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Chronologic Analysis of Gross and Histologic Lesions Induced by Field Strains of FAdV-1, FAdV-8b, and FAdV-11 in Six-Week-Old Chickens

生物 病理 粗检 解剖 兽医学 医学
作者
Penelope A. Steer-Cope,J. R. Sandy,Denise O’Rourke,Peter Scott,Glenn F. Browning,Amir H. Noormohammadi
出处
期刊:Avian Diseases [American Association of Avian Pathologists]
卷期号:61 (4): 512-512 被引量:10
标识
DOI:10.1637/11718-072317-reg.1
摘要

Inclusion body hepatitis (IBH) is a disease affecting broiler chicken flocks worldwide. Several serotypes of fowl adenovirus (FAdV) have been implicated in disease outbreaks, with and without immunosuppression as a predisposing factor. IBH usually occurs in flocks up to 30 days of age; it is seldom seen in older birds. The objective of this study was to determine whether the pathogenicity for older birds of three FAdV field strains, belonging to serotypes 1, 8b, and 11, in the absence of immunosuppressive factors, was akin to that for younger birds, and to establish an effective and economical disease model for assessing cross-protection between serotypes. To achieve this objective, the gross pathology, histopathology, and dissemination of virus were examined at multiple time points after inoculation of 6-wk-old, specific-pathogen-free chickens via intraperitoneal injection. Both FAdV-8b and FAdV-11 generated lesions typical of those associated with outbreaks of IBH, and they were shown to be primary pathogens. The presence and severity of hepatic lesions were used to define two disease stages: degeneration (1–5 days postinoculation) and convalescence (6–14 days postinoculation). During the degenerative stage, FAdV-8b was detected in the liver, kidney, and gizzard of most birds, whereas FAdV-11 was predominantly detected in the liver, and both viruses persisted in the gizzard into convalescence. The pathogenesis of two IBH-associated FAdV strains in 6-wk-old chickens confirms their high level of virulence and also provides an effective experimental model for investigation of cross-protection between FAdVs. It also demonstrates persistence of the virus in the gizzard long after infection, supporting the notion that it is a site of viral shedding.

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