ciguatoxins and Bradycardia

The aim of the present review was to collect the main observations reported until now concerning the cardio-circulatory effects of polyether toxins, called ciguatoxins, which are involved in an endemic intoxication named ciguatera found in tropical and subtropical countries. Ciguatera is caused by the ingestion of fishes contaminated with the dinoflagellate Gamberdiscus toxicus. Due to both tropical fish exportation destined for food and tourism, the disease has now spread out to temperate areas. Several toxins have been isolated and purified from different fish species living in different geographical areas. They are classified into three main groups by the nature of certain cycles of their carbon skeleton. Clinical reports show evidence that ciguatera intoxication affect both electrocardiograms and blood pressure. In most cases, ciguateric intoxication mainly evoked bradycardia, hypotension, and the alteration of S-T segment in the electrocardiogram. Isolated and purified ciguatoxins strongly altered the morphology of cardiac tissue inducing swelling of the cells and alterations of cellular organelles. These toxins impair the conduction of cardiac nerves and increase the opening probability of Na+ channels in intracardiac ganglions. Depending on the concentration applied, the substances exerted either a fast positive inotropic effect or a negative inotropic effect on the contraction of mammalian atrial and ventricular cardiac muscle. These effects were attributed to a release of noradrenaline and acetylcholine from neural terminals of the autonomic nervous system present in cardiac tissue. They also exert a slow delayed inotropic effect on the contraction which has been attributed to a direct effect of the toxins on tetrodotoxin-sensitive voltage-dependent Na+ channels of cardiac membranes. Ciguatoxins depolarized the membrane of mammalian atrial and ventricular preparations and shifted the threshold of sodium current activation to more negative membrane potentials. In conclusion, the inotropic effects of ciguatoxins on cardiac tissues mainly depend on the toxin concentration sensitivity of autonomic nerve terminals, which released noradrenaline and/or acetylcholine, while the ciguatoxin-induced increase of the sodium influx could be involved in the cardiac cell swelling which coincides with reports in which ciguatoxins induced a mannitol-inhibited swelling of the Node of Ranvier.

Topics: Animals; Bradycardia; Cardiovascular System; Cell Size; Ciguatoxins; Electrocardiography; Guinea Pigs; Heart; Heart Conduction System; Humans; Hypotension; Membrane Potentials; Mice; Molecular Structure; Myocardial Contraction; Ranidae; Rats; Sodium Channels; Synaptic Transmission

Ciguatera results when ciguatoxin-contaminated coral reef fish from tropical or subtropical waters are consumed. The clinical features that present in affected persons are mainly gastrointestinal, neurological, general, and much less commonly, cardiovascular. We report the case of a 50-year-old man who developed the characteristic combination of acute gastrointestinal and neurological symptoms after the consumption of an unidentified coral reef fish head. In addition to those symptoms, he developed dizziness, severe bradycardia (46 bpm) and prolonged hypotension, which required the administration of intravenous atropine and over three days of intravenous fluid replacement with dopamine infusion. Patients with ciguatera can develop severe bradycardia and prolonged hypotension. Physicians should recognise the possible cardiovascular complications of ciguatera and promptly initiate treatment with intravenous atropine, intravenous fluid replacement and inotropic therapy if such complications are observed.

Topics: Animals; Bradycardia; Ciguatera Poisoning; Ciguatoxins; Fishes; Humans; Hypotension; Male; Middle Aged

We report an outbreak of ciguatoxin poisoning after barracuda fish ingestion in southern Taiwan. Three members of a family developed nausea, vomiting, watery diarrhea, and myalgias about 1 hour after eating three to ten eggs of a barracuda fish. Numbness of the lips and extremities followed the gastrointestinal symptoms about 2 hours after ingestion. Other manifestations included hyperthermia, hypotension, bradycardia, and hyperreflexia. Bradycardia persisted for several days, and one patient required a continuous infusion of intravenous atropine totaling 40 mg over 2 days. Further follow-up of the patients disclosed improvement of neurologic sequelae and bradycardia, but sensory abnormalities resolved several months later. In conclusion, ciguatoxin poisoning causes mainly gastrointestinal and neurologic effects of variable severity. In two patients with ciguatoxin poisoning after barracuda fish egg ingestion, persistent bradycardia required prolonged atropine infusion.

Topics: Aged; Animals; Bradycardia; Ciguatera Poisoning; Ciguatoxins; Diagnosis, Differential; Disease Outbreaks; Female; Fishes; Food Contamination; Humans; Male; Middle Aged; Seafood; Taiwan

Epidemiologic characterization of ciguatera fish poisoning has been limited by lack of laboratory confirmation, absence of prospective follow-up, and incomplete analysis of age-related factors. A 1985 outbreak on the island of Kauai in the state of Hawaii that involved 15 persons of various ages was investigated to determine factors associated with disease severity. The presence of ciguatoxin was detected in leftover portions of the implicated fish by enzyme immunoassay. All cases were medically and epidemiologically investigated and followed prospectively. Ten of the 15 cases demonstrated bradycardia; seven were hospitalized, including two requiring placement in intensive care. Bradycardia was associated with increasing age and body weight (P < 0.01 and < 0.05, respectively) as well as the amount of toxic fish consumed (P < 0.01). Duration of illness ranged from two to 132 days. Increasing duration of illness was correlated with both increasing age and weight (rs = 0.64 and rs = 0.72, respectively, both P < 0.01) and was independent of amount and components of toxic fish consumed. The correlation between increasing age and weight with duration and severity of symptoms may be explained by prior subclinical toxin exposure and is consistent with the observation that repeated ciguatoxin exposures are associated with more severe illness. The association between amount of toxic fish consumed and bradycardia is consistent with an increased dose of ciguatoxin. The findings of this outbreak investigation support previously unconfirmed observations.

Topics: Adolescent; Adult; Age Factors; Aged; Animals; Body Weight; Bradycardia; Child; Child, Preschool; Ciguatera Poisoning; Ciguatoxins; Cohort Studies; Disease Outbreaks; Eating; Female; Fishes; Food Analysis; Foodborne Diseases; Hawaii; Humans; Immunoenzyme Techniques; Male; Middle Aged; Prospective Studies; Time Factors