Ciguatera is a widespread ichthyosarcotoxaemia with dramatic and clinically
important neurological features. This severe form of fish poisoning may pr
esent with either acute or chronic intoxication syndromes and constitutes a
global health problem. Ciguatera poisoning is little known in temperate co
untries as a potentially global problem associated with human ingestion of
large carnivorous fish that harbour the bioaccumulated ciguatoxins of the p
hotosynthetic dinoflagellate Gambierdiscus toxicus. This neurotoxin is stor
ed in the viscera of fish that have eaten the dinoflagellate and concentrat
ed it upwards throughout the food chain towards progressively larger specie
s, including humans. Ciguatoxin accumulates in all fish tissues, especially
the liver and viscera, of "at risk" species. Both Pacific (P-CTX-1) and Ca
ribbean (C-CTX-1) ciguatoxins are heat stable polyether toxins and pose a h
ealth risk at concentrations above 0.1 ppb. The presenting signs of ciguate
ra are primarily neurotoxic in more than 80% of cases. Such include the pat
hognomonic features of postingestion paraesthesiae, dysaesthesiae, and heig
htened nociperception. Other sensory abnormalities include the subjective f
eatures of metallic taste, pruritis, arthralgia, myalgia, and dental pain.
Cerebellar dysfunction, sometimes diphasic, and weakness due to both neurop
athy and polymyositis may be encountered. Autonomic dysfunction leads to hy
potension, bradycardia, and hypersalivation in severe cases. Ciguatoxins ar
e potent, lipophilic sodium channel activator toxins which bind to the volt
age sensitive (site 5) sodium channel on the cell membranes of all excitabl
e tissues. Treatment depends on early diagnosis and the early administratio
n of intravenous mannitol. The early identification of the neurological fea
tures in sentinel patients has the potential to reduce the number of second
ary cases in cluster outbreaks.