Ciguatera poisoning occurs due to eating ciguatoxin-contaminated reef fish.
Generally, the contaminated fish shows no odor, color, or taste thus it is difficult to identify any major contamination.
Poisoning from tropical fish causes ciguatera toxicity food poisoning. Toxins accumulate in food chain from herbivorous fish to cause illness in humans.
The primary toxin and ciguatoxin is a lipid-soluble neurotoxin produced species. These toxins are heat-stable in nature while cooking, freezing, or drying activities do not neutralize them.
Gambierdiscus species produce ciguatoxin, it is a heat-stable neurotoxin while cooking or freezing cannot neutralize.
Predatory fishes are slowly built-up high levels of ciguatoxins which is derived from small fish those consumes algae and dead coral.
Epidemiology
Travelers shows high estimated incidence rate of 3 per 100 cases reported in US.
>50000 cases are diagnosed every year as per global estimation. Ciguatera is common in tropical waters regions between north and south latitudes.
The incidence and geography both rises with climate change. Ciguatera risk rises with coral reef destruction due to environmental impacts and construction.
Ciguatera poisoning in tropical and subtropical waters including Caribbean, India, and Pacific seas in coral reef areas.
Anatomy
Pathophysiology
Gambierdiscus toxic produces ciguatoxin precursors, but newer species have similar toxins.
Dinoflagellates on seaweed and corals feed small herbivorous fish, which consume large number of carnivorous fish.
CTx and toxins in fish are heat stable, lipid soluble, unaffected with temperature or cooking.
Chemists create ciguatoxins for research, immunoassay and mouse assay available to detect toxin in fish for biological studies.
Etiology
The causes of ciguatera toxicity are:
Types of ciguatoxins
Environmental factors
Source of ciguatoxins
Human exposure
Genetics
Prognostic Factors
A Miami study found 12 patients recovered fully from ciguatera poisoning in 6 months but could become hypersensitive to future exposure.
Ciguatoxin ingestion may cause bradycardia, hypotension, and T-wave abnormalities with symptoms resolve within 5 days.
In mothers it shows premature labor, spontaneous abortion, and harmful effects on fetus.
Ciguatera poisoning may cause high and prolonged morbidity in children.
Clinical History
Collect details including food and medical history to understand clinical history of patient.
Intervention therapies include mannitol therapy along with plasmapheresis, hemoperfusion, cardiac pacing for their potential refractory symptoms to prevent long-term complications.
use-of-phases-in-managing-ciguatera-toxicity
In the initial treatment phase, evaluation of patient history, physical examination and laboratory testing to confirm diagnosis.
Pharmacologic therapy is effective in the treatment phase as it includes use of antidotes, antihistamines, antidepressants, diuretics, anticonvulsants, and analgesics.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and intervention therapies.
The regular follow-up visits with the physician are scheduled to check the improvement of patients along with treatment response.
Ciguatera poisoning occurs due to eating ciguatoxin-contaminated reef fish.
Generally, the contaminated fish shows no odor, color, or taste thus it is difficult to identify any major contamination.
Poisoning from tropical fish causes ciguatera toxicity food poisoning. Toxins accumulate in food chain from herbivorous fish to cause illness in humans.
The primary toxin and ciguatoxin is a lipid-soluble neurotoxin produced species. These toxins are heat-stable in nature while cooking, freezing, or drying activities do not neutralize them.
Gambierdiscus species produce ciguatoxin, it is a heat-stable neurotoxin while cooking or freezing cannot neutralize.
Predatory fishes are slowly built-up high levels of ciguatoxins which is derived from small fish those consumes algae and dead coral.
Travelers shows high estimated incidence rate of 3 per 100 cases reported in US.
>50000 cases are diagnosed every year as per global estimation. Ciguatera is common in tropical waters regions between north and south latitudes.
The incidence and geography both rises with climate change. Ciguatera risk rises with coral reef destruction due to environmental impacts and construction.
Ciguatera poisoning in tropical and subtropical waters including Caribbean, India, and Pacific seas in coral reef areas.
Gambierdiscus toxic produces ciguatoxin precursors, but newer species have similar toxins.
Dinoflagellates on seaweed and corals feed small herbivorous fish, which consume large number of carnivorous fish.
CTx and toxins in fish are heat stable, lipid soluble, unaffected with temperature or cooking.
Chemists create ciguatoxins for research, immunoassay and mouse assay available to detect toxin in fish for biological studies.
The causes of ciguatera toxicity are:
Types of ciguatoxins
Environmental factors
Source of ciguatoxins
Human exposure
A Miami study found 12 patients recovered fully from ciguatera poisoning in 6 months but could become hypersensitive to future exposure.
Ciguatoxin ingestion may cause bradycardia, hypotension, and T-wave abnormalities with symptoms resolve within 5 days.
In mothers it shows premature labor, spontaneous abortion, and harmful effects on fetus.
Ciguatera poisoning may cause high and prolonged morbidity in children.
Collect details including food and medical history to understand clinical history of patient.
Persistent paresthesia, fatigue, joint pain, and muscle weakness
Mushroom Toxicity
Botulism
Shellfish Toxicity
Supportive and activated charcoal therapies are effective if given within 3 to 4 hours.
Ipecac syrup should be avoided because it causes fluid loss. Amitriptyline shows good results to decrease severity of residual symptoms.
Administer dose through IV fluids once diagnosis is confirmed. Patients with mannitol therapy should maintain good hydration.
Use of gabapentin helped in some patients and high vitamin B-12 intake may relieve symptoms.
Avoid orogastric lavage for ciguatera poisoning as risks outweigh benefits.
Emergency Medicine
Arrange coral transplantation and reef rehabilitation programs to repair damaged ecosystems.
Control agricultural runoff and fertilizers that cause eutrophication.
Give protection to herbivorous fish species to keep algae under control.
Proper storage and refrigeration should be done of fishes to prevent histamine formation.
Raw seafood and seawater should be avoided in individuals with chronic liver disease.
Proper awareness about ciguatera toxicity should be provided and its related causes with management strategies.
Appointments with a physician and preventing recurrence of disorder is an ongoing life-long effort.
Emergency Medicine
Activated charcoal:
It absorbs the drug in the intestine with multidose charcoal to interrupt enterohepatic recirculation.
Emergency Medicine
Cyproheptadine:
It prevents histamine release in blood vessels.
Hydroxyzine:
It inhibits respiratory and GI smooth-muscle constriction.
Emergency Medicine
Amitriptyline:
It blocks fast sodium channels that activate ciguatoxin.
Doxepin:
It inhibits histamine and acetylcholine activity with chronic and neuropathic pain.
Emergency Medicine
Mannitol:
It reduces symptoms to promote the excretion of ciguatoxin
Emergency Medicine
Gabapentin:
It acts through the alpha and delta auxiliary subunits of voltage-gaited calcium channels.
Emergency Medicine
Ibuprofen:
It inhibits inflammatory reactions and pain to decrease prostaglandin synthesis.
Diclofenac:
It inhibits prostaglandin synthesis to decrease cyclooxygenase activity.
Emergency Medicine
Intervention therapies include mannitol therapy along with plasmapheresis, hemoperfusion, cardiac pacing for their potential refractory symptoms to prevent long-term complications.
Emergency Medicine
In the initial treatment phase, evaluation of patient history, physical examination and laboratory testing to confirm diagnosis.
Pharmacologic therapy is effective in the treatment phase as it includes use of antidotes, antihistamines, antidepressants, diuretics, anticonvulsants, and analgesics.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and intervention therapies.
The regular follow-up visits with the physician are scheduled to check the improvement of patients along with treatment response.
Ciguatera poisoning occurs due to eating ciguatoxin-contaminated reef fish.
Generally, the contaminated fish shows no odor, color, or taste thus it is difficult to identify any major contamination.
Poisoning from tropical fish causes ciguatera toxicity food poisoning. Toxins accumulate in food chain from herbivorous fish to cause illness in humans.
The primary toxin and ciguatoxin is a lipid-soluble neurotoxin produced species. These toxins are heat-stable in nature while cooking, freezing, or drying activities do not neutralize them.
Gambierdiscus species produce ciguatoxin, it is a heat-stable neurotoxin while cooking or freezing cannot neutralize.
Predatory fishes are slowly built-up high levels of ciguatoxins which is derived from small fish those consumes algae and dead coral.
Travelers shows high estimated incidence rate of 3 per 100 cases reported in US.
>50000 cases are diagnosed every year as per global estimation. Ciguatera is common in tropical waters regions between north and south latitudes.
The incidence and geography both rises with climate change. Ciguatera risk rises with coral reef destruction due to environmental impacts and construction.
Ciguatera poisoning in tropical and subtropical waters including Caribbean, India, and Pacific seas in coral reef areas.
Gambierdiscus toxic produces ciguatoxin precursors, but newer species have similar toxins.
Dinoflagellates on seaweed and corals feed small herbivorous fish, which consume large number of carnivorous fish.
CTx and toxins in fish are heat stable, lipid soluble, unaffected with temperature or cooking.
Chemists create ciguatoxins for research, immunoassay and mouse assay available to detect toxin in fish for biological studies.
The causes of ciguatera toxicity are:
Types of ciguatoxins
Environmental factors
Source of ciguatoxins
Human exposure
A Miami study found 12 patients recovered fully from ciguatera poisoning in 6 months but could become hypersensitive to future exposure.
Ciguatoxin ingestion may cause bradycardia, hypotension, and T-wave abnormalities with symptoms resolve within 5 days.
In mothers it shows premature labor, spontaneous abortion, and harmful effects on fetus.
Ciguatera poisoning may cause high and prolonged morbidity in children.
Collect details including food and medical history to understand clinical history of patient.
Persistent paresthesia, fatigue, joint pain, and muscle weakness
Mushroom Toxicity
Botulism
Shellfish Toxicity
Supportive and activated charcoal therapies are effective if given within 3 to 4 hours.
Ipecac syrup should be avoided because it causes fluid loss. Amitriptyline shows good results to decrease severity of residual symptoms.
Administer dose through IV fluids once diagnosis is confirmed. Patients with mannitol therapy should maintain good hydration.
Use of gabapentin helped in some patients and high vitamin B-12 intake may relieve symptoms.
Avoid orogastric lavage for ciguatera poisoning as risks outweigh benefits.
Emergency Medicine
Arrange coral transplantation and reef rehabilitation programs to repair damaged ecosystems.
Control agricultural runoff and fertilizers that cause eutrophication.
Give protection to herbivorous fish species to keep algae under control.
Proper storage and refrigeration should be done of fishes to prevent histamine formation.
Raw seafood and seawater should be avoided in individuals with chronic liver disease.
Proper awareness about ciguatera toxicity should be provided and its related causes with management strategies.
Appointments with a physician and preventing recurrence of disorder is an ongoing life-long effort.
Emergency Medicine
Activated charcoal:
It absorbs the drug in the intestine with multidose charcoal to interrupt enterohepatic recirculation.
Emergency Medicine
Cyproheptadine:
It prevents histamine release in blood vessels.
Hydroxyzine:
It inhibits respiratory and GI smooth-muscle constriction.
Emergency Medicine
Amitriptyline:
It blocks fast sodium channels that activate ciguatoxin.
Doxepin:
It inhibits histamine and acetylcholine activity with chronic and neuropathic pain.
Emergency Medicine
Mannitol:
It reduces symptoms to promote the excretion of ciguatoxin
Emergency Medicine
Gabapentin:
It acts through the alpha and delta auxiliary subunits of voltage-gaited calcium channels.
Emergency Medicine
Ibuprofen:
It inhibits inflammatory reactions and pain to decrease prostaglandin synthesis.
Diclofenac:
It inhibits prostaglandin synthesis to decrease cyclooxygenase activity.
Emergency Medicine
Intervention therapies include mannitol therapy along with plasmapheresis, hemoperfusion, cardiac pacing for their potential refractory symptoms to prevent long-term complications.
Emergency Medicine
In the initial treatment phase, evaluation of patient history, physical examination and laboratory testing to confirm diagnosis.
Pharmacologic therapy is effective in the treatment phase as it includes use of antidotes, antihistamines, antidepressants, diuretics, anticonvulsants, and analgesics.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and intervention therapies.
The regular follow-up visits with the physician are scheduled to check the improvement of patients along with treatment response.
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