A Generalized Inclusion Body Disease in the Budgerigar (Melopsittacus undulatus) Caused by a Papovavirus-Like Agent

Abstract

High mortality rates have been reported in budgerigars between one and 15 days of age in 19 aviaries in the Province of Quebec. The most consistent signs of disease were abdominal distention, lack of down feathers on the back and abdomen, lack of filoplumes on the head and neck, and retarded growth of the tail and contour feathers in birds that either survived or died later. Internal gross lesions were hydropericardium, enlarged heart and liver with multiple pinpoint white spots or large, yellow foci, pale or congested kidneys, congested lungs, and ascites. Histologic examination revealed large, slightly basophilic inclusion bodies in the enlarged nuclei of many different cells. These inclusion bodies were composed of viral particles. Multiple foci of coagulation necrosis were scattered in the myocardium and liver parenchyma, and granulovacuolar degeneration was common in renal tubular epithelial cells. Ballooning degeneration was multifocal in the epidermis and very extensive in the epithelial cells of developing feather follicles, and this led to their partial or complete destruction. Viral particles 50 to 55 nm in diameter were observed in negatively stained preparations from different organs of affected birds. These particles had the size and morphology of a papovavirus. In experimentally infected 25-day-old budgerigars, histologic examinations revealed the presence of intranuclear inclusions in hepatocytes, epithelial cells of the kidney tubules, and reticular cells of the spleen, despite the absence of clinical signs. We feel that this disease is caused by a papovavirus-like agent that can replicate in many tissues of the body, causing widespread lesions responsible for the high mortality rate of very young budgerigars and for the absence and/or incomplete development of feathers.

Proliferative Pododermatitis Associated with Virus-like Particles in a Northern Gannet

“…Papillomaviruses are common among mammalian species but have been identified less frequently in avian species, where they have been associated with proliferative epidermal lesions on the head, legs and feet, characterized microscopically by acanthosis and hyperkeratosis (Ritchie, 1995). Avian polyomaviruses are best known as the cause of budgerigar fledgling disease, a systemic and often fatal infection of young budgerigars (Melopsittacus undulatus) characterized microscopically by multifocal cellular hydropic degeneration and necrosis in the epidermis (including developing feather follicles) and internal organs, often with large intranuclear basophilic or amphophilic viral inclusion bodies (Bernier et al, 1981). Ultrastructurally, the viral particles may be accompanied by ''tubular structures'' (Bernier et al, 1981) or ''elongated forms'' (Dykstra and Bozeman, 1982), comparable in diameter to, but much longer than, the intranuclear rods observed in this gannet.…”

“…Avian polyomaviruses are best known as the cause of budgerigar fledgling disease, a systemic and often fatal infection of young budgerigars (Melopsittacus undulatus) characterized microscopically by multifocal cellular hydropic degeneration and necrosis in the epidermis (including developing feather follicles) and internal organs, often with large intranuclear basophilic or amphophilic viral inclusion bodies (Bernier et al, 1981). Ultrastructurally, the viral particles may be accompanied by ''tubular structures'' (Bernier et al, 1981) or ''elongated forms'' (Dykstra and Bozeman, 1982), comparable in diameter to, but much longer than, the intranuclear rods observed in this gannet. Systemic infection by avian polyomavirus has also been reported in nonbudgerigar psittacine birds and other avian families (Gerlach, 1994;Ritchie, 1995).…”

A concurrent outbreak of psittacine beak and feather disease virus, and avian polyomavirus infection in budgerigars(Melopsittacus undulatus)

“…Most of the lesions observed in both groups of birds (1-week-old birds and 2-month-old-birds) and the detection of PBFDV and APV viralspecific DNA had been previously described in the scientific literature about PBFDV (Latimer et al, 1991a;Ritchie & Latimer, 1995a) and APV (Bernier et al, 1981;Davis et al, 1981;Dykstra & Bozeman, 1982;Ritchie & Latimer, 1995b) as single infections. However, the lesions observed in smooth muscle fibres in arterial walls associated with basophilic nuclear inclusions (APV probe positive) had never been described previously in APV infections.…”

“…APV clinical presentation, distribution of lesions and epidemiology are dramatically different among susceptible species. In young budgerigars (Melopsittacus undulatus) the clinical process is named budgerigar fledgling disease (BFD) due to the marked abdominal distension observed in young birds, discoloration of the skin and loss of feathers; mortality is high and birds that survive beyond 15 days usually show delayed growth of tail and contour feathers (Bernier et al, 1981;Davis et al, 1981;Gaskin, 1989).…”

Unusual fatal avian polyomavirus infection in nestling cockatiels (Nymphicus hollandicus) detected by nested polymerase chain reaction

“…In non-budgerigar psittacine species, fatal infections occur in hand-raised nestlings. APV infection was first described in 1981 in budgerigars in the USA Davis et al, 1981) and Canada (Bernier et al, 1981). Since then, it has been reported worldwide (Reece et al, 1992;Scott, 1994;Sandmeier et al, 1999;Ozmen and Dorrestein, 2004;Bert et al, 2005).…”