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Fish toxin ciguatera: Harmful Algal Blooms: Ciguatera Fish Poisoning: Home

Food Poisoning from Seafood | Travelers’ Health

 

Generally, eating fully cooked food that is served hot helps you avoid foodborne disease, sometimes called food poisoning. However, there are a few types of foodborne diseases you can get from fish that cannot be prevented by cooking.

During travel if you think you have food poisoning from seafood seek medical care immediately.

Shellfish Poisoning

There are several types of toxins in contaminated shellfish that can cause illness. Toxins may be in found in mussels, oysters, clams, scallops, cockles, abalone, whelks, moon snails, Dungeness crab, shrimp, and lobster.

Shellfish usually become contaminated during or after algae blooms. Shellfish poisoning symptoms differ in severity and depend on the type of toxin in the shellfish. If you’ve recently eaten shellfish and develop the following symptoms, seek medical care.

Symptoms

Symptoms usually appear 30–60 minutes after eating contaminated shellfish, but it could be a few hours before you start to feel sick. Severe cases may be fatal. Symptoms vary based on the type of toxin in the shellfish and can include:

  • Numbness and tingling
  • Headache
  • Nausea
  • Vomiting
  • Diarrhea
  • Confusion
Prevention

Avoid potentially contaminated shellfish. If you’re visiting an area that’s recently experienced an algae bloom, sometimes called “red tide” or “brown tide,” avoid eating shellfish. You may want to avoid shellfish completely if you are traveling in a low-income country or if you aren’t confident of the water quality where the shellfish are from.

Ciguatera

You can get ciguatera (sig-wah-TARE-ah) poisoning by eating fish contaminated with toxins produced by tiny algae found around coral reefs. It can be difficult to tell if fish is contaminated as the toxins that cause ciguatera do not change the appearance, taste, or smell of the fish. Cooking does not destroy the toxins.

Ciguateria can accumulate in reef fish that eat other fish. Fish you may want to avoid include barracuda, moray eel, grouper, amberjack, sea bass, sturgeon, parrot fish, surgeonfish, and red snapper.

Signs and Symptoms

Ciguatera symptoms usually develop 3–6 hours after eating contaminated fish but may start up to 30 hours later. If you’ve recently eaten fish and develop symptoms, seek medical care.

Common symptoms include:

  • Nausea
  • Vomiting
  • Diarrhea
  • Stomach pain

Less common symptoms can include:

  • Tingling
  • Tooth pain or feeling as if teeth are loose
  • Itching
  • Metallic taste in the mouth
  • Blurred vision
  • Increased sensitivity to hot and cold

Symptoms usually last a few days but, in some cases, can linger for months. There is no cure for ciguatera, however there are treatments for some of the symptoms. After recovering you may want to avoid fish, nuts, alcohol, and caffeine for at least 6 months to prevent symptoms from returning.

Prevention

Avoid or limit eating fresh reef fish, especially barracuda and moray eel, as they are more likely to cause ciguatera. Do not eat the fish’s liver, intestines, eggs, or head because they have the highest concentration of toxins.

Scombroid

Scombroid (SKOM-broyd) poisoning is caused by eating fish that has not been properly refrigerated after being caught.

Scombroid occurs worldwide and is one of most common fish poisonings. Scombroid poisoning can occur from eating tuna, mackerel, mahi-mahi (dolphin fish), sardines, anchovies, herring, bluefish, amberjack, and marlin.

Signs and Symptoms

Scombroid symptoms usually develop within a few minutes to an hour after eating contaminated fish. They often resemble an allergic reaction and may include the following:

  • Flushing of the face
  • Headache
  • Heart palpitations (fast-beating, fluttering, or pounding heart)
  • Itching
  • Blurred vision
  • Cramps
  • Diarrhea

Symptoms can be treated with antihistamines. Even without treatment, people usually get better within 12–48 hours

Prevention

The best way to avoid scombroid is to only eat fish that you know has been properly stored. Contaminated fish usually look and taste normal, but may taste peppery, sharp, or salty. Keep in mind that cooking, smoking, or freezing the fish does not prevent scombroid.

More Information

CDC Yellow Book: Food Poisoning from Marine Toxins

Harmful Algal Bloom-Associated Illness

Safe Food and Drinks

Ciguatera Toxicity – StatPearls – NCBI Bookshelf

Continuing Education Activity

Ciguatera toxicity is a food-borne illness caused by eating fish contaminated with Ciguatoxin. This toxin is a potent neurotoxin, and it is produced by Dinoflagellates, such as Gambierdiscus toxicus. They adhere to algae, coral, and seaweed, where herbivorous fish eat them. Larger carnivorous fish will suffer a toxin build-up from consuming these herbivores. Ciguatera poisoning is endemic to tropical and subtropical regions, mainly in the South Pacific and Caribbean. However, it can be found anywhere fish is consumed. This activity reviews the etiology, presentation, evaluation, and management/prevention of Ciguatera toxicity, and reviews the role of the interprofessional team in evaluating, diagnosing, and managing the condition.

Objectives:

  • Describe the basic pathophysiology and toxicokinetics of ciguatera toxin in the human body.

  • Review the evaluation procedures for diagnosing ciguatera toxicity, including any applicable laboratory testing.

  • Summarize the treatment and management strategy for ciguatera toxicity.

  • Evaluate possible interprofessional team strategies for improving care coordination and communication to advance the evaluation and treatment of ciguatera toxicity and improve outcomes.

Access free multiple choice questions on this topic.

Introduction

Ciguatera toxicity is a food-borne illness caused by eating fish contaminated with ciguatoxin. This toxin is a potent neurotoxin, and dinoflagellates, such as Gambierdiscus toxicus, produce it. They adhere to algae, coral, and seaweed, where herbivorous fish eat them. Larger carnivorous fish will suffer a toxin build-up from consuming these herbivores. Ciguatera poisoning is endemic to tropical and subtropical regions, mainly in the South Pacific and Caribbean. However, it can be found anywhere fish is consumed. It affects other parts of the world where it is not indigenous through the import of contaminated fish. The fishes that most commonly cause ciguatera toxicity are barracuda, grouper, moray eel, amberjack, sea bass, sturgeon, parrotfish, surgeonfish, and red snapper. [1][2][3][4] 

Etiology

Gambierdiscus toxicus is a dinoflagellate responsible for the production of various toxins that can cause Ciguatera toxicity. These include ciguatoxin, maitotoxin, palytoxin, scaritoxin, and palytoxin. Predator species in tropical waters are most likely to cause ciguatera toxicity. Barracudas, groupers, moray eels, snapper, and amberjacks are commonly implicated, but it is also found in over 400 species of reef fish. Ciguatoxin is tasteless, odorless, lipid-soluble, and heat-resistant, so normal cooking cannot detoxify ciguatoxin-laden fish. [1][5][4][2]

Epidemiology

Ciguatera toxicity is the most common worldwide fish poisoning with up to 50,000 cases occur globally every year. This number is felt to be under-reported because most physicians do not realize that it is a reportable disease. While thought to be endemic to the South Pacific and Caribbean, it was recently isolated in the Red Sea and the Atlantic Ocean. It affects 3% of travelers to endemic regions.  It is the most common fish-related foodborne illness in the United States. Ciguatera toxicity is most commonly caused by eating barracuda, grouper, moray eel, amberjack, sea bass, sturgeon, parrotfish, surgeonfish, and red snapper. [3][6][7][1][2][8] 

Pathophysiology

Ciguatoxin decreases the threshold for opening voltage-gated sodium channels in synapses of the nervous system. Opening a sodium channel causes depolarization, which may cause muscle paralysis, cardiac dysfunction, and altered sensation of heat and cold. Cold allodynia is a unique symptom of ciguatera. Cooking or freezing the fish does not prevent ciguatera toxicity as these methods do not kill the ciguatoxin. It has no odor. Researchers are looking at the possibility of maitotoxins playing a larger role in ciguatera fish poisoning. When introduced to mice by intraperitoneal injection and oral consumption, it caused toxicity in the research trials. Further research is being done on ciguatoxins by introducing the toxin to human brain-derived cell lines to evaluate its toxicity. [7][1][2][8] 

History and Physical

Clinical symptoms of ciguatera toxicity include gastrointestinal and neurological effects. Gastrointestinal symptoms include nausea, vomiting, gastric upset, belching, and diarrhea, whereas neurological symptoms include headaches, muscle aches, perioral paresthesia, numbness, vertigo, metallic taste in the mouth, blurred vision, ataxia, pruritus, and hallucinations. Severe ciguatera toxicity can cause cold allodynia, which is a perception of a burning sensation on coming in contact with a cold object. Persistent ciguatera toxicity may be misdiagnosed as multiple sclerosis due to its symptomatology. Dyspareunia has been reported following sexual intercourse suggesting the toxin may be sexually transmitted. Breastfeeding mothers have reported diarrhea and facial rashes in their infants. This supports the theory that ciguatera toxins are secreted into breast milk. Cardiovascular effects can include bradycardia and hypotension. Cardiac symptoms are only present in the early stages of the toxicity. Alcohol consumption during toxin ingestion has been found to increase the risk of developing bradycardia, hypotension, and altered skin sensation. Signs and symptoms can last from weeks to years and usually most recover with an occasional relapse. Relapse may be triggered by the consumption of alcohol, nuts, seeds, fish, chicken, and eggs. [9][2][10][4] 

Evaluation

Multiple tests are available to detect ciguatoxin, including liquid chromatography-mass spectrometry (LCMS), cytotoxicity assays, and receptor binding immunoassays. These tests are not readily available at the time of patient presentation in the emergency department. Routine laboratory testing is often non-specific and rarely helpful. Treatment is based on clinical findings, including history and physical examination, as well as disease progression. [3][2][4][11] 

Treatment / Management

The treatment of ciguatera poisoning is supportive care. There is no specific antidote for the toxin. If the patient’s nausea and vomiting are not severe, activated charcoal may be used in the first few hours of toxicity to prevent further absorption of the ciguatoxin. Antihistamines can be used for pruritus. Symptomatic relief of nausea and vomiting should also be provided. Dehydration can occur due to nausea and vomiting and should be treated with intravenous fluids. If intravenous (IV) fluid resuscitation is not sufficient, then IV vasopressor infusion may be added. There is evidence that calcium channel blockers such as nifedipine and verapamil are useful in treating some symptoms like headaches.  In rare cases, patients may experience respiratory failure and should be managed by traditional rapid sequence intubation. Symptomatic bradycardia is treated with intravenous atropine. Medications such as amitriptyline may reduce some symptoms, such as paresthesia and fatigue. Steroids and vitamin supplements support recovery but do not reduce toxic effects. Mannitol’s role is controversial in Ciguatera poisoning as a clinical trial found no difference between mannitol and normal saline. But at the same time, many trials have demonstrated improvement of neurologic symptoms after administrating mannitol. A mid approach can be followed by giving only one dose of Mannitol in addition to Normal Saline. [2][4][12][13] 

Differential Diagnosis

Diagnosis is often difficult, as physicians do not recognize symptoms and their hesitation to report.  Ciguatera has similar symptoms to scombroid and other enteroviruses. Ciguatera can be mistaken for organophosphate toxicity, botulism, multiple sclerosis, Guillain-Barre syndrome, and a wide range of other food poisonings.  [2][4] 

Prognosis

The toxicity of ciguatera is generally self-limiting, with symptoms only lasting a few days. However, a patient has to be counseled to avoid caffeine, fish, alcohol, and nuts within six months of poisoning as it may trigger a recurrence of symptoms. [2][4] 

Enhancing Healthcare Team Outcomes

Patients with ciguatera poisoning initially present to the emergency department. However, because of the lack of a rapid diagnostic test, clinical acumen is required to make the diagnosis. The poisoning is best managed by a team that includes the emergency department physician, infectious disease expert, internist, primary care provider, nurse practitioner, and specialty trained nurses.

The treatment of ciguatera poisoning is supportive care. There is no specific antidote for the toxin. If intravenous (IV) fluid resuscitation is not sufficient, then IV vasopressor infusion may be added. There is evidence that calcium channel blockers such as nifedipine and verapamil are useful in treating some symptoms like headaches.  In rare cases, patients may experience respiratory failure and should be managed by traditional rapid sequence intubation. Symptomatic bradycardia is treated with intravenous atropine. Toxicology pharmacists can be involved in the care and provide teaching to patients and their families. Nurses monitor patient status and provide updates to the team.

After recovery, the patient must be warned not to eat fish or related seafood as the symptoms may recur. The outlook for most patients is excellent.  [2][4][12][13] 

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References

1.

Hardison DR, Holland WC, Darius HT, Chinain M, Tester PA, Shea D, Bogdanoff AK, Morris JA, Flores Quintana HA, Loeffler CR, Buddo D, Litaker RW. Investigation of ciguatoxins in invasive lionfish from the greater caribbean region: Implications for fishery development. PLoS One. 2018;13(6):e0198358. [PMC free article: PMC6010213] [PubMed: 29924826]

2.

Traylor J, Mathew D. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Jun 27, 2022. Histamine Toxicity. [PubMed: 29763046]

3.

Clausing RJ, Losen B, Oberhaensli FR, Darius HT, Sibat M, Hess P, Swarzenski PW, Chinain M, Dechraoui Bottein MY. Experimental evidence of dietary ciguatoxin accumulation in an herbivorous coral reef fish. Aquat Toxicol. 2018 Jul;200:257-265. [PubMed: 29803968]

4.

Traylor J, Singhal M. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Feb 7, 2023. Ciguatera Toxicity. [PubMed: 29494117]

5.

Roué M, Darius HT, Ung A, Viallon J, Sibat M, Hess P, Amzil Z, Chinain M. Tissue Distribution and Elimination of Ciguatoxins in Tridacna maxima (Tridacnidae, Bivalvia) Fed Gambierdiscus polynesiensis. Toxins (Basel). 2018 May 10;10(5) [PMC free article: PMC5983245] [PubMed: 29747460]

6.

Pierre O, Misery L, Talagas M, Le Garrec R. Immune effects of the neurotoxins ciguatoxins and brevetoxins. Toxicon. 2018 Jul;149:6-19. [PubMed: 29360534]

7.

Soliño L, Costa PR. Differential toxin profiles of ciguatoxins in marine organisms: Chemistry, fate and global distribution. Toxicon. 2018 Aug;150:124-143. [PubMed: 29778594]

8.

Nakada M, Hatayama Y, Ishikawa A, Ajisaka T, Sawayama S, Imai I. Seasonal distribution of Gambierdiscus spp. in Wakasa Bay, the Sea of Japan, and antagonistic relationships with epiphytic pennate diatoms. Harmful Algae. 2018 Jun;76:58-65. [PubMed: 29887205]

9.

Wang B, Yao M, Zhou J, Tan S, Jin H, Zhang F, Mak YL, Wu J, Lai Chan L, Cai Z. Growth and Toxin Production of Gambierdiscus spp. Can Be Regulated by Quorum-Sensing Bacteria. Toxins (Basel). 2018 Jun 22;10(7) [PMC free article: PMC6071102] [PubMed: 29932442]

10.

Leung PTY, Yan M, Lam VTT, Yiu SKF, Chen CY, Murray JS, Harwood DT, Rhodes LL, Lam PKS, Wai TC. Phylogeny, morphology and toxicity of benthic dinoflagellates of the genus Fukuyoa (Goniodomataceae, Dinophyceae) from a subtropical reef ecosystem in the South China Sea. Harmful Algae. 2018 Apr;74:78-97. [PubMed: 29724345]

11.

Farrell H, Murray SA, Zammit A, Edwards AW. Management of Ciguatoxin Risk in Eastern Australia. Toxins (Basel). 2017 Nov 14;9(11) [PMC free article: PMC5705982] [PubMed: 29135913]

12.

Darius HT, Roué M, Sibat M, Viallon J, Gatti CMII, Vandersea MW, Tester PA, Litaker RW, Amzil Z, Hess P, Chinain M. Toxicological Investigations on the Sea Urchin Tripneustes gratilla (Toxopneustidae, Echinoid) from Anaho Bay (Nuku Hiva, French Polynesia): Evidence for the Presence of Pacific Ciguatoxins. Mar Drugs. 2018 Apr 06;16(4) [PMC free article: PMC5923409] [PubMed: 29642418]

13.

Chan TYK. Regional Variations in the Risk and Severity of Ciguatera Caused by Eating Moray Eels. Toxins (Basel). 2017 Jun 26;9(7) [PMC free article: PMC5535148] [PubMed: 28672845]

Disclosure: Jeremy Traylor declares no relevant financial relationships with ineligible companies.

Disclosure: Mayank Singhal declares no relevant financial relationships with ineligible companies.

Causes, Symptoms, Diagnosis and Treatment

Ciguatera is a disease that occurs when certain types of reef fish are eaten. The most common symptoms are neurological manifestations, such as paresthesia of the face, limbs, hallucinations, headache, loss of consciousness, delirium. Neuropsychological, cardiovascular, gastrointestinal disturbances are not uncommon. Diagnosis consists in the detection of a toxin in food, the characteristic symptoms of the disease. Treatment is pathogenetic and symptomatic; etiotropic therapy of ciguatera has not been developed, therapeutic measures are aimed at detoxification of the body.

General information

Ciguatera (fish food poisoning) – toxicosis associated with the action of the biological poison ciguatoxin. For the first time, the symptoms of ciguatera are found in the written sources of doctors of Ancient China (VII century AD), the clinic was described in more detail by the Englishman Locke in 1675. The toxin was isolated by the Hawaiian professor Scheuer (1967). More often, poisoning occurs in regions with a tropical, subtropical climate, water areas of the Indian, Pacific Oceans, and the Caribbean. It is believed that no more than 20% of cases of ciguatera are recorded annually, the real number of poisonings is not known for certain.

Ciguatera

Causes

The source of infection is phytoplankton, the dinoflagellate Gambierdiscus toxicus, which is food for small fish, which, in turn, are eaten by predatory relatives. The poison accumulates mainly in the liver and other internal organs of fish. Ciguatoxin is odorless and tasteless, and is not neutralized by heat treatment and freezing. To date, three species are known: Indian, Caribbean and Pacific ciguatoxin; the latter is more common and studied.

Main risk factors: eating reef fish species larger than 10 kg caught after the storm; viscera and heads are especially toxic. The destruction of reefs caused by typhoons and hurricanes significantly increases the toxicity of fish. The most dangerous include Spanish mackerels, yellow moray eels, sea bass, barracudas, sea basses, hamfeads. The danger of ciguatera increases significantly for the elderly, those with heart and arterial diseases, and obesity.

Pathogenesis

The pathogenesis is not fully understood. The main action of toxins (ciguatoxin, meitotoxin) is associated with disruption of the sodium channels of cell membranes, neuronal edema, blockage of potassium channels, which ultimately leads to impaired conduction of the nerve impulse. Uncontrollable and repetitive action potentials occur due to a single stimulus. Ciguatoxin is implicated in calcium channel dysregulation, nitrous oxide induction by cells.

Peripheral nervous system, sensory neurons, skeletal muscle, heart, gray matter become targets for exposure. It has been shown in an animal model that venom administration can lead to neuronal excitotoxicity of the cerebral cortex. It has been suggested that polyneural edema caused by the activity of the toxin and leading to degradation of the myelin sheath may be the cause of autoimmune neuronal aggression.

Symptoms

The incubation period of ciguatera is 1-24 hours. In a typical course, there is a feeling of numbness in the mouth, toothache, burning of the skin upon contact with cold water, a feeling of “loose” teeth. The disease is accompanied by nausea, spastic abdominal pain, vomiting, loose stools, severe muscle weakness. Often there is temperature dysesthesia – hot seems cold, and vice versa.

The severity of symptoms depends on the amount of toxin that has entered the body, and the duration of the disease usually does not exceed 4 days. There are frequent cases of a prolonged drop in blood pressure, accompanied by weakness and the impossibility of active actions in an upright position. In severe cases, shortness of breath appears, a decrease in the patient’s contact reaction to stimuli.

If the symptoms of the disease last 2-6 months or more, it is possible to talk about chronic ichthyotoxicosis. Manifestations of chronic ciguatera are mainly neurological (paresthesia, dysesthesia, cold allodynia, pruritus, headache), psychiatric (cognitive dysfunction, sleep disturbance, anxiety, memory loss, depression) and systemic (myalgia, severe asthenia, arthralgia).

Complications

The most common complication of ciguatera is acute cardiovascular failure, less often respiratory failure. With large fluid losses, dehydration shock and renal dysfunction develop. In severe cases, cerebral edema rapidly increases with the danger of wedging into the foramen magnum. Among 20% ​​of patients, there is a long course and subsequent chronicity of the pathology.

Due to the accumulation of toxin in adipose tissue and the slow rate of its excretion, recurrence of the disease is possible. Most often this is due to repeated intake of fish dishes, caffeine, chicken, nuts, alcohol, prolonged dehydration, stress. To the probable complications of the long course of ciguatera, modern infectology includes multiple sclerosis, chronic fatigue syndrome and brain tumors.

Diagnosis

Verification of the diagnosis of toxicosis and treatment is carried out by infectious disease specialists, often in intensive care units. Other medical specialists are involved according to indications. It is important to collect an epidemiological history, including stay in endemic areas, the nature of nutrition (eating fish). The main clinical, instrumental and laboratory signs of ciguatera are:

  • Physical data. Physical examination reveals symptoms of dehydration, diffuse abdominal tenderness, bradycardia, hypotension, severe muscle weakness, less commonly dyspnoea, and forced posture. The degree of impaired consciousness can change to coma, dysphoria is detected. Be sure to evaluate the presence of meningeal symptoms, the nature of vomiting and feces, the amount of urine.
  • Laboratory tests . There are no specific laboratory markers for ciguatera. With pronounced fluid losses in the general blood test, symptoms of hemoconcentration increase, the ratio of electrolytes changes, the activity of ALT, AST increases. General clinical analysis of urine – with signs of toxic damage in the form of proteinuria, microhematuria, increased concentration of urinary sediment.
  • Detection of infectious agents . There is only a toxicological analysis of probably toxic fish products; in some cases, a biological test on laboratory animals is used for differential diagnosis. A bacteriological examination of feces, washings, preserved suspicious food should be carried out.
  • Instrumental methods . Ultrasound examination of the internal organs is shown to exclude urgent surgical pathology, abdominal radiography to confirm or refute the symptoms of an acute abdomen; ECG, EEG – with a differential diagnosis with a gastric form of myocardial infarction and neurological pathologies, respectively.

Differential diagnosis is carried out with various poisonings, in which the only way to determine the source of the toxin is laboratory analysis. Pathologies of the central nervous system are rarely associated with a particular food. The clinic of ciguatera is similar with food poisoning, gastrointestinal salmonellosis, in which there is no neuronal dysfunction, and botulism, characterized by transient “top-down” lesions of the cranial nerves.

Treatment

There are currently no established protocols for the management of patients with ciguatera symptoms. Patients who are indicated for inpatient treatment are the elderly, pregnant women, people with chronic pathology of the heart and blood vessels, children, people with severe dehydration. Before contacting a doctor, it is recommended to wash the stomach, take medicinal sorbents, and perform siphon enemas to get rid of toxic food residues, provided that the patient is conscious.

Bed or semi-bed rest is prescribed. Specific nutrition for ciguatera has not been developed, it is recommended to exclude alcohol, nicotine, heavy, indigestible food, especially saturated with fats. The use of large amounts of water, detoxifying polyionic oral solutions is required for detoxification purposes, as well as to replenish fluid losses – which can be done in the absence of contraindications.

Conservative therapy

Treatment of ciguatera non-specific; many groups of pharmaceuticals have been proposed, while etiotropic agents have not yet been developed. It is necessary to start supportive measures in the first hours and days after the patient presents with suspected ciguatera; thus, manifest symptoms of severe damage to the heart muscle occur among 43% of patients. Most often, poisoning therapy is carried out with the help of:

  1. Pathogenetic treatment. It is carried out using infusion detoxification measures with succinate-containing, glucose-salt, polyionic solutions, cardioactive, vasopressor agents. In chronic course, antidepressants, cholestyramine, antiepileptic drug formulas, as well as non-steroidal anti-inflammatory drugs are indicated. Calcium channel blockers have proven themselves well. For the treatment of shock, plasma substitutes, dopamine preparations are used.
  2. Symptomatic therapy. Antiemetic, antispasmodic drugs are used, with severe diarrhea – astringents, sorbents; B vitamins are widely used. With skin itching, sedatives, antihistamines and desensitizing agents are indicated. Treatment with steroid hormones, opiates, barbiturates has little therapeutic potential with ciguatera.

Previously widely recommended and highly effective in vitro studies, mannitol should be administered within 24 hours of symptom onset, according to current research. When intravenous mannitol is administered later, its effect is comparable to the introduction of saline, respectively, the risk of side effects of the drug also increases.

Mannitol has been shown to help reduce swelling of nerve cells due to exposure to ciguatoxins and also acts as a scavenger of free radicals generated when cells are exposed to these poisons. Treatment of symptoms of paresthesia with ciguatera is carried out by physiotherapeutic methods (diadynamic currents, electrophoresis, magnetotherapy), course use of antihypoxants and antioxidants.

Experimental treatment

Local people in the South Pacific traditionally use a decoction of the leaves of the silver argusia (Heliotropium foertherianum) to treat the symptoms of ciguatera. In vitro studies have shown that this herbal preparation has the ability to compete with ciguatoxins, limiting their fixation on biological targets, so the remedy is considered most effective only when taken immediately after the first signs of poisoning.

Prognosis and prevention

The prognosis is favorable in most cases. Ciguatera rarely leads to death, however, with a burdened premorbid background and a high dose of toxin that has entered the body, untimely treatment, the lethality of this poisoning is 0.04-0.1%. The duration of neurological symptoms – paresthesia, depression, headaches, memory loss – after recovery can be weeks and months.

No specific prophylaxis of ciguatera has been developed. Non-specific measures are considered to be abstinence from the consumption of meat and viscera (liver, milk, caviar) of large predatory reef fish, especially in periods after natural disasters, spawning; it is necessary to exclude the purchase of fish from private individuals. In endemic zones, states carry out toxicological studies of fish products supplied for official sale.

Ciguatera – Pacific fish poisoning

09/18/2012

Cases of ciguatera poisoning are on the rise in Pacific island nations, scientists have found.

Small fish that feed on plankton growing on or near algae accumulate toxins produced by these plankton. When these small fish are eaten by larger species, the toxins move up the food chain, accumulating in even greater concentrations in the larger fish. If a person eats large fish, the toxins cause acute painful and destructive effects in the human nervous system, stomach, intestines and heart – ciguatera poisoning. Symptoms can last for months.

Scientists from Australia and the UK are examining the medical records of the Pacific Islands. They found that cigar fish poisoning has affected nearly half a million people over the past 35 years, posing a greater public health threat than previously thought.

Between 1973 and 2008, scientists clearly saw an increase in cases of ciguatera. Seven countries – Fiji, French Polynesia, Vanuatu, Kiribati, the Cook Islands and Tokelau – have reported more than 2,000 cases of poisoning per 100,000 population per year. The total number of cases of ciguatera reached 40 thousand in eleven years at the time of 2008.

“Everything points to a significant increase, and this makes cigautera more than a minor health problem,” says study co-author Tom Brewer of James Cook University.

“Although fatal cases are rare, ciguatera poisoning makes people seriously ill, unable to work for weeks or months, losing their livelihood. Therefore, it has major social and economic implications. Also, because of the poisoning, the variety of seafood that can be eaten narrows. What’s more, the numbers indicate that if you live in the Pacific, you have a 25 percent lifetime risk of ciguatera poisoning,” added Brewer.

Algae are replacing coral reefs throughout the Pacific as corals are impacted by human activities. Scientists suspect the increase in ciguatera is due to coral shrinkage and algae growth, land wash, overfishing, shipwrecks and microscopic algae that spread in ships’ ballast water.

However, the biggest contributor is the increase in sea surface temperature, which has risen to 28-29°C and above. This factor may be exacerbated by global warming, according to Foodprocessing.

“Ciguatera happens to over 400 different types of fish – and there’s no way to know if any particular fish is poisoned,” says lead author Mark Skinner of the University of Queensland.

“A detection test was already under development but proved to be unreliable, and any future tests are likely to be beyond the means of most Pacific Islanders.