Ciguatera is a foodborne illness caused by eating certain reef fish whose flesh is contaminated with toxins originally produced by dinoflagellates such as Gambierdiscus toxicus which live in tropical and subtropical waters. These dinoflagellates adhere to coral, algae and seaweed, where they are eaten by herbivorous fish who in turn are eaten by larger carnivorous fish. In this way the toxins move up the food chain and bioaccumulate. Gambierdiscus toxicus is the primary dinoflagellate responsible for the production of a number of similar toxins that cause ciguatera. These toxins include ciguatoxin, maitotoxin, scaritoxin and palytoxin. Predator species near the top of the food chain in tropical and subtropical waters, such as barracudas, snapper, moray eels, parrotfishes, groupers, triggerfishes and amberjacks, are most likely to cause ciguatera poisoning, although many other species cause occasional outbreaks of toxicity. Ciguatoxin is odourless, tasteless and very heat-resistant, so ciguatoxin-laden fish cannot be detoxified by conventional cooking.[1][2]
Researchers suggest that ciguatera outbreaks caused by cooling climatic conditions propelled the migratory voyages of Polynesians between 1000 and 1400.[3][4]
Contents
- 1 Signs and symptoms
- 2 Detection methods
- 2.1 Scientific detection
- 2.2 Folk detection
- 3 Treatment
- 4 Epidemiology
- 5 History
- 6 See also
- 7 Footnotes
- 8 References
Signs and symptoms[edit]
Hallmark symptoms of ciguatera in humans include gastrointestinal and neurological effects.[5][6] Gastrointestinal symptoms include nausea, vomiting, and diarrhea, usually followed by neurological symptoms such as headaches, muscle aches, paresthesia, numbness, ataxia, vertigo, and hallucinations.[1][6] Severe cases of ciguatera can also result in cold allodynia, which is a burning sensation on contact with cold.[5] Neurological symptoms can persist and ciguatera poisoning is occasionally misdiagnosed as multiple sclerosis.[7]
Dyspareunia and other ciguatera symptoms have developed in otherwise healthy males and females following sexual intercourse with partners suffering ciguatera poisoning, signifying that the toxin may be sexually transmitted.[8] Diarrhea and facial rashes have been reported in breastfed infants of poisoned mothers, suggesting that ciguatera toxins migrate into breast milk.[9]
The symptoms can last from weeks to years, and in extreme cases as long as 20 years, often leading to long-term disability.[10] Most people do recover slowly over time.[11] Often patients recover, but symptoms then reappear. Such relapses can be triggered by consumption of nuts, seeds, alcohol, fish or fish-containing products, chicken or eggs, or by exposure to fumes such as those of bleach and other chemicals. Exercise is also a possible trigger.[1] Filipino and Chinese people may possibly be more susceptible.[1]
Detection methods[edit]
Scientific detection[edit]
Currently, multiple laboratory methods are available to detect ciguatoxins, including liquid chromatography-mass spectrometry (LCMS), receptor binding assays, and neuroblastoma assays). Although testing is possible, in most cases, LCMS is insufficient to detect clinically relevant concentrations of ciguatoxin in crude extracts of fish.
Folk detection[edit]
In Northern Australia, where ciguatera is a common problem, two different folk science methods are widely believed to detect whether fish harbor significant ciguatoxin. The first method is that flies will not land on contaminated fish. The second is that cats display symptoms after eating contaminated fish. A third, less common testing method involves putting a silver coin under the scales of the suspect fish. Only if the coin turns black, is it contaminated. It is not known whether any of these tests produce accurate results.
On Grand Cayman island the locals will test barracuda by placing a piece of the fish on the ground and allowing ants to crawl on it. If the ants continue to move then the fish is safe to eat.
Treatment[edit]
There is no effective treatment or antidote for ciguatera poisoning. The mainstay of treatment is supportive care. There is some evidence that calcium channel blocker type drugs such as Nifedipine and Verapamil are effective in treating some of the symptoms that remain after the initial sickness passes, such as poor circulation and shooting pains through the chest. These symptoms are due to the cramping of arterial walls caused by maitotoxin[6][12][13][14] Ciguatoxin lowers the threshold for opening voltage-gated sodium channels in synapses of the nervous system. Opening a sodium channel causes depolarization, which could sequentially cause paralysis, heart contraction, and changing the senses of hearing and cold. Nifedipine is a calcium channel blocker.[6] Some medications such as Amitriptyline may reduce some symptoms, such as fatigue and paresthesia,[15] although benefit does not occur in every case.[16] Steroids and vitamin supplements support the body's recovery rather than directly reducing toxin effects.
Mannitol was once used for poisoning after one study reported symptom reversal.[6][17] Follow-up studies in animals[18] and case reports in humans[19] also found benefit from mannitol. However, a randomized, double-blind clinical trial found no difference between mannitol and normal saline,[20] and based on this result, mannitol is no longer recommended.[5]
Folk remedies[edit]
Various Caribbean folk and ritualistic treatments originated in Cuba and nearby islands. The most common old-time remedy involves bed rest subsequent to a guanabana juice enema.[citation needed] Other folk treatments range from directly porting and bleeding the gastrointestinal tract to "cleansing" the diseased with a dove during a Santería ritual[citation needed]. In Puerto Rico, natives drink a tea made from mangrove buttons, purportedly high in B Vitamins, to flush the toxic symptoms from the system[citation needed]. The efficacy of these treatments has never been studied or substantiated.
An account of ciguatera poisoning from a linguistics researcher living on Malakula island, Vanuatu, indicates the local treatment: "We had to go with what local people told us: avoid salt and any seafood. Eat sugary foods. And they gave us a tea made from the roots of ferns growing on tree trunks. I don't know if any of that helped, but after a few weeks, the symptoms faded away."[21]
Senescent leaves of Heliotropium foertherianum (Boraginaceae) also known as octopus bush, a plant used in many Pacific islands as a traditional medicine to treat ciguatera fish poisoning, contain rosmarinic acid and derivatives, which are known for their antiviral, antibacterial, antioxidant and anti-inflammatory properties.[22] Rosmarinic acid may remove the ciguatoxins from their sites of action, as well as being an anti-inflammatory.
Epidemiology[edit]
Due to the limited habitats of ciguatoxin-producing microorganisms, ciguatera is common in only subtropical and tropical waters, particularly the Pacific and Caribbean, and usually is associated with fish caught in tropical reef waters.[5] Ciguatoxin is found in over 400 species of reef fish. Avoiding consumption of all reef fish (any fish living in warm tropical waters) is the only sure way to avoid exposure.[2] Imported fish served in restaurants may contain the toxin and produce illness which often goes unexplained by physicians unfamiliar with the symptoms of a tropical toxin.[2][23] Ciguatoxin can also occur in farm-raised salmon.[24] Furthermore, species substitution, labeling a reef fish as a non-reef fish at restaurants and retail, can complicate efforts by consumers to avoid ciguatera.
In 2007, ten people in St. Louis, Missouri developed the disease after eating imported fish.[25]
In February 2008, the U.S. Food and Drug Administration (FDA) traced several outbreaks to the Flower Garden Banks National Marine Sanctuary in the northern Gulf of Mexico, near the Texas–Louisiana shoreline. The FDA advised seafood processors that ciguatera poisoning was "reasonably likely" to occur from eating several species of fish caught as far as 50 miles (80 km) from the sanctuary.[26]
From August 2010 to July 2011, there were six outbreaks of Ciguatera Fish Poisoning in New York City. Outbreaks were linked to barracuda and grouper purchased at a fish market in Queens, New York.[27]
In Q1 2012, two restaurants in Lanzarote are thought to have been the source of ciguatera poisoning, leading to new fishing regulations issued 18 April 2012. The first outbreak was reported after eating amberjack in February 2012. The diners suffered with vomiting, diarrhoea and abdominal pain several hours later. The second case was in early April affecting six people who live in Lanzarote and had all eaten amberjack at a local restaurant.[28]
History[edit]
Ciguatera was first described by one of the surgeon's mates, William Anderson, on the crew of HMS Resolution in 1774.[29]
See also[edit]
- Algal bloom
- Dinoflagellate (see "neurotoxins" and "red tide" under Ecology and fossils and see "phosphate" under Life Cycle)
- Red tide
- Yessotoxin
[edit]
- ^ a b c d Swift A, Swift T (1993). "Ciguatera". J. Toxicol. Clin. Toxicol. 31 (1): 1–29. doi:10.3109/15563659309000371. PMID 8433404.
- ^ a b c Schep LJ, Slaughter RJ, Temple WA, Beasley DM (2010). "Ciguatera poisoning: an increasing occurrence in New Zealand". N. Z. Med. J. 123 (1308): 100–2. PMID 20173810.
- ^ Abstract at Wiley Online Library
- ^ Article at MongaBay.com
- ^ a b c d Isbister G, Kiernan M (2005). "Neurotoxic marine poisoning". Lancet. Neurol. 4 (4): 219–28. doi:10.1016/S1474-4422(05)70041-7. PMID 15778101.
- ^ a b c d e Clark RF, Williams SR, Nordt SP, Manoguerra AS (1999). "A review of selected seafood poisonings". Undersea Hyperb Med 26 (3): 175–84. PMID 10485519. Retrieved 2008-08-12.
- ^ Ting J, Brown A (2001). "Ciguatera poisoning: a global issue with common management problems". Eur. J. Emerg. Med. 8 (4): 295–300. doi:10.1097/00063110-200112000-00009. PMID 11785597.
- ^ Lange W, Lipkin K, Yang G (1989). "Can ciguatera be a sexually transmitted disease?". J. Toxicol. Clin. Toxicol. 27 (3): 193–7. doi:10.3109/15563658909038583. PMID 2810444.
- ^ Blythe D, de Sylva D (1990). "Mother's milk turns toxic following fish feast". JAMA 264 (16): 2074. doi:10.1001/jama.264.16.2074b. PMID 2214071.
- ^ Gillespie N, Lewis R, Pearn J, Bourke A, Holmes M, Bourke J, Shields W (1986). "Ciguatera in Australia. Occurrence, clinical features, pathophysiology and management". Med. J. Aust. 145 (11–12): 584–90. PMID 2432386.
- ^ Pearn J (2001). "Neurology of ciguatera". J. Neurol. Neurosurg. Psychiatr. 70 (1): 4–8. doi:10.1136/jnnp.70.1.4. PMC 1763481. PMID 11118239.
- ^ Attaway D, Zaborsky O (1993). Marine Biotechnology. p. 8.
- ^ Fleming L. "Ciguatera Fish Poisoning |[1]".
- ^ Schlossberg D (1999). Infections of leisure. p. 13. ISBN 3-540-94069-3.
- ^ Davis R, Villar L (1986). "Symptomatic improvement with amitriptyline in ciguatera fish poisoning". N. Engl. J. Med. 315 (1): 65. doi:10.1056/NEJM198607033150115. PMID 3713788.
- ^ Hampton M, Hampton A (1989). "Ciguatera fish poisoning". J. Am. Acad. Dermatol. 20 (3): 510–1. doi:10.1016/S0190-9622(89)80094-5. PMID 2918120.
- ^ Palafox N, Jain L, Pinano A, Gulick T, Williams R, Schatz I (1988). "Successful treatment of ciguatera fish poisoning with intravenous mannitol". JAMA 259 (18): 2740–2. doi:10.1001/jama.259.18.2740. PMID 3128666.
- ^ Mattei C, Molgó J, Marquais M, Vernoux J, Benoit E (1999). "Hyperosmolar D-mannitol reverses the increased membrane excitability and the nodal swelling caused by Caribbean ciguatoxin-1 in single frog myelinated axons". Brain Res. 847 (1): 50–8. doi:10.1016/S0006-8993(99)02032-6. PMID 10564735.
- ^ Williamson J (1990). "Ciguatera and mannitol: a successful treatment". Med. J. Aust. 153 (5): 306–7. PMID 2118229.
- ^ Schnorf H, Taurarii M, Cundy T (2002). "Ciguatera fish poisoning: a double-blind randomized trial of mannitol therapy". Neurology 58 (6): 873–80. PMID 11914401.
- ^ Dimock, L (2010). "Rescue mission for fading tongue". New Zealand Education Review. ([3]): 3.
- ^ Protective effect of Heliotropium foertherianum (Boraginaceae) folk remedy and its active compound, rosmarinic acid, against a Pacific ciguatoxin. Rossi F, Jullian V, Pawlowiez R, Kumar-Roiné S, Haddad M, Darius HT, Gaertner-Mazouni N, Chinain M and Laurent D, J Ethnopharmacol., 30 August 2012, volume 143, issue 1, pages 33-40, doi:10.1016/j.jep.2012.05.045
- ^ Geller R, Olson K, Senécal P (1991). "Ciguatera fish poisoning in San Francisco, California, caused by imported barracuda". West. J. Med. 155 (6): 639–42. PMC 1003121. PMID 1812639.
- ^ DiNubile M, Hokama Y (1995). "The ciguatera poisoning syndrome from farm-raised salmon". Ann. Intern. Med. 122 (2): 113–4. PMID 7992985.
- ^ Bizarre fish poisoning sparks alarm
- ^ "FDA Advises Seafood Processors About Ciguatera Fish Poisoning in the Northern Gulf of Mexico Near the Flower Garden Banks National Marine Sanctuary" (Press release). U.S. Food and Drug Administration. 2008-02-05. Retrieved 2008-02-07.
- ^ http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6204a1.htm?s_cid=mm6204a1_e
- ^ http://www.lanzaroteinformation.com/content/isolated-cases-ciguatera-poisoning-lanzarote
- ^ Sanders, Lisa (April 5, 2010). "Fish Tale". New York Times. Retrieved 2010-04-10. "The illness was first described in 1774 by a surgeon's mate on the crew of Captain Cook's South Pacific exploration aboard the HMS Resolution. The crewman, John Anderson, documented the symptoms described by several shipmates who had eaten a large fish caught in the tropical waters." (The New York Times incorrectly gives William Anderson's first name as John.)
References[edit]
- Ciguatera fish poisoning CDC
- Ciguatera fish poisoning—Florida, 1991. MMWR June 4, 1993;42(21):417-8
- Ciguatera fish poisoning—Texas, 1997. MMWR August 28, 1998;47(33):692-4
- Epidemiologic notes and reports ciguatera fish poisoning—Bahamas, Miami. MMWR July 23, 1982;31(28):391-2
- Epidemiologic notes and reports ciguatera fish poisoning—Vermont. MMWR April 25, 1986;35(16):263-4
- Ciguatera fish poisoning
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