Summary An adult blue-fronted Amazon parrot ( Amazona aestiva) was presented for a six-week history of ataxia and weight loss. Diagnostic results including a complete blood count, plasma chemistry panel, bile acids, and radiographic imaging were normal or considered unremarkable. The patient was hospitalized and supported with subcutaneous fluids, vitamin B complex, meloxicam, enrofloxacin, gavage feeding, and fenbendazole. While hospitalized, the ataxia significantly improved, and the bird began eating on its own and gaining weight. The bird was discharged from the hospital and prescribed enrofloxacin, meloxicam, and fenbendazole to be administered by the owner, with a recommended reexamination in 14 days. However, the owner did not bring the bird back to the hospital until three weeks later. Medications were discontinued prior to presentation; at the time of reevaluation, the patient’s condition had progressed. The patient’s weight was significantly lower and the ataxia more pronounced than on initial presentation. Given the poor prognosis, the owners elected for euthanasia. No gross abnormalities were noted on postmortem examination. Liver and kidney tissue zinc levels in this bird were measured at 125 ppm; normal limit is less than or equal to 25 ppm. Histopathologic changes to the brain were consistent with severe zinc toxicity, demonstrated by vasculopathy of the cerebral arteries and arterioles along with multifocal areas of hemorrhage and swelling of astrocytes. These findings have been reported in humans and other mammals, but not in birds. While the source of this bird’s heavy metal exposure is unknown, the high tissue zinc concentrations imply chronic exposure. This case presentation and unusual pathologic findings will be beneficial to the further understanding of avian zinc toxicosis.

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