Proventricular Dilitation Syndrome

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Reprinted in part from material submitted for publication to the Journal Association of Avian Veterinarians

Summary: Involvement of central and peripheral nervous tissues with lymphoplasmacytic inflammatory infiltrates is characteristic of proventricular dilatation syndrome (PDS). An etiologic agent has not been found for PDS, although recent findings are increasing the likelihood that the syndrome is caused by a virus. Suspicion of PDS is based upon historical information, clinical signs and radiographic evidence of proventricular enlargement or dysfunction. Definitive diagnosis of PDS requires the demonstration of characteristic lymphoplasmacytic infiltrates within nervous tissue. The syndrome cannot be diagnosed by clinical abnormalites or necropsy findings. Microscopic examination of the ventriculus, proventriculus, crop or brain of affected birds is currently the only way to confirm the syndrome.

late 1970's.1-5 Initially, the disease seemed to be limited to macaws. This fact, in conjunction with an unknown etiology, gave rise to the terms macaw wasting or fading syndrome, wasting macaw syndrome and gastric distension of macaws.5-7 As it became apparent that the disease occurred in psittacines other than macaws, a more general terminology was used to describe the syndrome, including proventricular dilatation, proventricular dilatation syndrome, psittacine proventricular dilatation syndrome, psittacine wasting syndrome, proventricular hypertrophy, proventricular dilatation of macaws or psittacines and proventricular dilatation disease.1,5,7-17 Various terminology also has been used to encompass the pathological features of this disease, including neuropathic gastric dilatation of Psittaciformes, myenteric ganglioneuritis, proventricular and ventricular myositis, psittacine encephalomyelitis and infiltrative splanchnic neuropathy.4,5,7,18

Various case reports have demonstrated lymphoplasmacytic inflammation in both central and peripheral nervous tissues, especially of the proventriculus and other digestive organs including crop, ventriculus and small intestine. Additionally, the possibility of sequelae other than proventricular dilatation, such as serositis and central nervous system (CNS) involvement without changes in the nerves of the ventriculus or proventriculus, has been reported.1,14,15 Myocarditis also has been observed.1,2,4,5,7,10,14,15,17,21,22

In the order Psittaciformes, PDS has been reported in more than 50 species, including members of families Cacatuidae (Cockatoos and Cockatiels) and Psittacidae (Lovebirds, Macaws, Parakeets, Parrots, Amazon Parrots, Conures). Pacific, South American and Afro-Asian species have been described with characteristic lesions. Some species of Psittaciformes are commonly affected (e.g.,Blue and Gold macaws, Ara ararauna; African Grey parrots, Psittacus erithacus ) but this may reflect a population bias rather than a species predisposition to PDS. Suggestive lesions also have been reported in two Canada Geese (Branta canadensis, Order Anseriformes),20 and spoonbills, toucans and weavers. (Dr. Robert Schmidt, personal communication) Other non-psittacine birds also may prove to be susceptible to this disease as improved tests are developed to accurately diagnose affected individuals (Table 1).

A review of available literature suggests a predisposition for adults (3:1, adults: juveniles) of both sexes (1:1, males: females). In a study of 127 birds diagnosed with PDS, birds of known age ranged from 10 weeks to 17 years (mean age= 3.8 years, median age= 2 years). Gender was determined in eighty-nine of these, with a ratio of 35 males to 54 females (0.6:1).22 A majority of affected birds were of undetermined gender and/or age; therefore, the above ratios may not accurately reflect the population parameters. Of 12 recent specimens diagnosed with PDS in the Department of Veterinary Pathology at the University of Georgia College of Veterinary Medicine (UGACVM), the ratios of adults to juveniles and of males to females approximates that reported in the literature.

The most common clinical signs of PDS include depression, weight loss (with or without decreased appetite), constant or intermittent regurgitation, and/or passage of undigested seeds in the feces indicating a malabsorptive or maldigestive disorder.1,5-12,14,15,17,18,21,23 Proventricular impaction,7,12 muscle atrophy,7,10,14 abdominal enlargement,6 lethargy,11,14,15,17 weakness,12,14,23 polyuria,9,10 diarrhea,9,15 scant feces9 or hypotension14 also have been reported in affected birds.

Concomitant CNS signs may include ataxia, abnormal head movements, seizures, and proprioceptive or motor deficits.1,6,8,10,14,15,,21,23 Some affected birds may only exhibit CNS signs.1,14,15 Of 89 birds described in the literature with confirmed PDS, 77 (86.5%) presented with one or more of the four most common clinical signs including depression, weight loss, regurgitation or passage of undigested seeds in the feces.

Clinical laboratory findings in PDS-affected birds are inconsistent. Hypoproteinemia,9,10,18,21 hypoglycemia,9 heterophilia1,9,14,17,21 and anemia9,10, 17,18 have been reported. Mycotic or bacterial opportunistic infections are common in affected birds and may complicate the laboratory picture.1,2,9,10,12,14,17

Survey and contrast radiographs are useful diagnostic techniques.4,9 Distension of the proventriculus and increased transit time of barium are common findings.1,9,10,12,14,24 Ultrasonic examination may be used to demonstrate dilatation and impaction of the proventriculus.8 Endoscopic examination may show impaction, ulceration, and dilatation of the proventriculus.10

Emaciation,1,11,15,20 pectoral muscle atrophy,7,10,14 and dilatation of the esophagus,1,6 proventriculus,1,6,7,10-12,14,15,17,20,21 ventriculus,7,10,12,20 or small intestine10,14,18 are observed commonly. The proventriculus may appear thin-walled and friable.6,9,11,15 None of the aforementioned physical, laboratory, radiographic or gross changes are pathognomonic for PDS. Microbial infections, parasitism, gastrointestinal obstructions, neoplasms, trauma, malassimilation disorders, toxin ingestion or malnutrition may cause similar changes and also must be considered.5,10,12,20,21 Presence of characteristic histopathological (microscopic) lesions in central and peripheral nervous tissues remains the most definitive diagnostic technique at present. 2

A presumptive diagnosis of PDS often is based on historical information, clinical signs, and radiographic evidence of proventricular dilatation or dysfunction. Antemortem biopsy of the ventriculus22,24 or post-mortem histologic evaluation of the proventriculus and ventriculus can be used to confirm the disease through the demonstration of lymphoplasmacytic ganglioneuritis.2 Antemortem techniques are invasive and potentially fatal in sick birds. Also, small biopsy samples may not contain affected nerve plexuses and may be non-diagnostic.24

In a study of 421 psittaciforme birds submitted for necropsy, sixteen (3.8%) had proventricular dilatation.11 Of these 16 birds, four (25%) had lymphoplasmacytic infiltrates in the proventriculus. In another study of 7 psittaciforme birds diagnosed with PDS, 100% had lymphoplasmacytic infiltrates in the proventriculus and 66% had similar infiltrates in the ventriculus.7 In addition, 100% had lymphoplasmacytic infiltrates in the pons, medulla, and midbrain, 47% in the cerebrum, and 16% in the cerebellum. Twenty-eight percent had cardiac lesions consisting of focal lymphocytic myocarditis and fibrosis. In a retrospective study of 10,640 pet, exotic, and wild birds necropsied over a 10-year period, 127 (1.2%) had diagnostic histopathological lesions consistent with PDS.22 Of 89 birds in the literature that had lymphoplasmacytic infiltrates in the proventriculus, 80 (89.9%) had proventricular dilatation and 67 (75.3%) had lymphoplasmacytic infiltrates and perivascular cuffing in the brain. At UGACVM, in 15 post-mortem specimens with lymphoplasmacytic infiltrates in the proventriculus, all had ventricular infiltrates, 73% had infiltrates in the heart, 67% had infiltrates in the brain, and 67% had proventricular dilatation.

The etiologic agent and pathogenesis of PDS are unknown. Some findings suggest that the disease is infectious.1,3,24,27 The disease may occur sporadically or may affect several psittacine birds in a group in a brief period of time.2,22,25 Disease does not develop in all exposed birds,1,22 which suggests that some birds have an innate resistance, develop a protective immune response, lack factors that are required for inducing the disease, possess factors which prevent development of the disease, or develop a carrier state. The disease apparently has subacute, acute and chronic stages; however, the majority of diseased birds die within several months to a year after developing clinical signs.1,3,10,14,15,17,18 Histopathological lesions are most consistent with an inflammatory response to viral infection.1,4,5,7,18,21,27 Viral isolation to date generally has been unsuccessful.2,6,7,11,21,27 Serum antibody titers to paramyxovirus types 1-4, 6, 7, avian herpesviruses, avian papovaviruses, and avian encephalitis virus have been negative.7,26

Initial isolates of Avian Viral Serositis (AVS) were from a group of various psittacine species from a single aviary with a history of PDS. The only reported association between the two diseases originates from this aviary. Three offspring were produced from a mating between a Blue and Gold macaw (Ara ararauna ) and a Military macaw (Ara militaris ).19 Of the three hybrid offspring, two died of lesions suggestive of AVS. The remaining sibling died of PDS approximately 8 months later.19 Based on this finding, it was speculated that AVS and PDS may be different manifestations of the same disease.19,30, 31 Birds with lesions suggestive of AVS and experimentally-infected chicks had lesions in the proventriculus, heart, and CNS that were histologically similar to those described with PDS.19 In addition, hepatocellular and bursal lymphoid necrosis, epicarditis, splenitis, and serofibrinous ascites were present in AVS-affected psittacine birds.19 Initial isolates from the AVS-affected birds were suggestive of a Togavirus19 and the isolate has been speculated to be a member of the Eastern encephalitis virus complex.31

Currently, there is no specific therapy for PDS; however, some clinicians report that birds with suspecious clinical changes respond favorably to interferon. 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.4 Until the virus that is likely to be causing this syndrome can be characterized, preventative measures such as quarantine of new birds, avoidance of direct or indirect contact between isolated groups of psittacine birds and appropriate hygiene seem prudent.

ACKNOWLEDGMENTS: Dr. Christopher Gregory is a clinical pathology resident at the University of Georgia College of Veterinary Medicine and is funded by Zoo Atlanta and Riverbanks Zoological Park. Additional major funding for PDS research has been provided by the Cowan International Avian Health Foundation, International Avian Research Foundation, International Aviculturists Society, Midwest Avian Research Exposition, Bird Clubs of Virginia, Inc. and the Association of Avian Veterinarians.

1. PHALEN DN: An outbreak of psittacine proventricular dilatation syndrome (PDS) in a private collection of birds and an atypical form of PDS in a Nanday Conure. Proc Assoc Avian Vet, Miami, FL, 1986, pp 27-34.

2. GERLACH S: Macaw wasting disease- a 4 year study on clinical case history, epizootiology, analysis of species, diagnosis, microbiological, and virological results. Proc Eur Chapt Assoc Avian Vet, Vienna, Austria, 1991, pp 273-281.

3. ROSSKOPF WJ, et al: Pet avian conditions and syndromes- an update. Proc Assoc Avian Vet, 1986, Miami, FL, pp 377, 392-393, 399.

4. MANNL A, et al: Neuropathic gastric dilatation in psittaciformes. Avian Dis 31:214-221, 1987.

5. GRAHAM DL: Infiltrative splanchnic neuropathy: a component of the "wasting macaw" complex. Int Conf Avian Med, Toronto, Canada, 1984, p. 275.

6. TURNER R: Macaw fading or wasting syndrome. Proc 33rd West Poultry Dis Conf, Davis, CA, 1984, pp 87-88.

7. HUGHES PE: The pathology of myenteric ganglioneuritis, psittacine encephalomyelitis, proventricular dilatation of psittacines, and macaw wasting syndrome. Proc 33rd West Poultry Dis Conf, Davis, CA, 1984, pp 85-87.

8. MALLEY DM: Case report: a case study of a Moluccan Cockatoo with proventricular dilatation. Proc Eur Chapt Assoc Avian Vet, Vienna, Austria, 1991, pp 271-272.

9. RIDGWAY RA, GALLERSTEIN GA: Proventricular dilatation in psittacines. Proc Assoc Avian Vet, San Diego, CA,1983, pp228-230.

10. DEGERNES LA, et al: Proventricular dilatation syndrome in a Green-Winged Macaw. Proc Assoc Avian Vet, Chicago, IL, 1991, pp 45-49.

11. CLARK FD: Proventricular dilatation syndrome in large psittacine birds. Avian Dis 28:813-815, 1984.

12. WOERPEL RW, ROSSKOPF WJ: Clinical and pathological features of macaw wasting disease (proventricular dilatation syndrome). Proc 33rd West Poultry Dis Conf, Davis, CA, 1984, pp 89-90.

13. WOODS L: Exotic avian disease trends seen at the California Veterinary Diagnostic Laboratory System: July 1988-July 1989. Proc Assoc Avian Vet, Seattle, WA, 1989, p. 220.

14. LUTZ ME, WILSON RB: Psittacine proventricular dilatation syndrome in an Umbrella Cockatoo. J Am Vet Med Assoc 198:1962-1963, 1991.

15. CAZAYOUX-VICE CA: Myocarditis as a component of psittacine proventricular dilatation syndrome in a Patagonian Conure. Avian Dis 36:1117-1119, 1992.

16. CLUBB SL: Appendix 2. Diseases of imported birds as related to country of origin and species. In Harrison GR and Harrison LR (eds.): Clinical Avian Medicine and Surgery. Philadelphia, WB Saunders Co, 1986, pp 656-657.

17. RICH G: Classic and atypical cases of proventricular dilatation disease. Proc Assoc Avian Vet, New Orleans, LA, 1992, pp 119-125.

18. JOYNER KI, et al: Encephalitis, proventricular and ventricular myositis, and myenteric ganglioneuritis in an Umbrella Cockatoo. Avian Dis 33:379-381, 1989.

19. GASKIN JM, et al: Preliminary findings in avian viral serositis: a newly recognized syndrome of psittacine birds. J Assoc Avian Vet 5:27-34, 1991.

20. DAOUST PY, et al: Proventricular impaction associated with nonsuppurative encephalomyelitis and ganglioneuritis in two Canada geese. J Wildl Dis 27:513-517, 1991.

21. SUEDEMEYER WK: Diagnosis and clinical progression of three cases of proventricular dilatation syndrome. J Assoc Avian Vet 6:159-163, 1992.

22.GRAHAM DL: "Wasting/proventricular dilatation disease" A pathologist's view. Proc Assoc Avian Vet, Chicago,IL,1991, pp 43-44.

23. SPENSER EL: Common infectious diseases of psittacine birds seen in practice. Vet Clin of N. Am/Small AnimPract 21:1227,1991.

24.BOND MW, et al: Screening for psittacine proventricular dilatation syndrome. Proc Assoc Avian Vet, Nashville, TN,1993,pp 92-97.

25. CLIPSHAM R: Trends in proventricular dilatation syndrome? J Assoc Avian Vet 3:73,1989.

26. WOERPEL RJ, ROSSKOPF WJ: Proventricular dilatation and wasting syndrome: myenteric ganglioneuritis and encephalomyelitis of psittacines: an update. Proc Intl Conf Avian Med, Toronto, Canada,1984, pp 25-28.

27. ROSSKOPF WJ, et al: Pet avian disease syndromes. Proc Assoc Avian Vet, Boulder, CO, 1985, pp 299-317.

28. BUSCHE R, et al: Zur pathologie des macaw wasting- syndroms. Internatl Symp Dis Zoo Anim, St. Vincent, Torino,1985, pp 325-329.

29. HELDSTAB A, et al: Pathologie einer endemieartag verlaufen neuritis im magen-darmberich bei grosspapageien. Internatl Symp Dis Zoo Anim, St. Vincent, Torino, 1985, pp 317-324.

30.GASKIN JM, HOMER BL: Some unofficial thoughts on Avian Viral Serositis. Proc Assoc Avian Vet, Chicago,IL,1991, pp 38-42.

31.GASKIN JM: Questions and answers about psittacine proventricular dilatation disease and avian viral serositis. Proc Midwest Avian Res Expo, Lexington, KY, 1992, pp. 69-71.

32. JOHNSON RT: The pathogenesis of acute viral encephalitis and postinfectious encephalomyelitis. J Inf Dis 155:359-364, 1987.

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