| Christopher R. Gregory, DVM, PhD Branson W. Ritchie, DVM, PhD Kenneth S. Latimer, DVM, PhD W.L. Steffens, PhD Raymond P. Campagnoli, MS Denise Pesti, MS Phil D. Lukert DVM, PhD |
Psittacine Disease Research Group University of Georgia College of Veterinary Medicine Athens, Ga |
IntroductionProventricular dilatation disease (PDD) was first discussed in the late 1970's in birds imported into the United States and Germany. 1-4 Subsequently, an epornitic of this disease has been occurring in psittacine birds in North America and Europe, probably as a result of the widespread importation and shipment of birds to satisfy the demands of the pet trade. 1-3,5-8
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. 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 syndrome, psittacine proventricular dilatation syndrome, psittacine wasting syndrome, proventricular hypertrophy and proventricular dilatation disease. 4-11
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. 1,4-6
Proventricular dilatation disease is used to describe 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. Inflammation of the heart also has been observed in some affected birds. 4,9,10
In the order Psittaciformes, PDD has been reported in more than 50 species. Suggestive lesions also have been reported in Canada Geese, spoonbills, toucans, honey-creepers and weaver finches. 11,12 (Dr. Robert Schmidt, personal communication) The description of PDD in multiple families of birds would suggest that its cause is not restricted to a particular host. It is expected that additional non psittacine birds will be diagnosed with this disease as improved diagnostic test are used to accurately detect affected individuals. There is no reference to spontaneous disease in free-ranging psittacine birds; however, there is every reason to assume that these birds would be susceptible. Given the severe nature of PDD and its apparent ability to affect a wide range of bird species, the importation of psittacine birds, or their eggs, into any region with indigenous Psittaciformes must be considered extremely dangerous.
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). 13 Of 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 continues to approximate 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. Proventricular impaction, muscle atrophy, abdominal enlargement, lethargy, weakness, polyuria, diarrhea, scant feces or hypotension also have been reported in affected birds. 9,12
Concomitant CNS signs may include ataxia, abnormal head movements, seizures, and proprioceptive or motor deficits. Some affected birds may only exhibit CNS signs. 9,12 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.
Diagnosis
Clinical laboratory findings in PDD-affected birds are inconsistent. Hypoproteinemia, hypoglycemia, heterophilia and anemia have been reported. However, concomitant mycotic or bacterial opportunistic infections are common in affected birds and may complicate the laboratory picture. 9,12
Survey and contrast radiographs are useful for demonstrating gastric dysfunction in suspect birds. Distention of the proventriculus and increased transit time of barium are common findings in chronically affected birds. The proventriculus of neonates is normally dilated, a condition which should not be misinterpreted as PDD. The proventriculus of a neonate attains its adult tone and size as the bird enters and completes the weaning period. Ultrasonic examination may be used to demonstrate dilatation and impaction of the proventriculus. Endoscopic examination may show impaction, ulceration and dilatation of the proventriculus. 5,9 ,10,12,14
Fluoroscopy has been used to demonstrate reduced gastric motility which can be an indication of PDD. (Dr. Mike Taylor, personal communication) A presumptive diagnosis of PDD often is based on historical information, clinical signs (progressive weight loss, regurgitation, passing undigested food and/or neurologic signs), and radiographic evidence of proventricular dilatation or dysfunction. However, the presence of characteristic histologic lesions in nervous tissues is necessary for a definitive diagnosis. 1,5,9,10,12,14
In most cases, a post-mortem diagnosis is rendered when a complete set of tissues (including proventriculus, ventriculus and brain) are examined microscopically. In some suspect patients, it is possible to obtain a diagnosis before death by submitting a biopsy of the crop. An ingluvectomy is relatively simple and non-invasive compared to the alternative methods of confirming this disease (biopsy of the proventriculus or ventriculus). In one study, PDD was reliably diagnosed in 30 of 44 (68%) of crop biopsies collected from positive birds. 15
To further define the diagnostic value of a crop biopsy, samples of the crop, proventriculus and ventriculus from 29 psittacine birds with PDD were examined microscopically. Histologic evaluation of a crop biopsy correctly diagnosed PDD in 76% of the birds. Seven of the 29 birds did not have discernible crop lesions; therefore, the probability of a false negative result was approximately 24%. 16 Thus, a positive crop biopsy in a bird with suggestive clinical changes is of diagnostic value, but a negative crop biopsy in a bird with suggestive clinical changes does not rule out PDD. To increase the likelihood of histologic detection of PDD-associated lesions, practitioners should obtain full-thickness crop biopsies containing at least one large blood vessel and its associated ganglia. In addition, pathologists may require additional tissue sections from different levels in the paraffin block to obtain sufficient numbers of ganglia for histologic examination. Multiple sectioning may also increase the likelihood of detecting focal histologic lesions.
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