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Ulcerative Enteritis in Poultry

(Quail Disease)

ByRocio Crespo, DVM, MSc, DVSc, DACPV
Reviewed/Revised Oct 2024

Ulcerative enteritis is caused by Clostridium colinum. It affects primarily young quail, but also several other domestic and wild bird species. Clinical signs include watery to hemorrhagic diarrhea, lethargy, anorexia, and sudden death. The signs are less severe in chickens and nonquail game birds. Presumptive diagnosis is based on gross and histological evaluation. Final diagnosis is based on detection of C colinum via bacterial culture and PCR assay. Streptomycin is an effective treatment, and bacitracin in feed can be used as a preventative.

Ulcerative enteritis is a contagious clostridial disease that affects domestic and wild birds. It was first diagnosed in bobwhite quail (Colinus virginianus) and is also known as quail disease.It is an economically important disease in poultry production because of high mortality rates.

Etiology and Pathogenesis of Ulcerative Enteritis in Poultry

Clostridium colinum is the etiological agent of ulcerative enteritis. It is an anaerobic, fastidious-to-culture, gram-positive, spore-forming, slightly curved rod, approximately 1 × 3–4 mcm wide, with subterminal, oval spores.

Ulcerative enteritis is highly contagious. To induce experimental disease in bobwhite quail, > 106 viable bacterial cells must be administered orally; chickens administered similar inoculum sizes are not affected.

After infection via the oral route, 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.

Although toxigenicity tests have produced negative results in mice, the role of an in situ–produced toxin in the pathogenesis of ulcerative enteritis has been suggested but not demonstrated.

Epidemiology of Ulcerative Enteritis in Poultry

Ulcerative enteritis was first diagnosed in bobwhite quail (Colinus virginianus). The disease affects not only quail but also chickens, turkeys, pheasants, grouse, and other gallinaceous birds. Bobwhite quail are the most susceptible to infection. In addition, this disease has been reported in pigeons, psittacine birds, and Japanese quail (Coturnix coturnix japonica).

In Coturnix quail, disease caused by Clostridium perfringens infection can resemble ulcerative enteritis.

High population density is a predisposing factor for ulcerative enteritis. In chickens, the disease is a complex linked to stress, coccidiosis, infectious bursal disease, and other predisposing factors.

Ulcerative enteritis occurs worldwide.

Birds that develop chronic ulcerative enteritis or that have recovered from the disease remain lifelong carriers. Infected birds shed the bacterium in their droppings. Infection can be introduced by flies feeding on contaminated fecal material or by recovered birds that remain carriers.

Most ulcerative enteritis cases are reported in captive populations of bobwhite quail, suggesting that management plays a role in incidence of the disease.

Clostridium colinum spores can survive on a given premises for months. Clostridium spp have been isolated from water samples obtained from drinker pipes containing biofilm and mineral deposits.

Pearls & Pitfalls

  • Clostridium spp have been isolated from water samples obtained from drinker pipes containing biofilm and mineral deposits.

In affected bobwhite quail, the rate of mortality due to ulcerative enteritis is high (approaching 100%, in just 2–3 days). In contrast, the mortality rate in affected chickens rarely exceeds 10%.

Clinical Findings of Ulcerative Enteritis in Poultry

Ulcerative enteritis can cause acute or chronic disease.

In bobwhite quail, acute ulcerative enteritis results in death without clinical signs or weight loss. Acute lesions include hemorrhagic enteritis of the duodenum.

In chickens and other game birds, the course of ulcerative enteritis is less severe and is accompanied by anorexia. Affected chickens recover within 2–3 weeks.

Clinical signs of ulcerative enteritis are similar to those of coccidiosis: lethargy, humped backs, ruffled feathers, diarrhea, and sometimes bloody or watery white droppings, especially in quail in the prolonged course.

Lesions

In early disease stages, the most common lesions of ulcerative enteritis include small, round ulcers surrounded by hemorrhages in the small intestine, ceca, and upper large intestine (see ulcer and hemorrhage images). Small ulcers later coalesce to form larger, sometimes perforating ulcers, producing local or diffuse peritonitis.

As with coccidiosis, with ulcerative enteritis there is blood in the gut. Characteristic yellow to gray necrotic foci are the predominant lesions in the hepatic parenchyma. Splenomegaly with hemorrhage and necrosis can be present.

Diagnosis of Ulcerative Enteritis in Poultry

  • Gross and histological evaluation

  • Bacterial culture

  • PCR assay

Gross postmortem lesions, including intestinal ulcerations and yellow to gray necrotizing hepatic lesions, support a diagnosis of ulcerative enteritis. Clostridium colinum, which appears singly as rod-shaped bacteria, is evident in Gram-stained smears of hepatic and intestinal lesions. In bacteremic birds, the microorganism can also be found in blood and splenic smears.

Differentiating ulcerative enteritis from coccidiosis can be difficult because the two diseases usually occur simultaneously. Necrotic enteritis and histomoniasis are differential diagnoses; however, the hepatic lesions of ulcerative enteritis help differentiate it from these other diseases.

C colinum can be isolated from liver samples cultured in strict anaerobic conditions in prereducedblood glucose-yeast medium with 8% horse plasma added. Identification can be made by conventional biochemical tests, matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS), and PCR assay.

Prevention, Treatment, and Control of Ulcerative Enteritis in Poultry

  • Bacitracin as a preventative

  • Streptomycin as treatment

Bacitracin in feed (220 g/tonne [200 g/ton]), which acts as a preventative for clostridial diseases in general, can prevent ulcerative enteritis in quail. Streptomycin (0.006% in feed, or 0.26 g/L of water) is an effective treatment.

Prevention of ulcerative enteritis involves good management practices, such as the following:

  • Avoidance of predisposing factors such as coccidiosis and high population density

  • Avoidance of the introduction of new birds into existing flocks

  • Because transmission of the bacteria is fecal-oral, the use of cages in quail breeding

  • Immediate removal of sick and dead birds

  • Thorough cleaning of premises between flocks

  • Pest control in and around the premises

  • Periodic treatment of watering systems with innocuous chemicals that dissolve mineral and biofilm buildup

  • Adherence to appropriate withdrawal times and residue avoidance standards for food-producing birds, per local regulations and restrictions

Key Points

  • A key sign of acute ulcerative enteritis in bobwhite quail is sudden death, without premonitory signs, and a high mortality rate (approaching 100% within just 2–3 days).

  • The most important lesions at necropsy are deep intestinal ulcers that are visible from the serosal surface.

  • Prompt removal of dead birds is an important control measure.

  • Ulcerative enteritis propagates rapidly throughout a colony. Treatment must start promptly to avoid large losses of birds.

For More Information

  • Boulianne M, Uzal, FA, Opengart K. Clostridial diseases. In Swayne DE, ed. Boulianne M, Logue CM, McDougald LR, Nair V, Suarez DL, assoc. eds. Diseases of Poultry. 14th ed. Wiley Blackwell; 2020:966-994.

  • Smith, JS. Clostridial diseases. In: Brugère-Picoux J, Vaillancourt J-P, Shivaprasad HL, Venne D, Bouzouaia M, eds. Manual of Poultry Diseases. AFAS; 2015:342-351.

  • Cooper KK, Songer JG, Uzal FA. Diagnosing clostridial enteric disease in poultry. J Vet Diagn Invest. 2013;25(3):314-327.

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