Ulcerative enteritis was first diagnosed in bobwhite quail (Colinus virginianus). It also affects chickens, turkeys, pheasants, grouse, and other gallinaceous birds. The disease has also been reported in pigeons. Japanese quail (Coturnix coturnix japonica) are resistant, as only experimentally induced cases were reported in highly inbred populations. Marked differences in mortality between males and females suggest that susceptibility is an inheritable trait in Coturnix quail. Ulcerative enteritis occurs worldwide and may be acute or chronic.
Clostridium colinum is the etiologic agent. It is an anaerobic, fastidious to culture, gram-positive, spore-forming, slightly curved rod, ~1 × 3–4 μm wide, with subterminal, oval spores. In chickens, the disease is a complex that is linked to stress, coccidiosis, infectious bursal disease, and other predisposing factors. To induce experimental disease in quail, >106 viable bacterial cells must be administered PO; chickens inoculated at the same levels are not affected.
Birds that develop chronic ulcerative enteritis or that have recovered from the disease remain carriers. Infection can be introduced by flies feeding on contaminated fecal material or by recovered carrier birds. Infected birds shed the bacterium in their droppings. Bobwhite quail are the most susceptible to this highly contagious disease. Most cases are reported in captive populations of bobwhite quail, suggesting that management plays a role in the incidence. C colinum spores can survive in the premises for months.
After oral infection, the bacterium adheres to the intestinal villi, producing enteritis and ulcers in portions of the small intestine and upper large intestine. Bacilli migrate to the liver via portal circulation, producing necrotic foci that later coalesce into extensive hepatic necrosis. Infarcts of the spleen are common. Stained smears of the lesions reveal the rod-shaped C colinum microorganism. Although toxigenicity tests in mice have been negative, the role of an in situ-produced toxin in the pathogenesis has been suggested but not demonstrated.
In susceptible bobwhite quail, sudden death occurs without signs or weight loss and with up to 100% mortality in just 2–3 days. Acute lesions include hemorrhagic enteritis of the duodenum. In chickens, as well as other game birds, the course of the disease is less severe and is accompanied by anorexia. Signs are similar to those seen in coccidiosis: depressed, listless birds with humped backs, ruffled feathers, diarrhea, and sometimes bloody or watery white droppings, especially in quail in the prolonged course. Chickens recover within 2–3 wk and mortality rarely exceeds 10%.
In early disease stages, the most common lesions include small, round ulcers surrounded by hemorrhages in the small intestine, ceca, and upper large intestine. Small ulcers later coalesce to form larger, sometimes perforating ulcers, producing local or diffuse peritonitis. The presence of blood in the gut resembles coccidiosis. Characteristic yellow to gray necrotic foci are the predominant lesions in the hepatic parenchyma. Spleen enlargement with hemorrhages and necrotic areas may be present.
Gross postmortem lesions including intestinal ulcerations and yellow to gray necrotizing lesions in the liver assist in diagnosis. C colinum can be seen in gram-stained smears of the liver and intestinal lesions. In bacteremic birds, the microorganism can also be found in blood and spleen smears. In chickens, differentiating ulcerative enteritis from coccidiosis (see Coccidiosis) may be difficult as both diseases may be present simultaneously. Necrotic enteritis (see Necrotic Enteritis) and histomoniasis (see Histomoniasis) may also present a diagnostic problem, but the hepatic lesions of ulcerative enteritis help differentiate it from these diseases. C colinum can be isolated from liver samples cultured in strict anaerobic conditions in prereduced blood glucose-yeast horse plasma medium. A fluorescent antibody test also has been used to accurately diagnose ulcerative enteritis.
Prevention, Treatment, and Control
Bacitracin in the feed at 200 g/ton is used for prevention in quail. Streptomycin (0.006%) and furazolidone (0.02%) in the feed are effective for treating the disease. Prevention must start with good management practices (eg, avoiding the introduction of new birds into existing flocks). High population density is a predisposing factor. The use of cages is recommended in quail breeding. Sick or dead birds should be removed promptly. Total cleanup between flocks and pest control in and around the premises are good preventive measures.
Last full review/revision March 2012 by Raul E. Otalora, DVM