| Abstract: | This report investigates the interrelatedness, biology, pathogenesis, and control of avian polyomavirus (APV) infection and disease in the budgerigar and nonbudgerigar parrots. It was demonstrated that APV from budgerigar and nonbudgerigar parrots are genetically similar and may be identical. Polymerase chain reaction analysis using primers derived from the sequence of budgerigar APV efficiently amplified the target DNA sequence from viral isolates and infected tissues of both budgerigar and nonbudgerigar parrots. APV in the budgerigar was found to be highly infectious. Also, despite the development of neutralizing antibody, once the infection was established, it was found to be continuous. Both antibody and tissue virus titers were found to be highest in the nestlings and young adult birds but rapidly decreased with the onset of breeding. Despite fluctuations associated with breeding, neutralizing antibody could be detected in all infected budgerigars. Breeding trials also suggested that the disease could be mitigated within endemic aviaries by the use of older breeding stock instead of young replacement birds. The protective value of maternally-derived anti-APV antibody was investigated in day-old budgerigar nestlings. Neither anti-APV or anti-Newcastle disease antibodies were detected in nestling serum. Immunodiffusion and western blot analysis of nestling serum demonstrated that maternal IgG, in general, was not transferred to the nestling. Characterization of the glomerulopathy frequently associated with APV disease in nonbudgerigar parrots revealed that it was an acute immune-complex glomerulopathy. Dense deposits of immune complexes containing both IgG and APV-antigen were found in the mesangium, subendothelially, and within capillary lumens. Affected birds had both circulating virus and neutralizing serum antibody at the time of their death suggesting that viremia preceded infection and that the acute fatal form of this disease developed only with rising anti-APV IgG titers. Based on these observations, it is proposed that 1) rising anti-APV titers permit intravascular formation of immune complexes, 2) soluble or insoluble immune complexes simulanteously result in the glomerular disease and antibody-mediated infection of macrophages, and 3) that macrophage infection stimulates release of cytotoxic factors triggering a dengue virus-like hemorrhagic shock syndrome. |
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