The aetiology and pathogenesis of avian inclusion body hepatitis : a thesis presented in partial fulfilment of the requirements for the degree of Doctor of Philosophy in Veterinary Virology, Massey University

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dc.contributor.authorSaifuddin, Mohammed
dc.date.accessioned2013-06-19T23:27:12Z
dc.date.available2013-06-19T23:27:12Z
dc.date.issued1990
dc.description.abstractNaturally occurring inclusion body hepatitis (IBH) in broiler flocks in New Zealand, and the experimental disease were characterized by a sudden onset of illness resulting in up to 30% mortality and severe liver damage associated with the formation of intranuclear inclusion bodies in the hepatocytes. Other features were anaemia and atrophy of the bursa and thymus associated with lymphoid depletion. Serotype 8 avian adenoviruses (AAVs) were isolated from several affected broiler and one breeder flock. High titres of virus neutralizing (VN) antibodies were demonstrated in flocks which had recovered from the disease. By restriction endonuclease fingerprint analysis, two of the New Zealand isolates were found to be similar to each other and to the reference strain HVI, but markedly different from three Australian isolates of the same serotype. Fatal disease resembling IBH was reproduced in 30% of broiler chickens following oral administration of one of the local isolates. Immunosuppression was demonstrated in both natural and experimental infections. An enzyme-linked immunosorbent assay and an immunocytochemical technique were developed for the detection and quantification of adenoviral antigens in various chicken tissues. Both techniques detected less than 100 mean tissue culture infective doses per gram of infected tissue and a group-specific antigen common to the 12 serotypes of AAV. A study of the pathogenesis of IBH infection was conducted following oral administration of AAV. Virus first multiplied to a high titre in the intestinal organs and passed into the blood by way of the lymphatics. Viral antigens were subsequently detected in phagocytic cells in the liver and then in the hepatocytes. Extensive replication resulted in severe liver damage, with release of virus into the blood stream and spread to other organs. Recovery was associated with the appearance of VN antibody from 7 days post inoculation. Viral antigens were detected by ELISA directly in yolk and albumin of eggs derived from 50-60-week-old breeder flocks, although all birds had high titres of VN antibody in their blood. The inclusion bodies found in hepatocytes were characterized antigenically and ultrastructurally.en
dc.identifier.urihttp://hdl.handle.net/10179/4651
dc.language.isoenen
dc.publisherMassey Universityen_US
dc.rightsThe Authoren_US
dc.subjectHepatitisen
dc.subjectPoultry diseasesen
dc.titleThe aetiology and pathogenesis of avian inclusion body hepatitis : a thesis presented in partial fulfilment of the requirements for the degree of Doctor of Philosophy in Veterinary Virology, Massey Universityen
dc.typeThesisen
massey.contributor.authorSaifuddin, Mohammeden
thesis.degree.disciplineVeterinary Virologyen
thesis.degree.grantorMassey Universityen
thesis.degree.levelDoctoralen
thesis.degree.nameDoctor of Philosophy (Ph.D.)en
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