Make your own free website on

The following article was published in the Z.A.P. newsletter -- an excellent newsletter providing up-to-date information on avian health & diseases.  Should you wish to subscribe to this newsletter, please contact Elaine at ZAP96EK

Use of an Inactivated Virus Vaccine to Control Polyomavirus Outbreaks in Nine Flocks of Psittacine Birds

Branson W Ritchie, DVM, PhD; Samuel B. Vaughn, DVM; Judy St. Leger, DVM; Gregory A. Rich, DVM; Dave J. Rupiper, DVM; Gina Forgey, DVM; Cheryl B. Greenacre, DVM; Kenneth S. Latimer, DVM, PhD; Denise Pesti, MS; Raymond Campagnoli, MS; Phil D. Lukert, DVM, PhD

Polyomavirus infection is a major cause of death in young psittacine birds. Use of an inactivated polyomavirus vaccine can help control outbreaks of polyomavirus infection among flocks of psittacine birds.

Nine flocks of psittacine birds were examined because of sudden death of neonates in each of the flocks. Adult birds in flock I had been purchased from multiple sources during a 2-year period and were congregated in a single location. The flock consisted of approximately 230 birds, including African grey parrots (Psittacus erithacus), macaws (Ara spp), conures (Pyrrhura spp and Aratinga spp), Amazona spp, cockatoos (Cacatua spp), eclectus parrots (Eclectus roratus), cockatiels (Nymphicus hollandicus), lovebirds (Agapornis spp), rosellas (Platycercus spp), Psittacula spp, Quaker parakeets (Myiopsitta monachus), parrotlets (Forpus spp). Polytelis spp, Neophema spp, Psephotus spp, lorikeets (Trichoglossus spp), and Pionus spp, most of which were maintained in breeding pairs in an indoor/outdoor aviary. Birds were not quarantined Or examined by a veterinarian prior to introduction to the flock. The aviary nursery was contained within a modified kitchen/den area of a house.

During 1993 and 1994, the flock experienced an outbreak of psittacine beak and feather disease (PBFD), which was traced to introduction of a group of infected lovebirds to the facility. The outbreak was controlled by use of a PBFD virus-specific DNA test to detect and remove persistently infected birds.

Nursery management was also changed, and the aviary was maintained as a closed flock and did not have any substantial health problems for 1.5 years. During the winter of 1995, however, approximately 12 neonatal (6- to 10-weeks-old) birds died during a 2-week period. Because of unusually cold weather, the aviculturist assumed that the deaths were weather related. During the subsequent week, however, approximately 7 additional chicks died, and the aviculturist requested that a necropsy be performed on a blue-and-gold macaw (Ara ararauna) chick and a blue-crowned conure (Aratinga acaticaudata) chick that had died without premonitory signs. At necropsy, the chicks were considered to be of normal weight for their age. The crop of each chick was full. Dried food on the rhamphotheca and feathers around the face and neck of the macaw suggested that this chick had regurgitated prior to death. Petechial to ecchymotic hemorrhages were evident throughout the subcutis and on serosal surfaces of the heart, liver, and spleen. Other gross abnormalities included hepatomegaly, splenomegaly, and pale kidneys. Histologic abnormalities included multifocal to coalescing hepatocellular necrosis and rare discrete foci of necrosis in the spleen. The blue-and-gold macaw had large amphophilic intranuclear inclusion bodies in sections of the liver and spleen; inclusion bodies were not seen in sections from the blue-crowned conure. Polyomavirus nucleic acid was found by means of in situ hybridization in sections of liver and spleen from both birds, and a diagnosis of polyomavirus infection was made.

At this time, there were 27 chicks in the nursery. In addition, 2 siblings of the blue-and-gold macaw chick that died had been shipped to a pet retailer. In an effort to control a possible outbreak of polyomavirus infection, all disposable goods (eg, syringes, wood shavings, paper, goods) in the nursery were discarded, and durable goods (eg, enclosures, refrigerator, brooders) were cleaned and disinfected. Five swab specimens were then collected from various areas in the nursery and submitted for DNA testing for polyomavirus nucleic acid. While these results were pending, new chicks that hatched were placed in a temporary nursery in a separate house that did not house any other birds. A new brooder and supplies were used to equip this temporary nursery.

Swab specimens from the nursery were negative for polyomavirus nucleic acid, and no additional birds died during the next several weeks. However, even though there were no further changes in management, several neonatal birds in the original nursery and several chicks that were moved to the new nursery immediately after hatching died without premonitory signs. All of these birds had subcutaneous or serosal hemorrhages, and birds that were sent for histologic evaluation were confirmed to have polyomavirus infection. The 2 blue-and-gold macaw chicks that had been shipped to a pet retailer died, and within several weeks, 2 other neonatal birds in the pet shop also died. These 4 birds were all confirmed to have polyomavirus infection by means of in situ hybridization. The pet shop owner imposed a quarantine and cleaned and disinfected the bird room, which was separated by walls from the dry goods portion of the shop.

Continued death of birds in the original nursery along with death of birds transferred to the new nursery and an inability to detect polyomavirus nucleic acid in swab specimen from the old nursery suggested 3 possibilities: the nursery had been adequately cleaned but there was subsequent shedding of the virus by a chick that was subclinically infected, the nursery had not been adequately cleaned and swab specimens were inadequate to detect environmental contamination or results were falsely negative, or neonatal birds were exposed to the virus through some other source than the nursery environment. On further questioning, the aviculturist revealed that approximately 1 month before the onset of the outbreak, an incubator had been purchased from an aviary that had gone out of business because of chronic polyomavirus-induced problems. Viral nucleic acid was detected in swab specimens from the incubator, therefore, at this time, eggs were no longer removed from nest boxes for artificial incubation, and chicks that were removed from nest boxes were placed in a third nursery and tended to by an aviculturist who did not have any direct or indirect contact with the affected flock.

During the period of this outbreak, an inactivated avian polyomavirus vaccine was approved for use by the USDA, and all birds in the flock were vaccinated. Birds weighing more than 200 were given 0.5 ml, SC, over the caudolateral third of the sternum; birds weighing less than 200 g were given 0.25 ml in the same location. Adult birds were vaccinated twice, with a 2-week interval between vaccinations. Neonatal birds were first vaccinated when they were 10 to 20 days old (birds expected to weigh < 200 g at maturity were vaccinated earliest) and were booster vaccinated 2 and 4 weeks later. A few neonatal birds that had been exposed to the virus-contaminated incubator died after the vaccination program was initiated, but no neonatal birds died more than 2 weeks after the last booster vaccination was given. Birds in the pet shop were also vaccinated, and no additional birds in this facility died. During the outbreak, 69 of 74 (93%) at-risk neonatal birds died, including 9 blue-and-gold macaws, 6 green-winged macaws (A chloroptera), 4 blue-crowned conures, 25 cockatiels, 1 yellow-naped Amazon parrot (Amazona ochrocephala auropalliata), 4 Princess of Wales parakeets (Polytelis alexandrae), 8 lovebirds, 6 rosellas, and 6 Bourke’s grass parakeets (Neophema bourkii). Twenty-three of 69 were examined histologically, and all 23 were confirmed to have died of polyomavirus infection.

The flock has produced more than 500 neonatal birds since the vaccination program was initiated, and only 1 six-week-old eclectus parrot has died of polyomavirus infection. This chick was produced by a hen that had been introduced to the flock without being quarantined or vaccinated. Fortunately, this was the only bird that died, even though approximately 40 young birds (in
various stages of the vaccination protocol) were in the nursery at the time. The eclectus hen was vaccinated and has since produced 6 healthy chicks. 

Flock 2 consisted of birds that had been obtained from multiple sources during a 10-year period and were congregated in a single location without being quarantined or examined by a veterinarian. The flock consisted of approximately 280 birds, including African grey parrots, cockatoos, macaws, conures, eclectus parrots, caiques (Pionites spp). Pionus spp, and Poicephalus spp, most of which were maintained in breeding pairs in an indoor/outdoor aviary. The flock had been moved to a newly constructed aviary starting in 1994, with the last birds being reintroduced to the flock in the summer of 1995. The nursery was maintained within a room in the building that housed the aviary.

In the fall of 1995, the aviculturist attended a bird fair and returned unsold chicks directly, to the nursery. Seven days later, chicks in the nursery began to die, and within 3 days, 21 of 92 (23%) chicks in the nursery died, including 1 blue-headed pionus (Pionus menstruus), 15 sun conures (A solstitialis), 2 blue-and-gold macaws, 1 military macaw (A militaris), and 2 African grey parrots. Polyomavirus infection was confirmed by means of in situ hybridization in 3 chicks. In an effort to control the outbreak, the facility was cleaned and disinfected, and all neonatal birds were vaccinated, starting as early as 20 days of age. Neonatal birds more than 35 days old when first vaccinated were booster vaccinated once; neonatal birds that were less than 35 days old when first vaccinated were booster vaccinated twice, 2 weeks apart. Eighteen of 70 chicks in the nursery at the time the vaccination program was initiated died, including 14 sun conures, 1 African grey parrot, and 3
eclectus parrots. However, no birds died of polyomavirus infection more than 2 weeks after the last booster vaccination was given. During the subsequent 6 weeks, adults in the breeding flock were vaccinated according to the manufacturers recommendations.

In all, this outbreak resulted in the death of 39 of 92 (42%) at-risk chicks. During the 18 months since the flock was vaccinated, breeding adults have produced 386 chicks, all of which were vaccinated against polyomavirus infection and remained healthy.

Flock 3 consisted of approximately 250 primarily wild-caught birds that had been slowly obtained during a 12-year period. Cockatoos, macaws, Amazona spp, African grey parrots, Pionus spp, Piocephalus spp, Quaker parakeets, and conures in this flock were maintained in breeding pairs in an outdoor aviary. Chick production was considered to be moderate until 1989, when the flock reached an 80% fertility rate, which was maintained through the 1992 breeding season, following the 1992 breeding season, adults were moved to an outdoor aviary and birds were housed by genem.

Early in the 1993 breeding season, neonatal birds began dying. Clinical signs included lethargy, crop stasis, bruising of the subcutis, and death within 48 hours. Chicks that developed any clinical sign of disease were moved to a separate room, footbaths were installed, and workers were instructed to wash their hands after handling neonatal birds and to use separate syringes to feed chicks. Additionally, incubator-hatched chicks were housed in a room separate from parent-hatched chicks. During the 1993 outbreak, 75 of 200 (38%) chicks died with clinical signs suggestive of polyomavirus infection including 18 blue-and-gold macaws, 14 military macaws, 9 severe macaws (A severa), 6 Hahn’s macaws (A nobilis), 6 umbrella cockatoos (cacatua alba), 5 Moluccan cockatoos (C moluccensis), 3 lesser sulphur-crested cockatoos (C sulphurea), 4 double yellow-headed Amazon parrots (A ochi-ocephala), 2 orange-winged Amazon parrots (A amazonica), 2 yellow-naped Amazon parrots. 2 red-lored Amazon parrots (A autumnalis), 1 African grey parrot, and 3 sun conures: approximately 90% of the neonatal birds that died were hatched in an incubator. Early during the 1994 breeding season. 36 of 140 (26%) chicks died with clinical signs suggestive of polyomavirus infection, including 3 blue-and-gold macaws, 3 military macaws. 3 severe macaws. 4 Hahn’s macaws, 2 umbrella cockatoos, 2 Moluccan cockatoos, 2 lesser sulphur-crested cockatoos, 2 double yellow-headed Amazon parrots. 3 blue-fronted Amazon parrots (A acstiva), and 12 conures. Mortality rates for incubator and parent-hatched chicks were similar. Starting with the first chick hatched during 1995, all neonatal birds were vaccinated at 21 days of age followed by booster vaccination 2 weeks later. During 1995, the flock produced approximately 100 chicks, none of which died of polyomavirus infection. In the fall of 1995, breeding birds were vaccinated without problems. The vaccination program was continued during the 1996 breeding season, and the flock produced approximately 180 chicks, none died of polyomavirus infection.

Flock 4 consisted of approximately 300 birds, including African grey parrots, macaws, cockatoos, conures, Amazona spp, and Psittacula spp, most of which were maintained in breeding pairs in 2 indoor facilities. The nursery for 1 facility was totally separate from the area where adult birds were housed, but all birds were cared for by the same personnel. The nursery for the second facility was in the same building as the area where adult birds were housed, and the only physical separation between adults and chicks was a door. This flock was not attended to by a veterinarian. In May 1995, the aviculturist sold several young blue-and-gold macaws at a local bird show. These birds died 3 to 5 days later; polyomavirus nucleic acid was detected by means of DNA testing in tissue samples collected at necropsy.

The aviculturist who sold these birds was contacted and informed that the birds died of polyomavirus infection. At that time, the 2 nurseries contained approximately 205 chicks, of which 83 (40%) died within the subsequent 30 days. The aviculturist then vaccinated all chicks in both nurseries and adults in both flocks. Chicks did not die more than 2 weeks after the last booster vaccination was given. During this outbreak, 94 of 205 (45%) at-risk chicks died. Since the outbreak, the aviculturist has vaccinated all chicks, starting at 35 to 40 days of age, and has successfully raised 310 chicks without any deaths attributable to polyomavirus infection.

Flock 5 consisted of 80 cockatiels and 8 cockatoos that were housed for breeding purposes in the aviculturist’s basement. The last birds, a pair of cockatiels, had been added in 1991. The flock was relatively healthy, except for unexplained deaths of several Moluccan cockatoo chicks during a 2- to
3-year period. Typically, 1 chick from a clutch of 2 to 3 would die. The aviculturist blamed these deaths on hand-feeding errors and repeatedly refused histologic evaluation of dead chicks. In 1995, all 3 Moluccan cockatoo chicks from a clutch developed ascites and severe respiratory disease. The first chick that developed these clinical signs did not respond to treatment and was euthanatized. Tissue samples were sent for histologic evaluation, and on the basis of gross findings at necropsy, the bird was suspected to have died of avian viral scrositis.1 However, histologic lesions suggested that this chick died of septicemia secondary to yolk sac infection. The adult Moluccan cockatoos produced 2 additional chicks, which developed ascites at 5 weeks of age. The chicks responded to antibiotic treatment for 2 weeks, but 1 developed malformation of the pin feathers, which were suggestive of PBFD. Results of DNA testing for PBFD virus were negative, however, polyomavirus nucleic acid was detected in a dystrophic feather.

The aviculturist was instructed to collect swab specimens for DNA testing from the cockatiel aviary, the kitchen where chicks were raised, and the cockatoo breeding area. Polyomavirus nucleic acid was detected in specimens from all 3 areas. Virus-contaminated areas were cleaned, and a flock vaccination program was instituted. Subsequently, there have not been any additional deaths
attributable to polyomavirus infection. Vaccinated chicks from this flock were transported to a bird fair, where they were apparently exposed to other birds infected with polyomavirus. Vaccinated chicks did not develop any clinical signs of disease, but a group of unvaccinated macaw chicks housed approximately 4.5 m away died of polyomavirus infection.

Flock 6 consisted of 6 pairs of macaws and 4 pairs of African grey parrots.  The last birds, a pair of macaws, had been added in 1991. The flock had few problems until 1993, when a blue-and-gold macaw chick that %vas purchased at a bird fair and housed in a pet shop owned by the aviculturist died of polyomavirus infection. Subsequently, 1 chick from each of 3 different clutches of blue-and-gold macaws housed in the pet shop died of polyomavirus infection, which was confirmed by means of in situ hybridization. Although the aviculturist was initially skeptical of the diagnosis, he did initiate a vaccination program for all neonatal birds after the third chick died of polyomavirus infection. The flock has produced 63 neonatal birds since the vaccination program was initiated, and there have not been any deaths in the nursery or pet shop attributable to polyomavirus infection.

Flock 7 consisted of 28 breeding cockatiels maintained in a room in the aviculturists home. This aviculturist practiced excellent hygiene and husbandry practices and had not added any new birds during a 5-year period. However, in March 1995, 8 cockatiel chicks died during a 2-week period, and in situ hybridization of samples from the last chick that died indicated that the chick died of polyomavirus infection. The flock was vaccinated in May 1995 and, during the 2 subsequent breeding seasons, produced 62 neonatal birds, none of which died of polyomavirus infection.

Flock 8 consisted of 408 breeding birds, including 140 African grey parrots, 60 macaws, 200 eclectus parrots, 4 conures, and 4 Leadbeater’s cockatoos (C leadbeateri). The flock was developed primarily from imported birds during a 15-year period: new birds had not been added to the flock during the previous 5 years. Breeding birds were maintained in an indoor/outdoor facility in hanging wire enclosures placed above a concrete pad. Most eggs were removed from nests and artificially incubated. A single mature imported jenday conure (A jandaya) introduced with a group of 40 pairs of sun and jenday conures died of polyomavirus infection in 1984. These conures were housed in a quarantine area that was completely separate from the established flock. When this conure died, the remaining 40 pairs of birds were removed from the premises. In 1991, results of DNA testing of random swab specimens from the aviary’s environment for polyomavirus nucleic acid and serologic screening of 4 recently weaned eclectus parrots for polyomavirus neutralizing antibodies were negative. The flock produced approximately 650 neonatal birds annually, 90% of which were eclectus parrots.

There were no additional polyomavirus-associated deaths in this aviary:  however, approximately 50 of 500 (10%) eclectus chicks that were sent to potentially polyomavirus-contaminated areas (eg. pet retailers and brokers) died of polyomavirus infections. A program for vaccination of eclectus chicks before they left the nursery was initiated, and none of approximately 450 properly vaccinated chicks (initial vaccination at 20 days of age, followed by 2 booster vaccinations or initial vaccination at 40 to 45 days of age, followed by 1 booster vaccination) subsequently died of polyomavirus infection. However, 8 eclectus chicks that were vaccinated at 20 days of age, given 1 booster vaccination at 34 days of age, and shipped to pet stores at 40 days of age died of polyomavirus infection.

Because new adults were not being added to the flock and there have not been any nursery problems attributable to polyomavirus infection, the aviculturist elected not to vaccinate adult birds. The aviculturist has been advised of the risk associated with polyomavirus amplifying in unvaccinated adult birds.  Flock 9 consisted of approximately 400 birds, including African grey parrots, macaws, conures, Amazona spp, cockatoos, and Poicephalus spp. The birds had been acquired during a 15-year period and were maintained as breeding pairs in covered outdoor aviaries. Adult and neonatal birds were frequently added to this flock. New birds were purchased from multiple sources and were congregated in a single area without being quarantined or evaluated by a veterinarian. The aviary also bought and sold thousands of smaller psittacine birds, including cockatiels, love-birds, and budgerigars. The nursery consisted of four 3 X 3.6-m rooms separated from areas that housed adult birds. Attempts were made to segregate neonatal birds into nursery, rooms by species; however, chicks produced by the flock were placed in the same nursery rooms as were chicks acquired from other breeders. Once in the nursery, chicks were maintained as clutches and kept in glass aquariums. Prior to 1995, the chick mortality rate had been considered too low to warrent necropsy of dead chicks.

In May 1995, several chicks developed delayed crop emptying that was unresponsive to treatment with fluids, antibiotics (piperacillin sodium and enrofloxacin), and an antifungal agent (nystatin). Mortality rate was highest in 3- to 7-week-old birds, and eventually, chicks in all 4 nursery rooms were dying. At this time, the aviculturist sought assistance, and intranuclear inclusion bodies suggestive of polyomavirus were demonstrated in tissue samples from a Moluccan cockatoo chick. A DNA test revealed polyomavirus nucleic acid in tissue samples from an affected scarlet macaw chick. Beginning in August 1995, all chicks that died were necropsied; many had serosal hemorrhages, hepatomegaly, and splenomegaly.

In the fall of 1995, a polyomavirus vaccination program was initiated. Adults were vaccinated according to the manufacturers recommendations. Chicks were vaccinated beginning at 14 to 25 days of age and received 1 to 3 booster vaccinations, 2 weeks apart. Approximately 8 conures died during the 2 weeks after the vaccination program was initiated, but no chicks died more than 2 weeks after the last booster vaccination was given. In all, 38 of 194 (20%) chicks between 2 and 7 weeks of age died.

During the 1996 breeding season, the flock produced 134 chicks, all of which were vaccinated. Chicks purchased from other breeders were placed in a separate room and were vaccinated at least once. Despite these changes, 3 incompletely vaccinated chicks died of polyomavirus infection between 2 and 7 weeks of age. To minimize the risk that birds purchased from multiple sources would continue to serve as potential sources of polyomavirus, the aviculturist began to require that all chicks accepted for hand feeding be fully vaccinated against polyomavirus. Using this strategy, the aviculturist has added approximately 150, vaccinated chicks to the nursery, without any additional polyomavirus associated deaths.

In 1997, flock production was typical, and none of the chicks in the nursery died of polyomavirus infection. However, a few Senegal parrot (Piocephalus senegalus) chicks less than 2 weeks of age died of polyomavirus infection while still in the nest box. In discussions with the aviculturist, it was
determined that nest boxes in which affected chicks hatched had not been changed since the initial outbreak in 1995, and polyomavirus nucleic acid was detected by means of DNA testing in swab specimens from the nest boxes. Nest boxes were replaced, and this pair of Senegal parrots successfully fledged 7 chicks. To prevent further problems associated with persistence of polyomavirus in the aviary, an environmental monitoring program was initiated, and all new breeding birds were vaccinated during a 6-month Quarantine period before being introduced into the aviary.

For more than 13 years, polyomavirus infection has been a major cause of death in young psittacine birds and a frustrating problem for aviculturists and veterinarians because of difficulties in controlling spread of the causative virus. The recently approved inactivated polyomavirus vaccine is an important tool for preventing polyomavirus-associated death of psittacine birds, and experiences from the 9 flocks described in this report suggest that the vaccine will be useful for controlling outbreaks of polyomavirus infection among flocks of companion birds.

Vaccination programs for controlling polyomavirus infection in birds are similar to those used to control other viral diseases in companion animals. Neonatal birds should be vaccinated to reduce their susceptibility to infection. Adult birds should be vaccinated to decrease the population of birds at risk for development of infection and reduce the likelihood that a progressive cycle of transmission among adult birds will develop. This, in turn, lessens the chances that adult birds will serve as a source of virus for neonatal birds.

Polyomavirus is environmentally stable and is most often introduced into an aviary through careless management practice, such as bringing new birds into the flock without an appropriate quarantine period, bringing birds from other aviaries into the nursery, and allowing visitors with direct or indirect contact with birds access to the nursery. If polyomavirus is introduced to an aviary nursery from an outside source, as probably occurred in flocks I and 9, it is possible for the virus to spread to unvaccinated adults. The likelihood that polyomavirus will spread from chicks in the nursery to adults in the breeding aviary, or vice versa, is higher when the nursery is in the middle of the breeding facility, food preparation and storage areas are in the same airspace as the nursery, and the same personnel care for neonatal birds and adults.

Although vaccination can play a pivotal role in reducing the incidence of polyomavirus infection in birds, no vaccine is 100% effective. Thus, vaccination programs should not be considered as a substitute for good management and hygiene. As was evident in the flocks in this report, controlling a polyomavirus outbreak requires vaccinating adult and neonatal birds, as well as cleaning and disinfecting the contaminated facility. In addition, instituting a vaccination program during a polyomavirus outbreak will decrease the mortality rate; however, some neonatal birds may still die until flock immunity is sufficiently high, generally 2 to 3 weeks after the last booster vaccination is given.

Although the vaccine manufacturer-does not recommended vaccinating a flock during the breeding season, experiences from the flocks in this report suggest that vaccination programs can be used to help stop an outbreak even while birds are breeding. Many adult birds from flocks 1, 2, 3, 4, and 9 were incubating eggs, feeding chicks, or preparing nest boxes at the time they were vaccinated and resumed normal activities immediately after vaccination. Several pairs of birds produced fertile eggs within 2 weeks after being vaccinated.

The vaccine’s manufacturer recommends that birds be at least 35 to 40 days of age before being vaccinated; however, results from this report suggest that chicks could be safely vaccinated at 10 to 20 days of age. Chicks first vaccinated when they are less than 35 to 40 days of age should receive 2 booster vaccinations 2 to 3 weeks apart. A bird should receive the last booster vaccination at least 2 weeks before leaving the aviary.

We suspect that environmentally stable polyomavirus was introduced to flock 1 through a contaminated incubator. The aviculturist who managed this flock had not added any birds following a PBFD virus outbreak and did not consider acquisition of equipment from another aviary to be a breach of the closed aviary concept.

As with other inactivated virus vaccines, inactivated polyomavirus vaccine should not be expected to help or hurt birds that are already infected at the time of vaccination. Some of the chicks in flocks 1, 2, 4, 8, and 9 were exposed to polyomavirus before a vaccination program was initiated and died several days to several weeks after being vaccinated. Although such deaths were unfortunate, they were not unexpected, and most likely resulted from infection of birds prior to vaccination.

Results for these flocks suggest not only that the vaccine is efficacious, but also that it is safe, even when used during an outbreak. On the basis of previously reported seroprevalence studies, 1-7 we would suspect that between 10 and 63% of adult birds in these flocks had been infected with polyomavirus prior to vaccination. However, vaccination did not induce immediate or delayed adverse systemic reactions in any of approximately 4,500 vaccinates, many of which were followed up for 2 years after vaccination. The type and prevalence of adverse local reactions were similar to those reported by other investigators 3,4,8 who conducted field trials to evaluate the safety of the vaccine. The few local reactions that did develop resolved without treatment and were considered to be unimportant by the aviculturists and attending veterinarians.

Because most at-risk birds discussed in this report were vaccinated, there were no unvaccinated control birds, making it impossible to definitively determine what role vaccination had in controlling these outbreaks. However, several findings suggest that vaccination altered the course of outbreaks, for instance, after birds in flock 1 were vaccinated, a single eclectus parrot chick produced by an unvaccinated hen died of polyomavirus infection, but approximately 40 vaccinated neonatal birds that were potentially exposed to this chick remained clinically normal. This mortality rate of 2.5% (1/40) was substantially less than that in previous reports 9,10 (27 to 41%) and in the flocks described in this report (10 to 93%). Additionally, after this eclectus parrot hen was vaccinated, it produced 6 chicks, none of which died of polyomavirus infection. In flocks 3, 5, 6, 8, and 9, polyomavirus infections had been causing death of chicks for multiple years. After a vaccination
program was initiated, however, polyoma associated deaths stopped or were dramatically reduced. In flock 8, chicks properly vaccinated and shipped to an apparently contaminated area remained clinically normal, but chicks shipped to the same location before completing the Vaccination protocol died. In flock 9, fully vaccinated chicks remained clinically normal, but chicks hatched in a contaminated nest box or chicks potentially exposed to virus prior to vaccination died.

When all 9 flocks in this report are considered together, the mortality rate for at-risk chicks prior to initiation of vaccination programs was 29% (422/1,474). After the outbreaks were controlled, the cumulative mortality rate for chicks that were partially vaccinated was only 1% (21/2,081). Fully
vaccinated chicks did not die of polyomavirus infection. Although these results are not conclusive, they do suggest that vaccination was useful in controlling polyomavirus infection in these flocks.

PBFD virus and polyomavirus DNA dectection assays are currently available through the Infectious Diseases Laboratory, Athens, GA.  Polyomavirus in situ hybridization is currently available thorugh the Infection Diseases Laboratory, Athens, GA. Autogenous avian polyomavirus vaccine, Biomune, Inc., Lenexa, KA.  Avian polyomavirus vaccine, Biomune, Inc. Lenexa, KA


1. Ritchie, BW, Carter K. Togaviridae. In: Avian VIruses: function and control, Lake Worth, FL: Wingers Publishing Inc., 1995:379-411.
2. Schmidt RE, Geographic pathology of pet avian diseases, in Proceedings, Assoc. Avian Vet Annu. Meet 1997; 11-22
3. Ritchie BW, Niagro FD, Latimer KS, et al. an inactivated avian polyomavirus vaccin is safe and immunogenic in various psittaciformes. Vaccine 1996; 14; 1103-1107
4. Ritchie BW, Latimer KS, Leonard J. et al. Safety, immunogenicity and effacy of an inactivated avian polyomavirus vaccine. AmJVet Res 1998; 59; 143-148
5. Ritchie BW. Pritchard N. Pesti D, et al. Susceptibility of avian polyomavirus to inactivation. J Assoc Avian Vet 1993:7;193-195.
6. RItchie BW, Carter K. Papovaviridae. In: Avian viruses: function and control. Lake Worthl FL. Wingers Publishing Inc. 1995: 127-170
7. Wainwright PO, Lukert PD, Davis RB, et al. Serological evaluation of some psittaciformes for budgerigar fledgling disease virus. Avian Dis 1987; 31;673-676.
8. Ritchie BW, Niagro FD, Latimer KS, et al. Antibody response and local reactions to adjuvanted avian polyomavirus vaccines in psittacine birds. J Assoc Avian Vet 1994; 8:21-26.
9. Jacobson ER, Hines SA, Wuesenberry K, et al. Epornitic of papova-like virus-associated disease in a psittacine nursery. J Am Vet Med Assoc 1984:185:1337-1341.
10. Clubb SL, Davis RB, Outbreak of papova-like viral infection in a psittacine nursery - a retrospective view, in Proceedings. Assoc Avian Vet Annu Meet 1984: 121-129.


wpe2.jpg (1473 bytes)