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Overview of Coronaviral Enteritis of Turkeys

(Bluecomb, Mud fever, Transmissible enteritis)

By James S. Guy, DVM, PhD, Professor, Department of Population Health and Pathobiology, College of Veterinary Medicine, North Carolina State University

Coronaviral enteritis is an acute, highly contagious disease of turkeys characterized by depression, anorexia, diarrhea, and decreased weight gain. Mortality may be high, particularly in young poults, but failure to gain body weight in adult birds may be more important economically. The causative agent is turkey coronavirus (TCV), but clinical disease usually is complicated by other enteric viral, bacterial, and protozoal infections.


Coronaviral enteritis has been identified in turkeys in the USA, Canada, Brazil, Italy, UK, and Australia. The disease has been reported in most turkey-producing regions of the USA. Turkey coronavirus affects turkeys of all ages; however, clinical disease most commonly is seen in young turkeys during the first few weeks of life. Turkeys are believed to be the only natural host for TCV.

TCV is shed in feces of infected birds and spread horizontally through ingestion of feces and feces-contaminated materials. Virus is shed in droppings of turkeys for several weeks after recovery from clinical disease. Infection generally spreads rapidly through a flock and from flock to flock on the same or neighboring farms. Mechanical movement of the virus may occur by people, equipment, vehicles, and insects. Darkling beetle larvae and domestic house flies are potential mechanical vectors. Wild birds, rodents, and dogs also may serve as mechanical vectors. There is no evidence that TCV is egg transmitted; however, poults may become infected in the hatchery via contaminated personnel and fomites such as egg boxes from infected farms.

Clinical Findings:

Clinical signs occur suddenly, usually with high morbidity. Birds exhibit depression, anorexia, decreased water consumption, watery diarrhea, dehydration, hypothermia, and weight loss. Droppings typically are green to brown, watery, and frothy, and may contain mucus and urates. Affected flocks have increased mortality, growth depression, and poor feed conversion. Morbidity generally approaches 100%, but mortality is variable; mortality may be high depending on the age of the birds, concurrent infection, management practices, and weather conditions.

In breeder hens, egg production drops rapidly. Egg quality also is affected; hens produce white, chalky eggs lacking normal pigmentation.


Gross lesions are seen primarily in the intestines. The duodenum and jejunum generally are pale, thin-walled, and flaccid; ceca are distended with gas and watery contents. Emaciation, dehydration, and atrophy of the bursa of Fabricius also may be seen.

In the intestines, microscopic lesions consist of a decrease in villous length and increase in crypt depth; the columnar epithelium changes to a cuboidal epithelium, and these cells exhibit a loss of microvilli. There is a decrease in the number of goblet cells, separation of enterocytes from the lamina propria, and infiltration of the lamina propria with heterophils and lymphocytes.

In the bursa of Fabricius, the normal pseudostratified columnar epithelium is replaced by a stratified squamous epithelium, and intense heterophilic inflammation is seen within and underneath the epithelium.


Diagnosis generally requires laboratory assistance, because other enteric pathogens of turkeys may cause similar clinical signs and lesions. Laboratory diagnosis is based on virus isolation, electron microscopy, serology, or detection of viral antigens or viral RNA in intestinal tissues, the bursa of Fabricius, or intestinal contents. Preferred clinical samples for diagnostic analyses include serum, intestinal contents, and fresh tissues (intestines and bursa of Fabricius); these samples should be kept cold (on ice at 4°C or frozen) at all times. Coronaviral enteritis must be distinguished from other enteric viral, bacterial, and parasitic infections, including those caused by astrovirus, rotavirus, reovirus, Salmonella spp, and crytosporidia.

Prevention and Treatment:

Prevention is the preferred method to control TCV. No commercial vaccine is available. Infected turkeys shed virus in feces for prolonged periods after recovery; these turkeys, their feces, and the materials their feces contact are potential sources of infection for other susceptible turkeys. Feces from infected turkeys can be carried on a variety of fomites, including clothing, boots, equipment, feathers, and trucks. Other potential vectors, such as wild birds, rodents, dogs, and flies, also may be involved in transmission. Biosecurity measures must be instituted to prevent introduction of TCV via potentially contaminated personnel, fomites, animal and insect vectors, and infected turkeys.

TCV may be eliminated from contaminated premises by depopulation followed by thorough cleaning and disinfection of houses and equipment. After cleaning and disinfection procedures, premises should remain free of birds for a minimum of 3–4 wk.

There is no specific treatment for TCV enteritis. Antibiotic treatment reduces mortality but not growth depression, most likely by controlling secondary bacterial infections. No beneficial effect was seen when glucose, electrolytes, or calf milk replacer was added to drinking water. Effective management procedures to reduce mortality include raising brooder house temperatures and avoiding crowded conditions.