SUMMARYTwo-day-old specific-pathogen-free chicks were inoculated intranasally with the MA-87 strain of infectious bronchitis virus, and trachea and kidney lesions studied histologically and immunohistochemically. Lesions and viral antigen were first detected in the trachea; severe damage was then observed in the kidney. Viral antigen appeared prior to the development of renal lesions and was detected in the cytoplasm of epithelial cells by 4 days post-inoculation (p.i.). The epithelial cells of the collecting ducts, collecting tubules and distal convoluted tubules were first affected, followed by involvement of Henle's loops, whereas the proximal convoluted tubules were only minimally affected. Antigen-positive cells of ducts and tubules were degenerated and desquamated. The severe epithelial cell damage resulted in infiltration of heterophils and macrophages in the interstitium, ducts and tubules. The detection of viral antigen was consistent with the distribution of histological lesions at 6 to 8 days p.i. At a later stage, antigen-positive cells disappeared and repair of epithelial cells was seen, accompanied by interstitial lymphoplasmacytic infiltration and lymphoid nodular formation.

The renal ducto-tubular epithelial cells of chicks infected with the MA-87 strain of avian infectious bronchitis virus (IBV) were examined ultrastructurally. Infected epithelial cells containing IBV particles were more numerous in the collecting ducts, collecting tubules, distal convoluted tubules and Henle's loops than in the proximal convoluted tubules. Virus particles invaded host cells through endocytotic vesicles. Cytopathologic changes in the infected epithelial cells were manifested by a variety of organlle alterations including swelling of mitochondria, dilation of Golgi vesicles and an increase in the amount of rough endoplasmic reticulum (RER). Virus particles were produced by budding into RER and, rarely, toward the perinuclear space. As virus replication progressed, virus particles were enclosed mainly in the dilated RER, cytoplasmic vesicles or virus-containing electron-dense bodies. Virus particles were also found in vesicles of Golgi complex, the dilated perinuclear space, in some autophagic vacuoles or free in the cytoplasm. Virus particles were released by exocytosis through cytoplasmic vesicles, or appeared to be discharged through disrupted cell membranes. It was concluded that epithelial cells of lower nephron and ducts are the primary target cells in IBV-infected kidneys.

SUMMARYA nephropathogenic strain of infectious bronchitis virus (IBV) was inoculated intra-tracheally into 14-day-old specific-pathogen-free chicks or ones previously inoculated with highly virulent infectious bursal disease virus (IBDV) at 7 days of age. The renal lesions were examined histopathologically and immunohistochemically at intervals up to 30 days post-inoculation. The mortality was 20% in the IBDV + IBV-inoculated group, but not in the IBV-inoculated one. Swollen and pale kidneys due to IBV infection were more severe and of longer duration in dually infected chicks. At the early stage of infection, the histopathological changes in the kidneys were similar in both groups, but the ducto-tubular damage was more severe in the dually infected chicks. At the late stage of infection, the renal lesions were characterized by chronic interstitial nephritis with formation of lymphoplasmacytic nodules in IBV-inoculated chicks and by chronic active nephritis which consisted of tubular degeneration, lymphoid cell reaction and interstitial fibrosis in IBDV + IBVinoculated ones. More IBV antigen-positive cells persisted longer in the kidneys of dually infected chicks than in those of IBV-inoculated ones.