CHICKEN CHOLERA. FOWL CHOLERA. CHICKEN TYPHOID. CHICKEN PASTEURELLOSIS.
Definition. Historic notes. Bacteriology: Bacterium choleræ gallinaceæ, nonmotile, with polar stain, bleached by iodine, non-liquefying, causes septicæmic lesions. Lignieres’ bacillus, culture features non-gasogenic, acidifies dextrose; vitality in disinfectants; survives drying. Accessory causes: new birds in flock, or eggs for hatching, mingling of flocks, manure, watershed, streams, ponds, dust, wild birds, buzzards, rabbits, insects, infected soil. Susceptible animals: hens, doves, peafowl, pheasants, parrots, ducks, small birds, guinea pigs, rabbits, white and gray mice. Effect on sheep, horse, man, cow, frog. Incubation 18 to 48 hours. Symptoms: in fulminant cases rarely seen, in acute, anorexia, depression, debility, apathy, ruffled feathers, sunken head, neck, wings, tail, tremors, nasal and buccal discharge, hyperthermia, sighing, violet comb and wattles, thirst, pultaceous fæces, later glairy, green and fetid. Temperature becomes subnormal, inability to rise, stupor, convulsions, death in 1 to 3 days. Mild cases last 7 days. Cases caused by one microbe have slough only. Lesions: congested, petechiated, hæmorrhagic intestinal mucosa; contents of bowels watery, frothy, bloody; epithelial degeneration and desquamation; abrasions, croupous exudates, enlarged congested lymph glands, fermenting contents of crop. Petechiæ general, spleen and liver swollen, congested, friable; kidneys congested; lungs hyperæmic or blood gorged. Blood diffluent with microbe. Anæmia. Emaciation. Arthritis. Diagnosis: by rapid spread, infection origin, early excessive mortality, hæmorrhagic lesions, microbe in blood and liquid ingesta. Prognosis: Mortality 90 to 95 per cent. at outset. Prevention: Quarantine new birds, inside screens in summer; burn or acidify manure; exclude buzzards, vermin, wild birds, and visitors; separate sick, kill, burn, disinfect; divide infected flock in small lots; prevent wandering in fowls, destroy insects. Phenic acid subcutem. Immunization: inoculate in breast with one microbe (Salmon): or with weakened virus (Pasteur). Limitations. Treatment: gastric and intestinal disinfection—copperas, mineral acids, carbolic or salicylic acids, aromatics, quinine, naphthol, tar, phenic acid subcutem.
Definition. A febrile hemorrhagic septicæmia of chickens and other fowls (pigeons, ducks, geese, parrots, etc.) communicable to certain rodents and other animals, and characterized by a short incubation, rapid progress, great prostration, violent diarrhœa usually greenish, and a high mortality (90 to 95 per cent.).
History, Geographical distribution. It is quoted as prevalent in Lombardy in 1789, in East India in 1817, in France in 1825, and generally in Europe and America in the last half century.
The losses from the ravages of this disease are far greater than the average value of the individual animal would lead one to suppose, but with domestic fowls numbering 300,000,000 and a yearly egg crop bordering on a billion dozens it may well be called enormous.
Bacteriology. Chicken cholera is caused by a very small ovoid bacterium (B. Choleræ gallinaceæ) about 0.3 to 1.8μ long, as found in the blood and tissues of the fowl. It has the general characters of the groups which cause hemorrhagic septicæmia, thus: 1. It fixes, above all at the poles, the ordinary anilin colors; 2. It is decolorized by the methods of Gram and Wiegert (iodine solutions); 3. It grows on gelatine without liquefying it; 4. It produces acute septicemic lesions; 5. It tends to polymorphism when grown under different conditions. In the peritoneum of the guinea pig it forms cocco-bacilli tending in acute and violent cases to diplococci. Fed to rabbits it appears in the fæces as a minute bacillus. Even the mode of staining causes a difference in appearance. Fixed in alcohol-ether, and then stained in Ziehl’s phenated preparation, coloring is polar, and the central area clear. If in place of Ziehl’s fluid, hot fuchsin solution is used warm for ½ a minute, bacillus or cocco-bacillus is shown (Lignieres). It is nonmotile, though some observers have been misled by Brownian movements. There are no flagella. In old bouillon cultures short chain forms are met with. No spores are formed.
From fresh cultures, in flask or in animals, the bacterium grows readily in alkaline culture media. In bouillon a turbidity ensues, and after some days pellicles form on the surface and walls, and the liquid slowly clears. The addition of a little blood serum, sugar or glycerine encreases and hastens the growth, while acid retards or prevents. This is common also to other septicemic germs. In gelatine growth is tardy, but in two or three days there are whitish glistening colonies, becoming opaque later, and appearing granular if slightly magnified. In punctures minute colonies form along the line of culture and one at the surface, at first translucent; later opaque. On agar the colonies grow faster with similar appearance. On gelose at 37° C. the colonies are blueish and iridescent, at first, and later opaque. If the germ has been repeatedly passed through the Guinea pig, they are more translucent. On potato with alkaline surface, there is a delicate grayish yellow growth after 48 hours; if acid, growth ceases. In milk there is no coagulation nor acidification for four weeks; then it becomes slowly clear and opalescent. With sugars it is not gas producing. With dextrose it forms an acid solution; with saccharose or lactose an alkaline one. Cultures in peptone gave a strong indol reaction (V. A. Moore). Lignieres found no indol in cultures in pancreatic bouillon.
The bacterium perishes when heated to 58° C. for fifteen minutes. It dies in carbolic acid solution (1:100) in five minutes; in sulphuric acid solution (0.25:100) in ten minutes; in lime water in ten minutes; and in sulphur fumes in three hours. Easily destroyed by disinfectants, it remains potent for months in flasks or buildings that are not subjected to disinfection. It is not killed by drying (T. Smith and V. A. Moore) nor by zero temperature maintained for seventeen hours.
The cultures, especially those made in agar have a very characteristic odor.
Accessory Causes. Birds sent to poultry shows will often contract the disease and introduce it into the home flock on their return. It may also be imported in newly purchased birds, or on eggs obtained for hatching. It is even alleged that it has been propagated by feeding healthy hens on the eggs of diseased ones. When chickens run at large it passes easily from flock to flock in the immediate vicinity. The infected manure is, however, the most common channel of infection. Carried on the feet or bill this contaminates the food and drinking water, and washed into streams and ponds, it finally in any case reaches the alimentary canal of the susceptible bird. Or drying up and raised as dust it is inhaled into the lungs. Or finally from any such source it infects any open sore. As granivorous birds, wild and tame, suffer from fowl cholera, it is often introduced by the wild, especially coming from infected poultry yards. Predatory birds, like hawks and buzzards, but the latter especially, are common bearers of infection. Rabbits, which contract the affection so readily, transmit it equally with birds, but man or beast, soiled by the manure will convey it. Insects are among the most prolific bearers, hence, as noted by Salmon, the infection may fail to overstep a close fence in winter, but is subject to no such limitation during the fly season. In this respect chicken cholera agrees with Asiatic cholera, typhoid fever and other affections in which the virus abounds in the alvine discharges. The sale and transportation of the guano from the infected poultry yard is a direct cause of new outbreaks. Feeding on the carcasses or offal of the infected birds is a further cause. It must not be forgotten that the microbe is largely saprophytic, living indefinitely in the organic matter in soils, and determining new outbreaks when brought in contact with susceptible animals. Thus a period of immunity may be followed by infection when new birds are brought in or when young and susceptible ones grow up.
Susceptible Animals. Fowl cholera is preëminently a disease of chickens, but the microbe is successfully transferred to pigeons, peafowl, pheasants, parrots, ducks, canaries, sparrows and other small birds, also to Guinea pigs, rabbits, white and gray mice. Guinea pigs have abscesses in the seats of inoculation (Pasteur); the same is alleged of sheep and horses (Kitt), and man (Marchiafava, Celli). Injection into a cow’s teat caused chronic catarrhal mammitis in which the microbe persisted for a long while (Kitt). Like other members of the group of microbes causing septicæmia hæmorrhagica, the pathogeny and even the morphology are liable to material modification as grown in different environment (genera). Some of the forms of cholera occurring among domesticated birds and held to be distinct diseases may find in this an explanation. Rabieaux claims that under favorable conditions it has been transmitted to the frog.
Incubation. This varies from 18 to 48 hours, the usual being 24 hours.
Symptoms. In some fulminant cases the animal is found dead a few hours after apparently blooming health; it may even have died on the nest or fallen dead from the roost. Cadeac speaks of transient symptoms even in such cases—extreme dulness, prostration, somnolence, seclusion in a cool, dark place, ruffling of feathers, sinking of the head between the wings, drooping, trailing wings and tail, violet comb, gaping, discharge of glairy mucus from the bill, convulsions and death. These symptoms last from two to five hours.
In acute but less fulminant forms there is loss of appetite, depression, debility, apathy, erection of the feathers, sinking of the head, swaying when made to walk, drooping wings and tail, sitting on the breast, convulsive tremblings, discharge of filmy or frothy mucus by the nose or mouth, vomiting, hyperthermia (108° to 111° F. ), sighing, breathing, inflation of the crop, violet colored comb, wattles and mucosæ, great thirst and diarrhœa, at first pultaceous and light yellow, later glairy, green and fetid. The feathers round the anus become soaked and matted with the discharge. Temperature becomes subnormal, the patient falls and is unable to rise, and finally dies in a stupor or convulsions, the illness having lasted 1 to 3 days.
Milder cases occurring chiefly towards the end of an outbreak when the less susceptible animals only are left, or when the microbe has become less virulent, show a larger ratio of recoveries. These show a lack of spirit and vigor, impaired appetite, diarrhœa, emaciation, dulness, prostration, moping, ruffling of the plumes, dark discoloration of the comb, and often swelling of one or more important joints (femoro-tibial, etc.). These may burst and discharge a reddish pus, or simply form dark or grayish swellings. These cases may drag along for a week or more and finally die in marasmus. The minute bacillus is not obtainable from these (Lignieres).
Cases inoculated in the pectoral muscles with only one or two microbes usually have only a circumscribed slough, with loss of condition, and after the elimination of the slough and the healing of the sore the bird proves immune.
Lesions. The alimentary canal is the main seat of morbid changes. The intestinal walls, and especially the mucosa, have points and patches of blood extravasation, extensive areas of congestion with ramified redness, exudation and thickening. The intestinal contents are watery, frothy, browned or blackened by effused blood, and swarming with ferments including the specific bacterium. The mucous surface is brownish or blackish, and epithelial degeneration and desquamation with abrasions are not uncommon especially on the summits of the duodenal folds and villi. Croupous exudates and swelling or ulceration of the follicles are met with. The lymph glands at the base of the cæcum are often enlarged and congested. The crop is full of watery, pulpy, frothy or slimy contents, and its mucosa and that of the pharynx may be deeply congested.
Elsewhere the lesions suggest rather the action of destructive toxins and the profound changes in the blood. Pericardium and endocardium are usually studded with dark petechiæ, and congestion and even slight exudation may be present. The spleen is enlarged, soft, and gorged with blood. The liver is swollen, congested, extremely friable, and mottled, grayish white from degenerations. The kidneys are dark red, and friable. The lungs may show slight hyperæmia only, or a blood engorgement and consolidation, and are then easily reduced to a dark red pulp. Friedberger and Fröhner say that respiratory changes are most frequent in land birds; and intestinal and cardiac in water fowl.
The blood is diffluent coagulating loosely if at all, of a brownish red color, reddening slowly and imperfectly in contact with air, and like the tissues contains an abundance of the characteristic bacterium staining deeply at the poles and clear in the center.
In birds that survive a few days there are marked anæmia and emaciation, and the muscular system is of a grayish red color, with fatty degeneration. In acute and fulminant cases on the other hand the muscles may be full and of the normal red color.
In arthritic cases the congestion and thickening of the soft tissues, and the excess of synovia, are supplemented by destruction of the articular cartilage and by areas of bone abrasion. In the more tardy cases collections of caseous matter are found.
Diagnosis. This is based on the demonstrably highly contagious character of the disease, its rapid spread in a flock, and from the first to nearby adjoining flocks in summer, the short period of incubation, the constancy and nature of the diarrhœa, the speedy and great mortality, and the hemorrhagic lesions of comb, bowels, heart, lungs, liver, kidneys, spleen, and serous membranes. The demonstration of the bacterium in the blood and affected tissues is conclusive. Kitt points out that inoculation of a pigeon kills the bird in 12 to 48 hours, with dry yellow exudate in patches of from ½ to ¾ inch in diameter on the surface of the muscles, and yellow discoloration and nodular induration beneath.
Prognosis. The mortality reaches 90 to 95 per cent. The negative chemiotaxis exerted on the leucocytes by the microbe, precludes defensive phagocytosis, and the progress of the deadly microbe is comparatively unhindered. Toward the end of a severe outbreak, and in certain mild epizoötics the recoveries are much greater.
Prevention. All birds bought or otherwise acquired and all birds returning from shows should be quarantined for one week before being allowed to mingle with the flock. In summer this should be conducted inside fly screens. The manure should be burned, carefully secluded, or treated with dilute sulphuric acid. Buzzards and vermin as possible bearers of the infection should be excluded from poultry yards. So with human beings, dogs, etc., coming from infected places. In an infected flock the sick should be at once separated, killed and burned or treated with sulphuric acid. All manure should be treated in the same way. Buildings, yards and runs should be thoroughly cleaned and liberally sprinkled with a dilute sulphuric acid (2:100). If the birds can be divided up in small groups (say of 5) the appearance of the disease will only endanger that group. In small flocks or with very valuable birds it may even be well to take the body temperature morning and night and separate at once any bird showing a rise. Any diseased or suspected flock should be kept where its manure will not be washed into wells, running streams or ponds to which other birds have access. In a locality where the disease exists fowls should not be allowed to run at large. In winter this is very effective; in summer owing to the danger from insect bearers, it must be supplemented by the most scrupulous cleanliness of poultry houses and yards, and by a liberal sprinkling with dilute sulphuric acid, or other disinfectant, to be made especially abundant and frequent on the manure. Nocard cuts short the disease by injections, subcutem of a 5 per cent. solution of carbolic acid.
Immunization. With valuable birds it may be desirable to secure immunization by non-fatal inoculations. Salmon secured this by first estimating the number of microbes in an mm. of the blood, then diluting until five drops would contain but one, or at most two of these organisms, and injecting this amount into the pectoral muscles. A sequestrum forms in the muscle and is gradually sloughed out, and the cavity heals, with resulting immunity.
Pasteur produced a weakened virus by exposing the artificial bouillon cultures to air for from three to ten months, the strength decreasing with the length of exposure. The weaker form produces slight illness only, from which recovery is prompt. A second and stronger virus is used ten or twelve days later and produces a real immunity.
The drawbacks to these methods are: 1st; that fowls are of too little value, to warrant inoculation in healthy flocks; 2d; that in infected flocks, where it is employed, the more susceptible birds are usually already contaminated, and a large proportion die in spite of it; and 3d; that it becomes a means of planting the infection in new localities (Kitt).
Treatment. The disease is so deadly that little can be hoped from medicinal treatment. It has been directed mainly to gastric and intestinal disinfection. Copperas and sulphuric or hydrochloric acid in the drinking water ½ to 1 per cent. of each is at once prophylactic and curative. Friedberger and Fröhner add fennel or peppermint, and give a tablespoonful every hour to an affected chicken. Other agents recommended are: carbolic acid (5:100) by the mouth or subcutem (Nocard), salicylate of soda, quinia (Cadeac), tannic acid (2:100), salol, naphthol, tar water, etc.