Hog cholera, its nature and control

Front matter

fJass 3T"9T3 Book ^M^_

CQPXRIGHT DEPOSIT.

THE MACMILLAN COMPANY

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. Moreover 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 problems.

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 infectious diseases in that preventive vaccination against it has served to open the new field of swine practice.

VI PKEFACE

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 statistics especially on the numerous and excellent publications of the United States Bureau of Animal Industry. I am indebted to Dr. E. A. Cahill, Director of the Pitman-Moore Biological Laboratories, Zionsville, Indiana, for some of the illustrations.

Dr. y. A. Moore, Dean of the New York State Veterinary 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 suggestions which are deeply appreciated.

Great care has been taken to make the book a conservative 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 confidence 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. R. B.

Contents

CHAPTER PAGE

I History and Economic Importance .... 1

II Nature and Cause of Hog Cholera .... 7

Chapter I History And Economic Importance

Hog 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 originated 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 therefore 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 epizootic.

It is true that as early as 1822 an epizootic disease resembling hog cholera was reported in

France, and there is evidence that prior to 1833 outbreaks of a similar nature occurred in other parts of continental Europe. But even with present-day knowledge hog cholera and other infectious 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 shipment of boars. In this same year the disease appeared 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 mortality hog cholera has caused and is causing enormous 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 6

thousand hogs has been approximately 66. In 1897, the loss per thousand ran as high as 130. 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 importance has been the object of close and prolonged 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 Department to investigate the disease, he succeeded in transmitting it by inoculation experiments. Dr. Detmers, acting as a member of the same commission, isolated an organism which he regarded as its cause, but his findings were not confirmed.

In 1885, Dr. Daniel Elmer Salmon and Dr. Theobald Smith isolated an organism, now kno^vn 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 Europe, but all attempts to produce immunity to field outbreaks by using B. suipestifer as an immunizing agent ended in failure. Thus during the late nineties considerable doubt had developed among some scientists relative to the true significance 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, siiipestifer 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 cultures 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, NicoUe and Adil-Bey in producing a protective serum against rinderpest, a disease of cattle caused by a filterable virus. The work of Dorset and his associates was confirmed by numerous investigators, among whom were Uhlenhuth, Hutyra and Xylander, and the epochal field experiments conducted in this country by Dr. Niles and described by him in the report of the United States Bureau of Animal Industry, 1908, fully established the great practical

HISTORY AND ECONOMIC IMPORTANCE O

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 impotent. 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 supervision of the Bureau of Animal Industry. In the refinement of the serum the aim has been to produce, 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 biologies used as prophylactic or therapeutic agents that there has 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 diseases that complicate hog cholera present very real problems, and experimental work looking toward a deeper understanding of them is one of the immediate needs of the present day.

I

Chapter II

Hog cholera is an acute, communicable, febrile disease which attacks swine of all breeds and ages, but does not afPect other domesticated animals, or man. It is a septicemia. Occasionally a peracute 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 characterized 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 infected. The mortality ranges between 80 and 100 per cent with a strong tendency to approach the

latter figure.

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 Avith 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 immunity to the fact that they are exposed to cholera as young pigs, and suffering only a slight reaction, 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 possibly possessed of characteristics which prevent it from taking stains that render bacteria more plainly visible. The virus readily passes porcelain 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, measles, mumps, scarlet fever and smallpox are among the diseases caused by filterable viruses, while among animals rinderpest, foot-and-mouth disease 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 appears in the blood stream in about four days, and thus all vascular organs harbor it during the attack. 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 '^ carriers'' in harboring it. It is eliminated through the excretions. The urine is regularly infectious, the feces may or may not contain it, and the discharge from the eyes and skin ulcers is infectious at least in some instances. Just how any one of the filterable viruses operates to produce disease is quite unknowm, but it is certain that hog cholera virus has a selective action for epithelial and endothelial cells.

Virulence. Hog cholera virus produces specific disease only in swine, and very small quantities of infected material are sufficient to cause death in susceptible animals. According to King, subcutaneous 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 produced by subcutaneous, intravenous or intra-abdominal injections of small quantities of virulent material.

Resistance. Most of the natural influences to which hog cholera virus is subjected do not operate to destroy it rapidly. Drying, sunlight, and low temperatures seem to have no immediate attenuating 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 considerable 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.

Putrefaction is the only natural influence which operates to destroy the virus rapidly. According to Uhlenhuth it will live in putrefying carcasses for about eight days, but undoubtedly the many influences which govern putrefactive processes render data of this kind of value merely in establishing tendencies. It is certain that decomposing carcasses do not harbor the virus regularly, and likewise it is true that virus kept in bottles in the laboratory often is killed when putrefaction develops. When sufficient preservative is added to prevent the growth of putrefactive organisms, 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 prepared by the German Imperial Board of Health laboratories gives a fair idea of the effects produced by various degrees of heat.

Degrees Material Centigrade Time

Liquid serum filtrate 45 24 hours

Liquid serum

filtrate 46.5 24 hours

Results

Not killed or weakened

Not killed or weakened

HOG

CHOLERA

Degrees Material Centigrade

Time

Results

Not killed

1 hour

Dried blood

Not killed

Dried blood

1 hour

Dried blood

1/2 hour

Urine

1 hour

Urine

% 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 oami experiments, hams removed from cholera infected pigs and frozen hard ninety-three days still harbored virus sufficient to produce the disease when small portions of them Avere fed to susceptible pigs.

Disinfectants. Hog cholera virus readily resists ordinary disinfectants in dilutions that are rapidly fatal to most bacteria. When % per cent phenol is added to virulent blood, the virus mil 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 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 furnishes additional information relative to the efP ectiveness 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

applied Result

Disinfectant

Corrosive

sublimate

Corrosive sublimate

Corrosive sublimate

Carbolic acid

Carbolic acid

Carbolic acid

Carbolic acid

0.3 per cent solution Serum filtrate not

killed in 8 days.

0.5 per cent solution Serum filtrate virus

not killed in 4 days.

0.2 per cent solution Urine virus killed

in 15 minutes in one trial. In another trial not killed.

0.5 per cent solution Serum filtrate virus

not killed in 8 days.

1.0 per cent solution Serum filtrate virus

not killed in 4 days.

3.0 per cent solution Failed to kill blood

virus in 8 days.

2.5 per cent solution Failed to kill urine

virus in 15 minutes.

Dilution Disinfectant applied

Chloroform Full strength

Sodium taurocholate

Formaldehyd 2.5 per cent solution

Lugol 's solution

Urea

0.25 per cent solution

20.0 per cent solution

Glycerin 33.0 per cent solution

Ozone

Hydrogen

peroxid 10.0 per cent solution

Antiformin 5.0 per cent solution

Antiformin 2.0 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 1 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 minutes.

Antiformin 1.0 per cent solution Serum filtrate virus

not killed in 24 hours.

Disinfectant Antiformin

Milk of lime

Chlorid of lime

Lysol

Dilution

applied Result

2.5 per cent solution Serum filtrate virus

killed in 2 hours.

Blood virus not killed in two hours.

Failed to kill in one

hour. In other experiments killed in 20 min.

5.0 per cent solution 3.0 per cent solution

Serum virus killed in 114 hours.

Serum filtrate virus usually killed in 1 hour.

Cresol soap

solution 3 — 6 per cent solution Always killed virus

in 1 hour.

Cresol soap solution 3 — 4 per cent solution Serum filtrate virus

not killed in %

hour.

Cresol soap solution 3.0 per cent solution Killed urine virus m hour.

Since a filterable virus has been incriminated as the true cause of hog cholera, various investigators 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 spirochaete (Spirochaeta hyos) which to him has seemed to possess etiological significance, but his work has never been verified. More recently Proescher and Sell 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 appear 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 course of hog cholera and on the lesions which develop, but which should in no way be confused with the filterable virus that produces the disease. These will be considered in another chapter.

Chapter III Methods Of Disseminatioit

Hog 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 discouraged 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 responsible for more outbreaks of hog cholera than all other factors combined, and in the country as a whole this practice plays an exceedingly important part in the spread of the virus from locality 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 infected pork find their way into garbage which is fed to susceptible swine, and the cycle is complete.

The use of hog cholera virus in the field in serum- virus immunization has now become a routine measure, and despite the advantages that result 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" following serum-virus treatment are called, although it usually runs a less rapid course which invites secondary 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 distant 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 exchanging 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 cholera 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, sparrows, 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 probabilities 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 surprising 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 discuss in detail the various influences which occasionally are instrumental in carrying hog cholera virus from herd to herd, and like^\ise it is impossible to assign to each influence a relative importance. 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 usuall}^ the direct or indirect result of shipping or moving infected hogs, or else they originate from the practice of garbage feeding, or that of using hog cholera virus indiscriminately in seeking to immunize against the disease.

Chapter IV

Before 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 autopsies become a continual source of surprise and perplexity to the diagnostician. No attempt will be made to give complete morphological and cultural characteristics of these organisms, which information 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 producing 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 Schiitz 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 many healthy swine. In the absence of knowledge of the filterable hog cholera virus, all these investigators were inclined to regard the organism as the cause of epizootic swine plague, and to ascribe repeated failures in causing it to produce transmissible 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. Sometimes involution forms are observed. In coverglass preparations made direct from the tissues and stained with basic aniline dyes, Bact. suisepticum 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 cultures or suspensions containing it. Eabbits are especially susceptible, usually dying in less than thirty-six hours of an acute bacteremia. Like cultures 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 intravenous doses produce death from septicemia quite regularly. The pigs that die in less than seventytwo hours may show as lesions congestion of the lymph glands and various parenchymatous organs, 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 lesions. Earely do checks kept with these experimental 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 temperature 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.

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, rendering 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 emaciation 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 manifestation. These facts lead us to doubt that the organism, acting alone, is the cause of a rapidly transmissible disease in the field.