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Firefighters in Queensland are exposed to hot, humid weather conditions that contribute to the overall workload encountered during emergency operations. Responding to certain hazardous material incidents requires firefighters to wear fully encapsulated chemical protective suits for a maximum period of 20 minutes. The nature of these suits, combined with workload and environmental conditions, poses a potential heat stress problem for firefighters. This study evaluates the heat-induced physiological responses of firefighters while wearing fully encapsulated chemical protective suits in a series of controlled thermal environments. Heart rate, body (aural) temperature, blood pressure, fluid loss, and a rating of perceived exertion were measured to evaluate the effect of increasing ambient air temperature during the performance of standard tasks. The results of the study indicated that the significant increase in heart rate, body temperature, and blood pressure was directly related to the increase in air temperature. The research indicates that the recommended suit wearing time of 20 minutes provided adequate physiological protection under the research conditions.

Between July 1997 and August 1998 we investigated three clusters (26 cases) of ciguatera poisoning in the inner Sydney area. Tropical reef fish were implicated in each cluster. Most of those affected had musculoskeletal, neurological and gastrointestinal symptoms. The clusters raise questions about the need for rapid diagnosis and enhanced surveillance mechanisms, the regulation of fish supply, and the lack of testing facilities for ciguatera toxin.

This study reports the effects of mannitol on nerve conduction when used as a therapeutic agent in mammals following the administration of ciguatoxin. Electrophysiological studies were performed in vivo on the rat ventral coccygeal nerve. The absolute and relative refractory periods, conduction velocity and the supernormal response were measured in rats treated with i.p. ciguatoxin, both prior to, and following, the infusion of i.v. mannitol. Ciguatoxin induced significant prolongation of the absolute refractory period as well as significant slowing of the compound nerve conduction velocity. The magnitude of the supernormal response was significantly increased and the duration of the supernormal period extended in ciguatoxin-treated animals. Recordings collected following the infusion of mannitol in these ciguatoxin-treated animals showed that mannitol did not reverse the effects of ciguatoxin on nerve conduction in any of the parameters measured.

Electrophysiological studies were performed on the ventral tail nerve of adult rats following intraperitoneal injection of a crude extract of ciguatoxin from known toxic fish flesh. Ciguatoxin induced significant slowing of both mixed and motor nerve conduction velocities and also significant reductions in both motor and mixed nerve amplitudes. Both absolute and supernormal periods were significantly prolonged together with an increase in the magnitude of the supernormal response. These electrophysiological disturbances were modified or blocked by intraperitoneal lidocaine. These findings suggest that lidocaine may have a potential therapeutic application in the treatment of the neurological disturbance in acute ciguatera poisoning in humans.

A study of soluble protein from skeletal muscle of Scomberomorus commersoni was undertaken to elucidate aspects of ciguatoxin (CTX) bioaccumulation in marine teleosts. Skeletal muscle tissue samples from toxic and non-toxic specimens were subjected to fractionation, centrifugation, (NH4)2SO4 precipitation and Sephacryl S-200 chromatography of soluble proteins. Toxicity associated with various fractions was assessed by mouse bioassay, and toxic and non-toxic soluble protein fractions were compared using SDS-PAGE. CTX eluted from Sephacryl S-200 with soluble proteins of apparent mol. wt between 35,500 and 59,500. The toxic eluate contained 1.4% of total sample protein and 15% of total sample toxicity, with an associated 7.2-fold increase in specific activity. SDS-PAGE comparisons show two protein bands in the 37,400 and 40,600 mol. wt range which appeared in toxic soluble protein fractions, but were not detectable in control (non-toxic) samples. These findings are interpreted as being consistent with the association of CTX with at least one monomeric soluble protein of 37,000 to 40,600 mol. wt from toxic S. commersoni skeletal muscle.

A compound lethal to mice (i.p.) was extracted from samples of Oscillatoria erythraea, four species of mollusc and one species of molluscivorous teleost collected from the south-east coast of Queensland, Australia, during and shortly after O. erythraea blooms. The compound was chemically indistinguishable from ciguatoxin (CTX) on the basis of solvent extraction and partitioning and silicic acid chromatography. Residues derived from toxic samples elicited signs of intoxication, death and histopathological changes in mice, consistent with extracts of ciguatoxic material. Stick enzyme immunoassay tests and thin layer chromatography assessment of extracts indicated the presence of ciguatoxin-like polycyclic ether(s). O. erythraea is implicated as a potential elaborator of a CTX-like compound in the tropical marine biota.

The absolute refractory period, relative refractory period, and the duration and magnitude of the supernormal period were measured after incubation of fish nerves with ciguatoxin and other channel modifying compounds, tetrodotoxin, veratridine, verapamil, and lignocaine. In vitro electrophysiological studies were carried out on the lateral line nerve of the whiting, Sillago ciliata Cuvier. Electrophysiological changes in fish nerves after exposure to ciguatoxin (0.3 MU.ml-1) and veratridine (1 x 10(-5) M) are similar to changes that occur in mammalian nerves and include an increase in the absolute refractory period, the relative refractory period, and the magnitude and duration of supernormality. The effects of ciguatoxin (0.3 MU.ml-1) in fish nerves were antagonised by tetrodotoxin (5 x 10(-10) M), verapamil (5 x 10(-7) M), and lignocaine (1 x 10(-5) g/ml-1). The nerves of Sillago ciliata used in this study responded to ciguatoxin and its antagonists in a similar manner to mammalian nerves, suggesting that these teleost nerves have no specific electrophysiological mechanism to cope with this toxin.

Ciguatera poisoning is the most common fish food poisoning encountered in man. Electrophysiological studies were performed on the ventral nerve of the tail on adult rats following intraperitoneal injection of toxic fish extract. Significant slowing of both mixed and motor nerve conduction velocities and F wave responses were recorded. Motor and mixed nerve amplitudes were significantly reduced. Both absolute and supernormal periods were significantly prolonged together with an exaggeration of the supernormal response. These findings indirectly suggest that ciguatoxin acts on mammalian nerve by prolonging sodium channel activation.

Fifteen cases of acute ciguatera poisoning were subjected to electrical studies on the sural and common peroneal nerves. Significant slowing of sensory conduction velocity and prolongation of the absolute refractory, relative refractory and supernormal periods were recorded. These findings indirectly suggest that ciguatoxin causes an abnormally prolonged sodium channel opening in nerve membranes.