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 i nfections with Pasteurella multocida, Riemerella anatipestifer, and Escheri chia roll were frequently seen in affected ducks. The isolated virus was id entical to the prototype DEV by virus neutralization test but differed from the classic DEV by causing lymphoid organ atrophy and inconsistent hemorrh agic lesions in the intestinal annular bands. Attempts to reproduce the dis ease in white Pekin ducks were unsuccessful until the virulence of the viru s was increased by three passages in Muscovy ducklings. Significant thymic atrophy (P less than or equal to 0.001) was detected during the first 10 da ys postinfection (DPI), but thymus size returned to normal by 17-24 DPI. Ho wever, bursal atrophy increased significantly (P less than or equal to 0.00 1) from 4 DPI until the end of the experiment (39 DPI). Reduction in body w eight was significant (P less than or equal to 0.05) between 4 and 6 DPI. T here was massive depletion of thymic and bursal lymphocytes with lymphoid n ecrosis in the thymus, bursa, spleen, and Harderian gland. Eosinophilic int ranuclear inclusions were observed in thymus, bursa, spleen, esophagus, clo aca, liver, conjunctiva, and Harderian gland. Occasional intracytoplasmic i nclusions were also found scattered in the epithelial cells of conjunctiva, esophagus, bursa of Fabricius, and cloaca. Virus was recovered from experi mentally infected ducks from thymus, bursa, spleen, liver, kidneys, trigemi nal ganglion, and cloaca during the first 10 days of infection. These findi ngs suggest that a low-virulent DEV can cause a massive lymphoid atrophy an d can sustain immunosuppression as noted by the secondary bacterial infecti on.