Pathogenicity of a low-virulence duck virus enteritis isolate with apparent immunosuppressive ability.

Duck enteritis virus (DEV) was isolated from commercial 2-to-6-wk-old white Pekin ducks experiencing 25%-30% mortality and high morbidity. Secondary infections with Pasteurella multocida, Riemerella anatipestifer, and Escherichia coli were frequently seen in affected ducks. The isolated virus was identical to the prototype DEV by virus neutralization test but differed from the classic DEV by causing lymphoid organ atrophy and inconsistent hemorrhagic lesions in the intestinal annular bands. Attempts to reproduce the disease in white Pekin ducks were unsuccessful until the virulence of the virus was increased by three passages in Muscovy ducklings. Significant thymic atrophy (P < or = 0.001) was detected during the first 10 days postinfection (DPI), but thymus size returned to normal by 17-24 DPI. However, bursal atrophy increased significantly (P < or = 0.001) from 4 DPI until the end of the experiment (39 DPI). Reduction in body weight was significant (P < or = 0.05) between 4 and 6 DPI. There was massive depletion of thymic and bursal lymphocytes with lymphoid necrosis in the thymus, bursa, spleen, and Harderian gland. Eosinophilic intranuclear inclusions were observed in thymus, bursa, spleen, esophagus, cloaca, liver, conjunctiva, and Harderian gland. Occasional intracytoplasmic inclusions were also found scattered in the epithelial cells of conjunctiva, esophagus, bursa of Fabricius, and cloaca. Virus was recovered from experimentally infected ducks from thymus, bursa, spleen, liver, kidneys, trigeminal ganglion, and cloaca during the first 10 days of infection. These findings suggest that a low-virulent DEV can cause a massive lymphoid atrophy and can sustain immunosuppression as noted by the secondary bacterial infection.