Use of Avian Bornavirus Isolates to Induce Proventricular Dilatation Disease in Conures

The fulfillment of Koch’s postulates shows that the virus causes proventricular dilatation disease in parrots

Novel Borna Virus in Psittacine Birds with Proventricular Dilatation Disease

Pyrosequencing of cDNA from brains of parrots with proventricular dilatation disease (PDD), an unexplained fatal inflammatory central, autonomic, and peripheral nervous system disease, showed 2 strains of a novel Borna virus. Real-time PCR confirmed virus presence in brain, proventriculus, and adrenal gland of 3 birds with PDD but not in 4 unaffected birds

Avian bornavirus genotype 4 recovered from naturally infected psittacine birds with proventricular dilatation disease in South Africa

The occurrence of proventricular dilatation disease caused by avian bornavirus (ABV) in captive psittacine birds has long been suspected in South Africa. This report documents the first detection by polymerase chain reaction and gene sequence analyses of ABV from three clinical cases of proventricular dilatation disease (PDD) in captive bred blue and gold macaws (Araara rauna) resident in this country. Lymphoplasmacytic encephalitis, gastrointestinal myenteric gangioneuritis and leiomyositis were the most prominent histopathological changes and ABV genotype 4 was detected in tissues from all three birds. Immunohistochemical stains for ABV antigen revealed positive labelling of neurons and glial cells of the brain, myenteric ganglia and nerve fibres as well as smooth muscle cells of the gastrointestinal tract of all three birds. In one bird, positive labelling of the peripheral nerves was observed. The identical sequence of the analaysed genome fragment of all three samples, history that all of these birds had originated from the same breeding facility, and young age at presentation raise the question of possible vertical transmission

Pathological and Biochemical Studies of Mucopolysaccharidosis Type IIIB (Sanfilippo Syndrome Type B) in Juvenile Emus (Dromaius novaehollandiae)

Mucopolysaccharidosis (MPS) type IIIB was diagnosed in 14 juvenile emus (Dromaius novaehollandiae), ages 3 weeks to 6 months, based on pathological and biochemical analyses. The animals had a history of neurological signs or sudden death; one of the birds with neurological signs and 3 others experienced acute hemoabdomen. Histopathologically, neuronal swelling and vacuolation in the cerebrum, cerebellum, brainstem, and spinal cord (80%-92%); retina (100%); autonomic ganglia of the intestine (71%); gizzard (50%); adrenal gland (27%); and ear (50%) were noted in affected but not healthy emus. Cytoplasmic vacuoles were also observed in the pancreas, liver, intestine, adrenal glands, and kidneys. The intracytoplasmic inclusions were periodic acid-Schiff and Luxol Fast Blue positive, consistent with a storage disease. Foamy macrophages infiltrated the liver, intestine, tunica media of the aorta, and spleen. By transmission electron microscopy, typical lamellated cytoplasmic bodies were detected in neurons of the brain and retina, while electron-dense bodies consistent with glycosaminoglycan inclusions were observed in hepatocytes and/or hepatic macrophages. The livers of the 2 affected emus studied contained large amounts of heparan sulfate, which is suggestive of MPS type III. Compared with normal controls, hepatic and serum α-N-acetylglucosaminidase activity was very low (<8% of control), while other enzyme activities were normal to increased in the 2 affected emus studied. Moreover, affected emus were homozygous for a 2-bp deletion in the NAGLU gene. This study characterizes the pathology of MPS type IIIB in emus, which is one of the rare inborn errors in birds, showing the homology of this condition to Sanfilippo syndrome in humans

Pathology and immunohistochemical findings of West Nile virus infection in Psittaciformes

West Nile virus (WNV) infection was diagnosed in 38 psittacine birds based on histology, immunohistochemistry, and reverse transcriptase polymerase chain reaction (RT-PCR). Rosellas (Platycercus spp, n = 13), conures (Enicognathus, Aratinga, and Nandayus spp, n = 6), and lorikeets (Trichoglossus spp, n = 6) represented the most commonly affected species. Clinical signs ranged from lethargy, ruffled feathers, anorexia, and weight loss in most birds to sudden death in others. Except for mild to moderate enlargement of liver and spleen, there were no significant gross lesions at necropsy. Histopathologic findings included lymphoplasmacytic and histiocytic hepatitis, interstitial nephritis, myocarditis, splenitis, enteritis, pancreatitis, and occasionally, encephalitis. Viral antigen was detected by immunohistochemistry in 34 of 35 hearts (97.1%), 29 of 32 pancreata (90.6%), 33 of 37 kidneys (89.2%), 31 of 35 intestines (88.6%), 27 of 33 gizzards (81.8%), 8 of 10 ovaries (80%), 27 of 34 spleens (79.4%), 30 of 38 livers (78.9%), 23 of 32 lungs (71.9%), 21 of 31 proventriculi (67.7%), 14 of 21 adrenals (66.7%), 10 of 16 testes (62.5%), 17 of 30 brains (56.7%), 15 of 27 skins (55.5%), 3 of 6 oviducts (50%), 15 of 34 skeletal muscles (44.1%), 11 of 27 crop or esophagus (40.7%), and 1 of 6 thymuses (16.7%). Kidney was positive for WNV by RT-PCR in all the cases tested. In conclusion, Psittaciformes are susceptible to West Nile virus infection, and WNV infections are often associated with nonspecific clinical signs and widespread viral distribution in this order of birds[...