Avian Encephalomyelitis: A Chronological Study of the Histopathogenesis in Selected Tissues

Avian encephalomyelitis in naturally infected pigeons in Turkey

“…At necropsy, no gross lesions were seen, aside from occasional whiteÁ/greyish foci in the pancreas, proventriculus and myocardium of AEV-infected chicks (Burtscher, 1960;Malik, 1969;Springer & Schimittle, 1968;Butterfield et al, 1969). However, in the present study, macroscopic lesions described in the pancreas were frequently a prominent finding, associated with massive mononuclear infiltrations, as reported in chicks (Calnek et al, 1997).…”

“…Changes in the central nervous system (CNS) have been characterized as non-suppurative encephalomyelitis (Mohanty & West, 1968;Yamagiwa et al, 1969;Itakura & Goto, 1975;Hishida et al, 1986). Lesions in visceral organs consist of lymphoid aggregates that are either increased in size or frequency or are found in unusual places (Markson & Blaxland, 1958;Hoekstra, 1964;Springer & Schimittle, 1968;Butterfield et al, 1969;Malik, 1969;Toplu, 2000). Lymphoid aggregates in proventriculus are considered to be pathognomic, especially when coupled with central chromatolysis from lesions of the CNS (Calnek et al, 1997).…”

Avian encephalomyelitis: A review

“…Infection of susceptible embryos and young chickens with egg-adapted strains has been shown to induce histopathological changes in a number of tissues (Jungherr et al, 1956;Van Roekel et al, 1938;Springer & Schmittle, 1968). Lesions in chickens occur more frequently in the CNS than in other organs in the early stages of infection.…”

“…Six to 7-day-old embryos inoculated with non egg-adapted strains by the yolk-sac exhibit clinical signs of the disease 1 to 9 days after hatching, indicating that virus multiplication occurs during embryogenesis (Hoekstra, 1964;Springer & Schmittle, 1968;Braune & Gentry, 1971;. Hoekstra (1964) reported that maximum virus titres could be detected in the brain, liver and intestines of 20-day-old chicken embryos inoculated at 5 days.…”

“…The concentration of virus excreted in the faeces has been reported to be sufficient to induce clinical disease in susceptible chickens when administered by the oral route (Calnek et al, 1961;Westbury & Sinkovic, 1976). Following oral administration of non-eggadapted strains to susceptible chickens, virus can be first detected in the pancreas, liver and spleen within 3 days p.i., and on subsequent days in the CNS and enteric tissues such as the proventriculus, small intestine and caecum (Springer & Schmittle, 1968;Ikeda et al, 1976a,b). Similar patterns of virus distribution have been observed in the organs of laying hens inoculated with non-egg-adapted AEVs by the s.c. or oral routes, with highest titres of virus being detected in the liver, spleen, pancreas and ovarian follicle.…”