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Running head Ciguatera A Seafood Poisoning Problem
CIGUATERA A SEAFOOD POISONING PROBLEM
Oscar L. Rohena Santiago
801-74-886
Order Custom Ciguatera paper
SAAM 6545 Food Hygiene
October 4, 001
Introduction
Seafood poisoning covers a broad area and is caused by a variety of low molecular weight toxins coming from a wide variety of sources. Theses diseases result from the ingestion of fish, which have accumulated toxins of bacterial or algal origin (Juranovic and Park 11).
The best-known seafood poisonings are, pufferfish poisoning, scombroid fish poisoning, paralytic shellfish poisoning (PSP), neurotoxic shellfish poisoning (NSP), diarrheic shellfish poisoning (DSP) and ciguatera (Juranovic and Park 11).
Pufferfish poison is caused by the biotoxin tetrodoxin, which of is reported to be of bacterial origin (Taylor, 188). In addition to its presence in certain pufferfish species, it has been identified in certain species of salamanders and octopus. Scombroid fish poisoning results from the spoilage of pelagic fish tissues from bacteria that change certain amino acids to amines. Symptoms resemble clinical responses produced by histamine (Juranovic and Park, 11).
PSP, NSP, and DSP are associated with the consumption of shellfish that have filter fed on dinoflagellates that produce toxins, mainly gonyautoxins, saxitoxins, dynophysitoxin and closely related congeners (Juranovic and Park, 11).
The most common reported seafood-related disease in the world is ciguatera, associated with the consumption of contaminated reef fishes. Ciguatera poisoning was first reported by Peter Martyr, historian of the Americas, in the West Indies in 1555. In the Pacific it was first reported in 1606. Capt. James Cook also reported the disease in the South Pacific in 1774 with symptoms that coincide with those evident today (Juranovic and Park, 11, Baden et al., 15).
The term ciguatera originated in the Caribbean in the 18th. Century (Tosteson, 187) to designate the intoxication caused by the snail Turbo pica, that was known by the Cuban name "cigua" (Tosteson, 187, Juranovic and Park, 11). Presently, the term ciguatera is used to describe the particular illness caused by the consumption of certain reef fishes from tropical and subtropical areas of the Caribbean and the Pacific.
Current data indicates that these fishes have accumulated the heat resistant, acid resistant toxins, which are bio-concentrated through the food chain. Several different toxins, singly or in combination, have been associated with the ciguatera poisoning, including ciguatoxin, maitotoxin and scaritoxin (Baden, et al., 15). Ciguatoxin, a polyether toxin is the toxic identified as responsible for the majority of ciguatera cases. (Juranovic et al., 11, Baden et al., 15, Stinn, et al., 18).
This disease is characterized by gastrointestinal (diarrhea, abdominal cramps, and vomiting), cardiovascular (arrhythmias, heart block, etc.), and neurological (paraesthesias, pain in the teeth, pain on urination, blurred vision, temperature reversal, etc.) symptoms. Some of the neurological symptoms can persist for months or even years (Colwell, 18, Juranovic and Park, 11).
It is estimated that 10,000 to 50,000 people per year are suffer from ciguatera poisoning around the world (Colwell, 18, Baden et al., 15). Under reported and under diagnosed, especially in endemic areas where people do not seek medical attention, make it difficult to know the true worldwide incidence of ciguatera. The Center for Disease Control in Atlanta estimates that only to 10% of Ciguatera cases in the United States are reported. In the US Virgin Islands, it is estimated that % of the population suffers from the illness each year. In Puerto Rico this estimate is of 7%. (Baden, et al., 15).
Toxic outbreaks of ciguatera are sporadic and unpredictable. The threat of this contamination results in enormous economic losses in the recreation and commercial exploitation of fishery resources in the affected areas. The growth of an international fish market and massive tourism has resulted in the expansion of the disease to all parts of the industrialized world (Baden, et al., 15).
This document covers several areas of progress in the ciguatera research. We will be focusing in the available information regarding the following areas
• Sources
• Biology
• Chemistry
• Pharmacology
• Clinical Information
• Diagnosis
• Treatment
• Prevention
Occurrence
Ciguatera is considered a world health problem. The disease is the predominant fish poisoning in the endemic tropical regions of the Pacific and Caribbean. In the past the outbreaks were limited to the endemic areas. With the increasing international travel, trade, as well as increasing fish consumption, ciguatera is being imported to traditionally non-endemic areas (Escalona de Motta, et al., 186, Bangis et al., 17). Ciguatera outbreaks have been documented in Canada, Egypt, Sri Lanka, Italy, Japan, Venezuela, French Polynesia, French Antilles and Australia. In the United States cases have been reported in Florida, Louisiana, Texas Kansas, Hawaii, Samoa, US Virgin Islands, Puerto Rico, New York, Tennessee, Vermont and Washington, DC. The most exposed area for ciguatera risk appears to be the French Polynesia (Bangis, 170). Juranovic, and Park (11) suggest that one factor involved may be the reduced diversity of fish species in this area with more favorable conditions for the proliferation of the macro algae and dinoflagellate community complex responsible for ciguatera.
More than 400 species of fish have been reported to be associated ciguatera poisoning. The most common species are amberjack, red snapper, barracuda, grouper, surgeonfish, horse eye jack, crevalle jack, bar jack, hogfish, moray eel, dog snapper, sea bass and Spanish mackerel. In Puerto Rico and Florida (Craig, 180) more than one third of the barracudas tested have been found to contain the toxins. Between 185 to 187, (Tosteson, 1) determined that from 1 specimens of barracuda caught in the southwest of Puerto Rico, % were toxic with ciguatera. Additionally, monthly frequencies of ciguatoxic barracuda showed seasonal variability, with peak values (60 to 70% of captured fish were poisonous) in the fall and late winter-early spring.
Ciguatoxic fish are usually bottom dwellers or shore fish, usually found at depths of less than 00 feet. In most cases herbivorous species consume algae and detritus of the coral reef. Larger fish eat these herbivores. Disease is transmitted to humans by the consumption of both the herbivore and carnivorous fishes (McMillan, 186).
Ciguatoxin has been detected in the intestinal contents, liver, skin, mucus, gonads, and the muscle tissues of certain species by the means of the mouse assay and column chromatography. The highest concentrations of the toxin have been found in the liver. Not all fish of a single population contain the same amount of the toxin. Apparently this level will vary depending on the amount of dinoflagellates in the area (Bagnis, et al., 10).
Biology
In 177, it was discovered that the dinoflagellate, Gambiediscus toxicus helped to expand the food chain cause of ciguatera poisoning (Yasumoto, et. al., 177). The dinoflagellate collected from its natural environment produces ciguatoxin and maitotoxin. Additionally to G. toxicus there are other species of benthic dinoflagellates that are major contributors of ciguatera. Several species of the genus Prorocentrum, Otreopsis, Coolia monotis, Thecdinium sp., and Amphidinium carterae have been identified. Similar active toxic compounds have been extracted from the motile dinoflagellates Gymnodinium sanguineum and Gonyaulax polyhedra (Juranovic and Park, 11).
Dinoflagellates associated with food poisoning are generally eukaryotic marine algae. They are among the primary producers of organic matter and a major component of the phytoplankton. Most are single celled motile organisms while other exist as filaments or coccoid cells and can be autotrophic, auxotrophic, or hetrotrophic (Juranovic and Park, 11).
G. toxicus cells are lenticular, flattened cells. Reproduction is thought to occur be binary fission. It is suspected that G. toxicus has a sexual cycle because isogametes and a planozygote have been partially described (Taylor, 17).
Several macroalgae species have been identified where G. toxicus and other dinoflagellates grow. Potentially, any red, green or brown algae are good substrate for these dinoflagellates. Humans are susceptible both to herbivores, which eat the dinoflagellates when they consume the algae, and from carnivores that eat contaminated herbivores. (Juranovic and Park, 11).
Natural and human made disturbances of the coral reef maybe directly related to the increase in ciguatera due to the re-colonization by G. toxicus. This species appears to grow better after disturbances than under normal conditions (Tosteson, 1).
Chemistry
Ciguatera has been reported after the consumption of fish contaminated by several different heat and acid stable polyether marine toxins, all produced by the dinoflagellate G. toxicus. The two most common toxins are ciguatoxin and maitotoxin. They are some of the most lethal natural substances known. In mice, ciguatoxin is lethal at 0.45 ug/kg ip., and Maitotoxin at a dose of 0.15 ug/kg ip. In humans oral intake as little of 0.1 ug can cause illness in adults. (Tindall, et al., 11, Baden, et al., 15).
Additionally to ciguatoxin and maitotoxin, other toxins have been identified as been involved in ciguatera poisoning, scaritoxin, palytoxin, and okadaic acid are the most important. Ciguatoxin is a lipid soluble substance that opens voltage dependent sodium ions in the cell membrane, which induces membrane depolarization. It causes prolonged symptoms indicative of nerve blockage or damage, requiring regeneration of nervous tissue. Maitotoxin is water-soluble, it increases the calcium ion influx trough an excitable membrane, and this is not affected by tetrodoxin or sodium. Scaritoxin is similar to ciguatoxin. Okadaic acid is a lipid soluble toxin with LD50 of 10 ug/kg in mice. It is a sodium ionophore. Palytoxin is a water soluble polyether which causes severe tonic contractions in muscles, it is also a strong skin irritant and potent tumor activator ( Baden et al., 15).
Pharmacology
Ciguatoxin has direct effects on excitable membranes. It has a powerful depolarization action due to selective increases on sodium permeability in nervous and striated muscle cells. This depolarization is counteracted by tetrodoxin and calcium ions (Tosteson, 10, Juranovic and Park, 11, Baden, et al., 15).
Ciguatoxin induces a two-phase cardiovascular response. In the first phase hypotension and bradycardia are produced, which cannot be antagonized with anthicholynergics. In the second phase it induces hypertension and tachycardia. These two later effects can be suppressed with adrenergic blockers. The effects on the smooth muscle are very complex. It causes a potent release of endogenous norepinephrine from adrenergic nerve terminals and a potentiating effect on the postsynaptic membrane. Respiratory arrest induced by lethal doses of ciguatoxin results from blocking phrenic nerve conduction. It is believed that this depression comes from the central respiratory center. (Juranovic and Park, 11, Baden, et al, 15).
Maitotoxin possesses a specific Ca+ dependent action, which causes a release of norepinephrine from rat pheochromicytoma cells. This action occurs in the absence of Na+ ions and in the presence of tetrodoxin, precluding the participation of sodium channels. Maitotoxin appears to exert its effect on endogenous membrane calcium ions (Ohizumi, 10).
Based on studies made on guinea pig vas deference and ileum, that showed the releasing action of norepinephrine and acetylcoline from adrenergic and cholinergic nerve endings in the presence scaritoxin, it is suggested that the action of scaritoxin is similar to ciguatoxin (Juranovic and Park, 11).
The okadaic acid, being a polyether presents ionopheric properties, as does ciguatoxin. It has two separate effects; activation of calcium channels and activation of contractile elements to induce smooth muscle contraction.. It also has been found that is a tumor promoter (Juranovic and Park, 11, Baden, et al, 15).
Clinical presentation
The clinical picture of ciguatera poisoning appears to vary among individuals, different ethnic groups, and possibly among different type of fish or geographical location. Additionally, it appears that ciguatera from the consumption of carnivorous fish is more toxic than that from herbivores due to exposure to more than one toxin or transformation of the toxins or and increased dose response (Baden, et al., 15).
The attack rate has been reported to be from 7 to 100% with the ingestion of contaminated fish. Acute fatality, usually due to respiratory failure, circulatory collapse, or arrhythmias ranges from 0.1 to 1% of the reported cases (Baden et. al. 15). Lethality is usually seen with the ingestion of the most toxic parts of the fish (liver, visceras, roe, and other organs.
Currently, ciguatera poisoning clinical diagnosis is based on a constellation of symptoms temporarily related to ingestion of suspect fish products. Onset of symptoms may be within 15 minutes or as late as 4 hours after ingestion of the toxins. Generally symptoms are noted within 6 to 1 hours. (Juranovic and Park, 11, Arnold, 001). Reported symptoms are numerous but commonly affect three major organ systems; gastrointestinal, neurologic and cardiovascular.
Gastrointestinal symptoms are often the first to appear and may last from 1 to days with a range of 1 hour to 7 days (Arnold, 001). They may include the following abdominal pain, nausea, vomiting, and diarrhea.
Neurologic symptoms usually are multiple, varied, and at times bizarre (Arnold, 001). They may begin within few hours to days after the ingestion of the contaminated fish, and can last days, weeks and months (Bagnis, et al., 17). The most common symptoms are lingual and circumoral paresthesias, painful paresthesia of the extremities, temperature reversal, dental pain, pruritus, arthralgiasias, weakness, vertigo, ataxia, respiratory paralysis, and coma. Chronic effects of ciguatera can also present some neurological symptoms, like psychiatric disorder of general malaise, depression, headaches, and peculiar feeling in extremities. It is reported that those with chronic symptoms seem to have recurrence with ingestion of fish, alcohol, caffeine, and nuts (Juranovic and Park, 11, Baden, et al., 15, Arnold, 001).
The cardiovascular symptoms are less common but can be severe. Patients may exhibit dyspnea, bradycardia, hypotension and tachycardia (Palafox, et al., 188, Juranovic and Park, 11, Arnold, 001).
Ciguatera can be sexually transmitted. Baden et al (15) cites one case that reports painful ejaculation of an affected male followed by dyspareunia in a previously unexposed female. The toxins can cross the placenta. Children born of mothers who have been affected late in pregnancy may manifest strange fetal movements in uterus and facial patsies after delivery. Ciguatera has been reported to be transmitted by breast milk. (Juranovic and Park, 11, Baden, et. al., 15).
Distinguishing ciguatera from other forms of seafood poisoning can be difficult. Scombroid and neurotoxic fish poisoning can have overlapping symptoms with ciguatera. Food poisonings due to organophosphates, type E botulism, monosodium glutamate and bacterial poisonings also have similar clinical signs (Baden, et al., 15).
Diagnosis
Ciguatera toxins are odorless, tasteless, and generally undetectable by any simple chemical tests. Many native tests like the discoloration of silver coins, or copper wire, the repulsion of flies or ants and rubbing the liver of the fish on the sensitive tissues of the mouth have proven invalid. In some places household pets or elderly relatives are given samples of any suspect fish as a screening test (Juranovic and Park, 11, Baden et al., 15). The following methods have been used and developed in the past years
Mouse bioassay (Kimura et al., 18) traditionally this is the technique that is used to detect ciguatera. Concentrated lipids extracts of fish tissue are injected intraperitoneally into a 0g mouse and the mouse is observed for toxic symptoms for 4 to 48 hours. This test has the disadvantage that mice colonies of 1 to g have to be maintained, the onset of symptoms is subjective, there is a high incidence of false positives, it is expensive and labor intensive, and cannot be used in the field.
Mosquito bioassay (Chungue et al., 184) Toxins are extracted from fish and injected intrathoracically into mosquitoes. The mosquitoes are observed for one hour for signs of death.
Radio immunoassay (Hokama et al., 177) Sheep anti-ciguatoxin serum coupled with iodine-15 is added to a sample of fish tissue extract. Excess antibody is removed and the samples are analyzed using a scintillation counter. If ciguatoxin is present, the DPM will be high.
Enzyme bioassay (Hokama et al., 18) Sheep anti-ciguatoxin serum coupled with horseradish peroxidase is added to a sample fish tissue extract and incubated at room temperature for 1 hour. The amount of toxin is determined by measuring the absorbance at 405 nm.
Stick test (Hokama et al., 187) Perhaps the most simple of al tests. Bamboo sticks, pretreated to help absorb the toxin, are stuck into the fish flesh for 1 second. The sticks are then fixed with methyl alcohol and immersed in a solution of blue latex beads and ciguatoxin antibody. A positive result will change the bamboo stick to a dark-blue or puyrple color within 10 minutes. This procedure does not require the extraction of tissue, gives rapid results and is inexpensive.
Treatment
There is no curative treatment presently known for ciguatera poisoning. Medical treatment has been symptomatic. A variety of agents, including vitamins, antihistamines, anticholynesterases, steroids, and tryciclic antidepressants are used (Juranovic and Park, 11).
It is counterproductive to administer antidiarrheal and antihemetics, because they will cause the retention of the toxins in the system. Forced emesis and purgation may actually help eliminate any remaining fish. Gut emptying and decontamination with charcoal is recommended. Atropine is indicated for bradycardia and dopamine or calcium gluconate for shock. Fluid and electrolytes should be replenished by oral or IV crystalloid infusion. Cool showers or H1 histamine antagonists may relieve the itching and pruritus (Baden, et al., 15).
Recently mannitol appears to have success in the treatment of ciguatera. Palafox et al. (188) administered mannitol to 4 patients with acute ciguatera. These patients were treated with intravenous mannitol and each patient's condition improved dramatically. All exhibited marked lessening of neurologic and muscular dysfunction within minutes of the administration of mannitol. Gastrointestinal symptoms disappeared more slowly.
Prevention
Ciguatera toxins impart no unusual taste, odor or color to fish, and ciguateric fish cannot be made safe to eat by cooking, freezing, drying or smoking (Tosteson et al., 188).
It is recommended that at least the following measure be taken to try to avoid the ciguatera intoxication (as cited in Juranovic and Park, 11)
• Avoid eating fish caught in endemic regions.
• Avoid eating fish considered harmful by natives; do not eat scaleless fish or moray ells.
• Avoid abnormally large carnivorous fishes, such as groupers, barracudas, snappers, and jacks.
• Avoid the liver, head gonads, or viscera of any fish.
• Beware of eating reef fishes after any aggression or disturbance to their environment
• Choose fish harvested from the leeward side of an oceanic island, if possible.
• If possible, the flesh of freshly caught fish should be filleted into barrow strips and soaked in several changes of saltwater over a 0-minute period.
If ciguatera, or any other type of fish poisoning is suspected, the following measures should be followed
• Call a doctor immediately for treatment. If not available call the poison center.
• Do not take drugs or medications without the physician's advice.
• Save the remainder of the fish in the refrigerator (Including the head and the guts).
• Call the department of Health, Poison Center or any suitable organization to report cases of fish poisoning.
Discussion
Ciguatera is a serious health and socio-economic problem, involving the fisheries in tropical and sub-tropical areas of the world. Due to the international and interstate commerce and tourism, the disease is spreading to others parts of the world. The absence of reliable and accurate diagnostics to identify and evaluate clinical cases makes it difficult to assess its health impact.
More than 400 species of reef fishes associated to ciguatera poisoning have been identified. The majority are bottom dwellers or shore fishes in depths of less than 00 feet. The disease gets to human through the food chain. Herbivores fishes forage on the algae and detritus of the coral reef. Large carnivorous fishes eat these herbivores. Humans acquire the disease consuming both the herbivore and carnivorous fishes. In Puerto Rico the disease is most commonly associated by the consumption of the barracuda. The toxin has been identified in the intestinal contents, liver, skin, mucus, gonads, and the muscle tissues of infected fishes. The highest concentrations have been found in the liver.
The most common substances associated with ciguatera are ciguatoxin and maitotoxin, and they are some of the most common lethal natural poisons known. Scaritoxin, palytoxin and okadaic are other secondary toxins that have been identified to be involved in ciguatera poisoning.
The dinoflagellate, Gambierdiscus toxicus has been identified as the most probable source of ciguatera. The dinoflagellate collected from its natural environment produces ciguatoxin and maitotoxin. Additionally to G. toxicus there are other species of benthic dinoflagellates that are major contributors of ciguatera. All these benthic dinoflagellates can use as substrate to grow; green, red or brown macroalgae and apparently growth is promoted by natural and man-made disturbances in the coral reefs.
Generally the pharmacological action of these toxins is to act as ionophores. Studies suggest that these toxins affect the cell membrane producing electrolyte imbalances. These actions cause severe symptoms in humans, affecting the neurological (paraesthesia, dysaethesia), gastrointestinal (vomiting, diarrhea, cramps, nausea), and cardiovascular (hypotension, bradycardia, and tachycardia) systems. These clinical symptoms begin after a few hours of consumption of contaminated fish and can last for several months and even years. Substances like alcohol, caffeine and nuts appear to promote the recurrence of symptoms.
The treatment of ciguatera is a difficult issue. Up to date the treatment of the disease has been symptomatic. No specific treatment or antidote has been found. The only hope at this moment are studies performed using mannitol to treat patients, which have demonstrated a rapid recovery and elimination of many of the symptoms.
The majority of the techniques for the detection of ciguatera contaminated fishes are inaccurate, expensive and time consuming. The only test that appears to give rapid results and is inexpensive is the stick test, although it gives a considerable number of false positives.
The ciguatera poisoning is a very complex problem with serious health and socio economic implications. The publicity associated with the devastating long effects of the illness and the methods of prevention have had a dramatic impact on the tropical fishing industry. The lack of efficient and low cost detection techniques severely affects the efforts of prevention, which in turn affect directly the fishing industry.
The long lasting, multi-systems effects of the ciguatera on human health present a challenge to the medical community. More research is needed to completely identify all the vectors that produce the poisonings. The development of inexpensive and efficient detection methods will have a positive effect in prevention. The complete identification of the pharmacological action of the toxins, including their changes through the food chain may help to develop better treatment protocols and maybe an antidote.
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