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Poultry
Coronaviral Enteritis of Turkeys
Overview of Coronaviral Enteritis of Turkeys
Epidemiology
Clinical Findings
Lesions
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Prevention and Treatment
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Topics in Coronaviral Enteritis of Turkeys
  • Overview of Coronaviral Enteritis of Turkeys
         
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        Overview of Coronaviral Enteritis of Turkeys(Bluecomb, Mud fever, Transmissible enteritis)

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        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.

        Epidemiology

        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 observed in young turkeys during the first few weeks of life. Turkeys are believed to be the only natural host for TCV.

        Turkey coronavirus 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 have been shown to be 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, 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; high mortality may occur depending on the age of the birds, concurrent infection, management practices, and weather conditions.

        Breeder hens experience a rapid drop in egg production. Egg quality also is affected; hens produce white, chalky eggs lacking normal pigmentation.

        Lesions

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

        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 observed within and underneath the epithelium.

        Diagnosis

        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 for controlling TCV. No commercial vaccine is available. Infected turkeys have been shown to shed virus in feces for prolonged periods after recovery; these turkeys, their feces, and the materials that 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. Following 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 has been shown to reduce mortality, but not growth depression, most likely by controlling secondary bacterial infections. No beneficial effect was observed when glucose, electrolytes, or calf milk replacer was added to drinking water. Management procedures that have been effective in reducing mortality include raising brooder house temperatures and avoiding crowded conditions.

        Last full review/revision March 2012 by James S. Guy, DVM, PhD

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