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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.

A red fox (Vulpes vulpes) and a European badger (Meles meles) were found dead on a golf-course in October 1997 near Stockholm (Sweden). At necropsy, both animals were obese and the main finding was acute circulatory collapse. Theobromine intoxication was suspected as chocolate waste was available at a nearby farm and no other cause of death could be detected. Gastric contents and samples of liver from both animals were analyzed by reversed-phase high pressure liquid chromatography for the presence of methylxanthines. Theobromine and caffeine were detected in gastric contents and theobromine was identified in the liver samples from both animals. This appears to be the first report of theobromine intoxication in the red fox and the European badger.

Allergic and pseudo-allergic reactions were examined in penicillin factory workers exposed to the dust of preparations of pivampicillin and pivmecillinam. Among 14 workers basophils from five persons showed histamine release by challenge with penicillins, whereas no release was observed in controls of non-atopic individuals not working with the manufacturing of penicillin. Positive skin response was obtained in four workers by path testing and in three persons by scratch test revealing late but no immediate response. All the eight workers who were also exposed to flavour additives used in the penicillin preparations showed histamine release by cocoa and peppermint. The release was not changed by removal of immunoglobulins from the basophil cell surface and the additives caused a similar release in the controls. The histamine release caused by cocoa and peppermint therefore depend on non-immunological mechanisms, i.e. pseudo-allergic reactions which might contribute to the symptoms in penicillin factory workers.

An outbreak of Salmonella napoli infection in England and Wales in 1982 was detected by the surveillance of routine reports of salmonella infections from hospital and public-health laboratories. Epidemiological investigation quickly identified two types of small chocolate-covered bars, imported from Italy, as the vehicles of infection, and subsequently both were found to be contaminated with the organism. The prompt recognition of this outbreak and rapid identification of the vehicle of infection enabled four-fifths of the consignment of contaminated chocolate to be withdrawn from the market. The 245 reported cases resulted from the sale of 600 000 bars; as these were presumably only a small fraction of the total number of cases, it is likely that many thousands of infections were prevented.