In our case report, it was the local port physician who suspected the disease in two sailors that were sent to his office by the ship’s LBH589 nmr agent. He promptly alerted the port health officer for further evaluation and preventative measures being aware that the toxins do not produce immunity but do accumulate, thus remnants of the poisonous fish might produce further disease. Confirmation of ciguatoxin in fish by appropriate laboratory diagnosis is not available as a routine test in most parts of the world.
At present, therefore, ciguatera fish poisoning diagnosis is based on the presentation of typical symptoms and time course, the history of having eaten a reef fish in a “ciguatera belt” region like the Caribbean, and the exclusion of other diagnoses that could account for the symptoms. Ciguatera fish poisoning has symptoms in common with paralytic and neurotoxic
shellfish poisonings, scombroid and pufferfish toxicity, botulism, bacteremia, and several neurologic conditions.[2] In our case the diagnosis was strongly supported by the fact that multiple seafarers from a single ship that consumed the same fish, all experienced typical signs, symptoms, and time course consistent with ciguatera fish poisoning. Ciguatoxins I BET 762 are known as highly potent natural substances that cause symptoms even in low doses. In our case study, we observed a relationship between severity of symptoms and amount of fish ingested. Owing to the preparation of food from a common source on ships, attack rates in crews are high. In a Norwegian cargo ship 85% of crew members got sick.[5] In a port in the UK, half of the crew (14 people) on a Colombian ship ate white snapper in the Caribbean; as a result,
all persons got sick with gastrointestinal symptoms and most with neurological symptoms.[7] In our case report from Hamburg, all 14 sailors that ate from the fish got sick. A varying degree of symptoms persisted for at least 2 weeks after the ciguatoxic fish meal in all but 1 affected sailors. While most authors describe the vanishing of symptoms after 1 to 4 days, others emphasize that neurological and neuropsychiatric symptoms may persist GBA3 for years.[1, 2, 9] On grounds of this uncertainty, the repatriation of the two most severely affected sailors was supported by the port medical officer (C. S.) for medical reasons. Published data on the case fatality rate of the disease vary between <0.1 and 7%.[1, 2, 7] Even if no fatality occurs, the disease may pose a threat to the ship’s operations and safety due to the neurological and neuropsychiatric symptoms that are associated with the intoxication. Hallucinations, giddiness, depression, or sleeping problems may potentially affect the function, vigilance, and judgment of the seafarers on duty. Costs to the ship operator may derive from diagnostic test and treatment.
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