Bacillus Coli Communis, the familiar bacillus of the healthy bowel, is charged by Lignieres with causing a fowl enteritis and probably does so as in mammals when the mucosa has become diseased and non-resistant. At the same time there are so many closely allied forms or varieties of this bacillus found in different intestinal diseases, that it may well be that the pathogenic agent is a modified form or “sport” from the parent microbe, though no clearly defined peculiarities can be established by cultures.
The typical colon bacillus is 2 to 3 μ long by 0.4 to 0.6 μ broad, with rounded ends, but it may be ovoid or even round, or it may be 5 μ long. It stains readily with aniline colors, bleaches with iodine. It is ærobic, facultative anærobic, non-motile, non-liquifying, and asporogenous. It ferments all sugars producing gas, acidifies its culture fluids, and coagulates milk. It grows freely at room temperatures in peptonized gelatine, agar and bouillon and on potato. Stab cultures in gelatine have a moss-like tufted appearance.
Pathogenesis. Injections subcutem, and into the veins and ingestion with food all failed to infect the chicken, while the pigeon died in 24 hours from intravenous injection and in 12 to 18 days from 1 c.c. given subcutem. In rabbits and guinea-pigs hypodermic injection caused abscess, while pleural and peritoneal injections killed in 24 to 48 hours. Rabbits are unaffected by intravenous injection, while guinea-pigs die in 1 to 3 days.
Bacillus of Duck Cholera found by Cornil and Toupet in the blood of ducks suffering from a diarrhœal enteritis, is 1 to 1.5μ long, by 0.5μ broad, with rounded ends. It is ærobic, non-liquifying, non-motile and asporogenous. Stains in the aniline colors and bleaches in iodine.
Pathogenesis. In morphology and cultures it resembles the bacillus of fowl cholera, but it fails to infect chicken, pigeon or rabbit. It infects ducks readily by ingestion or hypodermic inoculation.
Spirillum Metchnikowi was found in 1888, by Gamaleia in the ingesta of chickens dying in Russia of a choleræic enteritis. It resembles the cholera spirillum, but is shorter, broader and more curved. Its size varies, being twice as broad as the cholera spirillum, when found in pigeons. It may be 0.8μ long, by .5μ broad, furnished with one polar flagellum and very motile. It stains in aniline colors and bleaches in iodine. Grows readily in common media at room temperature, and is killed in five minutes by 122° F.; renders milk strongly acid, coagulating it, and perishes in the acid. In eggs turns the albumen yellow and the yolk black. In gelatine it forms transparent colonies and in potato pale brown.
Pathogenesis. By inoculation it infects chickens, pigeons and guinea-pigs, while rabbits and mice are refractory except to large doses. By ingestion it infects chickens and guinea-pigs but not pigeons. Infection takes place easily by the air passages. In all cases alike the lesions are concentrated in the intestines.
Lesions. These are very similar in the different forms. The intestine is violently congested and contains a quantity of yellowish green mucopurulent or serous fluid. The mucosa is infiltrated, softened and even abraded by the desquamation of epithelium. The liver is greatly enlarged and softened and gorged with blood, and the gall bladder filled. The spleen is enlarged and pale, contrary to what is seen in fowl cholera, and the kidneys are congested. The heart is flaccid, soft, petechiated, and the pericardium is the seat of serous effusion.
Symptoms. In the acute form there is dullness, langor, inappetence, ardent thirst, pale comb, and greenish fæces. Later the feathers are erect, the wings and tail droop, the head sinks, the patient gapes frequently, walks unsteadily, and a liquid bluish green diarrhœa sets in, which later becomes yellow and bloody. The somnolence increases, the walk becomes more unsteady, or the patient sinks down with eyes half closed and refuses to rise. As the disease advances the comb becomes violet, the dark shade constantly increasing and a glairy grayish mucus is discharged from the nose and bill. The temperature which was at first raised 1° or 2°, falls 2° or 3° below the normal prior to death, which may be deferred to near the end of the second week.
In the chronic cases the disease may drag along for three weeks, the emaciation, pallor and weakness constantly increasing and the feathers around the anus soiled and matted together by the fœtid liquid discharges. There may be remissions which go on to complete convalescence but more commonly an exacerbation occurs which proves fatal in a day or two.