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A 14-year-old unsexed African grey parrot ( Psittacus erithacus erithacus ) was presented with a 12-hour history of neurological signs and vomiting. The external physical examination of the patient revealed lethargy, moderate hypothermia, a head tilt, and horizontal nystagmus. Whole-body radiographic imaging and blood biochemistry parameters were unremarkable, and a serological test to detect bornavirus was negative. A computed tomography scan of the bird revealed a large cystic lesion located on the fourth ventricle of the brain. In spite of treatment (nonsteroidal anti-inflammatory drugs and antibiotic and antiparasitic therapy), the parrot's health continued to decline, and it was euthanatized 12 days after presentation. A complete postmortem examination was performed on the patient's brain. Histopathological interpretation of tissues submitted described a large neoformation composed of cells arranged in perivascular pseudorosettes. Hyperchromatic nuclei and marked anisokaryosis were suggestive of a malignant tumor. The tissue mass was associated with significant dilation of the fourth ventricle and a severe peripheral gliosis. The histopathological diagnosis of the neoformation was an ependymoma. Ependymomas are glial tumors of the ependymal cells that line the central canal and the ventricles of the brain and are rarely described in mammals. In birds, ependymomas were only described in budgerigars ( Melopsittacus undulatus ). In human medicine, the recommended treatment is surgical removal of the tumor when possible, followed by radiotherapy.

Treatment of avian renal disease relies on supportive care, such as fluid therapy and nutritional support. Analgesia and adaptations of the environment are indicated in cases of renal disease associated with painful joints. Other treatments vary with the underlying etiology and may include systemic antibiotics, antifungal therapy, vitamin A supplementation, or chelation therapy., (Copyright © 2019 Elsevier Inc. All rights reserved.)

To evaluate the toxicity of short-term high doses of meloxicam in American kestrels ( Falco sparverius ), 32 male captive-born, 1- to 4-year-old American kestrels were randomly assigned to 4 groups: 3 groups treated with meloxicam (n = 9 per group) and a control group (n = 5). Meloxicam was administered orally via feeding tube in the proventriculus at 2, 10, and 20 mg/kg every 12 hours for 7 days for the treatment groups, while the control group received saline solution. The birds were evaluated for the presence of clinical signs, abnormalities in the complete blood cell count and in the plasma biochemical panel for the 20-mg/kg group, and gross and histopathologic lesions. No clinical signs or mortality were observed in any group. No significant differences of clinical relevance were found in results of the packed cell volume, total solids, and biochemical panel, and no evidence of renal toxicity was found in the treatment or control groups. A significant correlation was found between hepatic lipidosis and meloxicam dose (P = .02). Two of 9 birds in the 20-mg/kg group developed gastric ulcers, although this result was not significant. None of the birds in the 2- and 10-mg/kg groups had similar lesions. Finally, meloxicam dosages up to 20 mg/kg did not result in nephrotoxicity in American kestrels. Further toxicologic studies to evaluate hepatotoxicity and gastrotoxicity of meloxicam in avian species are needed.

Microfilariae are considered non-pathogenic in wild birds. The objective of the current communication is to report host reactions to microfilarial infection of unusual intensity in emaciated boreal owls (Aegolius funereus). An unusually large number of boreal owls (n = 21) were submitted to the Canadian Cooperative Wildlife Health Center-Quebec Region for post-mortem examination during the winter of 2009. Nineteen out of 21 birds were considered emaciated based on atrophy of adipose tissue and pectoral muscles and suboptimal weight. A microscopic examination of a subset of nine owls revealed the presence of microfilariae in six owls. Three of the birds with a heavy parasite burden had masses of larval nematodes obstructing large vessels of the lungs. The emaciated owls are believed to have died from starvation due to a cyclic decrease in prey abundance in the boreal forest. This cycle also drives winter movements of boreal owls to urbanized areas of southern Quebec, presumably accounting for the large number of birds submitted in 2009. In the most severely infected owls, the extreme microfilarial burden might have caused an alteration in circulatory dynamics, gaseous exchanges and also probably some metabolic cost. Consequently, microfilariae could have significantly contributed to the death of some of these owls.