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

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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.

Proventricular dilatation disease (PDD) is a common infectious neurologic disease of birds comprising a dilatation of the proventriculus by ingested food as a result of defects in intestinal motility, which affects more than 50 species of psittacines, and is also known as Macaw wasting disease, neuropathic ganglioneuritis, or lymphoplasmacytic ganglioneuritis. Definitive diagnosis of PDD has been problematic due to the inconsistent distribution of lesions. Since its discovery, avian bornavirus (ABV) has been successfully cultured from the brains of psittacines diagnosed with PDD, providing a source of antigen for serologic assays and nucleic acid for molecular assays. This article provides evidence that ABV is the etiologic agent of PDD. Recent findings on the transmission, epidemiology, pathogenesis, diagnosis, and control of ABV infection and PDD are also reviewed.

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