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Ciguatera is a common form of fish poisoning, endemic in all nations of the Pacific region. Several thousand cases have been notified to Queensland authorities over a 10-year period. However, many cases remain undiagnosed and most go unreported. The public health implications include raising awareness of the condition, ensuring that ciguatera is considered in differential diagnosis and promoting better documentation and reporting.

Ciguatera is a type of food poisoning that results from eating certain tropical fish which have become toxic. It is common in Australia: 175 outbreaks, which involved 527 people, were reported in Queensland between 1965 and 1984. It seems restricted to certain areas around the Australian coastline. Most reports have involved the narrow-barred Spanish mackerel, Scomberomorus commersoni, most of which were caught in southern Queensland waters. Up to 2100 cases may have occurred in north Queensland between 1965 and 1984, which were not recorded by the writers. The symptoms of ciguatera in Australia are similar to those reported elsewhere in the South Pacific. Ciguatoxin acts by increasing the permeability of excitable membranes to sodium ions. This type of membrane is found throughout the body in nerve tissue as well as in heart and skeletal muscle. The treatment of ciguatera remains symptomatic and supportive only. Major advances in treatment for ciguatera and detection of ciguatoxin await the means of producing additional ciguatoxin.

Ciguatera is a distressing, hitherto-untreatable and not rare disease which results from the eating of ciguatoxin-contaminated fish from tropical and subtropical waters. We report here the results of a pilot study to assess the efficacy of mannitol therapy in ciguatera poisoning. Twelve adult patients (six men) have been treated, five of whom--who were ill acutely--experienced a significant benefit from this therapy, in three cases, with a hitherto-unexperienced dramatic reversal of symptoms. We conclude that an intravenous infusion of 1.0 g/kg of mannitol which is given over 45 minutes, after rehydration if required, can be of significant benefit to at least some acutely intoxicated victims. We postulate either a reduction of axonal oedema, or a scavenger effect, or both, as the mechanism of the beneficial effects of mannitol. Ciguatoxin is rich in hydroxyl groups, and causes microscopic oedema of neural tissue. If our conclusion of the beneficial effects of mannitol therapy is confirmed, this will offer the first effective therapy for acute phases of this disease, and has promise of preventing much long-term morbidity.