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.
It is ærobic (facultative anærobic), non-liquefying, and, in fluids, very actively motile, the movements lasting for months in preserved specimens (Smith). It grows luxuriantly in various culture media, and especially in alkaline ones, at the room temperature, and most actively at 85° to 100° F. It may grow as low as 60° to 70° F. and as high as 104°. (Swine plague bacillus grows at 55.4°).
On peptonized gelatine the surface colonies are usually round and flattened, those in its substance globular and smaller, and those at the bottom expanded next the glass and rising in the center into the gelatine like a knob. At 48 hours they appear as opaque whitish points and slowly increase to ½ to 2 mm. They may be brown by transmitted light, the depth of color increasing with age. On agar the colonies are grayish, shining and translucent and may reach the size of 4 to 6 mm. On potato (alkaline) a straw yellow film is formed, darkening with growth. In bouillon a turbidity appears in 24 hours, and in 1 or 2 weeks a precipitate and surface film.
The bacillus is usually larger in the gelatine and smaller in the bouillon than it is in the tissues. It seems to produce neither phenol nor indol.
Its behavior with sugars is significant. It ferments glucose producing acid and gas; does not ferment saccharose nor lactose, but turns the saccharose solution alkaline (no gas). In bouillon containing muscle glucose, it may without additional glucose form a little gas. The swine plague bacillus ferments saccharose producing acids but no gas: it ferments neither glucose nor lactose but turns the former acid.
Milk is neither coagulated nor soured by the hog cholera bacillus, but in 3 to 4 weeks it undergoes a change, becoming saponified.
Cultures have no special nor offensive odor. Some varieties in close tubes may cause a faint acid odor.
Oxygen is not essential to the success of a culture. The colonies form as promptly and as large in the depths of gelatine, or in a vacuum, as if in free air.
The following table will serve to show differences between the hog cholera bacilli, and related pathogenic microbes:
| Hog Cholera. | McFadyean’s. | Swine Plague. |
|---|---|---|
| B. Choleræ Suis | Swine Fever B. | B. Pestis Suis |
| 1.2 to 2μ × 5 to 0.8μ | 2 to 2μ × 0.6μ | 0.8 to 1.5μ × 0.6 to 0.8μ |
| Ends rounded | Ends rounded | Ends rounded |
| Involution forms | Involution forms | |
| Actively motile in liquids | Actively motile | Nonmotile |
| Flagella | No Flagella | |
| Stains throughout, lighter in center | Polar or uniform faint stain | From fresh organs polar stain, from old cultures uniform |
| Bleaches in Gram’s (I) Solu | Bleaches in Gram’s (I) Solu | Bleaches in Gram’s (I) Solu |
| Ærobic (Fac. Anærobic) | Ærobic | Ærobic, (Fac. Anærobic) |
| Vigorous growth in alkaline nutrient fluids | Slight growth in alkaline nutrient fluids | Weak growth in alkaline nutrient fluids |
| Active growth on potato yellowish, becoming darker | No growth on potato | On potato at 37° C. a slight, thin gray, waxy layer |
| On gelatine, small, round brownish colonies | On gelatine light bluish colonies shading off insensibly at edges | On gelatine feeble growth or none |
| Nonliquefying | Nonliquefying | Nonliquefying |
| On agar conical colonies, grayish, white, semi- translucent shining | On agar slight, transparent, almost invisible growth | On agar, grayish translucent, or brown, knobbed, waving edges |
| In milk grows freely, no acid, no clot: Saponifies in 3 or 4 weeks | Grows in milk, no clot | Grows in milk, no acid, no clot |
| Forms no indol in pancreatic bouillon | Forms no indol in pancreatic bouillon | |
| Ferments glucose, forming acid and gas | Does not ferment glucose, forms acid, no gas | |
| Lactose not fermented | Lactose not fermented | |
| Saccharose not fermented; alkalinity; no gas | Saccharose fermented, forms acid, no gas | |
| Thermal death point (moist) 58° C. in 15 minutes | Thermal death point 58° C. in 10 minutes | Thermal death point (moist) 58° C. in 7 minutes |
| Desiccated it dies according to bulk in 7 to 49 days | Dies quickly, if dried at body temperature | Dies in 3 days if dried |
| Dies in water in 3 to 4 months | Dies in water in 10 to 15 days | |
| Dies in soil in 2 to 3 months | Dies in soil in 4 to 6 days | |
| Pathogenic to swine, rabbits, guinea pigs, mice, pigeons | Pathogenic to swine and rabbits | Pathogenic to swine, hens, pigeons, pheasants, sparrows, mice, rabbits, cattle, deer, guineapigs, etc. |
| Guinea pigs immune | ||
| Swine Erysipelas. | B. Coli Commune. | Typhoid Fever. |
| B. of S. Erysipelas | B. Typhi Abdominalis | |
| 1 to 1.5µ × 0.1 to 0.2µ | 2 to 3µ × 0.4 to 0.6µ | 1 to 3µ × 0.6 to 0.8µ |
| Ends rounded | Ends rounded | Ends rounded |
| Involution forms | Involution forms | |
| Nonmotile in liquids | Nonmotile or very slightly so | Motile |
| No flagella | No flagella | Flagella |
| Stains readily and uniformly | Stains uniformly or polar | Stains uniformly (points clear) |
| Stains in Gram’s (1) Solu | Bleaches in Gram’s | |
| Anærobic (F. Ærobic) | Ærobic (F. Anærobic) | Ærobic (F. Anærobic) |
| Active growth in common nutrient liquids at 37° C. | Grows well in usual nutrient liquids, even if acid | Grows well in usual nutrient liquids |
| Usually no growth on potato; variable | Yellowish thick white growth on potato | Grows on potato; transparent glistening surface |
| In gelatine stab-culture delicate feathery branching growth | In gelatine amber colonies, becoming brown; may be bubbles of gas | On gelatine clear colonies with radiating and encircling lines |
| Nonliquefying | Nonliquefying | Nonliquefying |
| Grows in milk; acidifies, often coagulates it | Acidifies and clots milk in 8 to 10 days | Acidifies milk growing freely |
| Thermal death point (moist) 58° C. in 10 minutes | Thermal death point (moist) 60° C. in 10 minutes | Thermal death point (moist) 56° C. in 10 minutes |
| Loses virulence rapidly when dried | ||
| Dies in water in 18 to 20 days | ||
| Lives and even multiplies in rich soils, manure, etc. | Lives and grows in fæces | |
| Loses virulence slowly in light and air | ||
| Pathogenic to swine, pigeons, sparrows, rabbits, white and house mice, white rats | ||
| Guinea pigs, field mice and hens immune | ||
| Hog Cholera. | McFadyean’s. | Swine Plague. |
| Hen or pigeon has slough where inoculated, diarrhœa, ruffled plumage, somnolence | Hen or pigeon dies in 48 hours, after drowsiness, drooping wings, sunken head, ruffled plumage, liquid stools, soft black comb and wattles, prostration | |
| Rabbits getting 0.1cc. virulent culture subcutem die in 5 to 7 days with enlarged spleen and necrotic liver foci | Rabbits getting 0.5 to 1cc. culture subcutem had tumor like walnut but recovered | Rabbits getting 0.01cc. culture subcutem die in 16 to 20 hours, with inflamed serosæ and lung; Petechiæ |
| Weaker culture kills in 10 to 20 days with enlarged spleen, or recovery ensues | Weak cultures kill in 4 to 10 days, with inflamed serosæ and suppuration | |
| Guinea pigs die in 7 to 12 days | Not pathogenic to Guinea-pig | Guinea pigs die in 1 to 4 days |
| Swine inoculated subcutem have often local lesions and bacilli, also in lymph glands, only exceptionally fatal | Swine inoculated have local lesions only, only exceptionally fatal | |
| Ingestion of virulent cultures by fasting pig causes bowel lesions and death | Ingestion of 30cc. by pigs proved always fatal | Ingestion of virulent cultures by pigs is usually harmless |
| Intravenous inoculation in pig causes septicæmic lesions and death, or chronic diseases and typical bowel ulcers | Intravenous inoculation causes septicæmia and death in 1 or 2 days | |
| Intrapulmonary infection causes pleuro-pneumonia | ||
| Swine erysipelas kills inoculated pigeon in 3 to 8 days, and rabbit in 4 to 8 days. | ||
Accessory Causes. These are especially those conditions which favor the transmission of the germ from animal to animal. They include the reprehensible habit of allowing swine to run at large so that herd mingles with herd; the freedom to wander along the lines of railroad by which hogs are carried, and where the infected excretions fall on the ground; the scattering of infected litter or manure from a car or boat; the use of the same cars, boats or trucks for the conveyance of infected and sound pigs in succession, without intermediate disinfection; the use of the same loading banks, chutes, runways, yards, pens and feeding and watering troughs by strange pigs from all sources in succession, without constant disinfection; the purchase of stock swine at public markets; the return of swine from public fairs and exhibitions; the feeding and watering of pigs on the line of streams that have drained pig pens or pastures higher up; the use for pigs of premises that have harbored infected ones at an earlier (even distant) date; the supply of food or litter from barns where pigs have recently died; the admission to the pens or yards of butchers, dealers or others who are likely to carry infection on their persons; the admission even of wagons, dogs or other animals, including birds, tame and wild, which are liable to carry infection. Of all birds the buzzard is the most to be shunned as having presumably just come from infected carrion, but barnyard fowl and small birds that feed from the same trough with the pig are to be feared as well. The same remark applies to rats and mice, squirrels, skunks, woodchucks and rabbits which may easily carry the infection on their paws. If the infection is near, flies and other insects, in the warm season, will convey it for some distance from herd to herd. A common cause is the feeding of swine about abattoirs where they devour the offal and waste in a raw condition. Another is the feeding of boarding house, hotel or other kitchen slops, raw, or without the most exhaustive precautions in the way of cooking. Many outbreaks can be traced in this way to the consumption by the animals of the products of infected swine. Some indeed are fostered by the utter neglect of the parties in charge of an infected herd, in leaving the infected carcasses exposed so that they are eaten by wandering hogs, or portions are carried away by buzzards, carrion crows, dogs and other animals. In some cases a strong wind will carry the infection on dust, straw or other light object into sound herds at a distance. The introduction into a hitherto healthy herd of an apparently sound pig may be the occasion of a deadly outbreak. The strange new pig may have already had the disease, and in a condition of immunity, may without hurt to itself, carry the germ which becomes so fatal to the susceptible.
This susceptibility is one of the most important factors. It may be inherent in a given family or strain of blood. It may be enhanced by a constitutional weakness, engendered by too close breeding, by breeding from the young and immature, or from the old and worn out. It may be favored by a general debility from starvation, faulty or injudicious feeding, as exclusive feeding on corn (maize), an unbalanced ration, feeding cotton seed, irregular feeding, etc. It may result from parasitism, as round worms in the lungs, bowels, muscles, fat, kidneys or liver, from trichinosis, from cysticerci, echinococci, or from distomatosis. These not only lessen the force of constitutional and phagocytic resistance, but they also in many cases open the way for the entrance of the microbe by the wounds which they inflict. Perhaps nothing operates more effectively in this way than the attacks of other pathogenic microbes. The treatment of the domestic hog is often such that it would almost appear as if it were designed to destroy health and vitality. He is used to clear up the soiled and spoiled provender which has been rejected by other animals. Decayed vegetables and flesh of all kinds, which is no longer fit for other use, is supposed to be good for him and is furnished raw. Worse still, this is conveyed in barrels that are never washed, but are sent for each new supply reeking with abominations which render them a nuisance on the highway. It is left standing till wanted in these barrels, or in still larger receptacles, which are never emptied nor cleaned, but are allowed in the hottest weather, to continue a hotbed of the foulest fermentations. On a smaller scale the kitchen swill barrel becomes a similar centre of decomposition. Even at the creamery and cheese factory the surplus or waste products often remain in a common tank breeding larvæ, toxins and ptomaines, before they are fed to the hogs. In the hog pen, or yard, corn in the ear is thrown on the ground, already filthy with the solid and liquid excretions and is eaten with the rotting, if not infecting, filth in which it has been rolled. From grubbing in this filth with his snout, the pig plunges the latter in the liquid food in his trough and too often he gets his feet into the food as well, and further charges it with the injurious ferments. Again the kitchen swill is liable to contain various inorganic poisons and notably the carbonates and bicarbonates of potash and soda which are used to excess in the form of powdered soaps and, as shown by experiment, are deadly poisons to pigs.
The gastro-intestinal disorders caused by these poisons; (it may be botulism from stale or decomposing flesh, fish or fowl, the poisoning by mouldy bread or musty grain, or meal, or by the toxins of the many and varied saprophytic fermentations), often prove as deadly as outbreaks of genuine hog cholera, and are habitually mistaken for them. They do not, however, as a rule extend beyond the particular herd which has been exposed to the faulty management, and introduce no risk of a general spreading infection. The careless owner suffers and adjacent herds escape, unless exposed to similar causes. But if the hog cholera germ is present these pave the way for its destructive advance and tend to enhance the mortality. It may even be that the combination of the two factors is a condition of the eruption of a severe attack. The faulty feeding or food or poison by itself could be resisted, and the comparatively non-virulent hog cholera bacillus might have been resisted, but with the weakened system and digestive apparatus, the microbe finds a specially inviting field in which it can multiply destructively, and where it can gather a virulence which will enable it to invade and sweep away herd after herd in a deadly epizoötic.
I may add, as a prominent factor in the great modern extensions of hog cholera, the habitual aggregation of swine in large herds. This with the rapid steam transit of modern times, and the great aggregations of hogs in one common market, probably contributes more than anything else to the extraordinary diffusion of the infection. By accident, purchase or otherwise, a large herd becomes infected, and the owner, knowing that delay is ruin, at once ships the apparently healthy animals to market; these infect anything they or their excretions come in contact with; if sold in smaller lots they carry infection into every locality where they go, and along the route; if sold for slaughter, they still diffuse infection through the herds that receive their butcher and kitchen trimmings.
Finally other domestic animals may bring in an infection which becomes manifested by symptoms similar to those of hog cholera, and which if really different, yet serves to pave the way for such an outbreak. Galtier’s remarkable experience with a pneumo-enteritis in sheep, introduced into five separate flocks by infected pigs from the same market, is significant in this respect. It is further significant that the hog cholera bacillus is a very protean microbe. Th. Smith, to whom we owe more than to any one else the identification of the germ, gives seven varieties, which showed well-marked distinctions in their morphology, in their modes of growth on culture media, in the amount of gas they respectively produced in a glucose bouillon, or in their pathogenesis for rabbits. One of these modified germs which has largely parted with its virulence for pigs and some other animals, may under specially favorable conditions, resume its former potency and proceed on a new career of infection.
Lesions in the Acute or Septicæmic Form. The skin and subcutaneous fat are the seats of diffuse blotches or spots of a deep red varying from dark purple to light red, confined it may be to the inner sides of the arms and thighs the belly, the ears, eyelids, and muzzle, or it may be all but uniformly diffused over the body. When pressed so as to expel the blood, the greater part of the surface may be momentarily whitened, but red points remain representing the minute extravasations. Under the microscope the red points show tortuous and enlarged capillaries with here and there a rupture and minute clot. The visible mucosæ may show similar petechiæ, as may also the serosæ of the chest, cranium and abdomen. In the latter blood extravasations are liable to be more extensive. The spleen and lymph glands (particularly those of the bowels and omentum, the sublumbar and subdorsal regions) are usually enlarged, gorged with blood and softened. Many of the lymph glands may escape, and in others the congestion is largely confined to the cortical portion. The lungs may show petechiæ and even extensive hæmorrhages into their substance. The kidneys may show petechiæ in the glomeruli, the medullary substance, the papillæ or the pelvic mucosa, or there may be larger circumscribed hæmorrhages.
The stomach in its greater curvature especially is usually deeply congested and petechiated, with small submucous extravasations, and these conditions are liable to be still more marked in the small intestines and especially in the large, which may have a dark red or port wine hue. Blood may be present in clots among the contents. Necrotic ulcers are absent.
Lesions in the Protracted and Chronic Forms. The lesions of the skin are usually less extensive than in the acute type, and may be almost entirely absent. The lymph glands are enlarged and congested, though the discoloration may be largely confined to the cortical layer. The spleen is as a rule normal in size. The liver is firm, but it may show softening of the secreting acini and encrease of the fibrous framework. Petechiæ or circumscribed hæmorrhages may or may not be present on or under the serosæ or in the tissues.
The characteristic lesions belong to the gastric-intestinal organs. Congestions and ulcers may be found on the gastric mucosa, on that of the small intestine, and rectum, but they are above all common on the ileocæcal valve, cæcum and first half of the colon. In the earlier stages of these lesions the mucosa and submucosa are the seat of a congestion and exudation, but later the round button-like ulcer usually stands out prominently with its necrotic centre dirty white, brown or black, and composed of superposed layers, the whole resting on a congested and thickened submucosa. This contains small round and giant cells and may show considerable encrease in connective tissue. The ulcers may be seated on the agminated or solitary glands but do not show the same predilection for these parts which is seen in typhoid fever.
Incubation. This varies according to the dose and susceptibility from two or three to as many as thirty days. With the short incubation the disease tends to assume its most acute and deadly type, while the prolonged incubation bespeaks a milder form. During ordinary outbreaks from six to fourteen days represent the average interval between exposure and the onset of active symptoms. During the extreme heats of summer and the excessive cold of midwinter in our northern states incubation tends to be shortened.
Symptoms in Fulminant Type. In violent outbreaks some pigs are found dead without observed preliminary symptoms, and have been set down as fulminant examples of the disease. When these occur during very hot weather, in open yards or fields, there is reason to believe that insolation, acting on a system rendered specially susceptible by the toxic fever, has much to do with the early death. Though seldom observed during life, it has been said that such cases, show extreme dulness, prostration, stupor, weakness, unsteady gait, thirst, hyperthermia, persistent recumbency, and at times red blotching of the skin and even convulsions.
Symptoms in Acute Type. In contrast with erysipelas these may advance slowly and insidiously, there is a lack of the customary life and vivacity, the tail droops, appetite is impaired, the pig creeps under the litter and lies there, preferably on its belly, a great part of its time, there may even be tremors suggestive of slight chill, when moved it shows weakness, may stagger, or it may have difficulty in rising on its hind limbs and there is encreased thirst and heat of the skin. Even in the absence of shivering or chill, the skin is usually tender to the touch, calling out plaintive grunting or squealing, and the same is often true of manipulation of the belly. The temperature is raised, yet this must be compared with the previous temperature under the conditions in which the pig has been kept. That may have been anywhere from 100° F. in a confined, cold, draughty pen, to 104° F. in a warm, dry pen and with plenty of exercise. In hog cholera it may rise 1° to 3°. The patient is breathless under exertion, the circulation is accelerated and the mucosæ congested.
Sooner or later, (usually by the second or third day) the skin shows an erythematous blush, especially on the ears, breast, belly and inner sides of the thighs and forearms, in greater part effaceable by pressure but promptly reappearing and complicated by darker spots of extravasation which retain their color under pressure. The blush may appear in spots of ⅒ to ⅓ inch in diameter, or it may cover the region, or indeed the whole body uniformly. At first of a brighter red it tends to pass in succession through the different shades of purple and violet. Appetite becomes more and more impaired, and in exceptional cases vomiting may occur, but often the pig will drink liquid food to the last. A marked symptom is the enlargement of the inguinal lymph glands, which may even be tender. An early symptom is watering of the eyes, and later a muco-purulent exudate may form, and drying, gum the lids together. An abundant exudate appears on the skin as the disease advances, most abundantly about the eyelids, roots of the ears, axillæ and groins, but often covering the whole body, forming a foul greasy inunction, and later a black scaly covering.
The bowels may be costive at first, with fæces, firm, moulded, and covered with mucous, and this may continue to the end. In most cases, however, about the second or third day they become soft, pultaceous and finally liquid, profuse, fœtid, and mixed with abundance of mucous or even blood. The color varies, they may be whitish, yellowish (on maize diet), red, or black (on swill).
Petechiæ usually form on the mucosæ and small sloughs and ulcers may be found on the lips, tongue or elsewhere on the buccal mucosa.
A cough may be present but is by no means a marked symptom.
Emaciation advances with great rapidity, the patient arches the back, tucks up the abdomen, moves weakly and unsteadily or is unable to rise, and dies in one or several weeks, it may be quietly or in a state of coma, but usually without convulsions.
Symptoms in Subacute and Chronic Forms. In this type the disease may be obscure, and even overlooked, so that infected animals carry the microörganism into fresh herds, without rousing a suspicion as to its true source. In other cases, after a slow and progressive development, it takes on such a distinct pathognomonic character that its diagnosis becomes more easy.
In the slightest cases there may be only a capricious or irregular appetite, drooping tail, enlarged inguinal glands, and a progressive emaciation, with loss of life and strength and occasional irregularity of the bowels. The greasy exudation on the skin and black scaly encrustation is not uncommon. Such patients usually survive but they are liable to prove unthrifty and unprofitable.
In other cases the pig becomes dull and listless, leaves its fellows, creeps and lies much under the litter, has impaired or irregular appetite, some costiveness followed by a fœtid diarrhœa, abdominal tenderness, enlarged inguinal glands, progressive emaciation, arched loins, hollow flanks, skin exudation, and oftentimes in the end erythematous eruption with petechiæ and black scaly exudate on the skin. It is in these protracted cases especially that the formation and detachment of the necrotic intestinal sloughs take place and these may pass in the fæces as flattened rounded masses or more extensive plaques. Necrotic ulcers are also liable to show on the buccal mucous membrane or skin. The patient may finally die of colliquative diarrhœa, of exhaustion and marasmus, in a state of coma as in the more acute cases. The mortality may be high and the survivors are liable to prove unthrifty and unprofitable.
Diagnosis. With a group of plagues in swine bearing a strong family resemblance, and maintained by microörganisms, which, though maintaining distinct characters, yet show so much in common that it seems not impossible that they may have been originally derived from a common ancestor, and in face of the not infrequent complication of two of these microbes in one patient, it becomes a task of great difficulty to diagnose at once the particular outbreak that is met with in the field. In some outbreaks, however, the differential features are clear enough to allow the veterinarian to pronounce at once on the true nature of the disease. In others he must withhold his diagnosis until he can put it to the test of microscopic examination, bacteriological culture, the Widal test, or inoculation.
Hog Cholera may be decided upon, when upon wholesome food, in healthy environment, without any change of food, and in six to fourteen days after the introduction of pigs from outside, or the arrival of strange pigs in the near vicinity, or higher up on the watershed, sickness appears tardily, taking one or two daily, with or without a sudden hyperthermia, petechiæ on nose, eyes, belly, axilla, or groin, a general soreness of the skin and abdomen, stiffness or weakness, hiding much under the litter, enlargement of the lymph glands, costiveness with dark red rectum and glazed dung, followed by a profuse, watery, fœtid, bloody, black or yellow diarrhœa, and death mostly after one or two weeks or more. The absence of cough, and the presence of ulcers bearing necrotic sloughs on the lips, mouth or skin, and above all the presence of the button-like necrotic ulcers on the mucosæ of the cæcum, colon or ileum may be accepted as conclusive evidence on this point. So also its prompt fatality to rodents, but not to pigeons.
Swine erysipelas has a much shorter incubation, more rapid and violent onset, deeper, darker congestion of visible mucosæ, more extensive petechiæ of skin, mucosæ, serosæ, and tissues generally, a comparative absence of inflammatory and necrotic lesions of bowels, a very early and high mortality in swine, rabbits and pigeons, and a harmlessness toward the inoculated Guinea pig.
Swine plague also shows a shorter incubation, a speedy elevation of temperature, more mucous congestion, less indication of abdominal tenderness or of diarrhœa, more cough, dyspnœa, wheezing and objective symptoms of pulmonary consolidation, less congestion or engorgement of the spleen, or ulceration of the bowels, and finally is very much more fatal to pigeons, and spares neither rabbits nor Guinea pigs.
Widal test. The cessation of movements and the agglutination of the bacilli of hog cholera, noted by Dawson, is a valuable test, but as in the case of typhoid fever in man is not to be implicitly relied on in all cases. Some of the forms of bacillus coli commune and other allied microbes act in a similar way. It necessitates the maintenance of fresh (24 hours) active, artificial, agar cultures of the hog cholera bacillus and is thus virtually reserved for the bacteriological laboratory. A drop of blood is drawn from the suspected pig smeared very thinly on the cover glass and about 10 times the amount of sterile water added. Then the smallest possible addition of the agar culture of the bacillus is made. Immediately, or in ½ hour the bacilli cease their active motility and mass together in clumps in which they can be seen individually clear and distinct but absolutely still and crossing each other in all directions forming a kind of network. A few isolated bacilli remaining in the intervals between the clumps and even showing a slight motility are not to be considered as invalidating the reaction.
The table on the next page will serve to place in contrast the differential phenomena of the diseases caused by bacilli of hog cholera, swine plague and swine erysipelas in uncomplicated infections.
Prevention. As in all other contagious diseases, effective preventive measures imply the destruction of the pathogenic germ and all sanitary measures should aim at the early and final extinction of this organism and its subsequent exclusion from the country. This, however, entails an outlay and governmental control which it seems idle to expect in the very near future so that palliative measures, and those looking toward success over limited areas must still be resorted to. It should be here distinctly stated, however, that the extinction of a plague, though often the most expensive at the start, is in the end by far the most economical resort.
Removal of accessory causes. The health and vigor of the animal exposed is not without its influence in case of attempted invasion by a virus of diminished potency.
| DIFFERENTIAL SYMPTOMS AND PHENOMENA. | ||
|---|---|---|
| Hog Cholera. | Swine Plague. | Rouget. |
| Incubation 6 days + | Incubation 1 day to + | Incubation 1 day |
| Mucosæ not necessarily congested | Mucosæ congested | Mucosæ deeply congested, dark red, violet |
| Petechiæ on snout, eyes, mouth, etc. | Petechiæ on snout, eyes, mouth, etc. | Petechiæ extensive |
| Necrotic ulcers on snout, mouth, skin, etc. | Necrotic ulcers rare | Necrotic ulcers less frequent |
| Furred tongue, vomiting common | Vomiting less likely | Vomiting not uncommon |
| Temperature high in acute cases (104° to 108°) | Temperature high in acute cases | Temperature very high, 107° to 109° |
| Lies on belly mostly, abdomen hot, tender | May lie on side | May lie on side |
| Moves stiffly, feebly, unsteadily with grunting, may be paraplegic | Stiff but less so, Paretic. | Stiff, weak, paraplegic |
| Bowels 1st costive, fæces molded, glazed; 2d or 3d day, or before death, diarrhœa, profuse, watery, fœtid, bloody, black on slops,—yellow on corn (maize) | Diarrhœa less marked, may be entirely absent | Diarrhœa usually sets in |
| Everted anus dark red | Anus may not be deep red, less everted | Anus may be less red, less everted |
| Cough often present, hurried breathing | Cough, hard, frequent; wheezing breathing. Auscultation and percussion may show lung consolidation toward lower border. May bleed from nose | Cough absent, save in latter stages with pulmonary consolidation |
| Spleen slightly enlarged | Spleen usually little altered | Spleen enlarged, soft, grumous |
| When death is deferred 1 to 2 weeks, necrotic button-like ulcers on ilio-cæcal valve, cæcum, colon, or ileum | Necrotic, button-like ulcers on cæcum rarely marked | Necrotic ulcers on bowels rare |
| Lobar pneumonia uncommon | Lobar or lobular pneumonia a marked lesion | Pulmonary and enteric inflammation rare |
| Kills rabbits (5 to 7 days) and Guinea pigs (7 to 12 days). Pigeons sicken but survive | Kills rabbits (1 to 12 days), Guinea pigs (1 to 4 days), pigeon (48 hours) | Kills pigeon (3 to 8 days), rabbit (4 to 8 days), Guinea pig resists |
| Blood serum of hog cholera patient causes agglutination of bacilli in cultures; (not constant, occurs with other bacilli) | ||
Dry, warm beds with plenty of air and light are essential to vigorous health and the usual damp, filthy, dark pens are depressors of the vital forces and virtually invitations to hog cholera as to other diseases. The close packing of swine under manure or under rotten piles of straw where they often suffocate each other is to be carefully guarded against. It is a sufficient commentary on this to say that for every kilogramme of its body weight, the horse consumes daily 13,272 grammes oxygen, the cow, 11,040 grammes, and the pig, 29,698 grammes. This is in perfect keeping with the high normal temperature maintained by the latter animal. In the interest of health the pig requires twice the breathing space for every 100 lbs. of his weight that is demanded by either ox or horse. What violence is done to this demand of nature in the daily treatment of the hog!
Fresh, sound, wholesome food is no less a desideratum. Yet the omnivorous pig is condemned to become the scavenger for the kitchen, the stable, the feeding pen, the slaughter house, the creamery, the sugar works, the brewery and even the rendering works. Whatever is considered unfit for human use is thrown into a swill barrel, and as this is never emptied it becomes the field of endless decompositions with the production of the most varied toxins, ptomaines and enzymes. Many of these chemical toxic products cause gastro-intestinal inflammation with vomiting, bloody diarrhœa and tenesmus, and derangement of the nervous and other functions as manifested in weakness, staggering, dulness, stupor, etc. Death may follow in a few hours and the cases are set down as acute forms of hog cholera, rather than the simple poisoning that they are. All the same they pave the way for the attack of hog cholera if its germ is present even in a form of little potency. All such foods should, on the contrary, be fed fresh and after boiling.
Salt in excess, the brine of salt meats or fish (containing toxins), the powdered soaps used in kitchens and added to swill, mouldy bread, cotton seed meal fed in any considerable proportion in the food, and even an exclusive diet of corn (maize), must be guarded against.
The crowding of many pigs in a small yard where they root continually in each others’ droppings and their own, should be avoided. Individual pens, or pens holding two or three only and kept clean are to be preferred, and still more a wide grassy range where they may escape from their own filth. The long feeding trough should be discarded in favor of one into which the pig can introduce his nose only. The nose itself will introduce filth ferments, but, where there are not specific-plague-germs, it is the quantity that tells and the exclusion of the foul feet is an important consideration. To these various poisonous products of saprophytic ferments it often happens that the older swine have by continuous exposure, acquired a comparative immunity, while the young growing pigs perish in large numbers.
Feeding pigs in confinement, without green or animal food is very liable to induce costiveness and indigestion which pave the way for the inroad of the hog-cholera germ. A certain allowance of green food, slops, and, above all, a variety of food constituting a well-balanced ration are always desirable.
Again, the constitution of the pig is often material. On the continent of Europe it is the high bred English pigs that suffer most, and in all cases a lack of the rugged vigor attained through an active, open air life lays the system more open to a violent attack. Too close breeding must be similarly avoided, together with breeding from the immature, the weak and the debilitated. In this connection it is important to rid the herd of parasitisms which not only weaken the system and lessen the power of resistance, but by the bites or the inflammation induced, open channels for the introduction of the hog-cholera bacillus.
Prevent the Introduction of the Bacillus. The above precautions are important in obviating infection and favoring a milder type of the disease when the germ has been introduced, but they are but palliatives at best, and will not hinder the development of a plague in the presence of an active and potent virus. Adopted alone they are worse than useless as a means of extinction of the germ: they tend to preserve it. The exclusion of the hog-cholera germ is the one essential thing in prevention and whatever comes short of this must have at best but a partial effect.
Avoid pens, pastures or streams that drain swine enclosures higher up. Discard all provender or litter that has come in contact with other pigs or their products. Allow no visitors to the herd such as butchers, dealers, drovers, that have habitually come in contact with other herds. Exclude as far as possible domestic animals (dogs, sheep, cattle, fowls, pigeons), and even vehicles coming from places where hogs are kept. Wild animals such as buzzards, and other carrion feeders, must be especially guarded against. Wild rabbits and hares (jack rabbits), skunks, wood chucks, minks, rats and mice should be exterminated. Small birds and flies are difficult to deal with but the latter may be destroyed by acids, copperas, or sulphites on the manure and the former may even be exterminated when hog-cholera exists in the vicinity.
Sows should not be sent from herd to herd for service or otherwise, and any swine that have been hired out, or sent to an exhibition, and all that are acquired in any manner, should, on arrival, be excluded from the herd and held in quarantine, well apart for three or four weeks, and finally washed with carbolic acid soap before they are admitted.
The pestilential prevalence of hog cholera and other swine plagues to-day is largely the result of the great industrial and commercial activity of modern times. In America the disease was comparatively unknown until after 1830, and in Europe even later. But with the advent of steamboat and railroad, the few pigs raised in separate pens, or secluded localities, and killed and cured near by, gave place to the large herds, sent when fattened to great markets where pigs were collected from distances of many hundreds of miles, the stock animals and the fat occupied in succession the same boats, cars and yards, and, as a matter of course, the virulent germs were concentrated and diffused through the infected places and things. We cannot go back to the antiquated safer methods, but it would be possible to so regulate our commerce, that the evil could be reduced to a minimum. Separate cars, loading banks, chutes, alleyways, and yards can be reserved for fat swine going to immediate slaughter and no animal having passed through any of these should be allowed to be taken out for stock purposes, unless it has been passed through a rigid quarantine. The places and things used for such fat swine should be disinfected at intervals, and the manure and offal should be disinfected, or exposed to a boiling temperature for a sufficient length of time before removal from the premises. Stock swine on their part should be shipped only on a certificate of the complete immunity of the herd and locality from which they come from swine epizoötics, and of the roads or vehicles by which they reached the shipping point. They should be debarred from all yards, loading banks and cars or boats used for fat hogs, and admitted only to such as have just passed through a thorough disinfection. They should be sent directly to their destination, or if to a market, for purposes of sale, it should be well apart from that used for fat swine, and the loading banks, chutes and yards should be entirely distinct and should be thoroughly disinfected on every occasion after use. The millions now lost yearly from swine epizoötics might well warrant the inconvenience and expense entailed by such precautions. Heavy penalties should be imposed on those shipping pigs from infected localities, on those making false certificate, and on all who in any way violate the law.
Independently of State or local authorities the stock owner can do much to protect himself. He can make a number of pens large enough to hold 2 or 3 pigs each, safely fenced off from one another and so constructed that no drainage can take place from pen to pen. Then in winter in the absence of flies, and with rats, mice, and birds excluded the opportunity for the extension of infection from pen to pen can be kept at its minimum. All pigs must be kept apart from the manure heap, and in summer the manure must be so treated as to destroy the larvæ of flies. All food and water that might convey infection must be guarded against. Then if one pig is attacked it will only be necessary to destroy it and its two fellows in the same pen, and even if those in adjacent pens are killed or quarantined the loss will be a trifle as compared to the ruin of the whole herd, as usually happens. Prompt disinfection of the pens and manure is imperative, and the same would apply to the person and clothes of the attendant, and to all stable utensils.
Immunization by injection of sterilized products of the bacillus, has not proved satisfactory. In 1880 I applied this to two pigs, causing a transient fever, after recovery from which, the subjects resisted exposure to infected pens and pigs, and even virulent inoculations. But they failed to thrive well. Later experiments by Drs. Salmon and DeSchweinitz respectively, also proved unsatisfactory. The latter separated and injected the enzymes, but lost 50 per cent of his cases, the survivors proving immune, with the drawback of troublesome local lesions. The enzymes obtained from cultures in milk could be used safely on guinea pigs in the dose of 0.01 grams and in some cases even up to 0.04 securing immunity. But the great risk of an overdose, the frequent local lesions, and the subsequent unthrift, have prevented the adoption of the method.
Disinfection. The experiments of the Bureau of Animal Industry show that, apart from freezing, four months in the soil, serves to render the bacillus harmless.
From .75 to 1 per cent of quick lime added to soil in the form of lime water, destroyed the virulence in 11 days.
Lime can be employed as a thick whitewash on pens, fences, yards, etc., the precaution being taken to see that it is newly burned, caustic and applied in sufficient amount. Lime that has been kept absorbs carbon dioxide and loses its disinfectant property. If ¼lb freshly made chloride of lime is added to each gallon of the caustic lime white wash the certainty of success is insured. Lime water has the advantage of being applicable to grassy surfaces, without proving hurtful to the vegetation. For buildings and yards it furnishes a ready means of estimating the thoroughness of the application.
Sulphuric acid (1:100 or 1¼ oz. to 1 gallon) makes a good disinfectant for buildings and yards. Like lime this can be used freely without fear of poisoning the animals.
Carbolic Acid, 5 per cent, can be used with great safety. The Bureau of Animal Industry advises the combination of this with sulphuric acid, which adds greatly to its solubility.
Formalin may be employed, diluted one to forty of the solution (1 per cent of the gas) in buildings and on woodwork generally. It may also be applied in the form of gas by heating the solution in closed rooms. Like carbolic acid it is especially applicable to cars, boats, and other vehicles.
Corrosive Sublimate (1:500) makes a convenient and cheap disinfectant, with the drawback that it is poisonous, and destructive to metals. Mercuric Iodide though more potent is also more expensive. Blue stone (2:100) and zinc chloride (10:100) are also effective but poisonous.
The failure to stamp out hog cholera in England and America has been largely chargeable on the appointment of laymen to do the work of the expert, and no less so on the attempt to deal with the disease in hogs in transit or in the market rather than in the farm where they have been raised or kept. Let the fat and stock markets be kept rigidly apart, together with the means of conveyance to and from these, and let no stock swine start for a market or destination without a certificate of the soundness of the locality from which they came, and the purity of the means of transit, and we shall have taken a long step toward the final extinction of the pest.
State limits and rights stand in the way of successful work, but this can be partly met by a frontier supervision by national officials, and should be further, by a prompt and hearty coöperation of the sanitary officers of the two states involved. When it becomes possible to trace infecting hogs, back to the infected place in another commonwealth, and punish the offender who shipped them, we shall be within sight of a satisfactory control or extinction of hog cholera.
Extinction of Hog Cholera in Herds and Districts. As in all deadly plagues this should be a recognized governmental function to be carried out at public expense. It is a question of political economy and its neglect is subversive of prosperity not in Agriculture alone but in all public industries whose workers must subsist on the fruits of the soil. The $10,000,000 lost yearly by the farming community, is a dead loss, not to agriculture alone, but to the prosperity of the nation, the markets of which would be revived and improved by such a yearly sum expended.
The existence of the disease at any point should be reported by the stockowner or guardian, under penalty in case of failure. When the nature of the outbreak has been certified by the expert, the district should be scheduled, and the herd appraised, slaughtered and all products disposed of in such a way as to prevent any escape of infection. The carcasses may be burned, buried deeply, or boiled and rendered. The buildings, yards, utensils, fences, manure, cesspools, and infected fields should be thoroughly disinfected, or secluded from all animals for a year. The owners of the herd should be indemnified according to appraisment, and not to exceed ¾ths of the actual market value, provision being made that no award shall be made if the herd sickened within a fortnight after their arrival from another State, or in case the owner, has concealed the existence of the illness, or has otherwise deliberately or carelessly contributed to its spread.
Many minor rules and restrictions will be required to fit the general measures to individual cases and local conditions, and these require the direct supervision of an expert, and not of a mere business manager or layman.
Therapeutic Treatment. With state, county or municipal measures for the extinction of hog cholera, treatment is to be condemned, as calculated to encrease and spread the infection. But until the states can be educated out of the past wasteful system, into economical measures of extinction, the swine breeders are entitled to whatever salvage they can secure through therapeutics. For acute cases there is no hope. For the chronic a clean, dry, comfortable pen, well disinfected, and a moderate diet of varied and laxative food are essential. Wheat, bran or middlings, with corn, oat, barley or linseed meal may be allowed in form of a mash. A little green vegetable food may be added. Medicinal agents may be used to meet special indications, but when a whole herd must be treated at once, antiseptics and febrifuges have apparently proved the most generally helpful. The Bureau of Animal Industry especially recommends the following: Wood charcoal, sulphur, sodium sulphate and antimony sulphide, of each 1 lb.; sodium chloride, bicarbonate and hyposulphite, of each 2 lbs.; mix thoroughly and add to each feed in ratio with the size of the patient. In suitable cases, this is said to improve the appetite and contribute much to convalescence. Modifications will readily suggest themselves to meet individual conditions and different stages of the disease—antithermics, eliminants, calmatives. stimulants, tonics, etc.
Serum Therapy. This has been especially exploited and advocated in America by De Schweinitz of the Bureau of Animal Industry, and Dr. Peters of Lincoln, Neb. In Europe, Perroncito has prepared an antitoxin. The serum is produced in the body of the cow or other animal which is inoculated repeatedly with gradually encreasing doses of living hog cholera cultures and with solutions of the bacilli and their products, for a period of eight months, or until no reaction takes place from large doses, and the blood serum added to cultures of hog cholera bacilli causes agglutination of the latter. The serum is further tested as to its power of preserving Guinea pigs inoculated with a lethal dose of live hog cholera cultures. After separation from the blood the serum is concentrated until it reaches a standard at which 10cc. proves curative to a pig of 40 to 60 lbs. weight.
It proves most successful in animals in which the subacute or chronic form of the disease has just begun. One injection only was given to each animal. Of 1923 cases treated (1897–8) 30 per cent. died, and 70 per cent. recovered. Of 3197 in abandoned herds (checks), 81.24 per cent. were lost. (De Schweinitz.)
One drawback was found in the short period of immunity secured, the susceptibility reappearing as soon as the antitoxin had been eliminated from the body. This was met in part by using sterilized cultures (toxins) along with the serum.
Another desideratum was a speedy means of distinguishing in field work between hog cholera and swine plague, as the antitoxin of the one was not protective against the other. To meet this, serum was obtained from an animal immunized to both diseases, or a mixture was made of the sera of two animals respectively made resistant to the two affections.
De Schweinitz was very optimistic in the matter, claiming that the serum is absolutely harmless, can be used on pigs freely, and will cost but 15 cents for each animal. He estimated that of the $15,000,000 per annum lost by Hog Cholera and Swine Plague in Iowa alone, $11,000,000 can be saved at a comparatively small cost.
The method is scientifically sound in availing of the defensive products of the immunized system for imparting to the animal attacked, the power of vital resistance, and after allowing for enthusiasm, for the inevitable mistakes, when used on a large scale, of other deadly swine diseases for hog cholera, for the many accidents incident to its application by operators who are not specially trained like the employés of the Bureau, for its demand for acute and deadly outbreaks, as well as for chronic and mild ones, and taking into account that in other hands it has not fully borne out the promise made for it; yet it seems to have some measure of merit, and where no systematic attempt is made by the authorities for the extinction of the disease and its germ, it is an available resort for the owner of herds.
The fundamental objection is that it entails the preservation, encrease and spread of the poison, and like all temporizing measures, stands as a barrier to the complete extinction of the plague. Giving such a very transient protection, its repetition may be demanded in a few months or a year, and proceeding on the ground that the pest must continue for all time, the apparent economy of the process will prove, in the long run, but a permanent and grievous tax.
The soundest and only truly economical course in dealing with this and other deadly infections of swine is the radical extinction of the germ. When the people can be educated up to this we shall see the dawn of a brilliant future for our animal industries. Until then we must be satisfied to fall back upon, and make the best use of the temporizing measures now in vogue or that may hereafter be devised. Even if it should be shown that hog cholera is at long intervals developed from a ‘sport’ of the usually harmless bacillus coli commune, the fact remains that its great extensions and the resulting fatality are due to the contagion alone, so that extinction remains the true watchword of success and economy.