ciguatoxins and Nervous-System-Diseases

Ciguatera fish poisoning (CFP), the most prevalent seafood poisoning worldwide, is caused by the consumption of tropical and subtropical fish contaminated with potent neurotoxins called ciguatoxins (CTXs). Ciguatera is a complex clinical syndrome in which peripheral neurological signs predominate in the acute phase of the intoxication but also persist or reoccur long afterward. Their recognition is of particular importance in establishing the diagnosis, which is clinically-based and can be a challenge for physicians unfamiliar with CFP. To date, no specific treatment exists. Physiopathologically, the primary targets of CTXs are well identified, as are the secondary events that may contribute to CFP symptomatology. This review describes the clinical features, focusing on the sensory disturbances, and then reports on the neuronal targets and effects of CTXs, as well as the neurophysiological and histological studies that have contributed to existing knowledge of CFP neuropathophysiology at the molecular, neurocellular and nerve levels.

Topics: Action Potentials; Animals; Ciguatera Poisoning; Ciguatoxins; Diagnostic Errors; Humans; Nervous System Diseases; Prevalence

This review focuses on the neurobiological actions of ciguatoxins and brevetoxins which are phycotoxins produced respectively by the dinoflagellates Gambierdiscus toxicus and Ptychodiscus brevis. These actions are illustrated in particular by the effects of the toxins on myelinated nerve fibres and on skeletal neuromuscular junctions of vertebrates. Ciguatoxins and brevetoxins, through different vectors, are responsible for human intoxications characterized mainly by neurological disturbances. The molecular target of these families of lipid-soluble cyclic polyethers is the voltage-gated sodium channel, a fundamental transmembrane protein involved in cellular excitability. The different toxins share a common binding site (the receptor-site 5) located on the alpha sub-unit of this neuronal transmembrane protein. Electrophysiological studies of the mode of action of ciguatoxins and brevetoxins identify these toxins as specific sodium channel activators. Indeed, during the action of these phycotoxins, sodium channels remain permanently opened, at the resting membrane potential, which produces a continuous entry of sodium ions in most excitable cells. Such a sodium entry has various consequences on sodium-dependent physiological mechanisms, consisting in a membrane depolarization which, in turn, causes spontaneous and/or repetitive action potential discharges and thereby increases membrane excitability. These neuronal discharges may be transient or continuous according to the preparation and the toxin tested. The increase in membrane excitability during the action of ciguatoxins and brevetoxins is responsible for the different effects exerted by these toxins on various chemical synapses and secretory cells. Another consequence of the continuous entry of sodium ions into cells was revealed using confocal laser scanning microscopy and vital staining of plasma membranes with the fluorescent dye FM1-43. These techniques made feasible the dynamic study of morphological alterations produced by ciguatoxins and brevetoxins on various cellular preparations in situ. Thus, it has been possible to bring to the fore that these phycotoxins cause a marked increase in the volume of nodes of Ranvier of myelinated nerve fibres, motor nerve terminals innervating skeletal muscle and perisynaptic non-myelinating Schwann cell somata. This increase could be reversed by hyperosmotic external solutions and completely prevented by the blockade of voltage-gated sodium channels. The mech

Topics: Animals; Ciguatoxins; Humans; Marine Toxins; Nerve Fibers, Myelinated; Nervous System Diseases; Neuromuscular Junction; Neurotoxins; Oxocins

Topics: Animals; Ciguatoxins; Foodborne Diseases; Humans; Nervous System Diseases; Risk Factors; Travel; Tuna

Topics: Animals; Ciguatoxins; Dinoflagellida; Europe; Foodborne Diseases; Humans; Japan; Marine Toxins; Mollusca; Nervous System Diseases; Paralysis; Shellfish; Water Microbiology

In November 2012, 23 cases of ciguatera with typical combinations of gastrointestinal and neurological symptoms occurred in Germany after consumption of imported tropical fish (Lutjanus spp.). A questionnaire was used to gather information on the disease course and fish consumption. All patients suffered from pathognomonic cold allodynia. Aside from two severe courses of illness, all other cases showed symptoms of moderate intensity. During a three-year follow-up, seven patients reported prolonged paresthesia for more than one year. Two of them reported further neuropathies over almost three years. This is the first time that long-term persistence of symptoms has been documented in detail. Outbreak cases were allocated to eight clusters in seven German cities. A further cluster was prevented by the successful recall of ciguatoxic fish. Three clusters were confirmed by the detection of ciguatoxin in samples of suspicious and recalled fish. An extrapolation on the basis of ciguatoxic samples revealed twenty prevented cases of ciguatera. Further officially unknown cases should be assumed. During the outbreak investigations, inadvertently falsely labelled fish species and fishing capture areas on import and retail level documents were observed. The ascertainment of cases and the outbreak investigations proved to be difficult due to inconsistent case reports to poisons centers, local health and veterinary authorities. In Germany, many physicians are unaware of the disease pattern of ciguatera and the risks caused by tropical fish. The occurrence of further outbreaks during the following years emphasizes the increasing significance of ciguatera in Germany.

Topics: Animals; Ciguatera Poisoning; Ciguatoxins; Cluster Analysis; Comorbidity; Disease Outbreaks; Female; Fishes; Gastrointestinal Diseases; Germany; Humans; Incidence; Male; Nervous System Diseases; Population Surveillance; Risk Factors

To review the clinical features and laboratory investigations of ciguatera patients in Hong Kong between 2004 and 2007 in order to show the timely sampling of implicated fish from ciguatera victims and application of validated mouse bioassay for confirming suspected clinical cases of ciguatera.. Diagnosis of the ciguatera victims was based on history of coral fish consumption and clinical presentations stated in official guidelines for clinical diagnosis of ciguatera fish poisoning in Hong Kong. Food remnants of coral fish samples were collected swiftly from ciguatera victims between 2004 and 2007 for ciguatoxins (CTXs) analysis.. Major clinical symptoms in ciguatera patients included gastrointestinal and neurological effects including limb numbness and diarrhoea, which developed at 0.5 to 15 hours after consumption of fish. In most cases, neurological symptoms were more common than gastrointestinal symptoms. A broad range of attack rate (10%-100%) was observed in each ciguatera outbreak. Validated mouse bioassay on ether extracts of the food remnant samples confirmed that all were CTXs-positive (<0.5 - 4.3 MU/20 mg ether extract) and directly linked to the corresponding ciguatera cases.. Consistency between clinical and laboratory analysis for ciguatera poisoning illustrates the application of laboratory mouse bioassay in a timely fashion for confirming ciguatera poisoning cases and implementing effective public health measures. With further improvement in laboratory techniques, features of ciguatera fish poisoning cases can be better defined. Further studies are needed to determine the risk of each class of CTXs (Pacific-, Indian- and Caribbean-CTXs) in Hong Kong.

Topics: Animals; Biological Assay; Ciguatera Poisoning; Ciguatoxins; Disease Outbreaks; Fishes; Gastrointestinal Diseases; Hong Kong; Humans; Mice; Nervous System Diseases; Prevalence; Public Health; Risk Factors; Time Factors

Ciguatera is a widespread ichthyosarcotoxaemia with dramatic and clinically important neurological features. This severe form of fish poisoning may present with either acute or chronic intoxication syndromes and constitutes a global health problem. Ciguatera poisoning is little known in temperate countries as a potentially global problem associated with human ingestion of large carnivorous fish that harbour the bioaccumulated ciguatoxins of the photosynthetic dinoflagellate Gambierdiscus toxicus. This neurotoxin is stored in the viscera of fish that have eaten the dinoflagellate and concentrated it upwards throughout the food chain towards progressively larger species, including humans. Ciguatoxin accumulates in all fish tissues, especially the liver and viscera, of "at risk" species. Both Pacific (P-CTX-1) and Caribbean (C-CTX-1) ciguatoxins are heat stable polyether toxins and pose a health risk at concentrations above 0.1 ppb. The presenting signs of ciguatera are primarily neurotoxic in more than 80% of cases. Such include the pathognomonic features of postingestion paraesthesiae, dysaesthesiae, and heightened nociperception. Other sensory abnormalities include the subjective features of metallic taste, pruritus, arthralgia, myalgia, and dental pain. Cerebellar dysfunction, sometimes diphasic, and weakness due to both neuropathy and polymyositis may be encountered. Autonomic dysfunction leads to hypotension, bradycardia, and hypersalivation in severe cases. Ciguatoxins are potent, lipophilic sodium channel activator toxins which bind to the voltage sensitive (site 5) sodium channel on the cell membranes of all excitable tissues. Treatment depends on early diagnosis and the early administration of intravenous mannitol. The early identification of the neurological features in sentinel patients has the potential to reduce the number of secondary cases in cluster outbreaks.

Topics: Ciguatoxins; Humans; Nervous System Diseases

Societal awareness of toxins in general has been heightened in the past few decades with the increased focus on environmental concerns. The medical profession has been aware of the effects of some toxins such as lead and mercury for centuries, while other toxins have more recently been identified. Neuroscience nurses are challenged to be aware of the neurological effects of lesser known toxins, such as ciguatera and methyl bromide, and to meet the complex needs of patients who are suffering from the effects of toxic levels of these substances.

Topics: Adult; Agricultural Workers' Diseases; Air Pollutants, Occupational; Ciguatoxins; Critical Care; Humans; Hydrocarbons, Brominated; Male; Nervous System Diseases; Neurologic Examination; Neurotoxins; Nursing Diagnosis; Protective Clothing