Ciguatera poisoning

Abstract

Human ciguatera poisoning has a circumtropical distribution and a close association with coral reef fish. Cases of poisoning have been reported along the tropical coast of Queensland and in the Northern Territory. The largest single outbreak of ciguatera poisoning, in Australia, occurred in Sydney in 1987. Human intoxication follows consumption of a variety of tropical fish which contain a potent toxin, ciguatoxin, in their tissues. Ciguatoxin is believed to be elaborated by a benthic dinoflagellate Gambierdiscus toxicus and passed through the food chain to higher level carnivores such as Coral Trout. Human victims of Ciguatoxin usually present with gastrointestinal symptoms within six to twelve hours of ingestion of fish. Following the onset of gastrointestinal disturbances a variety of neurological symptoms are manifested. The duration and type of symptoms displayed by the Sydney victims of ciguatera poisoning will be presented. Ciguatoxin is believed to exert a fundamental physiological action on the voltage dependent sodium channels in nerve fibres. Electrophysiological studies performed on rat and human nerves indicate that ciguatoxin slows conduction velocity and prolongs the absolute and relative refractory periods. The duration and magnitude of the supernormal period is also increased. Identical changes in these nerve conduction parameters have also been recorded from fish nerves. Fish nerves, in vivo, may be protected from Ciguatoxin by Inherent partitioning mechanisms. Until recently there was no effective therapy for the ciguatera syndrome. Intravenous Infusion of mannitol has been reported to effectively alleviate symptoms by a number of workers, however the physiological mechanisms underlying this treatment are as yet not elucidated. Human ciguatera poisoning has a circumtropical distribution and a close association with coral reef fish. Cases of poisoning have been reported along the tropical coast of Queensland and in the Northern Territory. The largest single outbreak of ciguatera poisoning, in Australia, occurred in Sydney in 1987. Human intoxication follows consumption of a variety of tropical fish which contain a potent toxin, ciguatoxin, in their tissues. Ciguatoxin is believed to be elaborated by a benthic dinoflagellate Gambierdiscus toxicus and passed through the food chain to higher level carnivores such as Coral Trout. Human victims of Ciguatoxin usually present with gastrointestinal symptoms within six to twelve hours of ingestion of fish. Following the onset of gastrointestinal disturbances a variety of neurological symptoms are manifested. The duration and type of symptoms displayed by the Sydney victims of ciguatera poisoning will be presented. Ciguatoxin is believed to exert a fundamental physiological action on the voltage dependent sodium channels in nerve fibres. Electrophysiological studies performed on rat and human nerves indicate that ciguatoxin slows conduction velocity and prolongs the absolute and relative refractory periods. The duration and magnitude of the supernormal period is also increased. Identical changes in these nerve conduction parameters have also been recorded from fish nerves. Fish nerves, in vivo, may be protected from Ciguatoxin by Inherent partitioning mechanisms. Until recently there was no effective therapy for the ciguatera syndrome. Intravenous Infusion of mannitol has been reported to effectively alleviate symptoms by a number of workers, however the physiological mechanisms underlying this treatment are as yet not elucidated.