Turkey viral hepatitis is an acute, highly contagious, frequently subclinical disease of turkey poults 5 wk of age. The disease is widespread and common in some areas, with morbidity rates of as much as 100%. Mortality has been reported only in poults, is confined to a 4- to 8-day period, and may reach 25%.
A picorna-like virus from poults with typical lesions has been reported, but its etiologic role has not been conclusively established. The causal virus has not been fully classified, but a picornavirus from turkeys with typical lesions of turkey viral hepatitis has been molecularly characterized and proposed as a new species in the order Picornavirales. It is isolated without difficulty from the liver and a variety of other tissues, including the pancreas, spleen, and kidney, as well as feces. The virus is isolated less consistently from older birds. It grows readily in the yolk sac of 5- to 7-day-old chicken or turkey embryos. It is thermostabile; resistant to ether, phenol, and creolin but not formalin; and susceptible to high, but not low, pH.
Disease is usually subclinical and becomes apparent only when the birds are stressed. Affected birds are stunted and unthrifty. Morbidity and mortality vary according to the severity of stress. In poults <5 wk old, morbidity may reach 100% and mortality 10%–25%. Breeder flocks may exhibit decreased production, fertility, and hatchability.
Gross lesions are confined to the liver and pancreas. In the liver, foci of necrosis are 1–3 mm in diameter and may be confluent. Areas of hemorrhage or congestion are also present and frequently obscure the degenerative changes. Occasionally, the liver is diffusely bile-stained. Liver lesions may resemble those of bacterial infections, particularly from Salmonella spp, Pasteurella multocida, or Escherichia coli, and infections caused by Group 1 and Group 2 avian adenovirus and reovirus. The pancreas frequently exhibits relatively large, circular, gray areas of degeneration. In the subclinical form, lesions are less extensive, and hepatic hemorrhage or congestion is seldom prominent. Affected tissues return to normal in 3–4 wk.
Salmonella spp and other bacterial infections produce necrotic areas in the liver that can be confused with those of viral hepatitis. Bacterial infections must be differentiated by appropriate culturing techniques. Liver lesions may resemble those of histomoniasis, but the absence of cecal lesions in turkey viral hepatitis helps to differentiate the two diseases. With histomoniasis, histologic examination or demonstration of the respective etiologic agents is necessary. Diagnosis is aided by demonstration of picornavirus by immunohistochemical or molecular techniques from poults with typical lesions.
There is no known treatment. Secondary bacterial invasion does not appear to be important, but if it occurs, it should be treated on the basis of specific etiology. Although recovered birds demonstrate resistance to infection, neutralizing antibodies have not been detected. Improved sanitation may be of value in preventing dissemination of the agent.
Last full review/revision June 2013 by Willie M. Reed, DVM, PhD, DACVP, DACPV