Avian Polyomavirus Primer

Introduction

Polyomavirus is a small DNA virus belonging to family Papovaviridae. Polyomavirus typically causes asymptomatic infections in mammals, however avian polyomavirus can cause an acute infection that results in death.

 

Signalment

Among companion birds, polyomavirus infection is most common in order Psittaciformes. Avian polyomavirus infections have also been sporadically reported in a variety of species including members of order Passeriformes (finches), Caprimulgiformes (nightjars), Piciformes (aracaris), and Anseriformes (domestic geese, Muscovy ducks, mule ducks).

Avian polyomavirus is classically a disease of juvenile birds (Box 1). Avian polyomavirus (APV) type 1 is seen in budgerigar parakeets (Melopsittacus undulatus) and is also called “budgerigar fledgling disease”. Avian polyomavirus type 2 is seen in a variety of non-budgerigar psittacines. Species most commonly affected include macaws and eclectus parrots (= 14 weeks) and conures (= 6 weeks). Infected caiques (genus Pionites), ring-necked parakeets (Psittacula krameri), and lovebirds may be as old as 1 year of age (Box 1).

Budgie chick

Figure 1. Avian polyomavirus type 1 is a disease of the budgerigar parakeet (Melopsittacus undulatus). Image by kyoto5301. Click image to enlarge.

Box 1. Species Commonly Affected by APV Type 2

  • Caiques

  • Conures

  • Eclectus parrots

  • Lovebirds

  • Macaws

  • Ring-necked parakeets

Epidemiology

Avian polyomavirus is transmitted by the horizontal route in both budgerigar parakeets and non-budgerigar psittacine birds. Virus may be shed in feces, crop secretions, skin, and feather dander—even aerosol transmission has been proposed for APV type 1. Vertical transmission of APV does not occur in non-budgerigar psittacines, but has been confirmed in APV type 1.

 

Clinical disease

Avian polyomavirus has an affinity for epithelial, lymphoreticular, and endothelial cells.

Signs of APV type 1 in the budgerigar parakeet can be quite variable (Box 2). Feather dystrophy or abnormal feather growth can lead to deformed flight feathers. Affected birds are unable to fly and are called “runners” or “creepers”. “French molt” is a term sometimes used for this slow, debilitating disease in parakeets characterized by progressive development of abnormal feathers. Bleeding is another hallmark of clinical avian polyomavirus infection. Birds can bleed into subcutaneous tissues or from feather follicles. Regurgitation, coelomic distension caused by hepatomegaly and/or ascites, as well head tremors caused by cerebellar disease can also be signs of APV type 1. Avian polyomavirus can ultimately be fatal, causing acute death in budgerigar nestlings.

Box 2. Clinical signs of APV Type 1

  • Stunting

  • Feather abnormalities

  • Regurgitation

  • Coelomic distension

  • Head tremors

  • Bleeding

  • Death (10-25 days)

Although up to 60% of non-budgerigar psittacine birds can survive infection, APV type 2 can cause peracute death in susceptible species (Box 1). Some individuals can exhibit a brief period of illness lasting 12-24 hours (Box 3). Clinical findings can include non-specific signs of illness, signs of gastrointestinal distress, bleeding, as well as coelomic distension caused by hepatomegaly and/or ascites.

Box 3. Clinical Signs of APV Type 2

  • Depression

  • Weakness

  • Anorexia

  • Weight loss

  • Crop stasis

  • Vomiting

  • Diarrhea

  • Bleeding

  • Hematuria (Eclectus)

  • Coelomic distension

  • Death

More resistant species, such as cockatoos and African grey parrots (Psittacus erithacus), typically remain asymptomatic. Rare reports of clinical disease have also been reported in adult non-budgerigar psittacines. Adult birds typically suffer from transient lethargy, anorexia, and diarrhea.

 

Antemortem diagnosis

Available antemortem diagnostics include DNA probe testing and serology:

  • Antibody titers can be detected as early as day 9 post-infection in budgerigar parakeets. The existence of latent APV type 1 infections means that these titers can persist for life.
  • It usually takes 2-3 weeks post-infection for titers to rise in non-budgerigar psittacines. Titers can persist for months or even years.
  • Collect samples for polyomavirus-specific DNA probes from whole blood and/or cloacal swabs. If a single sample is used, pair blood and cloacal specimens.

Postmortem diagnosis

Gross necropsy findings can include hepatosplenomegaly, ascites, pallor, as well as subcutaneous and subserosal hemorrhages. Histopathology can reveal large, intranuclear inclusion bodies in affected tissues as well as membranous glomerulopathy of the kidneys.

Definitive diagnosis relies upon viral isolation from infected tissues but this test is time-consuming and expensive. Polyomavirus particles can also be identified in tissues using electron microscopy or polymerase chain reaction (PCR) testing. Commonly sampled tissues include the spleen, liver, and kidney.

 

Treatment

There is no treatment for avian polyomavirus. Immunostimulants such as interferon have been administered with variable success.

 

Prevention/control

An inactivated vaccine against avian polyomavirus is commercially available (Psittimune ® APV, Biomune). The vaccine is rarely administered to birds housed singly or in small, closed collections, but instead is given subcutaneously to adult breeder birds. Adverse vaccine reactions can include scab formation at the subcutaneous injection site as well as vaccine site granuloma formation.

Vaccination should never be a replacement for good management and hygiene. Disinfectants effective against polyomavirus include stabilized chlorine dioxide and 0.525% sodium hypochlorite (Clorox). Chlorine bleach should not be used around birds because of the strong fumes and it should be rinsed well. Chlorhexidine reduces, but does not eliminate, the infectivity of avian polyomavirus.

Like most non-enveloped viruses, polyomavirus is environmentally stable and is probably introduced into aviaries through careless management techniques. Therefore a closed flock system and traffic control are also crucial in nurseries (Box 4).

Box 4. Risk Factors Associated With APV Outbreaks

  • Mixed collections of birds, larger parrot species mixed with small parrot species such as lovebirds, budgerigar parakeets, cockatiels

  • Movement of birds in and out of aviary

  • Failure to test new birds brought into the aviary*
  • Chicks from various sources raised in same nursery

  • Failure to quarantine new birds or inadequate quarantine practices
  • Birds of susceptible ages in pet stores

  • Exposure to infected at bird shows, sales, fairs


  • Birds infected with psittacine beak & feather disease virus on the premises

*When new adults are brought into a breeding situation, the DNA probe can be used to identify and isolate birds shedding virus.

Since polyomavirus can be shed in crop secretions, non-budgerigar parent birds can transmit disease to their young during hand rearing. Therefore hand-feeding has also been used to break the cycle in some infected nurseries. This practice does carry the risk of transferring this infection to naive individuals.

 

Management in the face of an outbreak

The primary goal in the midst of an outbreak is to halt the movement of avian polyomavirus in the nursery by using “all in/all out” principles:

  • DO NOT allow new chicks to enter the epicenter of the die-off.
  • DO restrict traffic flow into and out of the nursery.
  • DO stop air recirculation.
  • DO introduce foot baths and clothes changing stations at the nursery’s entry.
  • DO institute strict sanitation practices within the nursery and between nursery bins.
  • DO NOT stir up dust or debris into the air.
  • DO pay careful attention to hand-feeding protocols (since there is potential for transfer of APV).
  • DO introduce new arrivals from the aviary into a biosecure nursery distant from the current nursery. DO tightly control all traffic into this new, secondary, biosecure area.

Summary

APV Type 1APV Type 2
SignalmentBudgerigar parakeetNon-budgerigar psittacines
TransmissionVertical or horizontalHorizontal only
Clinical pictureVARIABLE clinical signs
Latent infections common

Feather dystrophy
Gastrointestinal signs
Cerebellar disease
Bleeding
Hepatomegaly
Ascites
Susceptible species DIE
Peracute illness is sometimes observed:


Gastrointestinal signs

Bleeding
Hepatomegaly
Ascites
DiagnosisPCR
Serologic titer
PCR

References