Dinoflagellates associated with coral reefs produce ciguatoxin which is concentrated in the marine food chain and subsequently ingested by humans resulting in ciguatera poisoning.' It is an endemic and underreported* problem in Queensland. We present two cases of cardiac dysfunction temporally related to ciguatera poisoning.A 65-year-old Vietnamese male (Case 1) presented to the Princess Alexandra Hospital with findings consistent with ciguatera poisoning. He described paraesthesia of the tongue, abdominal skin, distal extremities and perioral region. Temperature sensation reversal, nausea, vomiting and mild diarrhoea were noted. These symptoms began within 24 hours of eating portions of a large reef fish, including the head and liver. Others who shared the meal had the same typical but milder symptoms of ciguatera poisoning.On examination the patient was shocked, without fever or signs of dehydration. Blood pressure (BP) was 75 mmHg systolic with a relative bradycardia of 60 beatshinute. The ECG showed only non-specific minor ST shift. Serial serum creatine phosphokinase levels were normal.The patient responded to fluid loading. The cardiac findings resolved over three days and the non-cardiac symptoms cleared over the subsequent 14 days.A 54-year-old Caucasian male (Case 2) was admitted to Townsville General Hospital with progressive dyspnoea, dizziness and peripheral oedema dating from his ingestion of several large portions from a large coral trout two weeks previously. He also complained of perioral paraesthesia, myalgia, arthralgia, and limb hyperaesthesia. Diarrhoea, abdominal pain and temperature sensation reversal were not described. Others from the group who had eaten the same fish had typical symptoms of ciguatera poisoning. Pulse rate was 110 beatdminute, BP 165/95 mmHg, third and fourth heart sounds were evident, the JVP was raised and the apex beat displaced. Diminution of light touch, pin prick and vibration sense was noted below the level of the knees with ankle and knee jerks being absent. Proprioception was impaired and the gait ataxic.

A case of meningitis due to Cryptococcus neoformans var. gattii coincident with disseminated Nocardia transvalensis infection is reported. Nocardia infection initially progressed despite high-dose antimicrobial therapy. Although a specific immunologic defect could not be defined, in vitro lymphocyte proliferation in response to stimulation with the Nocardia isolate was reduced. It is proposed that coinfection with Cryptococcus neoformans may have contributed to the observed impairment of lymphocyte function, leading to disseminated Nocardia disease and a suboptimal treatment response.

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