AVIAN POLYOMAVIRUS INFECTION
KEVIN EATWELL
Exotic Animal and Wildlife Service, Royal (Dick) School of Veterinary Studies, Edinburgh, Scotland Avian polyomaviruses (APV) are small double-stranded DNA viruses and were first described in budgerigars (Mel- opsittacus undulatus) in 1981.
Antigenically similar viruses have been since isolated from a variety ofpasserines and have been associated with high morbidity and mortality worldwide. APV have also been identified in dead wild buzzards (Buteo buteo) and a kestrel (Falco tinnunculus) in Germany1-9).The acute nature of polyomavirus infection is unusual for papovaviruses. In captive and recently imported fringil- lid and estrildid finches it has been associated with acute mortality in 2- to 3-day-old chicks, fledglings, juveniles and adult birds. Some birds die peracutely and others exhibit non-specific signs of illness 24 hours prior to death. Clinical signs can include anorexia, weakness, ataxia, diarrhoea and lethargy.
Birds surviving infections can have poor feather development and long, tubular, misshapen beaks. Surviving chicks may have delayed fledging and can also develop persistent infections followed by intermittent shedding of the virus from the cloaca.
Transmission is usually horizontal via faeces, urates, feather dust and respiratory droplets. Vertical transmission may be possible but has only been confirmed in budgerigars(10).
In pied flycatchers (Ficedula hypoleuca) in Spain, polyomavirus has been found in larval blowflies in the nesting site, leading to infection in the chicks. Adults are subsequently infected via cloacal shedding from the chicks when nest cleaning1-11). No association was found with other common nest parasites such as Dermanyssus. Infected parents did not appear to lead to a higher incidence of APV in the chicks compared with families with noninfected parents, suggesting that routes such as oral transfer or droplet transmission is of less importance in disease transmission1-11).
Underlying stress or concurrent diseases may cause subclinically affected birds to shed virus and result in outbreaks of clinical disease.Affected birds may have no gross or histological lesions, or may show swollen, pale mottled livers, splenic enlargement and internal haemorrhage.
Histological changes can include inflammation and necrosis of the liver, myocarditis, bone marrow necrosis, lymphoid necrosis and plasma cell infiltration of the intestine. Intranuclear inclusion bodies can be demonstrated in the spleen, bone marrow, intestines, kidneys, heart, cloacal bursa and liver. Most isolates are serologically related to the psittacine polyomavirus, but DNA probes used for psittacine virus are unlikely to detect the virus in passerines(12).
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