Part 4

Definition. A microbian disease of swine manifested by high fever, great prostration and muscular weakness, a violet tint of the visible mucosæ, red or violet discoloration of the skin in spots and patches or universally, enlarged lymph glands, encreased size of the spleen, and general congestion of the capillary plexus.

Contrary to the habit of hog cholera and swine plague, rouget attacks mature swine mainly, the sucking pig showing a remarkable power of resistance. It does not appear whether this is due to the animal (milk) diet or to the absence of infection from feeding in the trough used by the adult animals. Up to the present this disease has not been recognized in America.

Causes. The one essential cause of rouget is the presence of the bacillus. The other conditions are either such as predispose the animal to receive it, for example, mature age: or they are such as favor diffusion of the poison, such as the introduction of an infected animal, the feeding of the healthy from the same manger with the infected, the introduction into the manger of the feet or snout which have become soiled with the infected manure or urine, the distribution of the infection in dust, the introduction of the bacillus in the bodies of mice, rabbits, or pigeons, or on the feet of those animals, of men, dogs, birds, and vermin. We may add the distribution of infection in dried butcher’s scraps used in pig feeding, and in uncooked scraps from the kitchen or in hotel swill.

It has been noted that the highest mortality prevails in hot summer weather, in damp seasons, and in narrow, confined, badly ventilated pens. Under such circumstances the introduction of a diseased pig will lead to the infection of most of the others in a few hours. Infection is quite as prompt through public pens in stock yards and fairs, and in public conveyances (cars, stock wagons, steamboats, ferry boats, etc.) and public highways.

Symptoms. After a period of incubation of three days or more the subject is seized with shivering, the limbs are hot and cold alternately, respiration and heart beats are accelerated, the mucous membranes assume a dark violet tint and the rectal temperature rises to 104° to 108° F. From the first the pig tends to bury itself under the litter, and refuses to move unless absolutely forced to do so, and then only with painful grunts, swaying and staggering limbs (especially the hind ones), and straight drooping tail. There is inappetence, but thirst remains, and the bowels are at first costive, the manure being covered with a film of mucous or even streaks of blood; later they become relaxed and diarrhœa becomes often a prominent symptom. The pig seems to suffer and often squeals when handled, and he may give a weak, dry cough. The external inguinal glands may often be felt perceptibly enlarged. The red discoloration of the skin appears early and extends and deepens to the end in fatal cases. It may be of a bright red, or of a bluish red, violet or black. The first indications appear as spots, by preference around the roots of the ears, on the breast and abdomen, inside the arms and thighs, and in the perineum. These isolated spots run together into great patches, which extend over the whole ventral aspect of the body, and may cover the entire dorsal aspect as well. In some instances the skin is swollen and retains an impression made by the finger.

Course. The disease may reach a fatal termination in twelve hours: more commonly it endures for forty-eight hours, and at times it will last for four, five or six days. In the most rapidly fatal cases, the violet discoloration of the skin may be absent or only a little marked, while in the protracted cases it acquires its greatest extensions and its darkest shades. In the protracted cases too the prostration becomes extreme, the animal may find it impossible to raise himself on his hind limbs, the diarrhœa becomes profuse, liquid and fœtid, the respiration labored, cyanosis sets in and the temperature is reduced below the normal standard.

In case of recovery, convalescence is usually prompt and complete, differing in this from cases of swine plague and hog cholera. The more favorable issue in rouget probably depends on the comparative integrity of the intestinal mucosa and mesenteric glands, which are subject to slow healing lesions in swine plague and hog cholera. Slow convalescence is however not uncommon, yet in such cases, the concurrent, speedy and complete recoveries in other animals in the same herd serve to identify the disease as rouget.

Mortality. The mortality among grown hogs averages eighty per cent.

Morbid Anatomy. The most prominent lesion is the general congestion of the capillary blood vessels, and the numerous minute extravasations or petechiæ. The skin shows in the red patches a general dilatation of the capillaries which have become at the same time elongated and tortuous, with minute, often microscopic, ruptures and extravasations at frequent intervals. This usually extends to the whole thickness of the cutis, and to a considerable depth in the subcutaneous fat. Where swelling occurred or pitting on pressure, a serous infiltration of the tissues is found. The lymph glands are uniformly enlarged and discolored, of a dark red, almost black, color, the congestion and extravasation being extreme in the cortical substance, while the medullary is paler, soft and cellular. The lungs are usually gorged with black blood suggesting death by asphyxia. In tardy cases there may, though rarely, be centres of broncho-pneumonia. The spleen is enlarged, with dark color and uneven surface from rounded swellings, and is filled by a soft black, bloody pulp. The liver is congested, the kidneys congested, enlarged and petechiated, and the gastric and intestinal mucosa congested and thickened, with desquamating epithelium, and swollen solitary and agminated glands, the degree of alteration usually bearing a ratio to the duration of the disease. The serosæ are usually extensively petechiated and serous effusions occur into the serous cavities. The muscular substance of the heart and the endocardium are also the seats of petechial extravasations. Unless in some protracted cases the blood appears to be unaltered as regards its power of taking up oxygen, or coagulating.

Bacillus of Rouget. The germ of this disease is found in small numbers only, in the blood and vascular tissues, but very abundantly in the lymph glands, the spleen, the kidneys, and the red marrow of the bone. It is also present in enormous quantities in the urine and the bowel dejections, the former (urine) offering a ready means of diagnosing the disease microscopically.

The bacillus is 1µ to 1.5µ long by 0.1µ to 0.15µ broad, is nonmotile, and stains readily even in Gram’s solution. They occur either solitary or in pairs tending to unite at an angle. In old artificial cultures chains of considerable length may be formed. In the blood the bacillus is usually found in the leucocytes, as many as 20 or more being often present in a single cell. In the lymph networks of organs they also invade the leucocytes but are found in free masses as well. The bacillus is anærobic, but facultative ærobic, its preference being manifestly for the absence of oxygen. It is non-liquefying. In gelatine cultures no development takes place on the surface, but along the line of puncture a delicate cloud-like branching growth takes place which extends horizontally in parallel masses from the central puncture. This resembles but is not quite so delicate as that formed by the bacillus of mouse septicæmia with which it is supposed to be identical. It grows scantily on the surface of nutrient agar or blood serum, but not at all on bouillon, in the bottom of which, however, it forms a slight grayish white deposit. It does not grow on potato. The bacillus sometimes shows refrangent granules which have been supposed to be spores, but this idea appears to be negatived by the ease with which its vitality is destroyed by heat and disinfectants. The thermal death point is 68° C. (137° F.) maintained for 10 minutes (Sternberg). Boulton found that it was killed in 2 hours by mercuric chloride (1:10000), by carbolic acid solution (1:100), and by sulphate of copper solution (1:100).

It is killed by desiccation, by quick lime and by chloride of lime. At a temperature of 18° to 27° F. it perished in 13 days. In salted pork it lost vitality in one month.

Pathogenesis. The bacillus is pathogenic to swine, rabbits, white mice, house mice, white rats, pigeons and sparrows. Field mice, guinea pigs and chickens are immune.

Mice and pigeons take the disease most certainly, and die in three days to five, the whole body swarming with bacilli. Rabbits take the disease less certainly or rapidly, inoculation in the ear causing first an erysipelatoid inflammation and recovery with immunity often takes place.

Immunization. When inoculated continuously from rabbit to rabbit it encreases its potency for that animal, which it comes to kill in 24 to 48 hours, but in the same ratio it loses its virulence for swine upon which it can then be inoculated without danger to their life.

It was on this basis that Pasteur and Thuillier established in 1883, their preventive inoculation for rouget. The method has been most extensively employed in Europe, and where intelligently employed has prevented this disease. From the laboratory at Buda-Pest alone, there was sent out in one year material for 249,816 swine.

The objections to the method are: the danger of mistaking hog cholera and swine plague respectively for rouget, as the rouget mitigated germ would be in no sense protective against these; and the danger of spreading the germs of rouget in fresh localities and thus introducing a new plague instead of controlling and preventing an old one. In the Baden experiments 5.4 per cent. of inoculated pigs died, and of 118 unprotected pigs exposed to them 62 per cent. contracted the disease and one died. In France and Hungary, on the other hand, 1 to 1.45 per cent. died of the operation, instead of 20 per cent. when the disease was contracted in the ordinary way.

It is held that the danger lies largely in the inoculation of very young pigs, and Nocard advises to operate only on those of four months and upward.

The danger of spreading the germ by inoculation may be the more easily guarded against, considering that it is very destructible by disinfectant agents (heat, dryness, cold, chloride of lime, quick lime), and that it does not readily survive in a locality, where it cannot find a constant succession of victims. Yet the practice ought to be confined to herds exposed to infection, and under special precautions, as regards the exposure of other herds.

The technique of the Pasteurian inoculation is to inject, subcutem, on the inside of the thigh, 0.1cc. of the weaker preparation (premier vaccin), and twelve days after a similar dose of the stronger one (deuxieme vaccin).

This produces a mild attack of the disease from which the great majority recover, and though they still react somewhat to a second and third inoculation yet the disease so produced is rarely fatal.

CHOLERA SUIS; HOG CHOLERA.

Definition, Synonyms, History, Losses. Bacillus choleræ suis, 1.2–2μ., ærobic, biology, table of germs; accessory causes, roaming pigs, railways, car litter and manure, boats, trucks, loading banks, chutes, runways, stockyards, pens, fairs, watershed, butchers, dealers, etc., wagons, dogs, birds, vermin, insects, offal of abattoirs, butcher’s and kitchen scraps, unburied carcasses of dead hogs, convalescent and immune hogs, susceptibility, parasites and infection atria, putrid food, infection from ground carried into feeding trough by snout and feet, large herds, rapid carriage of swine for long distances. Lesions: hæmorrhagic spots and petechiæ on skin, mucosæ and serosæ, circumscribed capillary congestions, congestion of spleen, lymph glands, stomach, intestines, necrotic processes. Button-like ulcers on intestinal mucosæ. Incubation, 6 to 14 days. Symptoms: fulminant cases. Acute Cases: dulness, anorexia, recumbency on belly, weakness, paresis behind, thirst, tenderness of skin and abdomen, hyperthermia, easily blown, blush on skin, dark red spots and patches, enlarged inguinal glands, cutaneous exudate—greasy or drying black, bowels costive, later pultaceous and finally diarrhœaic, petechiæ on mucosæ, emaciation. Chronic Cases: symptoms more slight, but great loss of condition. Diagnosis: from swine erysipelas, swine plague, Widal test, table of differential symptoms. Prevention: expense of extinction prevents effective measures; removal of accessory causes, comfort, air, light, food, salt, powdered soaps, mouldy bread, cotton seed, space, green food, precautions against introduction of bacillus, special shipping provisions for fat hogs, exclusion of stock hogs from infected localities, precautions by purchasers. Immunization, Disinfection. Certificates. Extinction in herds and districts. Treatment: chronic cases, food, antiseptic medication, antithermics stimulants, tonics. Serum therapy, method, merits, demerits.

Definition. A contagious bacteridian disease of swine, acute or subacute, and characterized by hyperthermia and other febrile disorders,—congestion, exudation, ecchymosis and necrotic ulceration of the intestinal mucosa and of that of the stomach and of other parts,—by a profuse foul, liquid diarrhœa, by enlargement of the lymph glands with congestion and blood extravasation,—by effaceable blotches, and petechiæ (ineffaceable) of the skin, snout and visible mucosæ, with a tendency to necrotic changes—less frequently by pulmonary congestions, and degeneration,—and by a high mortality.

Synonyms. The earlier designations were mostly drawn from the red or black discoloration of the skin and mucosæ and applied indiscriminately to the other forms of hæmorrhagic septicæmia which we now differentiate as erysipelas (rouget, Rothlauf) and swine plague. They included measles, erysipelas, scarlatina, red soldier, purples, blue sickness, carbuncular fever, etc. Others basing their nomenclature on the prominent intestinal lesions, etc., designated it typhoid fever, pig typhoid, typhus, carbuncular gastro-enteritis, pneumo-enteritis, and diphtheria. Even in Europe while the pig erysipelas (rouget, Rothlauf) is now recognized as a distinct disease there is no clear distinction made between hog cholera and swine plague. In England we find these more or less confounded under the names of swine fever, swine plague and hog cholera, and on the continent of Europe under those of schweineseuche and schweinepest, or pneumo-enteritis infectieuses. Differences in different epizoötics or outbreaks are recognized, and the field is left open for the future identification of different forms of this common group of swine fevers, but the existence of constant bacteriological distinctions are not always insisted on, as we do in the United States in the case of the two great leading types swine plague and hog cholera.

History. Definite history of this disease may be said to begin with the discovery and demonstration of the actively motile hog cholera bacillus by the U. S. Bureau of Animal Industry in 1885. Yet in the history of animal plagues, even in early times, deadly epizoötics are described which undoubtedly represented one or other of the contagious affections of modern times. Among the more definite may be named a destructive gastro-enteritis (magen seuche) in Germany in 1817, a pleuro-pneumonia in France and Bavaria in 1821, a cholera with blotching of the skin (morbus niger) in Ireland, and an erysipelas in pigs in France and Switzerland in 1836, and in Ohio in 1833, there was a fatal affection afterward recognized as hog cholera. Writers conjecture that it was imported into America from Europe in improved pigs, and from one European country to another in the same way, but we have no absolute proof of times and shipments and their immediate effects, so that these theories are but more or less reasonable deductions from the familiar extensions of the disease in more recent cases. Under the great commercial activity of the latter half of the 19th century, the active movements of animals by canal, steamboat and rail, and the massing together in one market of many animals drawn from widely different sources, hog cholera has made extraordinary extensions on both sides of the Atlantic, until Friedberger and Fröhner pronounce the schweineseuche and schweinepest the most widely disseminated and dangerous of swine epizoötics, and Dr. Salmon estimates the losses in the United States at $10,000,000 to $25,000,000, per annum.

Bacteriology. Prior to 1885 bacteria had been found in the different outbreaks of contagious fevers in swine, and the bacillus of swine erysipelas had been demonstrated in 1882, but it was only two years later (1884) that the motile bacillus choleræ suis was first described by Klein, and in 1885 that Salmon and Smith demonstrated it as the essential cause of the disease, together with its biological and cultural peculiarities.

It is a short bacillus, 1.2 to 2μ × 0.5 to 0.8μ, but varying considerably in size according to the stage of its growth and the genera of animal or culture medium in which it is grown. It has rounded ends and is usually in pairs connected by an invisible band. It stains promptly in all the aqueous aniline colors, but loses the stain in a solution of iodine (Gram’s). Prolonged exposure of artificial cultures produces an uniform stain, while a transient exposure, and especially of bacilli obtained from the tissues, stains them most deeply at the ends (polar) and periphery, while the centre remains somewhat clear. This is less marked than in the bacillus of swine plague, yet serves to show the relation between this microbe and the colon group.