Histopathology and immunohistochemistry of renal lesions due to avian infectious bronchitis virus in chicks uninoculated and previously inoculated with highly virulent infectious bursal disease virus

Abstract

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.

Pathogenesis and Tissue Distribution of Avian Infectious Bronchitis Virus Isolate IRFIBV32 (793/B Serotype) in Experimentally Infected Broiler Chickens

“…These findings indicate IRFIBV32 isolate has a broad tissue distribution that includes respiratory, digestive, congenital, and urinary tract tissues; predominantly in urinary and digestive tracts. This result is in agreement with the previous studies about IBV distribution [6,22,24,25]. Chen and Itakura [24] reported that the tracheal lesions recovered faster in IBV inoculated groups.…”

“…This result is in agreement with the previous studies about IBV distribution [6,22,24,25]. Chen and Itakura [24] reported that the tracheal lesions recovered faster in IBV inoculated groups. The nephropathogenic property of their IBV was longer lasting than the respiratory involvement.…”

“…Chen and Itakura [24] reported that the clinical signs and gross and histological lesions in the trachea and kidneys due to IBV infection were more severe and of longer duration in dually infected chicks (with infectious bursal disease virus and IBV) than in ones inoculated with IBV. Our field observation indicates that flocks that are infected by IBV have shown an increase in mortality in recent years that could be due to increased pathogenicity of the virus or due to other undetected field infections.…”

Infectious Bronchitis

“…The kidney lesions of IB are principally those of an interstitial nephritis (Figure 4.7G and H) (35,36,155). The virus causes granular degeneration, vacuolation and desquamation of the tubular epithelium, and massive infiltration of heterophils in the interstitium in acute stages of the disease.…”

The avian coronavirus spike protein

“…From the respiratory tract, the virus spreads through the host via viremia (Jones and Jordan, 1972) to the epithelial cells of the renal tubuli (Chen and Itakura, 1996;Condron and Marshall, 1986;Purcell et al, 1976) and the ciliated epithelium of the oviduct (Crinion et al, 1971;Jones and Jordan, 1971). Here the virus causes respectively renal failure with urate obstruction due to tubular necrosis with mononuclear inflammation (Chen and Itakura, 1997;Jones, 1974), and oviductal necrosis and malformation leading to abnormal egg production and inability to lay (Chousalkar and Roberts, 2007). The severity of the disease in various organs depends on the IBV subtype and ultimately determines the mortality in chickens.…”