Continued from page 1Etiology of PDD
Since its initial description in the late 1970's, multiple etiologies have been proposed for the lymphoplasmacytic ganglioneuritis described as PDD. Adenovirus-like particles were demonstrated within intranuclear inclusion bodies in the cells lining the kidneys of one affected bird. 17
Paramyxovirus-like viral particles were demonstrated within inclusion bodies located in the neural cells of the spinal cord and in visceral nerve ganglia of another. 2,18,19 Similar inclusion bodies have been described in the nerves of pigeons with paramyxovirus infections. 1 Birds with PDD have been shown to lack detectable levels of antibodies to paramyxovirus (serotypes 1, 2, 3, 4, 6 and 7), Pacheco's disease virus (an avian herpesvirus), avian polyomavirus and avian encephalitis virus. 3,8
Because an infectious agent had not been recovered from affected birds, it was suggested that the observed changes in the nerves may be a result of an autoimmune process. 2 However, most autoimmune diseases that affect nerves cause demyelination which is uncommon in birds with PDD.
An eastern equine encephalomyelitis (EEE) virus was recovered from neonates with abdominal distention from an aviary with a history of PDD. The disease in these neonates was termed avian viral serositis. This finding was used to suggest that PDD may be caused by EEE virus, 20 even though EEE virus occurs primarily in the eastern portion of the United States, and PDD has been shown to occur throughout the United States, Canada and Europe. Our experimental studies have shown that PDD is not caused by EEE virus. 21 The lymphoplasmacytic ganglioneuritis that characterizes PDD can be induced when susceptible adult psittacine birds are given a tissue homogenate, derived from affected birds, which contains an enveloped virus approximately 80 nm in diameter.22 A DNA probe derived from the RNA of this virus can be used to demonstrate the presence of target nucleic acid in the tissues from birds with naturally or experimentally acquired PDD. With further study, this finding may lead to the availability of a test to detect birds which are shedding the PDD virus prior to the development of overt clinical signs.
The presence of lymphoplasmacytic ganglioneuritis and variable clinical signs (GI only, CNS only or GI and CNS ) have led several researchers to propose that PDD might be caused by more than one etiologic agent. Our studies suggest that the same virus containing inoculum can cause varying clinical changes even within birds of the same species. Additionally, a morphologically similar virus has been recovered from the tissues or excrement of birds that were diagnosed by crop biopsy with PDD, even though some of these naturally affected birds had predominately CNS signs, some had gastrointestinal signs and some had both.
We have also been able to demonstrate that PDD can have an extremely variable incubation period which can range from 1 week to 3 months. Further research is necessary to determine why some birds develop an acute form of the disease and die within 2 to 4 weeks while others develop a persistent form of the disease and survive for months to years. Additionally, further research will be necessary to determine why some birds infected with the same virus suspension develop varied clinical signs involving the gastrointestinal tract, the CNS or both.
Therapy and Prevention
Proventricular dilatation disease can occur in any aviary despite excellent hygiene, valid quarantine procedures and the absence of new additions to the flock. In some aviaries, numerous cases of PDD will occur simultaneously. In others, several affected birds may die, and the problem seemingly resolves, only to reappear 1 to 2 years later. 20 In a group of mixed species of wild-caught psittacine birds exposed to a bird confirmed by histopathology to have PDD, signs of disease were not noted in contact birds for up to a year following exposure. 14
In other cases, a single bird in a breeding pair may die, with no subsequent losses in the aviary even 4 to 5 years later. It is common for many birds exposed directly or indirectly to an affected bird to remain asymptomatic.
Mates, offspring or siblings of birds that are diagnosed microscopically with PDD should be considered at extra risk of developing the disease; however, they should not be euthanized. Many of the birds that are directly exposed to those with PDD never develop the disease. Until appropriate preventative measures can be developed, it would be prudent to place exposed birds in single bird households where they have no direct or indirect exposure to other birds.
Provided with an easily digested high energy diet, a stress-free environment and treatment for secondary bacterial or fungal infections, affected companion birds can survive for months or years. Any bird with the disease that is being treated should be placed in strict isolation with no direct or indirect contact with other birds. Some birds with clinical changes suggestive of PDD have been reported to recover when provided supportive care. However, a positive diagnosis of this disease requires the demonstration of microscopic lesions in the nerves and none of the reported recoveries have been in birds confirmed to have PDD.
Currently, there is no specific therapy for PDD. Some clinicians report that birds with suspicious clinical changes respond favorably to interferon. 14 The long-term prognosis in birds that do not respond to this therapy remains poor with death occurring in affected birds from emaciation, secondary infections, autointoxication or CNS disturbances. Nucleic acid probes show promise for detecting birds which are shedding viral nucleic acid in their excrement and studies are ongoing to document the sensitivity and specificity of this test as a screening tool to detect infected birds.
Acknowledgments
Major contributions that have allowed our research group to continue work on PDD have been provided by the Cowan Avian Health Foundation, the International Avian Research Foundation, Dr. Joe and Sue Still, Loro Parque Fundacion, Zoo Atlanta, Riverbanks Zoological Park, Veterinary Medical Experiment Station, Terry Clyne, Dr. Richard and Luanne Porter, Bobbi Brinker, Knick Enterprises, The National Aviary in Pittsburgh, International Aviculturist's Society, Midwest Avian Research Exposition, The Pet Care Trust, Aiken Bird Club, Jacksonville Avicultural Society, BERD Club, Georgia Cage Bird Society and Zeigler Brothers Inc. Hunderds of other bird clubs, aviculturist and veterinarians have also made contributions to help stop PDD.
REFERENCES
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2. Graham DL: Infiltrative splanchnic neuropathy, a component of the "wasting macaw" complex. Proc Assoc Avian Vet, pp 275, 1984.
3. Hughes E: The pathology of myenteric ganglioneuritis, psittacine encephlomyelitis, proventricular dilatation of psittacines, and macaw wasting syndrome. Proc 33rd West Poult Dis Conf, pp 85-87, 1984.
4. Clark FD: Proventricular dilatation syndrome in large psittacine birds. Avian Dis 28:813-815, 1984.
5. Phalen DN: An outbreak of psittacine proventricular dilatation syndrome (PPDS) in a private collection of birds and an atypical form of PDS in a nanday conure. Proc Assoc Avian Vet, pp 27-34, 1986.
6. Turner R: Macaw fading or wasting syndrome. Proc 33rd West Poult Dis Conf, pp 87-88, 1984.
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9. Gregory CR: Proventricular dilatation disease, In Ritchie BW (ed): Avian Viruses: Function and Control. Lake Worth, Wingers Publishing. 1995, pp 439-448.
10. Gerlach H: Viruses, In Ritchie BW, Harrison GJ, Harrison LR (eds): Avian Medicine: Principles and Application. Lake Worth, Fl, Wingers Publishing, Inc. 1994, pp 862-948.
11. Daoust PY, Julian RJ, Yason CV, et al: Proventricular impaction associated with nonsuppurative encephalitis and ganglioneuritis in two Canada Geese. J Wildl Dis 27:513-517, 1991.
12. Gregory CR, Latimer KS, Niagro FD, et al: A review of proventricular dilatation syndrome. J Assoc Avian Vet 8:69-75, 1995.
13. Graham DL: Wasting/proventricular dilation disease: A pathologist's view. Proc Assoc Avian Vet, pp 43-44, 1991.
14. Bond MW, Downs D, Wolf S: Screening for psittacine proventricular dilatation syndrome. Proc Assoc Avian Vet, pp 92-97, 1993.
15. Doolen M: A low risk diagnosis for neuropathic gastric dilatation. Proc Assoc Avian Vet, pp 193-196, 1994.
16. Gregory CR, Latimer KS, Campagnoli RP, et al: Histologic evaluation of the crop for diagnosis of proventricular dilatation syndrome in psittacine birds. J Vet Diag Invest 8:76-80, 1996.
17. Heldstab A, Morgenstern D, Ruedi A, et al: Pathologie einer endemieartig verlaufenden neuritis im magen/darmberich bei groBpapageien. Int Symp Zoo Animal, pp 317-324, 1985.
18. Busche R, Frese K, Weingarten M: Zur pathologie des macaw wasting-syndromes. Int Symp Zoo Animal, pp 325-329, 1985.
19. Mannl A, Gerlach H, Leipold R: Neuropathic gastric dilatation in Psittaciformes. Avian Dis 31:214-221, 1987.
20. Gaskin JM, Homer B, Eskelund K: Preliminary findings in avian viral serositis. A newly recognized syndrome of psittacine birds. J Assoc Avian Vet 5:27-34, 1991.
21. Ritchie BW: Avian Viruses: Function and Control. Lake Worth, Wingers Publishing, 1995, pp 379-411.
22. Gregory CR, Latimer KS, Niagro FD, et al: Characterization of a virus like particle observed in tissues from psittacine birds affected with proventricular dilatation syndrome. Southeastern Conf Avian Dis, 1996.
Psittacine Disease Research Group
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