Avian and Exotic Animal Medicine
with a passion!
with a passion!
Polyoma Virus
by Susan Horton, DVM
History
First described as Budgerigar fledgling disease in 1981, was called papovavirus
It is a nonencapsulated DNA particle
Avian polyoma viruses are apparently worldwide, but presentation of the disease is different between species
Effects Budgerigars, nonbudgerigar psittacines, finches and gallinaceous species
Clinical Features
Budgerigars
Nonbudgerigar psittacine birds
Passeriformes
Epizoology
All species should be considered susceptible to polyomavirus.
Most commonly effected species include young budgerigars, macaws, conures, Eclectus parrots, lovebirds, ring-necked parakeets, and caiques
First described as Budgerigar fledgling disease in 1981, was called papovavirus
It is a nonencapsulated DNA particle
Avian polyoma viruses are apparently worldwide, but presentation of the disease is different between species
Effects Budgerigars, nonbudgerigar psittacines, finches and gallinaceous species
Clinical Features
Budgerigars
- Feather abnormalities: reduced formation of down (Head and neck), contour feathers, and flight feathers; these birds are older then 15 days (runners, French molt)
- Develop normally for 10-15 days, then die
- Abdominal distension, hemorrhage under the skin, neurologic signs: ataxia, tremors of head and neck
- Mortality rates vary dependent on age of bird at time of exposure to virus
- Embryonic death
Nonbudgerigar psittacine birds
- Peracute death with no signs (most common in young birds)
- Acute infections: 12 to 24 hour period of clinical changes such as depression, anorexia, weight loss, delayed crop emptying, regurgitation, dehydration, diarrhea, polyuria, difficulty breathing, bleeding under the skin followed by death
- Subcutaneous hemorrhage over the crop and across the cranium-common in larger psittacines (any disease causing vasculitis, clotting disorders or damage to the liver)
- Yellowish urates
- Increased LDH, AST, AlkPhos
- Eclectus parrots may also exhibit gastrointestinal stasis, melena, hematuria, and abdominal pain
- Chronic form (Europe ): Weight loss, intermittent anorexia, polyuria, poor feather formation, and recurrent bacterial or fungal infections. Renal failure may follow
Passeriformes
- Acute death (fledglings, adults)
- Beak abnormalities (fledglings)
Epizoology
All species should be considered susceptible to polyomavirus.
Most commonly effected species include young budgerigars, macaws, conures, Eclectus parrots, lovebirds, ring-necked parakeets, and caiques
Birds considered naturally susceptible to avian polyomavirus
Psittaciformes
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Passeriformes
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Others
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Age Susceptibility/Mortality
Mortality rate with budgerigars less than 15 days may be as high as 100%, older birds range from 30-80%
Nonbudgerigar neonates are highly susceptible (parent or hand-raised)- usually signs show up at time of weaning; mortality rates from 31-41%
Older psittacine birds
Persistent Infections
These are individuals (budgies) that develop latent infections and shed virus periodically throughout their lives.
They are responsible for the persistence, transmission and spread of virus through budgie flocks as well as exposure to others.
Polyoma virus inclusion bodies can be detected in feathers, feather follicles and renal tissue in and may be protected in these areas from the neutralizing effects of antibodies.
Persistent (latent) infection has not been proven in other nonbudgie species.
Incubation
Budgerigars naturally exposed have peak mortality rates between day 15 and day 19
Incubation period in nonbudgie species has not been determined but is estimated to be as long as 14 days and as short as 2 days.
Transmission
Horizontal transmission- virus-contaminated feather dust, feces, urine, urates, respiratory secretions, crop secretions… Aerosolized virus: intranasal route of infection, ingestion
Vertically – Parent to offspring (infected embryos, Budgies only)
Pathology
In Budgerigars
In Nonbudgerigars
Immunity
Natural exposure to the virus can produce virus-neutralizing antibodies; titers usually decrease over a two to three month period
Diagnosis
Most accurate confirmation involves recovery of virus in cell culture from tissues of an infected bird
Electron microscopy
Four fold increase in antibody titer in paired samples
Specialized staining techniques of tissue sample
Detection of viral nucleic acid using polyoma-specific DNA probes (cloacal swabs)
DNA testing shows there is no correlation between active shedding of polyomavirus in feces and the titer of neutralizing antibodies… 98.2 % sensitivity, 100% specificity
Prevention and Control
Reduce exposure to virus
Sound hygienic practices
Disinfectants found to experimentally inactivate avian polyoma and their sources
Agent Active ingredient Dilution
Synphenol Synthetic phenol 1:256
Clorox Sodium hypochlorite 1:10
Dent-A-Gene Stabilized chlorine dioxide 1:400
Alcohol Ethanol 70% Undiluted
Treatment
To date, there is no effective treatment
Interferon, acyclovir and AZT have been tried, may show some promise.
Seriously effected birds need intensive supportive care
Vaccination
Adults (at risk breeding birds, birds going to shows)
Immature birds
Companion birds
References
Mortality rate with budgerigars less than 15 days may be as high as 100%, older birds range from 30-80%
Nonbudgerigar neonates are highly susceptible (parent or hand-raised)- usually signs show up at time of weaning; mortality rates from 31-41%
Older psittacine birds
- Can seroconvert and may be clinically normal (budgies over one month, and over five months of age in others)
- Exceptions seem to be Eclectus, caiques, grass parakeets and cockatoos
Persistent Infections
These are individuals (budgies) that develop latent infections and shed virus periodically throughout their lives.
They are responsible for the persistence, transmission and spread of virus through budgie flocks as well as exposure to others.
Polyoma virus inclusion bodies can be detected in feathers, feather follicles and renal tissue in and may be protected in these areas from the neutralizing effects of antibodies.
Persistent (latent) infection has not been proven in other nonbudgie species.
Incubation
Budgerigars naturally exposed have peak mortality rates between day 15 and day 19
Incubation period in nonbudgie species has not been determined but is estimated to be as long as 14 days and as short as 2 days.
Transmission
Horizontal transmission- virus-contaminated feather dust, feces, urine, urates, respiratory secretions, crop secretions… Aerosolized virus: intranasal route of infection, ingestion
Vertically – Parent to offspring (infected embryos, Budgies only)
- In Budgerigars- horizontally and vertically; ie both among members of the flock and between parent and offspring.
- In Nonbudgerigars-Just horizontally
Pathology
In Budgerigars
- Hydropericardium
- Cardiomegally
- Hepatomegally with multifocal yellow-white foci
- Ascites
- Splenomegally
- Hemorrhage under the skin, of the intestines and heart
- Feather dystrophy
- Histologically there is atrophy of the lymphoid tissue in the spleen and cloacal bursa; inclusion bodies can be found in most tissues
In Nonbudgerigars
- Clear fluid in the abdominal cavity
- Small, pale spleen
- Congested, hemorrhagic liver
- Splenomegally
- Pale, swollen kidneys
- Pale cardiac and skeletal muscles
- Feather dystrophy (rare)
- Ascites
- Hemorrhage under the skin and over any serosal surface
- Histologically there is hepatic necrosis, lymphoid depletion of the cloacal bursa, and membranous glomerulopathy
- Intranuclear inclusion bodies can be found in spleen and liver tissue most often
Immunity
Natural exposure to the virus can produce virus-neutralizing antibodies; titers usually decrease over a two to three month period
Diagnosis
Most accurate confirmation involves recovery of virus in cell culture from tissues of an infected bird
Electron microscopy
Four fold increase in antibody titer in paired samples
Specialized staining techniques of tissue sample
Detection of viral nucleic acid using polyoma-specific DNA probes (cloacal swabs)
DNA testing shows there is no correlation between active shedding of polyomavirus in feces and the titer of neutralizing antibodies… 98.2 % sensitivity, 100% specificity
Prevention and Control
Reduce exposure to virus
Sound hygienic practices
- Virus is shed in feces, urine, and feather dust
- Good disinfectants are Avinol-3 (Synthetic phenol), Clorox (Sodium hypochlorite), Dent-A-Gene (Stabilized Chlorine dioxide), and Alcohol (ethanol 70%)
- Nursery is cleaned and disinfected regularly
- Limited visitors
- Quarantine all new birds for 60-90 days
- Do not accept or ship unvaccinated birds
- Budgies are not in same airspace as other neonate psittacines
- Use biosecure shipping containers to prevent exposure
- Ship only weaned birds
- No Visitors in the Nursery
- Do not return neonates to nursery that have been exposed to other birds
- Separate feeding instruments for each bird
- Do not replace feeding utensil into common food container
- Vaccinate susceptible adults and neonates
- Do not ship unvaccinated birds
Disinfectants found to experimentally inactivate avian polyoma and their sources
Agent Active ingredient Dilution
Synphenol Synthetic phenol 1:256
Clorox Sodium hypochlorite 1:10
Dent-A-Gene Stabilized chlorine dioxide 1:400
Alcohol Ethanol 70% Undiluted
Treatment
To date, there is no effective treatment
Interferon, acyclovir and AZT have been tried, may show some promise.
Seriously effected birds need intensive supportive care
Vaccination
Adults (at risk breeding birds, birds going to shows)
- Vaccinated during nonbreeding season
- Series of 2 vaccinations, 2 to 3 weeks apart
- During the vaccination process, it is expected that 2 to 4 % of the breeding population will also be found to have serious pre-existing medical problems (even in best managed aviaries)
Immature birds
- In general, vaccination is started 4 weeks prior to weaning
- Series of 2 vaccinations 2 to 3 weeks apart
- Last vaccination 2 weeks before shipping
- If aviary has a history of polyoma disease, start vaccination at 40 to 50 days of age
- If having an outbreak, vaccine can safely be given at 20 days of age; these birds are boostered 2 additional times, 2 to 3 weeks apart
- Original certificate of vaccination should be sent with bird
Companion birds
- If kept in complete isolation, not necessary
- Dr. Ritchie points out that if the bird or it’s keeper leaves the home to go to the groomer, veterinarian, club meetings or anywhere else where direct or indirect exposure might occur, vaccination is not a bad idea.
- It is interesting to note that we protect our dogs and cats who are maintained in relative isolation with yearly boosters against common viruses
References
- Ritchie BW. Avian Viruses: Function and Control. Wingers Publishing, Inc., Lake Worth , Florida . 1995. Pp136-170
- Ritchie BW, Niagro FD, Latimer KS , et al: Avian Polyomavirus. An overview. J Assoc Avian Vet 5:147-153, 1991
- Clubb SL, Davis RB: Outbreak of papova-like viral infection in a psittacine nursery-a retrospective view. Proc Assoc Avian Vet, 1984, pp 121-129.
- Niagro FD, Ritchie BW, Lukert PD, et al: Avian Polyomavirus: Discordance between neutralizing antibody titers and viral shedding in an aviary. Proc Assoc Avian Vet, 1991, pp22-26.
