Farm-reared bobwhite quails less than 3 weeks of age experienced high mortality (250 of 400). At necropsy, these birds had multiple 1-to-2-mm pale foci throughout their livers. Histologically, these foci varied from acute hepatocellular necrosis without an inflammatory response to necrosis with infiltrates of mononuclear inflammatory cells and some heterophils. Hepatocytes adjacent to affected areas had large basophilic intranuclear inclusions. A group I avian adenovirus was isolated from affected livers.

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To determine the fate of virus and characterize the development of lesions, 1-week-old bobwhite quails (Colinus virginianus) were inoculated intratracheally with 10(6) mean tissue-culture-infective doses of quail bronchitis virus. Quails were killed and necropsied sequentially at 2, 4, 8, 16, and 24 hours postinoculation (PI) and on days 2-10 PI. Virus was first isolated from the lung as early as 2 hours PI, from cecal tonsils and bursa of Fabricius 4 hours PI, and from spleen and liver 8 hours PI. Tissue virus titers were highest on days 4 to 6 PI, corresponding with the severity of histologic lesions. Viral inclusions were present in tracheal mucosal epithelium by day 2 PI. On day 3 PI, tracheal epithelium was deciliated, formed an irregular luminal border, and had more frequent inclusions. On days 4 and 5 PI, tracheal epithelium was partially desquamated, but there were minimal leukocytic infiltrates. Bronchiolar epithelium underwent similar changes, but the leukocytic infiltration was more intense and included lymphocytes and heterophils. There was extension of leukocytic infiltrates into surrounding lung that was most extensive on day 3 PI. Hyperplasia of splenic macrophages was first identified on day 2 PI and peaked by day 5 PI.