Dedicated to the Birds
of the WorldProventricular Dilatation Disease (January 1996)
Dedicated to the Birds
of the World
Excerpted from the Proceedings of the International Aviculturists Society, January 1996, Orlando FL
Proventricular Dilatation Disease
Christopher R. Gregory, DVM, Branson W. Ritchie, DVM, PhD,
Kenneth S. Latimer, DVM, PhD, Raymond P. Campagnoli, MS,
Cheryl B. Greenacre, DVM, Phil D. Lukert DVM, PhD
Psittacine Disease Research Group
University of Georgia
College of Veterinary Medicine
Athens, Ga
Reprinted in part with permission from Avian Viruses: Function and Control
Wingers Publishing, Lake Worth, FL, 1995.
Introduction
Proventricular dilatation disease (PDD) has been reported since the
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 distention 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 an inflammatory response characterized by the accumulation of lymphocytes and plasma cells in the nervous system, especially the nerves that supply the muscles in 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 Inflammation of the heart also has been observed in some affected birds.1,2,4,5,7,10,14,15,17,21,22
In the order Psittaciformes, PDD 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., African grey parrots, eclectus parrots and blue and gold macaws ) but this may reflect a population bias rather than a species predisposition to PDD. Suggestive lesions also have been reported in two Canada Geese,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.
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 PDD, 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 PDD 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.
Clinical Features
The most common clinical signs of PDD 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 PDD, 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 PDD-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 Distention 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
Diagnosis and Etiology
Presence of characteristic histopathological (microscopic) lesions in nervous tissues remains the most definitive diagnostic technique. 2 A presumptive diagnosis of PDD often is based on historical information, clinical signs, and radiographic evidence of proventricular dilatation or dysfunction. Confirmation of the disease in a live bird requires biopsy of the crop or ventriculus.2, 22,24
Recent findings implicate an infectious agent as the cause of PDD. Further research is needed to characterized the virus that is suspected to be the cause of this disease. Interestingly, 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
Therapy and prevention
Currently, there is no specific therapy for PDD; however, some clinicians report that birds with suspicious 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.
Acknowledgements
Major contributions that have allowed our research group to start work on PDD have been provided by the Cowan Avian Health Foundation, the International Avian Research Foundation, Veterinary Medical Experiment Station, Terry Clyne, Richard and Luanne Porter, Knick Enterprises, Ted Lafeber, Kathleen Sazbo, Allen Berk, Bobbi Brinker, International Aviculturist's Society, Avian Research Associates, Midwest Avian Research Exposition and Zeigler Brothers Inc.
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