1/37. Ciguatera fish poisoning. Ciguatera fish poisoning is one of a variety of non-bacterial forms of human seafood poisoning. Consuming large predatory fish from tropical reef ecosystems may be hazardous. We describe a case that is typical of the disease, and illustrates the persistence of neurological symptoms that occur in some patients. ( info) |
| ciguatera poisoning causes mainly gastrointestinal and neurological effects of variable severity. However, symptoms of peripheral neuropathy with paresthesias and paradoxical disturbance of thermal sensation are the hallmark. Electrophysiological studies are often normal, except in severe cases. We report four people who developed mild ciguatera poisoning after barracuda ingestion. Electrophysiological studies documented normocalcemic latent tetany. These findings are consistent with ciguatoxin's mechanism of toxicity, which involves inactivation of voltage-gated Na( ) channels and eventually increases nerve membrane excitability. ( info) |
3/37. The transport of ciguatoxin: a case report. Ciguatera fish poisoning has been responsible for as many as half of all food poisonings in the united states due to fish. Because the initial symptoms often include gastrointestinal symptoms, such as nausea, vomiting, diarrhea, and abdominal pain, patients may be discharged from the Emergency Department with a diagnosis of "acute gastroenteritis," only to return soon thereafter. This is a case report of such a patient who was evaluated and discharged only to subsequently return because of worsening of symptoms. ( info) |
4/37. Chronicity of neurological features in ciguatera fish poisoning. A 43-year-old woman complained of colicky abdominal pain, followed by numbness, myalgias, and muscle weakness in the four limbs after eating a grouper (Epinepheius spp.). She presented to our hospital 36 hours later with increased myalgias, muscle weakness, and malaise. On examination, the muscle power and sensation in her four limbs appeared to be normal. She was given an intravenous infusion of mannitol 20% (200 ml over 1 hour) and an intramuscular injection of diclofenac (75 mg). Her myalgias then improved and she was discharged. She presented to our hospital again 1 week later with poor appetite, malaise, numbness of the four limbs, and increased muscle weakness. On examination, the muscle weakness was more marked in the lower limbs (4 /5) than in the upper limbs (5-/5) and proximally than distally. She also had some difficulty in getting up from a squatting position. She was given another intravenous infusion of mannitol 20% (200 ml over 1 hour), following which there was subjectively slight improvement in her muscle weakness. Herplasma creatine phosphokinase level was normal. electromyography performed 4 weeks later revealed no abnormalities. When she was reviewed 45 days after the consumption of the grouper, her muscle weakness and malaise had improved considerably. She could then stand up from a squatting position. However, mild impairment of finger grip was still present. Chronicity of neurological features in other reported cases (e.g., chronic fatigue, relapse of symptoms after exposure to ciguateric fish or alcohol, and peripheral neuropathy) may also indicate a lengthy persistence of ciguatoxins in the body. ( info) |
| Although ciguatera fish poisoning is generally a mild, self-limited disease, both life-threatening acute reactions and troublesome chronic symptoms can occur. Because ciguatera has been largely confined to tropical locations, a relative lack of recognition exists among many US physicians. As access to tropical locations has increased, so has the distribution of ciguatera. Herein, we present a case report and review the current literature on ciguatera. ( info) |
6/37. ciguatera poisoning: a global issue with common management problems. ciguatera poisoning, a toxinological syndrome comprising an enigmatic mixture of gastrointestinal, neurocutaneous and constitutional symptoms, is a common food-borne illness related to contaminated fish consumption. As many as 50000 cases worldwide are reported annually, and the condition is endemic in tropical and subtropical regions of the Pacific Basin, indian ocean and Caribbean. Isolated outbreaks occur sporadically but with increasing frequency in temperate areas such as europe and north america. Increase in travel between temperate countries and endemic areas and importation of susceptible fish has led to its encroachment into regions of the world where ciguatera has previously been rarely encountered. In the developed world, ciguatera poses a public health threat due to delayed or missed diagnosis. Ciguatera is frequently encountered in australia. Sporadic cases are often misdiagnosed or not medically attended to, leading to persistent or recurrent debilitating symptoms lasting months to years. Without treatment, distinctive neurologic symptoms persist, occasionally being mistaken for multiple sclerosis. Constitutional symptoms may be misdiagnosed as chronic fatigue syndrome. A common source outbreak is easier to recognize and therefore notify to public health organizations. We present a case series of four adult tourists who developed ciguatera poisoning after consuming contaminated fish in vanuatu. All responded well to intravenous mannitol. This is in contrast to a fifth patient who developed symptoms suggestive of ciguatoxicity in the same week as the index cases but actually had staphylococcal endocarditis with bacteraemia. In addition to a lack of response to mannitol, clinical and laboratory indices of sepsis were present in this patient. Apart from ciguatera, acute gastroenteritis followed by neurological symptoms may be due to paralytic or neurotoxic shellfish poisoning, scombroid and pufferfish toxicity, botulism, enterovirus 71, toxidromes and bacteraemia. Clinical aspects of ciguatera toxicity, its pathophysiology, diagnostic difficulties and epidemiology are discussed. ( info) |
7/37. Rabbitfish ("aras"): an unusual source of ciguatera poisoning. BACKGROUND: ciguatera poisoning is the commonest fish-borne seafood intoxication. It is endemic to warm water tropical areas and is caused by consumption of bottom-dwelling shore reef fish, mostly during spring and summer. The causative agent, ciguatoxin, is a heat-stable ester complex that becomes concentrated in fish feeding on toxic dinoflagellates. The common clinical manifestations are a combination of gastrointestinal and neurologic symptoms. Severe poisoning may be associated with seizures and respiratory paralysis. OBJECTIVE: To describe a series of patients who sustained ciguatera poisoning in an uncommon region and from an unexpected source. patients: Two families complained of a sensation of "electrical currents," tremors, muscle cramps, nightmares, hallucinations, agitation, anxiety and nausea of varying severity several hours after consuming rabbitfish ("aras"). These symptoms lasted between 12 and 30 hours and resolved completely. The temporal relationship to a summer fish meal, the typical clinical manifestations along with the known feeding pattern of the rabbitfish suggested ciguatera poisoning. CONCLUSIONS: The Eastern Mediterranean basin is an unusual region and the rabbitfish an unusual source for ciguatera poisoning. There are no readily available and reliable means for detecting ciguatoxin in humans. A high index of suspicion is needed for diagnosis and a thorough differential diagnosis is essential to eliminate other poisonings, decompression sickness and encephalitis. Supportive therapy is the mainstay of treatment. ( info) |
8/37. ciguatera poisoning after ingestion of imported jellyfish: diagnostic application of serum immunoassay. Ciguatera fish poisoning is an important public health problem wherever humans consume tropical and subtropical fish. It accounts for over half of fish-related poisonings in the united states but is uncommonly diagnosed and underreported. Produced by dinoflagellates, ciguatoxin accumulates up the food chain in herbivorous and carnivorous fishes. cnidaria jellyfish and related invertebrates) have not previously been associated with direct ciguatera intoxication in humans. We report the first case of ciguatera fish poisoning associated with cnidarian ingestion. A 12-year-old Tongan female presented to our Emergency Department with mid-abdominal pain, nausea, change in mental status, and new-onset movement disorder after ingestion of jellyfish imported from american samoa. Clinical diagnosis was confirmed by strongly positive serum identification of ciguatoxin and related polyether toxins (including okadaic acid) with a rapid extraction method (REM) and highly reliable solid-phase immunobead assay (S-PIA) performed by the Food toxicology research Group, University of arizona. Ciguatera pathophysiology, clinical presentation, differential diagnosis (including consideration of palytoxin poisoning), and treatment are briefly reviewed. We emphasize the growing incidence of ciguatera fish poisoning outside "high-risk" areas. In regions with immigrant populations, privately imported exotic fish may be toxin vectors. Marine species other than carnivorous fish are now suspect in human ciguatera intoxication. Reliable tests can aid in premarket fish testing, diagnosis, and follow-up of ciguatera fish poisoning. The global prevalence of marine toxins demands fishermen, consumers, and physicians maintain a high index of suspicion for ciguatera fish poisoning. ( info) |
9/37. Orthostatic hypotension in ciguatera fish poisoning. PURPOSE--The purpose of this study was to investigate the pathophysiology of persistent orthostatic hypotension in a patient with ciguatera fish poisoning. methods--A patient who became ill and who developed prolonged and symptomatic orthostatic hypotension with ciguatera fish poisoning after eating barracuda is described. Studies of autonomic function included measurements of plasma catecholamine levels in the supine and standing positions, and pressor responses to infusions of norepinephrine, atropine, and propranolol. RESULTS--Volume depletion was excluded as a cause for hypotension. Our patient showed low plasma catecholamine levels and marked pressor hypersensitivity to norepinephrine infusion. hypotension and bradycardia were reversed by atropine infusion. The heart rate freed from autonomic influences, ie, after atropine plus propranolol infusion, was normal. CONCLUSIONS--In ciguatera fish poisoning, orthostatic hypotension appears to be a result of both parasympathetic excess and sympathetic failure. ( info) |
10/37. Emergence of imported ciguatera in europe: report of 18 cases at the Poison Control Centre of Marseille. BACKGROUND: Ciguatera is a disease caused by the ingestion of fish containing the toxins of Gambierdiscus toxicus. This dinoflagellate is frequently found in damaged coral reef systems. Previously rare in europe, this disease entity is now seen in tourists returning from tropical countries. CASE SERIES: Eighteen patients were examined between 1997 and 2002. Nine poisonings occurred in atlantic ocean islands, eight in pacific ocean islands, and one in the Egyptian Red Sea coast. Gastrointestinal signs were always present in the Atlantic areas, but were less severe or absent in the Pacific areas. All patients had sensory disturbances, and two of them had motor disturbances affecting the respiratory muscles and leading to the death of a 73-year-old man in cuba. The 17 surviving patients returned to france and for 2 to 18 months suffered from arthralgias, myalgias, or pruritis. CONCLUSION: Ciguatera is a newly imported intoxication in europe. As the number of international tourists grows each year, this type of poisoning will be seen more frequently. Furthermore, as the condition of coral reefs declines around the world and the prevalence of G. toxicus increases, physicians in non-tropical countries should be prepared to manage such poisoned patients. ( info) |