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Ciguatera fish poisoning is characterized by gastrointestinal symptoms such as nausea, vomiting, and diarrhea and neurologic symptoms such as weakness, tingling, and pruritus (itching). The condition is caused by eating fish containing toxins produced by the dinoflagellate Gambierdiscus toxicus, a one-celled plantlike organism that grows on algae in tropical waters worldwide. Because these toxins are lipid soluble, they accumulate through the food chain as carnivorous fish consume contaminated herbivorous reef fish; toxin concentrations are highest in large, predatory fish such as barracuda, grouper, amberjack, snapper, and shark. Because fish caught in ciguatera-endemic areas are shipped nationwide, ciguatera fish poisoning can occur anywhere in the United States. This report describes ciguatera fish poisoning in four persons (two in 1998, two in 2004) who ate fish caught by recreational fishers in waters outside of ciguatera-endemic areas (e.g., the Caribbean Sea and the Atlantic and Gulf Coast waters off southern Florida). These cases underscore the need for physicians, regardless of whether they are in a ciguatera-endemic area, to consider ciguatera in patients who have gastrointestinal or neurologic symptoms after eating large, predatory fish.
South Carolina, 2004
Two cases of ciguatera fish poisoning, in a husband and wife, were reported to the South Carolina Department of Health and Environmental Control on August 10, 2004; the cases were associated with a barracuda caught approximately 60 miles southeast of Charleston, South Carolina, and are the first known cases caused by fish caught off South Carolina. Caribbean ciguatoxin was identified by high-performance liquid chromatography and mass spectrometry in a remaining portion of the barracuda fillet.
The husband, whose age was not known, had diarrhea and abdominal cramping approximately 5 hours after eating the fish. He then experienced weakness, tooth pain, and the feeling that his teeth were loose. He sought care from his family physician and recovered within a few days with no long-term effects; the treatment provided, if any, was unknown.
The wife, aged 36 years, experienced nausea, vomiting, severe abdominal pain, and diarrhea 2 hours after eating the fish. She then experienced a slowed heartbeat; hypotension; dizziness; severe, generalized pruritus; a reversal of hot and cold temperature sensations; and the feeling that the tops of her hands and feet were burning. She was hospitalized for 13 days; treatment included intravenous fluids, promethazine for nausea, gatifloxacin, and low doses of dopamine. Eighteen months after eating the barracuda, the patient reported that she still occasionally experienced slight tingling in her hands.
During January 2005–June 2006, CDC conducted a study of ciguatera fish poisoning among recreational fishers who fished from Texas Gulf Coast oil rigs. Various outreach materials were used to recruit sport fishers who became ill after eating a fish caught offshore in Texas; they were asked to call a toll-free number and complete a telephone survey detailing the symptoms and duration of their illness, the type and quantity of fish consumed, the location where they caught the fish, and details of their fishing practices.
Two cases of ciguatera fish poisoning were identified in attendees of a 1998 dinner party in Houston, Texas, where snapper and barracuda fillets, both caught from an oil-rig platform off the Texas Gulf Coast, were served. None of the fish was saved for laboratory testing, so whether only one or both fish species were ciguatoxic is unknown.
Within 4 hours of the meal, a woman aged 50 years had onset of generalized pruritus and severe gastrointestinal symptoms, including diarrhea, abdominal pain, nausea, and vomiting. The symptoms persisted into the following day; 24 hours after eating the contaminated fish, she began experiencing arm and leg weakness. Two days after the meal, she began to feel tingling in her arms and legs and around her mouth and had hot-cold temperature sensation reversal. Her illness persisted for several days (exact number of days is unknown). She visited her primary-care physician but did not receive any medication. She reported no long-term effects.
A man aged 56 years, a friend of the female patient, attended the same dinner party and became ill within 12 hours of eating the fish. He experienced muscle aches and stiffness, burning on urination, a metallic taste in his mouth, and hot-cold temperature sensation reversal. The patient also reported that his penis was extremely sensitive, which caused occasional ejaculations; although this phenomenon is a neurologic symptom, it is not characteristic of ciguatera. Because the patient, who was a fisherman, knew the symptoms of ciguatera, he assumed that he had the condition and did not seek any medical treatment. He reported no long-term effects.
These are not the first documented cases of ciguatera caused by fish caught off the Texas coast1; they provide additional evidence that ciguatoxic fish can be caught in Texas coastal waters, an area not typically associated with ciguatera fish poisoning. A recent study supports the hypothesis that oil-rig platforms can serve as sites for G. toxicus proliferation in the northwestern Gulf of Mexico.2
TA Villareal, PhD, Marine Science Institute, Univ of Texas at Austin. C Moore, MS, South Carolina Dept of Natural Resources, Charleston; P Stribling, MSN, South Carolina Dept of Health and Environmental Control, North Charleston; Fran Van Dolah, PhD, National Oceanic and Atmospheric Admin, Center for Coastal Environmental Health and Biomolecular Research, Charleston. G Luber, PhD, National Center for Environmental Health; MA Wenck, DVM, EIS Officer, CDC.
CDC Editorial Note:
Ciguatera fish poisoning generally begins with a gastrointestinal syndrome consisting of nausea, vomiting, diarrhea, and abdominal pain, with onset ranging from 2-30 hours after ingestion3,4; however, symptoms most commonly begin within 2-6 hours. Within approximately 3 hours of eating contaminated fish, neurologic symptoms can occur, including profound weakness, paresthesias (tingling), severe pruritus, tooth pain or the feeling that teeth are loose, pain on urination, and blurred vision. Hot-cold temperature sensation reversal is characteristic although not always present. Ciguatera often is associated with signs of cardiovascular dysfunction, such as hypotension, bradycardia (slowed heartbeat), or arrhythmia (irregular heartbeat), which typically occur 1-3 days after eating contaminated fish.3 Complete recovery usually occurs within a few weeks, but neurologic symptoms can recur periodically. No diagnostic tests for ciguatera fish poisoning exist; diagnosis is based on the presence of characteristic symptoms in a patient with a recent history of fish ingestion. The diagnosis can be confirmed through laboratory testing (i.e., high-performance liquid chromatography and mass spectrometry) indicating the presence of ciguatoxin in fish samples saved from a meal; the level of ciguatoxin in fish that causes human illness varies. In addition, no proven screening test exists for detecting ciguatoxin in fish before they are distributed and eaten. Ciguatoxins are odorless, colorless, and tasteless and cannot be eliminated or reduced by cooking or freezing.
Ciguatera has a low mortality rate (<0.5%), although it is a substantial cause of morbidity in areas where ciguatera is endemic.4,5 Ciguatera-endemic U.S. states and territories include Hawaii, Florida, Puerto Rico, Guam, the U.S. Virgin Islands, American Samoa, and the Commonwealth of Northern Marinana Islands; approximately five (Florida) to 70 (U.S. Virgin Islands) cases per 10,000 population are estimated to occur each year.5 Because of difficulties confirming cases and the absence of a reliable assay for human exposure, the number of cases reported to health departments is estimated at 2%-10% of the actual number of cases in the United States.4
Potentially ciguatoxic fish such as barracuda and amberjack migrate seasonally; therefore, they can acquire the toxin in one region and transport it to another. Migration of barracuda from south Florida waters and the Caribbean to South Carolina waters has been documented by the South Carolina Department of Natural Resources cooperative Marine Game Fish Tagging Program,6 and migration of barracuda from Florida to Texas waters has been documented by Fish Trackers, Inc., a volunteer fish-tagging organization that catches, tags, and releases certain fish species.7
The number of oil rigs in Gulf Coast waters is increasing, providing new habitats for Gambierdiscus species and the reef fish that feed on them. In addition, the oil rigs are popular sport-fishing sites and are being considered for experimental fish farming and mariculture operations, increasing the likelihood that humans will be exposed to ciguatoxic fish. In the western Gulf of Mexico, these structures already are becoming habitats for hard coral reefs, which in turn provide a surface for algae growth.2
The temperatures of the northern Caribbean and extreme southeastern Gulf of Mexico have been predicted to increase 4.5°F–6.3°F (2.5°C–3.5°C) during the twenty-first century, with greater temperature increases in higher latitudes.7 Higher temperatures favor G. toxicus growth8 and are likely to alter fish migration patterns. Ciguatera outbreaks previously have been correlated with sea-surface temperature increases in the south Pacific Ocean9 and Tahiti.10 These data suggest G. toxicus proliferation likely will continue and perhaps increase in the Gulf of Mexico2 and along the southern Atlantic coastline.
Persons living in or traveling to ciguatera-endemic areas should adhere to the following general precautions: (1) avoid consuming large, predatory reef fish, especially barracuda; (2) avoid eating the head, viscera, or roe of any reef fish; and (3) avoid eating fish caught at sites known to be ciguatoxic. Physicians everywhere who treat patients with gastrointestinal or neurologic symptoms after eating large, predatory fish should consider a diagnosis of ciguatera.
Ciguatera Fish Poisoning—Texas, 1998, and South Carolina, 2004. JAMA. 2006;296(13):1581–1582. doi:10.1001/jama.296.13.1581
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