B D Gartrell1, C Reid. 1. New Zealand Wildlife Health Centre, Institute of Veterinary, Animal and Biomedical Sciences, Massey University, Palmerston North, New Zealand. b.gartrell@massey.ac.nz
Abstract
CASE HISTORY: An adult male kea (Nestor notabilis) in good body condition was found dead at Aoraki/Mt Cook Village, in the Southern Alps of New Zealand. The bird had previously been involved in behavioural tests of problem-solving ability. CLINICAL AND PATHOLOGICAL FINDINGS: The bird had substantial subcutaneous and abdominal reserves of fat. The crop contained 20 g of what appeared to be dark chocolate; a conservative estimate of the dose of methylxanthines ingested by the bird was 250 mg/kg theobromine, 20 mg/kg caffeine and 3 mg/kg theophylline. Histopathological examination revealed acute degenerative changes to hepatocytes, renal tubules, and cerebrocortical neurons. DIAGNOSIS: Acute combination methylxanthine toxicity after opportunistic ingestion of chocolate. CLINICAL RELEVANCE: This is the first report of the pathological findings of methylxanthine toxicity in a wild parrot, and illustrates the need to ensure that kea are protected from the toxic by-products of human habitation, and the difficulties in ensuring this against a neophilic, inquisitive and innovative parrot.
CASE HISTORY: An adult male kea (Nestor notabilis) in good body condition was found dead at Aoraki/Mt Cook Village, in the Southern Alps of New Zealand. The bird had previously been involved in behavioural tests of problem-solving ability. CLINICAL AND PATHOLOGICAL FINDINGS: The bird had substantial subcutaneous and abdominal reserves of fat. The crop contained 20 g of what appeared to be dark chocolate; a conservative estimate of the dose of methylxanthines ingested by the bird was 250 mg/kg theobromine, 20 mg/kg caffeine and 3 mg/kg theophylline. Histopathological examination revealed acute degenerative changes to hepatocytes, renal tubules, and cerebrocortical neurons. DIAGNOSIS: Acute combination methylxanthinetoxicity after opportunistic ingestion of chocolate. CLINICAL RELEVANCE: This is the first report of the pathological findings of methylxanthinetoxicity in a wild parrot, and illustrates the need to ensure that kea are protected from the toxic by-products of human habitation, and the difficulties in ensuring this against a neophilic, inquisitive and innovative parrot.