Avian Polyomavirus: My Thoughts...

David N. Phalen

Abstract


Introduction

The avian polyomavirus (APV) is one of the most significant viral pathogens of cage birds. It results in substantial economic losses for aviculturists and pet store owners each year. The biology of this virus is complex and as a result veterinarians and aviculturists alike are often very confused about how to best prevent this virus infection and, once confronted with it, how to minimize its impact. The following article is an in depth discussion on APV from my perspective. In it I address issues surrounding the value of testing, what the various tests mean, vaccination, and the various factors that must be understood if the effects of APV are to be mitigated. I feel that this article is timely, as our knowledge of biology and behavior of this virus has grown significantly in the past few years.

Avian Polyomavirus:

A Definition and History

The avian polyomavirus was first recognized in the early 1980s in the southeastern and southcentral United States" 9· IO and in Ontario, Canada in budgerigars.2· 3 It was called the Budgerigar Fledgling Disease Virus. It was found to be a nonenveloped, DNA virus and based on its size, shape, and DNA content it was classified as a papovavirus.2· 3· 4· 9. IO. 49 The Papovaviridae contain two very different virus families, the papillomaviruses and the polyomaviruses. With further investigation, it was determined that the Budgerigar Fledgling Disease Virus is a polyomavirus.26• 29· 57 Subsequently, the virus was found to infect many different species of psittacine birds (parrots) and thus it is generally the convention to call it the avian poly-

 

omavirus (APV).5• 17 20• 35· 45 APV is wide spread and can be found in most countries of the world where psittacine birds are raised.29• 31• 32· 59· 61As will become clearly apparent, generalizations about this virus cannot be made and over simplification about the issues of infection and disease, while convenient, are often misleading.

Avian Polyomavirus Disease Budgerigars

In the Budgerigar, disease and death is confined to nestlings between 10 and 25 days of age.2· H 9 Budgerigar breeders first detect this problem in their flocks when there is a sudden increase in the number of dead nestlings in the nest boxes. The signs of APV disease in Budgerigar nestlings are somewhat variable. Most often, the young birds experience an abbreviated course of disease. At death, birds are found to be stunted, to have abnormal feather development, skin discoloration, abdominal distension, ascites (fluid in the abdomen), enlargement of the liver with localized areas of necrosis (cell death), and scattered areas of hemorrhage. In some outbreaks, the virus attacks the cerebellum (a portion of the brain) and these birds will show head tremors. Microscopic examination of the tissues from these birds reveals virus inclusion bodies in cells of multiple organ systems, including the liver, spleen, kidney, feather follicles, skin, esophagus, brain, and heart. 2. 3. 4. 9. 10. 23, }!)

Not every Budgerigar infected with APV will die. Some survivors will never become outwardly ill and will show no signs of infection. Other nestlings will fail to develop their primary and secondary wing feathers and/or their tail feathers.3· 18· 22 These

 

birds have been referred to as runners or creepers and this form of the disease has been described as French molt. It is extremely important to note that another virus, the Psittacine Beak and Feather Disease Virus (PBFDV), can also cause similar signs. It is possible that one or more additional diseases may also cause feather disease in nestling Budgerigars.

Not all Budgerigars appear to be equally susceptible to infection and disease. In one study in the United States, English Budgerigars were rarely found to be infected with APV although they were housed with other birds shedding the virus."

Nonbudgerigar Parrots

Nonbudgerigar parrots are also susceptible to avian polyomavirus infection." 17. zo, ;z .. i3. 53 Some are highly sus-

ceptible to disease, while others rarely if ever develop disease (Table I)." APV-disease in these birds occurs at different ages in different birds (Fig. 1). In conures, deaths typically occur in birds less than six weeks of age. Deaths in macaws and Eclectus Parrots occur in birds 14 weeks and younger. Most, possibly all, of the nestlings lost are being hand fed.5· 17· 20· -'9 Infected nestlings appear healthy, show very few premonitory signs, and then die suddenly. When signs do occur, they proceed death by only a few hours. Observant owners may notice delayed crop emptying, weakness, a generalized pallor, or bruising under the skin in the preceding hours before death. Yell ow discoloration of the urates is another rare observation.5· 17· 20 Dr. Susan Clubb was able to predict which birds would die, up to 24 hours before their death, by pulling out growing feathers. Birds developing disease would bleed extensively from the feather follicle.'

Necropsy findings commonly include generalized pallor with subcutaneous and subsersoal hemorrhage and enlargement of the spleen and liver. Less commonly, acites and pericardia! effusion may be present. Microscopic examination of the tissues reveals extensive areas of necrosis (cell death) in the liver. Virus inclusion bodies are found in the spleen, mesangial cells of the kidney, and Kupffer cells of

the liver. Necrosis of splenic cells is often massive. Less commonly, virus inclusions are found in other organ systems including the feather follicles.5· 11•20 An immune complex glornerulopathy occurs in a significant percentage of the birds with this disease. These complexes contain antibody and APV proteins. 36.43

 


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