Also known as: Avian Polyomavirus — APV — Budgerigar Fledgling Disease Virus — BFD — BFDV — French Moult
APV was first isolated from Budgerigars from aviaries in the US and Canada in the early 1980s experiencing a high incidence of nestling mortality. It was subsequently shown to cause disease in love-birds, parrots, several species of passerines and various other wild birds.
A second avian polyomavirus called Goose Haemorrhagic Polyomavirus (GHP) was found in farm-raised geese in France in the year 2000. It is closely related to APV.
Infection in wild and captive-raised birds is widespread. All psittacine birds and many other species of birds are susceptible to infection. Disease is generally limited to Budgerigar and lovebird nestlings and hand-fed nestling parrots. It is seen less commonly in Amazon parrots and cockatoos.
APV is a non-envelopped, icosahedral virus that has a circular double-stranded DNA genome. There is little evidence to suggest any host specificity of the virus.
Infections in susceptible non-Budgerigar species that are of the appropriate age result in a rapidly fatal disease, but slightly older nestlings survive and shed virus in faeces and possibly through feather dander for up to 16 weeks. The birds are important sources of infection for other birds.
In Budgerigars, shedding is believed to continue for up to 6 months. Concurrent APV and Psittacine Beak and Feather Disease virus infection may permit persistent shedding of APV.
Infection occurs through the respiratory tract and the mixing of birds at shows and sales and stocking pet shops with birds from multiple sources perpetuates infections.
The virus is also believed to be environmentally stable and can persist from one year to the next in nests.
The commonest presenting sign in Budgerigar aviaries is a sudden onset mortality in chicks 10-20 days old.
Live nestlings are stunted, have a distended abdomen and feather dystrophy.
Some nestlings survive with only feather dystrophy: grossly, primary wing feathers and tail feathers are either absent entirely or have thick sheaths and there may be haemorrhage in their shafts.
These birds are sometimes also infected with Psittacine Beak and Feather Disease Virus.
In nestling parrots, most affected birds die suddenly. Clinical signs last less than 24 hours and include: weakness, pallor, subcutaneous haemorrhage, anorexia, dehydration and crop stasis.
Histologically, finding the characteristic lesions and inclusion bodies is diagnostic. Within the growing feather there is often massive infection of the cells in the zone of differentiation with inclusion bodies in nearly every cell. Inclusions in the epidermis of the skin can also be present.
Swabbing affected organs and submitting the swab for DNA probe testing is definitive, and, in cases with poorly developed lesions, may be the only way of making a positive diagnosis.
Cloacal and oral swabs may be assessed by PCR for the presence of polyomavirus.
Serology is of little use in predicting virus shedding as antibody titres persist for years and possibly for life.
Treatment and Control
There is no known treatment for APV infection.
Control in captive populations of birds is done through management and testing.
Breeding facilities can prevent the introduction of the disease by keeping a closed nursery and the use of quarantine and testing. Birds should not be expected to be shedding virus after 16 weeks of quarantine.
Birds should also be tested for Psittacine Beak and Feather Disease as this can cause persistend APV shedding.
Budgerigars and lovebirds should not be kept in the same premises as other parrots unless they are all tested.
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Schmidt, R. E. (2003) Pathology of pet and aviary birds Wiley-Blackwell
Thomas, D. (2007) Infectious diseases of wild birds John Wiley and Sons
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