The fulfillment of Koch’s postulates shows that the virus causes proventricular dilatation disease in parrots.

A flock of 14 apparently healthy cockatiels, purchased from a single aviary, was tested for the presence of avian bornavirus (ABV). Twelve birds were found to be intermittently shedding ABV, predominantly genotype 4. Four of the cockatiels known to be shedding ABV4 were subsequently challenged with the tissue culture derived, virulent M24 strain of ABV4. The challenged birds remained in apparent good health until day 92 when one was found dead. The remaining three birds began to exhibit severe neurologic signs, ataxia and convulsions on day 110 and were euthanized. On necropsy, all four birds showed mild proventricular enlargement. In contrast, histopathological examination showed unusually severe and widespread tissue lesions. These included massive lymphocytic infiltration and lymphoid nodule formation within and around the ganglia throughout the gastrointestinal tract. There were similar lesions in the medullary cords of the adrenal gland, heart, spleen, liver, kidney, lungs, pancreas, testes and ovary. Immunohistochemistry demonstrated ABV P antigen not only in the cells of the central and autonomic nervous systems, but also within the mononuclear cells infiltrating the various organs. Two healthy cockatiels, one of which was a known ABV carrier, were inoculated with uninfected tissue culture cells and euthanized on day 150. These birds showed no gross lesions of proventricular dilatation disease but had a mild lymphocytic infiltration in their liver, spleen, and kidneys. Prior infection with ABV did not therefore confer significant immunity on these birds, and may have resulted in increased disease severity following challenge.

Avian bornavirus (ABV) is currently considered a probable etiologic agent of proventricular dilatation disease (PDD) of psittacines. We tested 24 stored avian brain samples, processed for histopathology and retained following their submission for necropsy or histopathology to the Schubot Exotic Bird Center diagnostic laboratory in 1992. Thirteen of these samples were from birds diagnosed at that time as suffering from PDD. The remaining 11 samples were diagnosed as suffering from diseases other than PDD. Immunohistochemistry was performed using an antiserum directed against the ABV nucleoprotein (Nprotein). Stained slides were read by an investigator unaware of their prior histopathology results. Cells containing ABV N-protein were present in the nervous tissues of all 13 PDD cases. One bird not previously diagnosed with PDD also had ABV N-protein in its brain. A review of this bird's necropsy report indicated that it was, most probably, also suffering from PDD. The remaining 10 non-PDD birds had no detectable Nprotein in their brains. The N-protein was present in the cerebrum, cerebellum and spinal cord. These findings support other studies that indicate that ABV is an etiological agent of PDD.

No abstract

An isolate of genotype 2 avian bornavirus (ABV) was recovered from a cockatiel (Nymphicus hollandicus) that was euthanatized for an unrelated lesion and showing no clinical evidence of proventricular dilatation disease (PDD). On histopathologic examination, mild inflammatory lesions were present in the heart and brain, but gastrointestinal lesions characteristic of classic PDD were not observed. To investigate if this ABV2 isolate had reduced virulence, the virus was propagated in duck embryo fibroblasts and inoculated into 2 adult cockatiels by the oral and intramuscular routes. One bird developed clinical signs on day 33 and was euthanatized on day 36. The second challenged bird developed clinical signs on day 41 and was euthanatized on day 45. At necropsy, the proventriculus of both birds was slightly enlarged. Histopathologic examination showed lesions typical of PDD in the brain, spinal cord, heart, adrenal gland, and intestine. A control, uninoculated cockatiel was apparently healthy when euthanatized on day 50. These results show that ABV2 is now the second ABV genotype to be formally shown to cause PDD.