent the growth of putrefactive or- ganisms, the virus regularly lives several months, and may even exist for years. Moderate degrees of heat attenuate or destroy the virus, and under no circumstances has it been found to survive temperatures near the boiling point. The following rather incomplete table pre- pared by the German Imperial Board of Health laboratories gives a fair idea of the effects pro- duced by various degrees of heat. Degrees Material Centigrade Time Results Liquid serum filtrate 45 24 hours Not killed or weakened Liquid serum filtrate 46.5 24 hours Not killed or weakened 12 HOG CHOLERA Degrees Material Centigrade Time Results Liquid serum filtrate 46 48 hours Killed Liquid serum filtrate 5D 24 hours Killed Liquid serum filtrate 60 10 hours Killed Liquid serum filtrate 58 2 hours Not killed Liquid serum filtrate 78 1 hour Killed Dried blood 65 2 hours Not killed Dried blood 72 1 hour Killed Dried blood 72 1% hour Killed Urine 58 1 hour Killed Urine 58 1% hour Not killed Low temperatures act to prevent growth of putrefactive organisms and are thus instrumental in prolonging the life of the virus. In our own experiments, hams removed from cholera infected pigs and frozen hard ninety-three days still har- bored virus sufficient to produce the disease when small portions of them were fed to susceptible pigs. Disinfectants. Hog cholera virus readily re- sists ordinary disinfectants in dilutions that are rapidly fatal to most bacteria. When 1% per cent phenol is added to virulent blood, the virus will remain alive for months, and all of the coal tar disinfectants must be prepared in strong solutions in order to destroy it. Liquor cresolis compositus NATURE AND CAUSE OF HOG CHOLERA 13 in 5 per cent aqueous solution, when allowed to act for an hour or more, has proved effective in killing it. Following is a table prepared by the German Imperial Board of Health laboratories, which fur- nishes additional information relative to the effec- tiveness of various disinfectants when used to kill hog cholera virus. Most of the tests were made by mixing 10 mils of the virus with an equal quantity of aqueous dilution of the disinfectant. Dilution Disinfectant applied Result Corrosive sublimate 0.3 per cent solution Serum filtrate not killed in 8 days. Corrosive subhmate 0.5 per cent solution Serum filtrate virus not killed in 4 days. Corrosive sublimate 0.2 per cent solution Urine virus killed in 15 minutes in one trial. In another trial not killed. Carbolic acid 0.5 per cent solution Serum filtrate virus not killed in 8 days. Carbolie acid 1.0 per cent solution Serum filtrate virus not killed in 4 days. Carbolie acid 3.0 per cent solution Failed to kill blood virus in 8 days. Carbolie acid 2.0 per cent solution Failed to kill urine virus in 15 minutes. 14 HOG CHOLERA Dilution Disinfectant applied Chloroform Full strength Sodium taurocholate Formaldehyd 2.5 per cent solution Lugol’s solution 0.25 per cent solution Urea 20.0 per cent solution Glycerin 33.0 per cent solution RZOME. Qo ate a Hydrogen peroxid 10.0 per cent solution Antiformin 5.0 per cent solution Antiformin 2.0 per cent solution Antiformin 1.0 per cent solution Result Serum filtrate virus not killed in 24 hours. Blood virus not killed in 4 days. Serum filtrate virus alive after one hour. Dead in 15 days. Failed to kill serum filtrate virus in 2 hours. Did not kill serum filtrate virus in 1 month. Failed to kill serum filtrate virus in l month. Blood virus not killed. Serum virus not killed in two hours. Serum filtrate virus killed in one hour. Urine virus. not killed in 10 minutes. Killed in 15 min- utes. Serum filtrate virus not killed in 24 hours. NATURE AND CAUSE OF HOG CHOLERA Dilution Disinfectant applied Antiformin 2.5 per cent solution Pea Ob WITNE: |. o ataeie te iivieru ate am ele Chlorid of lime 5.0 per cent solution Lysol 3.0 per cent solution Cresol soap solution 3—6 per cent solution Cresol soap solution 3—4 per cent solution Cresol soap solution 3.0 per cent solution 15 Result Serum filtrate virus killed’ im 2. hours. Blood virus _ not killed in two hours. Failed to kill in one hour. In other ex- periments killed in 20 min. Serum virus killed in 114 hours. Serum filtrate virus usually killed in 1 hour. Always killed virus in 1 hour. Serum filtrate virus not killed in &% hour. Killed urine virus in 14 hour. Since a filterable virus has been incriminated as the true cause of hog cholera, various investiga- tors have from time to time attempted to isolate it, stain it, and grow it on artificial culture media. King has made an exceedingly careful study of a spirochete (Spirocheta hyos) which to him has seemed to possess etiological significance, but his 16 HOG CHOLERA work has never been verified. More recently Proescher and Seil have described a diplococcus which they are inclined to regard as the virus of hog cholera, but as yet they have not submitted substantial proof to justify such a claim. Certain cell inclusions which in cholera-infected hogs ap- pear in the epithelial cells of the conjunctival sac have also been regarded as possible possessors of pathogenic powers, but it now seems probable that these exist as an effect rather than as a cause. There are various organisms which, acting as secondary invaders, exert profound influence on the eourse of hog cholera and on the lesions which develop, but which should in no way be confused with the filterable virus that produces the dis- ease. These will be considered in another chap- ter. CHAPTER III METHODS OF DISSEMINATION Hoe cholera virus exists only in infected hogs and in material contaminated by their excretions, and this is the fundamental fact to which we must repeatedly refer in accounting for new outbreaks. There are numerous exceptions to the rule, but the individual outbreak can usually be traced to a definite source, and this fact is important in its relation to measures for control. Shipping infected animals is probably the one practice responsible for most new herd infections. It is not uncommon for a breeder to become dis- couraged when his hogs begin to die and to ship all seemingly well animals to a distant market. During the fall of the year especially one has but to stand for a few hours at the unloading chutes of some of our large stockyards in order to realize how nearly universal this practice has become. Thus most public stockyards harbor hog cholera virus, and all hogs unloaded in them and later taken to farms for feeding or breeding become potential sources of danger. In the eastern states garbage feeding is re- sponsible for more outbreaks of hog cholera than 1 Y 18 HOG CHOLERA all other factors combined, and in the country as a whole this practice plays an exceedingly im- portant part in the spread of the virus from local- ity to locality. Many hogs are killed while they are in the incubation period of cholera, and pork that comes from their carcasses, even though it is fit for human food, will produce hog cholera when fed in small portions to hogs. Bits of this in- . fected pork find their way into garbage which is fed to susceptible swine, and the cycle is com- plete. The use of hog cholera virus in the field in serum-virus immunization has now become a rou- tine measure, and despite the advantages that re- sult from this practice, it must in truth be said that it is responsible for many new outbreaks of hog cholera. The practice of giving feeding shoats serum-virus treatment and shipping them immediately to distant points operates to infect much new territory, and is often the cause of heavy losses among the hogs thus handled. ‘‘Vaccination cholera,’’ as these ‘‘breaks’’ follow- ing serum-virus treatment are called, although it usually runs a less rapid course which invites sec- ondary infection, is not fundamentally different from hog cholera contracted as a result of natural infection, but there is a marked tendency in some quarters to avoid the issue and attribute the deaths to causes other than hog cholera virus. METHODS OF DISSEMINATION 19 The practice of taking breeding hogs to dis- tant points to mate them is a fruitful source of new herd infections, and in more than one instance we have known the virus to be carried from one farm to another as a result of neighbors exchang- ing help during butchering time. Small streams to which many hogs have access may also become polluted and carry destruction to herds below the one in which the original infection occurs. Show hogs returned from fairs often contract hog chol- era en route or during their contact with other hogs in the show ring, only to infect the herds they represent when they return home. Besides the regular channels of infection which we have already indicated, and which severally are responsible for most new outbreaks of hog cholera, there are almost an infinite number of casual carriers of the virus, such as crows, spar- rows, buzzards, pigeons, and various predatory animals. These, by feeding in infected yards or on carcasses of hogs dead of cholera, may carry the infection to clean territory, but the probabili- ties are that in most localities the number of herds thus infected is relatively small. In recent experiments Dr. Marion Dorset has found it difficult to transmit hog cholera from herd to herd by employing attendants, pigeons and sparrows as agents of transmission, and in our own experiments we have failed in a surpris- 20 | HOG CHOLERA ing percentage of cases to infect yards with hogs sick of cholera so that susceptibles placed in them subsequently will contract the disease. In spite of these facts, though, we must in handling hog cholera be guided by the practically universal clinical experience which teaches that when hog cholera once finds its way into a farm herd it will eventually infect all individuals in it, irrespective of the fact that the herd may consist of several pens of hogs kept some distance apart. It is impossible, and indeed unnecessary, to dis- cuss in detail the various influences which occa- sionally are instrumental in carrying hog cholera virus from herd to herd, and likewise it is impos- sible to assign to each influence a relative import- ance. It is much more important, in concluding this chapter, to call attention again to the fact that in the great majority of cases hog cholera virus travels in certain quite definite channels, and that new outbreaks are usually the direct or in- direct result of shipping or moving infected hogs, or else they originate from the practice of garbage feeding, or that of using hog cholera virus indis- criminately in seeking to immunize against the disease. — CHAPTER IV COMPLICATIONS BeroreE we consider the symptoms, lesions and diagnosis of hog cholera, it is necessary that we shall discuss briefly some of the organisms that complicate the disease, and which at times exert _ such profound influence on its course that autop- sies become a continual source of surprise and perplexity to the diagnostician. No attempt will be made to give complete morphological and cul- tural characteristics of these organisms, which in- formation may be found in various standard works on bacteriology. The scope and purpose of this book require that we shall deal only in a general way with most biological characteristics, confining our attention chiefly to disease produc- ing power, especially in swine. Bact. suisepticum is the most important of the organisms that complicate hog cholera. It was isolated and described by Loeffler and Schttz in 1885, and in 1886 Dr. Theobald Smith recovered it from various organs of many hogs dead of an epizootic disease in this country. Moore showed that it is present in the upper air passages of 21 22 HOG CHOLERA many healthy swine. In the absence of knowledge of the filterable hog cholera virus, all these investi- gators were inclined to regard the organism as the cause of epizootic swine plague, and to ascribe repeated failures in causing it to produce trans- missible disease, to the fact that field conditions could not be duplicated in the laboratory. The organism is rod-shaped varying in length from .8 to 2 microns, and in width from .4 to 1.2 microns. Often the ends are rounded giving it an oval shape, but it is not uncommon for the rods to be so short as to resemble micrococci. Some- times involution forms are observed. In cover- glass preparations made direct from the tissues and stained with basic aniline dyes, Bact. suisepti- cum often stains heavily at the ends and around the periphery, and very lightly or not at all in the center. Preparations made from cultures do not as a rule exhibit this bipolar staining. The organism is subject to wide variation in virulence. Rabbits, mice and guinea-pigs readily succumb to injections of minute quantities of cul- tures or suspensions containing it. Rabbits are especially susceptible, usually dying in less than thirty-six hours of an acute bacteremia. Like cul- tures or suspensions injected subcutaneously into cholera immune pigs produce as a rule a transient local reaction. Small doses injected intravenously may or may not prove fatal, but large intrave- COMPLICATIONS 23 nous doses produce death from septicemia quite regularly. The pigs that die in less than seventy- two hours may show as lesions congestion of the lymph glands and various parenchymatous or- gans, or, more rarely, petechial hemorrhages in the kidneys and heart, indistinguishable from those observed in acute hog cholera. In the cases in which the disease runs a less rapid course, there is a rather constant tendency for joint lesions of an inflammatory nature to form, and, contrary to what might be expected, pleuritis and pneumonia appear much less frequently than these joint le- sions. Rarely do checks kept with these experi- mental animals contract disease.! The symptoms that appear in pigs artificially infected with large intravenous doses of Bact. suisepticum are observed in a very few hours after the injection. There is rapid breathing, sometimes an extreme degree of dyspnea, or the respiratory disturbance may manifest itself in ‘‘thumping.’’ The appetite is suspended, the tem- perature is moderately high (104°-105.5° F.) and there is an anxious facial expression. A general stiffness is practically always observed, and *In our own experiments, in which more than 100 pigs were exposed in pens with pigs artificially infected with intravenous injections of Bact. suisepticum, 3 contracted disease and 2 died. Bact. suisepticum was recovered from the blood and various parenchymatous organs of the dead animals. We know of no other well authenticated instances in which like transmission has occurred. 24 HOG CHOLERA lachrymation often is pronounced. If death or recovery does not take place in two or three days, the tendency is for the disease to assume a chronic type. One or more of the joints, usually the knee or hock, becomes hot, painful, and swollen, render- ing it difficult or impossible for the animal to stand. In spite of this, the temperature falls and is maintained close to normal, the appetite returns and is surprisingly good considering the condition of the animal and the fact that progressive ema- ciation is taking place. Pneumonia sometimes appears in these chronic cases, adding its train of symptoms, but it fails to develop in a surprising percentage of cases, thus presenting a striking comparison with field outbreaks formerly thought to be caused solely by Bact. suisepticum, in which pneumonia is the most constant manifesta- tion. These facts lead us to doubt that the or- ganism, acting alone, is the cause of a rapidly transmissible disease in the field. Field observations are in almost perfect accord with these experimental data. We have frequently had outbreaks of ‘‘pure swine plague’’ reported to us, and in those we have investigated, in which there was evidence of transmissible disease, we have without exception succeeded in positively demonstrating or establishing the probable pres- ence of the filterable hog cholera virus. It is also significant that in the Hast, at least, cholera im- COMPLICATIONS 20 mune hogs do not suffer from ‘‘swine plague”’ if we except the cases in which it is said to appear in the first month subsequent to serum-virus treat- ment, and which in reality have their origin in the hog cholera virus used. Acting as a secondary invader in hogs suffering with cholera, in those badly infested with lung worms, and very probably as a primary microbian cause in those weakened as a result of shipping, Bact. suisepticum regularly produces a rather characteristic bronchopneumonia, and hastens or causes death. In those cases in which it acts as a secondary invader it produces pneumonia so rap- idly and regularly that the lesions due to the pri- mary cause are often obscured or overlooked. Cholera immune farm hogs kept in exceedingly bad sanitary surroundings and exposed regularly to damp and inclement weather, have not been shown to suffer from a rapidly transmissible and fatal pneumonia caused by this organism. There is, though, some experimental evidence that it oc- casionally produces pleuritis or possibly slight pneumonic lesions from which most hogs recover. B. suipestifer (B. cholere suis) is another or- ganism which may often be isolated from various parenchymatous organs of hogs dead in outbreaks of cholera. It is a short, motile rod, belonging to the colon group. In 1885 it was described by Salmon and Smith as the cause of epizootic hog 26 HOG CHOLERA cholera. In later years Uhlenhuth and his co- workers reported finding it in the intestinal tracts of many healthy swine. Jordon, in this country, was unable to identify it in any normal hogs which he examined, and neither was Tenbroeck. Both of these investigators regard Uhlenhuth’s work as inconclusive owing to the fact that he did not differentiate correctly between B. suipestifer and B. paratyphord B. Smith states that the only dis- tinction that can be made between the two is that the former is pathogenic for rabbits, while the latter is not. Rabbits and guinea-pigs succumb to small sub- cutaneous injections of cultures of B. suipestifer, rabbits being somewhat more susceptible. Swine are not easily infected with subcutaneous injec- tions, but large intravenous doses prove fatal. According to Welch, small doses may lead to for- mation of the ‘‘button ulcers’’ observed in chronic hog cholera, and Smith secured like results by feeding pigs bouillon cultures. | The part played by this organism in producing swine disease in the field is not well defined, as most work with it ceased as soon as the filterable virus was accepted as the cause of epizodtic hog cholera. There is good evidence that it is one cause of the ‘‘button ulcers’’ just mentioned, and it is likewise probable that, acting in the role of secondary invader, it is responsible for the en- COMPLICATIONS oat larged, dark, and somewhat pulpy spleens ob- served in individual hogs dead in outbreaks of cholera. It also seems to intensify hemorrhagic lesions produced by the filterable virus. Its pathogenic powers in relation to cholera immune pigs will bear further investigation, but it is prob- able that for the most part it acts to complicate diseases produced by other causes. B. pyocyaneus, or, according to Migula’s classi- fication, Pseudomonas pyocyaneus, is a motile rod 2 to 6 microns long and .8 to 1 micron broad. Itis widely distributed in nature, and there has been a tendency to regard it chiefly as a saprophyte. It is included frequently in the flora of wounds, it appears at times in abscesses in swine and other animals, and it has been described as the cause of an outbreak of dysentery in man. In Germany it is said to be the cause of an infectious nasal catarrh in pigs, and we have found it associated with outbreaks of pneumonia in swine, as the prob- able cause. The organism is an aerobe, it grows luxuriantly on the common culture media, tending to over- whelm other bacteria associated with it. It has a marked tendency to produce green color in any cul- ture medium, and the sweetish odor produced by it in bouillon cultures is quite characteristic. It takes the aniline stains regularly, and is Gram negative. 28 HOG CHOLERA B. pyocyaneus is pathogenic for pigeons, guinea pigs and rabbits. In swine, it is not regularly so, but under certain conditions it assumes great pathogenic significance. We have failed to pro- duce disease by feeding cultures of it or by spray- ing them into the nostrils of healthy pigs, while subcutaneous doses produced nothing more than an occasional local abscess. Moderate intrave- nous doses of suspensions containing it cause dyspnea, chilling or spasms to appear immedi- ately, and death, preceded by paralysis, usually of the hind quarters, often takes place in a day or two. This paralysis is observed in rabbits as well, and must be regarded as a more or less constant but nevertheless specific action on the part of the organism. According to Hutyra, cultures of B. pyocyaneus inoculated directly into the ethmoid mucosa in young pig's, produce disease similar to the catarrhal rhinitis observed in Germany. Under natural conditions certain predisposing factors, among which early age, lung worms, hog cholera virus and long confinement in very dusty quarters are most important, prepare the ground so that B. pyocyaneus exerts its pathogenic pow- ers. We have observed its effects following hyperimmunization during the process of anti-hog- cholera serum preparation, the hypers developing a fatal pneumonia in a few days following a large intravenous dose of hog cholera virus. COMPLICATIONS 29 The lesions produced in swine experimentally infected by means of intravenous injections of material containing Bb. pyocyaneus are those char- acteristic of septicemia, congestion and dark col- oration of the lymph glands, lungs, kidneys and other organs appearing regularly. We have ob- served no such effects where natural infection rules. Here the constant lesion produced is pneu- monia, acute or chronic, and the constant symp- toms that appear are those that may be referred to this condition. Dyspnea, abdominal breathing and_ other marked evidence of respiratory distress charac- terize the disease. Paroxysms of coughing occur when the hog is required to move, the ale of the nostrils are drawn backward, giving the snout a peculiar pointed appearance, and it is not uncom- mon for the affected animals to assume a dog- sitting position, with the forelegs placed widely apart. Thumping appears frequently. Some- times there is a yellowish purulent discharge from the nostrils. The appetite may or may not be affected, while the temperature, as a rule, remains normal or is only slightly elevated. The typical lesion which we have found associ- ated with natural infection due to B. pyocyaneus consists of a semi-chronic type of bronchopneu- monia, affecting first the ventral and cephalic portions of the lungs, or if lung worms are pres- 30 HOG CHOLERA ent, the posterior border of the diaphragmatic lobe as well. The solidified portions may be red but are often rather light in color, macroscopically resembling the surface of a salivary gland. There is a marked tendency for necrosis to develop from numerous foci, and multiple abscesses occur, appearing as slightly elevated yellow areas dotted over the surface of the pneumonic lung. Pleuritis is somewhat constant, and a high degree of em- physema appears in the dorsal nonpneumonie por- tion, giving it a pale white color as compared to the normal pink. Often there is distinct evidence that as a final cause of death an acute pneumonia 1S superimposed over a more chronic type, in which cases all parts of the lungs are pneumonie, while the lesions in the dorsal and posterior por- tions are of more recent origin. B. necrophorus is another organism that some- times complicates hog cholera. Although subject to wide variations in form, it usually appears as a long, slender, nonmotile rod. It is a strict anaér- obe, it stains with the ordinary aniline dyes, and is Gram negative. Evidently it is quite widely distributed in nature, for it appears in numerous necrotic lesions in practically all domesticated ani- mals. It is regarded as a normal inhabitant of the intestinal tract in swine, and it exists in soil con- taminated with manure. It is the exciting cause of calf diphtheria, lip and leg ulceration in sheep, COMPLICATIONS ot and a necrotic stomatitis of calves and pigs, each of which partakes somewhat of the nature of a specific infectious disease, but none of which, with the possible exception of calf diphtheria, tends to be reproduced regularly, in typical form, by arti- ficial means. In swine, B. necrophorus may be the. primary, and usually is the exciting cause of various ne- eroses which appear in the mouth, stomach and intestines, nasal passages, skin, and lungs, and are designated, respectively, according to loca- tion, necrotic stomatitis, enteritis, rhinitis (bull nose), dermatitis and pulmonary bacillosis. The typical lesion consists of a dark brown necrotic patch which spreads slowly and tends to penetrate the deeper structures. Frequently a yellowish- brown scab or false membrane is formed. In ne- erotic stomatitis and enteritis especially, numer- ous lesions often coalesce until large areas are af- fected, and, depending on location, even the man- dible itself may be involved or the intestinal wall penetrated. A foul odor is usually detected. In the mouth, the lesions usually take origin from teething wounds or other slight abrasions; in the stomach and intestines, hog cholera lesions and various irritants prepare the ground for their development; in the nasal passages they follow rhinitis due to other causes; in the skin, they ap- pear especially on the teats and udders of sows Oe HOG CHOLERA which are chapped or wounded as a result of nurs- ing litters. We know less regarding the primary cause of necrotic lesions that appear in the lungs. It is still an open question whether B. necropho- rus is really capable of penetrating normal mu- cous membrane and producing its characteristic effects, but usually it does not. Likewise there is doubt as to whether it releases a toxin, the prob- ability being that at times it does, for especially in young pigs suffering with necrotic stomatitis, death often takes place suddenly, before it can be explained on the basis of the existing local lesion. On the other hand, some pigs will harbor surpris- ingly extensive lesions without marked systemic disturbances. Some regard B. necrophorus as a secondary invader that may cause the ‘‘button ulcers’’ which appear in chronic hog cholera, but there is at least a distinct difference between the button ulcer in which degenerative and regenera- tive processes coexist, and the usual lesion pro- duced by B. necrophorus, in which a progressive necrosis prevails as long as the exciting cause re- mains active. There is also somewhat meager evidence that the organism may in rare instances cause petechial hemorrhages in the serous mem- branes and kidneys. Bact. swsepticum, B. suipestifer, B. pyocya- neus, and Bact. necrophorus have two characteris- Ce -_ COMPLICATIONS 33 tics in common. All are of a subvirulent nature, usually depending on other influences or predis- posing causes to enable them to exert their patho- genic powers, and all frequently take advantage of the lesions produced by hog cholera virus, in which they establish themselves, changing the course of the disease, and rendering autopsies puzzling and inconclusive. There are several other organisms that have been associated with hog cholera, either as com- plicating influences or probable causes, but some of these normally lead a saprophytic existence, and with our present knowledge we are unable to assign to any one of them a definite pathogenic role. B. colt communis and other members of the group, together with various streptococci and micrococci may often be found in lungs of hogs that have died of a terminal pneumonia brought on by hog cholera. Spirocheta hyos (King) is sometimes found in the blood and intestinal le- sions of hogs suffering with cholera, and B. py- ogenes suis is found in various suppurating lesions in swine, some of which have died in hog cholera outbreaks. The collective primary and secondary effects of all the organisms considered in this chapter, together with the changes produced by hog cholera virus go to make up the symptom- complex which, conveniently but unfortunately, has come to be known as ‘‘mixed infection,’’ and 34 HOG CHOLFRA handled as a single entity. Only when we begin to inquire more closely into the disease-producing powers of each organism will real progress be made. CHAPTER V SYMPTOMS AND LESIONS Fottowine the subcutaneous injection of a small quantity of hog cholera virus, or the feeding of material containing it, symptoms of the disease usually appear between the fifth and eighth days. In herds through which the disease is spreading, several weeks are often required for it to reach all individuals, but this delay must be regarded as due to failure of some of the hogs to take up the virus, rather than as a prolonged incubation period. The incubation period usually given va- ries between four and twenty-one days, but in the vast majority of cases symptoms will appear in less than nine days following definite exposure (feeding or inoculation) of susceptible pigs. Three forms of hog cholera are recognized, per- acute, acute and chronic. The peracute form is relatively infrequent, but it occurs occasionally among the first few hogs that succumb in an out- break. No definite symptoms have been asso- ciated with this form of the disease, for the af- fected animals are found dead with no history of previous sickness. 35 36 HOG CHOLERA The acute form, which includes the great ma- jority of cases, begins with high fever (105°-109° F.), arched back, chilling, rough coat, drooping ears and tail, and general depression. The appe- tite is impaired. The affected animals may crowd to the trough in the usual greedy fashion, but after drinking sparingly of any liquid that may be ~ contained in the feed, they return languidly to the nest in advance of their associates, slowly draw the litter backward with alternating fore- feet, and then settle to sternal recumbency with the snout hidden beneath the litter, seemingly in an effort to keep warm. Intermittent attacks of chilling shake the body, the reflexes are dulled, the eyes closed, and a general stupor prevails. Conjunctivitis, mild or severe, is practically al- ways present, causing an exudate of a seromucous or seropurulent type to appear, gumming the eye- lids together, or forming crusts which remain in the internal canthus and on the margins of the lids. Early in the attack, constipation is noted. The fecal balls, usually dark in color and often cov- ered with mucus, are voided with difficulty. Later, if death does not ensue, diarrhea sets in, and continues pending the advent of death or con- valescence. The character of the food determines the color of the feces. As the sick hog les undisturbed in the nest B1ajoyoa soy oynoe qT JIM popyooye syevoys T v1 d 37 38 HOG CHOLERA there is often noted a scarcely audible, high- pitched, complaining expiratory grunt, but if the animal is seized suddenly it struggles feebly and emits a weak, hoarse squeal. The gait may be unchanged, but often staggering is noticed, and sometimes there is a characteristic unsteadiness or weaving in the hind quarters, best observed in well advanced cases when the animals are caused to move without undue excitement. Convulsions appear somewhat infrequently, and may be regarded as the only violent hog cholera symptom. The attack usually occurs at feeding time or under stress of other excitement, more often in young pigs. The pig comes to the trough as if to eat, but suddenly backs away, squealing, with the snout drawn low between the forelegs. The muscles stiffen in spasm, the pig falls on its side, the eyeballs roll upward, the legs are in con- stant motion, and the snout is gradually extended with a jerky, convulsive movement. The attack lasts less than a minute and terminates either in death or complete return of nervous function. Early in an attack of hog cholera, the skin is flushed, hot and sensitive, the flush being appar- ent only in clean white pigs. Later, as death ap- proaches, a diffuse purplish discoloration some- times appears in the skin covering the ears, snout, belly and inner surfaces of the legs, and is less frequently observed at the extremity of the tail, SYMPTOMS AND LESIONS 39 on the vulva, and in the perineal region. Depend- ing on whether the color results from hyperemia or hemorrhage, it will or will not disappear on pressure. Sometimes congestion and hemorrhage coexist, in which case the color disappears for the most part, revealing the presence of ecchymoses in the pressure-whitened area. Less frequently ecchymoses exist alone. Somewhat infrequently skin ulcers appear on the throat and between the forelegs, very rarely elsewhere on the body. 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