Ciguatera Fish Poisoning

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Ciguatera fish poisoning

AUTHOR: Erin N Marcus, MD, MPH, FACP
SECTION EDITORS: Daniel F Danzl, MD, Erica L Liebelt, MD, FACMT
DEPUTY EDITOR: Michael Ganetsky, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jan 2024.

This topic last updated: Jun 22, 2023.
INTRODUCTION
This topic describes the clinical manifestations, diagnosis, and management of ciguatera
poisoning. Poisoning caused by ingestion of other seafood (eg, scombroid fish, shellfish, or
pufferfish) is discussed in detail separately.
● (See "Overview of shellfish, pufferfish, and other marine toxin poisoning".)

● (See "Scombroid (histamine) poisoning".)
EPIDEMIOLOGY
Ciguatera fish poisoning is a foodborne illness that is caused by ingestion of reef fish (eg,
barracuda, amberjack, moray eel, and certain types of grouper, snapper, or parrotfish) that
are contaminated with toxins that arise from Gambierdiscus toxicus, a single-celled organism
that grows on coral reefs. Ciguatera fish poisoning accounts for approximately 20 percent of
the fish-related foodborne disease outbreaks in the United States [1], and is a common fish
food poisoning in tropical coastal regions [2]. Approximately 10,000 to 50,000 people develop
this poisoning annually worldwide [3,4], although this is not precise and may be an
underestimate because of missed diagnoses and underreporting [5,6]. In the United States,
an estimated 16,000 cases occur annually, resulting in more than 300 hospitalizations but
fewer than five deaths. This may be an underestimate since cases are not rigorously tracked
by the United States National Office for Harmful Algal Blooms [6,7].
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Most cases originate in the tropics and subtropics, between 35 degrees north latitude and 35
degrees south latitude. However, cases of ciguatera toxicity may also occur in more
temperate regions because of increasing tourism, fish exportation, and unusual fish
migration. Multiple cases of ciguatera fish poisoning have also been reported after ingestion
of imported fish purchased at markets in New York City [8] and in northern Germany [9], as
well as fish imported to Paris from Guadeloupe [10]. In addition, two cases of ciguatera fish
poisoning have been reported following consumption of fish (barracuda) caught off the
coast of South Carolina, well north of the typical location for such poisoning [11]. More
recently, cases have been reported in the Canary Islands [12].
More than 400 different fish species have been associated with ciguatera fish toxicity. Reef-
dwelling tropical fish such as barracuda, moray eel, amberjack, and certain types of grouper,
mackerel, parrotfish, and red snapper are the most common sources. Rare cases exist of
ciguatera fish poisoning occurring after the ingestion of temperate fish, including farm-
raised salmon [13]. In general, however, toxicity from nontropical fish is extremely rare.
The overall fatality rate from ciguatera fish poisoning is about 0.1 percent, with death usually
due to cardiovascular collapse or respiratory failure [3,14-17]. Mortality is lowest in the
Caribbean and areas of the world where the healthcare system is able to rapidly treat the
rare episodes of coma, bradycardia, or hypotension.
PATHOGENESIS
Ciguatera fish poisoning is caused by several distinct toxins, of which ciguatoxin is the best
known. These toxins are formed by dinoflagellates of the genus Gambierdiscus, which are
single-celled algae-like organisms that grow on and around coral reefs. Gambierdiscus
toxicus, which produces ciguatoxin, tends to proliferate on denuded coral surfaces [18].
The dinoflagellates are consumed by large, predatory fish (eg, barracuda, amberjack, moray
eel, snapper, and certain types of grouper) that concentrate the toxin in their organs and
flesh but are not affected by it. Ciguatera toxin-containing fish do not taste, smell, or appear
unusual. Cooking, marinating, freezing, and stewing fish do not destroy the toxins.
Ciguatoxin is a lipid-soluble, heat-stable, acid-resistant neurotoxin. It opens voltage-

dependent sodium channels in cell membranes, triggering membrane depolarization.
Ciguatoxin exposure in an animal model has caused long-term disruption of cerebral
function in association with upregulation of sodium channel expression in astrocytes [19].
Maitotoxin and scaritoxin, other ciguatera associated toxins, increase calcium ion influx
through excitable membranes [14] and permeability of sodium channels resulting in
norepinephrine and acetylcholine release, respectively [20].
CLINICAL MANIFESTATIONS
The patient affected with ciguatera fish poisoning frequently develops the following
constellation of clinical findings:
● Gastrointestinal – Gastroenteritis, including vomiting, diarrhea, and abdominal

cramping, typically begins three to six hours after eating contaminated fish, but can be
delayed up to 30 hours [15,16,21,22].
● Neurologic – Neurologic abnormalities usually appear 3 to 72 hours after the meal.

Clinical findings include peri-oral paresthesias, pruritus without urticaria or erythema, a
metallic taste in the mouth, painful dentition, a feeling that the teeth are loose, painful
urination, blurred vision, ataxia, and temperature-related dysesthesias (cold stimuli
perceived as hot or producing an abnormal, unpleasant sensation) [21-24].
Temperature-related dysesthesias are regarded by some as a specific finding of
ciguatera toxicity although it can also be seen in patients with neurotoxic shellfish
poisoning. In the South Pacific, paresis may occur in up to 10 percent of patients [25].
Reversible cerebellar dysfunction also can occur [26].
● Cardiovascular – Cardiovascular signs, including bradycardia, heart block, and

hypotension, can occur within hours of consumption [21,22].
The types and frequencies of presenting signs and symptoms vary according to locale and
likely reflect geographic differences in the various toxins and local food habits (eg, ingestion
of visceral or reproductive organs where the toxin is concentrated) that may increase toxin
consumption ( table 1) [5]. In Pacific and Indian Ocean regions, patients often display early
neurologic, gastrointestinal, and cardiovascular findings with neurologic findings
predominating [27]. Mental status changes, such as hallucinations or giddiness, and ataxia
may also be noted [28]. Although infrequent, life-threatening signs including coma and
respiratory distress have also been described [25,29].
By contrast, in the Caribbean, ciguatera fish poisoning usually presents with gastroenteritis
followed by a neurologic illness without mental status changes and is usually not life-
threatening [3,5,21,22,30,31].
A number of other clinical findings have been associated with ciguatera toxicity as follows:
● Chronic neuropsychiatric illness with fatigue and malaise [32]
● Fibromyalgia [33]
● Premature labor and spontaneous abortion [14]
● Painful sexual intercourse in men and women [34]
● Painful ejaculation in an affected male, followed by dyspareunia in the previously

unaffected female [14]
The course of ciguatera fish poisoning is variable. Gastrointestinal and, if present,

cardiovascular signs frequently resolve within 24 to 48 hours and rarely persist beyond four
days [5,21]. Neurologic abnormalities typically are more persistent, lasting from a few days
to several weeks. About 20 percent of patients have neurologic signs and symptoms that
persist for months; and up to 2 percent report findings, such as fatigue, weakness,
headache, or depression, that last for years [22,30,35]. However, patients who continue with
symptoms beyond one year warrant investigation for other potential etiologies [32].
Several case reports and series describe exacerbation or relapse of ciguatera toxicity in
patients who consume alcohol, caffeine, nuts, pork, chicken, or fish, including fish that did
not cause poisoning symptoms in other individuals sharing the meal [25,36-38]. In one case,
a patient developed neurologic symptoms (perioral paresthesia, myalgia, and malaise) and
arthralgia similar to his original ciguatera poisoning symptoms two years later after drinking
one beer [36]. Excessive physical exertion or dehydration within six months of original
symptoms has also been reported to cause worsening or relapsing symptoms [39].
Pregnant and nursing mothers — Perinatal transmission of ciguatera toxicity may occur. As
an example, a baby born by caesarean section to a mother with ciguatera poisoning
exhibited left sided facial palsy, possible hand myotonia, and respiratory distress [18]. These
symptoms resolved within six weeks.
Toxins can also be transmitted via breast milk [14]. Thus, nursing mothers with ciguatera fish
poisoning should be advised to stop breast feeding while symptomatic. To maintain
lactation, they can pump and discard breast milk. Though evidence is lacking, resumption of
breast feeding is probably safe once the mother's symptoms have completely resolved.
However, careful monitoring of the infant is warranted in such situations.
DIAGNOSIS
No clinical test is available to diagnose ciguatera fish poisoning. The diagnosis is established
clinically using the following criteria:
● A history of ingestion of a large reef fish commonly associated with ciguatera toxicity
(eg, moray eel, amberjack, barracuda, red snapper, or grouper)
● Gastrointestinal and neurologic features consistent with ciguatera fish poisoning,

especially temperature-related dysesthesia (see 'Clinical manifestations' above)
● Exclusion of other potential causes (see 'Differential diagnosis' below)
● Confirmation of ciguatoxin in the consumed fish, if possible. The United States National
Oceanographic and Atmospheric Administration helped to develop a fluorescent
receptor binding assay for detecting ciguatoxins in fish, which is now available
commercially [40,41]. If the fish is not available for analysis, ciguatera poisoning in
other individuals who consumed the same fish is also supportive.
Fish can be tested using a mouse bioassay and an IgG immunoassay, but these tests are
costly and time consuming and are not widely used [20]. Alternatively, cytotoxicity assays or
liquid chromatography-mass spectrophotometry can be employed although these
techniques are also not widely or rapidly available, other than through the US Food and Drug
Administration (FDA) or similar government agency in other countries [21,42].
Reporting of ciguatera poisoning is variable depending upon region. In the United States,
ciguatera is a reportable condition in many states, including California, Florida, Hawaii, North
Carolina, New York, Rhode Island, and South Carolina, as well as the US Virgin Islands [43].
Regardless of region, suspected cases should be reported to public health authorities when
diagnosed so that outbreaks can be identified and investigated. Ciguatera fish poisoning is
believed to be widely under-reported [43].
DIFFERENTIAL DIAGNOSIS
Ciguatera fish poisoning has a distinct clinical presentation and is often readily identified
once a careful food history is obtained. However, several other illnesses may have similar
features as follows [21]:
● Neurotoxic shellfish poisoning – Ingestion of shellfish contaminated by dinoflagellate

species Karenia brevis (formerly Gymnodinium breve), which is associated with red tides
in temperate waters, can produce gastrointestinal distress and neurologic symptoms
such as paresthesias of the face, mouth, and extremities, dizziness, ataxia, and muscle
aches. Patients may also experience temperature-related dysesthesia and seizures. All
symptoms, including neurologic toxicity, typically resolve within three days. The
development of symptoms soon after ingestion of shellfish helps to differentiate
neurotoxic shellfish poisoning from ciguatera poisoning. However, the diagnosis may
be clouded if the patient has also ingested reef fish. (See "Overview of shellfish,
pufferfish, and other marine toxin poisoning", section on 'Neurotoxic shellfish
poisoning'.)
● Paralytic shellfish poisoning – Paralytic shellfish poisoning is caused by ingestion of

bivalve mollusks, such as mussels, clams, scallops, and oysters, as well as crabs and
snails that are contaminated with dinoflagellates of the genus Alexandrium. These algae
are also associated with red tides in temperate waters. Physical findings occur within
hours of ingestion and include neurologic symptoms ranging from perioral tingling,
ataxia, difficulty swallowing, dizziness, paresthesias, weakness, paralysis, brainstem
dysfunction, and respiratory failure. The rapid onset of weakness and paralysis
distinguishes paralytic shellfish poisoning from ciguatera fish poisoning. (See "Overview
of shellfish, pufferfish, and other marine toxin poisoning", section on 'Paralytic shellfish
poisoning'.)
● Pufferfish poisoning – Pufferfish poisoning results in paresthesias of the face and

extremities, nausea, dizziness, weakness, loss of reflexes, paralysis, and hypotension
caused by tetrodotoxin, which blocks sodium channels. This poisoning is primarily
encountered in Japan where "Fugu" or blowfish is considered a delicacy. As with
paralytic shellfish poisoning, the development of weakness and paralysis differentiates
pufferfish poisoning from ciguatera fish poisoning. (See "Overview of shellfish,
pufferfish, and other marine toxin poisoning", section on 'Pufferfish poisoning
(tetrodotoxin)'.)
● Scombroid fish poisoning – Signs and symptoms of scombroid toxicity usually begin
within an hour of eating contaminated fish. The symptoms resemble an IgE-mediated
allergic reaction. The patient may suddenly experience flushing, a sensation of warmth,
an erythematous rash, palpitations, and significant tachycardia. The rash often is
especially prominent on the upper torso and face. Although the timing of symptoms
after eating fish is similar to ciguatera toxicity, scombroid otherwise shares very few of
its clinical features. (See "Scombroid (histamine) poisoning", section on 'Clinical
manifestations'.)
● Foodborne botulism – Ingestion of preformed botulinum toxin, typically found in

home canned foods, causes vomiting, diarrhea, abdominal pain, cranial nerve
dysfunction, and descending paralysis beginning hours to days after consumption. The
disease presentation can vary from mild complaints to death within the first 24 hours of
symptoms. Demonstration of the toxin in the blood is diagnostic. The lack of sensory
changes helps to distinguish foodborne botulism from ciguatera fish poisoning. (See
"Botulism", section on 'Clinical manifestations'.)
● Guillain-Barré syndrome – The acute inflammatory demyelinating polyneuropathy

variant of Guillain-Barré syndrome produces extremity paresthesias followed by
ascending weakness with associated hypo- or areflexia. In some patients, the
paresthesias may precede signs of weakness and suggest the diagnosis of ciguatera
fish poisoning. The diagnosis of Guillain-Barré syndrome is based upon the clinical
features of the characteristic development of weakness. Lack of pleocytosis on
examination of the cerebrospinal fluid and nerve conduction studies consistent with a
demyelinating polyneuropathy provide confirmation of the clinical impression. (See
"Guillain-Barré syndrome in adults: Pathogenesis, clinical features, and diagnosis",
section on 'Clinical features' and "Guillain-Barré syndrome in adults: Pathogenesis,
clinical features, and diagnosis".)
● Multiple sclerosis – Sensory symptoms of multiple sclerosis (MS) can include

paroxysmal onset of extremity paresthesias, pruritus dysesthesia, ataxia, fatigue, and
alteration of facial sensation that may be mistaken for early signs of ciguatera toxicity.
However, unlike ciguatera fish poisoning, MS causes vertigo, bowel and bladder
dysfunction, transverse myelopathy, and weakness. However, clinical findings vary
significantly in patients with MS and considerable overlap with neurologic symptoms of
ciguatera fish poisoning may occur. The diagnosis of MS is based upon clinical findings
and demonstration of demyelinating central nervous system lesions distributed over
space and time. (See "Manifestations of multiple sclerosis in adults" and "Evaluation
and diagnosis of multiple sclerosis in adults".)
● Eosinophilic meningitis – Similar to findings of ciguatera toxicity, patients with

eosinophilic meningitis commonly have nausea, vomiting, and paresthesias.
Paresthesias with residual areas of hyperesthesia can persist for several weeks, even
after other symptoms have resolved. However, unlike ciguatera fish poisoning, these
patients typically have suggestive features of meningitis including neck stiffness and
excruciating headache, which is usually frontal, occipital, or bitemporal. The diagnosis
of eosinophilic meningitis is made based upon clinical presentation and cerebral spinal
fluid eosinophilia, defined as the presence of more than 10 eosinophils/mm³ in the
cerebrospinal fluid (CSF) and/or eosinophils accounting for more than 10 percent of CSF
leukocytes. (See "Eosinophilic meningitis".)
● Organophosphate poisoning – Organophosphate poisoning has some features in

common with ciguatera toxicity including vomiting, diarrhea, and abdominal pain. It
can also uncommonly cause delayed neurotoxicity consisting of "stocking-glove"
paresthesias and ascending flaccid weakness after acute toxicity has resolved. However,
unlike ciguatera fish poisoning, organophosphate toxicity also has additional
cholinergic findings of salivation, bronchorrhea, and bronchospasm with accompanying
nicotinic features of muscle fasciculations, weakness, and paralysis. Lack of
anticholinergic response to atropine challenge and decreased red blood cell
acetylcholinesterase activity support the clinical diagnosis of organophosphate
poisoning. (See "Organophosphate and carbamate poisoning", section on 'Clinical
features' and "Organophosphate and carbamate poisoning", section on 'Diagnosis'.)
● Acute arsenic poisoning – Gastrointestinal symptoms, including diarrhea, vomiting,

and abdominal pain, are common early findings in acute arsenic poisoning and may be
accompanied by mental status changes and prolongation of the QT interval on
electrocardiogram. A sensorimotor peripheral neuropathy may occur one to three
weeks following acute exposure. Unlike ciguatera, however, arsenic poisoning may be
associated with excessive salivation, rash, acute kidney injury, and respiratory failure.
Acute exposure is usually established through urinary arsenic testing. (See "Arsenic
exposure and chronic poisoning", section on 'Arsenic concentrations'.)
In addition to the above diagnoses, chronic fatigue syndrome (CFS), also known as myalgic
encephalomyelitis/chronic fatigue syndrome (ME/CFS); or depression may develop as
comorbidities after ciguatera fish poisoning. (See "Clinical features and diagnosis of myalgic
encephalomyelitis/chronic fatigue syndrome" and "Unipolar depression in adults:
Assessment and diagnosis".)
TREATMENT
Gastrointestional decontamination — Although some experts have suggested activated

charcoal (AC) administration to bind ciguatoxins [21], vomiting frequently prevents its use
and most patients seek medical attention more than one hour after fish ingestion. Thus,
activated charcoal is not warranted. Similarly, because vomiting is a prominent feature of
ciguatera fish poisoning, syrup of ipecac also has no role in its treatment.
Initial supportive care — Initial treatment of ciguatera fish poisoning is primarily

supportive and consists of the following [21,44]:
● Airway and breathing – In the rare patients with respiratory distress, coma, or
weakness, the airway should be assessed and if not maintainable, secured by
endotracheal intubation [21,44]. (See "Rapid sequence intubation in adults for
emergency medicine and critical care" and "Rapid sequence intubation (RSI) in children
for emergency medicine: Approach".)
● Circulation – Hemodynamic instability caused by dehydration is frequently seen in

patients with ciguatera fish poisoning. Bradycardia and toxin-induced hypotension also
occur infrequently in some patients. Management for these conditions is as follows
[21]:
• Dehydration – Dehydration from vomiting and diarrhea warrants rapid fluid

repletion with isotonic saline (eg, 20 mL/kg normal saline, intravenously, maximum
initial volume, 1 L). Further fluid therapy should be guided by the degree of
dehydration and serum electrolyte values. (See "Treatment of hypovolemia
(dehydration) in children in resource-abundant settings" and "General principles of

disorders of water balance (hyponatremia and hypernatremia) and sodium balance
(hypovolemia and edema)".)
• Bradycardia – Intravenous atropine, including atropine infusion has been used to

treat symptomatic bradycardia. Dosing in these cases varies, but anecdotal evidence
from case reports suggests that high doses may be required (eg, 0.5 mg atropine
intravenously every five minutes to maintain a goal heart rate ≥60 beats per minute
in adults with no maximum total dosage) [22,45,46].
Management according to Advanced Cardiac Life Support (ACLS) and Pediatric

Advanced Life Support (PALS) guidelines is appropriate for patients who do not
respond to atropine ( algorithm 1 and algorithm 2). (See "Temporary cardiac
pacing".)
• Hypotension – In the rare patient for whom hypotension does not respond to initial
fluid resuscitation, vasopressors may be administered.
● Vomiting and diarrhea – Vomiting can be treated with antiemetics (eg, ondansetron).
Because diarrhea may be beneficial in removing ingested toxin and is typically self-
limited, antimotility agents should be avoided [21].
● Pruritus – Pruritus may be intense after ciguatera fish poisoning and can be treated
with antihistamines (eg, diphenhydramine, hydroxyzine, or cetirizine) [21].
Neurologic symptoms — Neurologic symptoms of ciguatera fish poisoning can be

prolonged and debilitating. Although several treatments have been proposed, evidence is
limited regarding benefit of any specific medical regimen.
● Paresthesias (polyneuropathy) – Ciguatoxins have complex actions on ion channels in

cell membranes which may explain some of the neuropathic pain in ciguatera fish
poisoning. Medications used to treat ciguatera fish poisoning are as follows:
• Mannitol – We suggest that fluid-repleted patients with significant neurologic

symptoms caused by ciguatera fish poisoning receive a single dose of mannitol (1
g/kg infused over one hour) [47]. Because mannitol can cause additional volume
loss, it should not be given to patients with significant dehydration or signs of shock.
The use of mannitol for the treatment of ciguatera fish poisoning is controversial.
Mannitol is known to reverse prolonged opening of sodium channels and to reduce
Schwann cell periaxonal edema in animal models [48]. Multiple uncontrolled trials
have found that intravenous mannitol, given at a dose of 0.5 to 1 g/kg, reduces
neurologic symptoms when given within the first 48 hours [21,49]. In addition, case
reports describe significant benefit from mannitol administration several weeks

after onset of symptoms [50,51].
However, the only randomized, placebo-controlled trial, conducted in 50 patients

with ciguatera fish poisoning, found that treatment with a single intravenous dose
of mannitol was no better in alleviating the acute signs and symptoms of ciguatera
poisoning than intravenous normal saline, and was associated with increased local
discomfort at the infusion site [52]. Significant improvement (50 percent reduction
on a subjective symptoms scale) was seen in both treatment groups with equal
frequency at 1, 3, and 24 hours after the infusion. However, the small size of this
study may have prevented detection of a clinically important difference.
Taken together, although the evidence base is weak and contradictory, a single dose
of mannitol is unlikely to be harmful if given to patients who are not dehydrated or
in shock and may be beneficial.
• Gabapentin – Gabapentin was reported to improve polyneuropathic symptoms in

two patients approximately one month after onset of symptoms [53]. However, it is
a relatively expensive therapy which limits its usefulness in the tropical regions
where ciguatera fish poisoning is most prevalent.
• Amitriptyline – Small case series suggest that amitriptyline can provide relief for
chronic paresthesias and pruritus but may not be effective for temperature-related
dysesthesias [39,54,55].
• Pregabalin – Two Australian travelers were treated with pregabalin titrated from 75
mg daily to a maximal dose of 150 mg twice daily, with resolution of their painful
peripheral neuropathy and cold dysesthesia after 17 weeks [56]. As with gabapentin,
pregabalin is expensive. It has numerous side effects, most notably sedation, and a
risk for dependency and abuse. If used, it should be tapered slowly [57].
● Headaches – Acetaminophen has been used for the treatment of headaches associated
with ciguatera toxicity [21]. Limited evidence from case reports suggest that nifedipine
also may provide benefit [55,58]. However, nifedipine should be avoided during the
acute phase of illness as it may cause or exacerbate hypotension.
● Chronic fatigue syndrome (CFS) and symptoms of depression – Although one case
report suggests that fluoxetine may benefit ciguatera patients suffering from CFS,
insomnia, and depression [58,59], these conditions may reflect comorbidity rather than
chronic ciguatera toxicity and warrant careful evaluation by a clinician with expertise in
their diagnosis and treatment [21]. (See "Clinical features and diagnosis of myalgic
encephalomyelitis/chronic fatigue syndrome" and "Unipolar depression in adults:
Assessment and diagnosis".)
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Diet and activity modification — Patients should be counseled that consumption of fish,
alcohol, caffeine, and nuts within six months of poisoning may trigger a recurrence of
symptoms and elimination of these foods from their diet is prudent [3,60,61]. Patients
should understand that future attacks of ciguatera fish poisoning might be worse than the
initial illness. Ciguatera is not an infectious disease, and individuals do not develop immunity
to the toxin [25].
Given the potential for painful sexual intercourse, including dyspareunia in previously
unaffected female sexual partners, the male patient should curtail sexual activity until
symptoms resolve [34]. Although not specifically studied, the use of condoms may present
an alternative to abstinence [62].
Overexertion with dehydration may also cause a relapse of ciguatera symptoms and should
be avoided until toxicity has resolved. The patient should then gradually increase activity
over time.
PREVENTION
The best way to prevent ciguatera fish poisoning is to avoid eating all high-risk fish, such as
barracuda, moray eel, and certain types of grouper, red snapper, and amberjack.
Unfortunately, no accurate analytical field test for caught fish is available [63]. Development
of such tests is difficult because of the lack of effect of ciguatoxin on live fish and the minute
amounts of ciguatoxin necessary to render a fish poisonous.
Traditional methods of identifying toxic fish, such as excessive hemorrhage when cutting
into a fish (bleeding test) and lack of rigor mortis several hours after the death of a fish (rigor
mortis test), can identify some fish that contain toxic levels of ciguatoxin in selected regions
(eg, French Polynesia), but have significant interobserver variability and poor discrimination
[63].
Fish mislabeling is common, and conscientious consumers may be unaware of the type of
fish they are consuming. DNA testing of more than 1200 commercially purchased fish
samples found that a third were mislabeled. Fish sold as snapper was the most commonly
mislabeled [64].
When in the tropics, it may be less risky to eat smaller fish and avoid eating fish organs, such
as the liver and the head, where the toxin concentrates [3]. Recreational fishermen should
also travel with experienced local guides who often know which reefs to avoid [65].
Community outreach and education can also help to warn travelers and increase recognition
and investigation of ciguatera fish poisoning outbreaks [21,66]. Some mass ciguatera fish
poisonings with mortalities occur when ciguatoxic fish species are shared in gatherings or
parties. Monitoring reef fish toxicity is particularly important when reef fish are collected
following large storms [67].
Upon diagnosis of ciguatera fish poisoning, clinicians should contact their local health
department and, if applicable, their regional poison control center so that investigation of
the fish source can prevent consumption of other toxic fish from the same reef.
ADDITIONAL RESOURCES
Regional poison control centers — Regional poison control centers in the United States are
available at all times for consultation on patients with known or suspected poisoning, and
who may be critically ill, require admission, or have clinical pictures that are unclear (1-800-
222-1222). In addition, some hospitals have medical toxicologists available for bedside
consultation. Whenever available, these are invaluable resources to help in the diagnosis and
management of ingestions or overdoses. Contact information for poison centers around the
world is provided separately. (See "Society guideline links: Regional poison control centers".)
Society guideline links — Links to society and government-sponsored guidelines from

selected countries and regions around the world are provided separately. (See "Society
guideline links: Envenomation by snakes, arthropods (spiders and scorpions), and marine
animals".)
SUMMARY AND RECOMMENDATIONS
● Pathogenesis – Ciguatera fish poisoning is caused by consumption of fish

contaminated with several distinct toxins (eg, ciguatoxin, saitotoxin, scaritoxin) that are
formed by dinoflagellates of the genus Gambierdiscus, single-celled algae-like
organisms that grow on and around coral reefs. These toxins are concentrated in the
organs and flesh of large, predatory reef fish (eg, moray eel, amberjack, barracuda, red
snapper, or grouper). Ciguatera toxin-containing fish do not taste, smell, or appear
unusual. Cooking, marinating, freezing, and stewing fish do not destroy the toxins. (See
'Pathogenesis' above.)
● Clinical manifestations – Although signs and symptoms vary according to locale

( table 1), the patient affected with ciguatera fish poisoning frequently develops the
following constellation of clinical findings (see 'Clinical manifestations' above):
• Gastrointestinal – Gastroenteritis, including vomiting, diarrhea, and abdominal

cramping.
• Neurologic – Neurologic abnormalities include peri-oral paresthesias, a metallic

taste in the mouth, painful dentition, a feeling that the teeth are loose, painful
urination, blurred vision, and temperature-related dysesthesias (cold stimuli
perceived as hot or producing an abnormal, unpleasant sensation). Temperature-
related dysesthesias are regarded as a specific finding of ciguatera toxicity. In the
South Pacific, paralysis may occur in up to 10 percent of patients.
• Cardiovascular – Less commonly bradycardia, heart block, and hypotension may

occur.
The course of ciguatera fish poisoning is variable. Gastrointestinal and, if present,

cardiovascular signs frequently resolve within 24 to 48 hours and rarely persist beyond
four days. Neurologic abnormalities typically are more persistent, lasting from a few
days to several weeks. Ingestion of alcohol, caffeine, nuts, or fish as well as excessive
physical exertion can cause exacerbation or recurrence of ciguatera toxicity.
● Diagnosis – The diagnosis of ciguatera fish poisoning is made using the following
clinical criteria (see 'Diagnosis' above):
• A history of ingestion of a large reef fish commonly associated with ciguatera

toxicity (eg, moray eel, amberjack, barracuda, red snapper, or grouper).
• Signs and symptoms consistent with ciguatera poisoning, especially temperature-

related dysesthesia (see 'Clinical manifestations' above)
• Exclusion of other potential causes (see 'Differential diagnosis' above)
• Confirmation of ciguatoxin in the consumed fish, if possible. If the fish is not

available for analysis, ciguatera fish poisoning in other individuals who consumed
the same fish is also supportive.
There is no clinical diagnostic test for ciguatera fish poisoning. Toxins can be detected
in cooked fish, but the various techniques are costly and not widely available. (See
'Diagnosis' above.)
● Management
• Initial supportive care – Initial treatment of ciguatera fish poisoning is primarily

supportive and consists of expectant management of dehydration, pruritus, and
hemodynamic instability. (See 'Initial supportive care' above.)
• Treatment of neurologic symptoms – In a patient with significant neurologic

symptoms caused by ciguatera fish poisoning who is fluid repleted, we suggest
administering a single dose of mannitol (1 g/kg infused over one hour) (Grade 2C).
Neurologic symptoms of ciguatera fish poisoning can be prolonged and debilitating.

Agents that have been effective in the treatment of other painful neuropathic
syndromes (eg, gabapentin, pregabalin, or amitriptyline) may improve symptoms of
chronic polyneuropathy, but should be used cautiously with close monitoring. (See
'Neurologic symptoms' above.)
• Diet and activity modification – In addition to avoiding excessive physical exertion,

patients with ciguatera toxicity should be counseled that consumption of fish,
alcohol, caffeine, and nuts within six months from onset of illness may trigger a
recurrence of symptoms and that it is prudent to avoid these foods. The male
patient should curtail sexual activity until symptoms resolve or, alternatively, may
use condoms. (See 'Diet and activity modification' above.)
● Prevention – The best way to prevent ciguatera fish poisoning is to avoid eating all
high-risk fish, such as barracuda, moray eel, and certain types of grouper, red snapper,
and amberjack. No accurate analytical field test for caught fish is available. When in the
tropics, it may be less risky to eat smaller fish and avoid eating fish organs where the
toxin is concentrated. Recreational fishermen should also travel with experienced local
guides who often know which reefs to avoid. (See 'Prevention' above.)
Upon diagnosis of ciguatera fish poisoning, clinicians should contact their local health
department and, if applicable, their regional poison control center so that investigation
of the fish source can prevent consumption of other toxic fish from the same reef. (See
'Prevention' above and 'Regional poison control centers' above.)
Use of UpToDate is subject to the Terms of Use.
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Topic 88331 Version 26.0
GRAPHICS
Clinical findings of ciguatera fish poisoning by geographical region
Relative frequency
Clinical features Geographical region (Ocean)
Caribbean Atlantic Pacific Indian
Gastrointestinal
Diarrhea +++ +++ ++ +
Vomiting ++ +++ ++ ++
Abdominal pain ++ Not reported ++ +
Neurologic
Extremity paresthesia ++ ++ +++ +++
Circumoral paresthesia ++ ++ +++ +++
Temperature dysesthesia ++ Not reported +++ ++
Pruritus ++ ++ +++ +
Dental pain or teeth feeling loose + Not reported + Not reported
Headache ++ ++ ++ +
Vertigo ++ ++ ++ Not reported
Myalgia or arthralgia ++ +++ +++ +
Weakness +++ + ++ +++
Hallucinations Not reported Not reported 0/+ +
Giddiness Not reported Not reported + +
Cardiovascular
Bradycardia Not reported Not reported + Not reported
Hypertension Not reported Not reported + Not reported
* Estimates of relative frequencies are based upon reports from series with at least 100 patients.
Data from: Friedman MA, Fleming LE, Fernandez M, et al. Ciguatera fish poisoning: treatment, prevention and management.
Mar Drugs 2008; 6:456.
Graphic 88891 Version 1.0
Adult bradycardia algorithm 2020 update
Reprinted with permission. ACLS Provider Manual. Copyright © 2020 American Heart Association, Inc.
Pediatric bradycardia with a pulse 2020 update
BP: blood pressure; ABCs: airway, breathing, circulation; ECG: electrocardiogram; CPR:
cardiopulmonary resuscitation; HR: heart rate; IV: intravenous; IO: intraosseous; AV: atrioventricular;
ET: endotracheal.
Reprinted with permission. Circulation 2020; 142:S469-S523. Copyright © 2020 American Heart Association, Inc.

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21/2/24, 19:53 Ciguatera fish poisoning - UpToDate

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Ciguatera fish poisoning

Literature review current through: Jan 2024.

● (See "Overview of shellfish, pufferfish, and other marine toxin poisoning".)

Ciguatoxin is a lipid-soluble, heat-stable, acid-resistant neurotoxin. It opens voltage-

● Gastrointestinal – Gastroenteritis, including vomiting, diarrhea, and abdominal

● Neurologic – Neurologic abnormalities usually appear 3 to 72 hours after the meal.

● Cardiovascular – Cardiovascular signs, including bradycardia, heart block, and

● Chronic neuropsychiatric illness with fatigue and malaise [32]

● Premature labor and spontaneous abortion [14]

● Painful sexual intercourse in men and women [34]

● Painful ejaculation in an affected male, followed by dyspareunia in the previously

The course of ciguatera fish poisoning is variable. Gastrointestinal and, if present,

● Gastrointestinal and neurologic features consistent with ciguatera fish poisoning,

● Exclusion of other potential causes (see 'Differential diagnosis' below)

● Neurotoxic shellfish poisoning – Ingestion of shellfish contaminated by dinoflagellate

● Paralytic shellfish poisoning – Paralytic shellfish poisoning is caused by ingestion of

● Pufferfish poisoning – Pufferfish poisoning results in paresthesias of the face and

● Foodborne botulism – Ingestion of preformed botulinum toxin, typically found in

● Guillain-Barré syndrome – The acute inflammatory demyelinating polyneuropathy

● Multiple sclerosis – Sensory symptoms of multiple sclerosis (MS) can include

● Eosinophilic meningitis – Similar to findings of ciguatera toxicity, patients with

● Organophosphate poisoning – Organophosphate poisoning has some features in

● Acute arsenic poisoning – Gastrointestinal symptoms, including diarrhea, vomiting,

Gastrointestional decontamination — Although some experts have suggested activated

Initial supportive care — Initial treatment of ciguatera fish poisoning is primarily

● Circulation – Hemodynamic instability caused by dehydration is frequently seen in

• Dehydration – Dehydration from vomiting and diarrhea warrants rapid fluid

(dehydration) in children in resource-abundant settings" and "General principles of

• Bradycardia – Intravenous atropine, including atropine infusion has been used to

Management according to Advanced Cardiac Life Support (ACLS) and Pediatric

Neurologic symptoms — Neurologic symptoms of ciguatera fish poisoning can be

● Paresthesias (polyneuropathy) – Ciguatoxins have complex actions on ion channels in

• Mannitol – We suggest that fluid-repleted patients with significant neurologic

reports describe significant benefit from mannitol administration several weeks

However, the only randomized, placebo-controlled trial, conducted in 50 patients

• Gabapentin – Gabapentin was reported to improve polyneuropathic symptoms in

Society guideline links — Links to society and government-sponsored guidelines from

SUMMARY AND RECOMMENDATIONS

● Pathogenesis – Ciguatera fish poisoning is caused by consumption of fish

● Clinical manifestations – Although signs and symptoms vary according to locale

• Gastrointestinal – Gastroenteritis, including vomiting, diarrhea, and abdominal

• Neurologic – Neurologic abnormalities include peri-oral paresthesias, a metallic

• Cardiovascular – Less commonly bradycardia, heart block, and hypotension may

The course of ciguatera fish poisoning is variable. Gastrointestinal and, if present,

• A history of ingestion of a large reef fish commonly associated with ciguatera

• Signs and symptoms consistent with ciguatera poisoning, especially temperature-

• Exclusion of other potential causes (see 'Differential diagnosis' above)

• Confirmation of ciguatoxin in the consumed fish, if possible. If the fish is not

• Initial supportive care – Initial treatment of ciguatera fish poisoning is primarily

• Treatment of neurologic symptoms – In a patient with significant neurologic

Neurologic symptoms of ciguatera fish poisoning can be prolonged and debilitating.

• Diet and activity modification – In addition to avoiding excessive physical exertion,

Use of UpToDate is subject to the Terms of Use.

3. Whittle K, Gallacher S. Marine toxins. Br Med Bull 2000; 56:236.

travel. CMAJ 2017; 189:E19.

33. Bilic E, Hajnsek S, Kello N, et al. Neurotoxin-induced fibromyalgia or fibromyalgia after

45. Senthilkumaran S, Meenakshisundaram R, Michaels AD, et al. Cardiovascular

64. https://oceana.org/reports/oceana-study-reveals-seafood-fraud-nationwide (Accessed o

66. Ciguatera fish poisoning poster. Florida Department of Health. http://www.floridahealth.

Clinical findings of ciguatera fish poisoning by geographical region