ciguatoxins and Acute-Disease

Ciguatera is an important form of human poisoning caused by the consumption of seafood. The disease is characterised by gastrointestinal, neurological and cardiovascular disturbances. In cases of severe toxicity, paralysis, coma and death may occur. There is no immunity, and the toxins are cumulative. Symptoms may persist for months or years, or recur periodically. The epidemiology of ciguatera is complex and of central importance to the management and future use of marine resources. Ciguatera is an important medical entity in tropical and subtropical Pacific and Indian Ocean regions, and in the tropical Caribbean. As reef fish are increasingly exported to other areas, it has become a world health problem. The disease is under-reported and often misdiagnosed. Lipid-soluble, polyether toxins known as ciguatoxins accumulated in the muscles of certain subtropical and tropical marine finfish cause ciguatera. Ciguatoxins arise from biotransformation in the fish of less polar ciguatoxins (gambiertoxins) produced by Gambierdiscus toxicus, a marine dinoflagellate that lives on macroalgae, usually attached to dead coral. The toxins and their metabolites are concentrated in the food chain when carnivorous fish prey on smaller herbivorous fish. Humans are exposed at the end of the food chain. More than 400 species of fish can be vectors of ciguatoxins, but generally only a relatively small number of species are regularly incriminated in ciguatera. Ciguateric fish look, taste and smell normal, and detection of toxins in fish remains a problem. More than 20 precursor gambiertoxins and ciguatoxins have been identified in G. toxicus and in herbivorous and carnivorous fish. The toxins become more polar as they undergo oxidative metabolism and pass up the food chain. The main Pacific ciguatoxin (P-CTX-1) causes ciguatera at levels=0.1 microg/kg in the flesh of carnivorous fish. The main Caribbean ciguatoxin (C-CTX-1) is less polar and 10-fold less toxic than P-CTX-1. Ciguatoxins activate sodium ion (Na ) channels, causing cell membrane excitability and instability. Worldwide coral bleaching is now well documented, and there is a strong association between global warming and the bleaching and death of coral. This, together with natural environmental factors such as earthquakes and hurricanes, and man-made factors such as tourism, dock construction, sewage and eutrophication, may create more favourable environments for G. toxicus. While low levels of G. toxicus are found th

Topics: Acute Disease; Animals; Caribbean Region; Ciguatera Poisoning; Ciguatoxins; Cnidaria; Demography; Dinoflagellida; Disease Outbreaks; Fishes, Poisonous; Foodborne Diseases; Humans; Incidence; Indian Ocean Islands; Muscles; Pacific States; Prevalence; Risk Factors; Socioeconomic Factors

Ciguatera fish poisoning arises from consumption of any of the 400 species of tropical marine reef fish containing polyether toxins. No laboratory method is available for clinical diagnosis of acute ciguatera poisoning. The objective of this pilot study was to ascertain the potential usefulness of a bioassay to detect ciguatoxins in humans suspected of acute intoxication. We analyzed plasma of healthy volunteers (asymptomatic negative controls), participants with gastrointestinal (GI) illness but without recent fish consumption (symptomatic negative controls), and participants with GI illness who had recently consumedfish.. Blood samples, questionnaires, and consent forms were collected from 11 symptomatic negative controls and 86 patients that visited emergency rooms in southern Puerto Rico over a 1-year period. Patients had consumed fish within 24 hour prior to the symptoms. Plasma samples were analyzed by a neuroblastoma cell bioassay that detects seafood toxins active at the sodium voltage-gated channel in a dose-dependent fashion. Concentrations were expressed in terms of brevetoxin-1 equivalents (ng PbTx-1 equiv/mL).. The mean plasma concentration of 14 asymptomatic negative controls was 39.4 ng PbTx-1 equiv/mL (range 2-74). Of 86 potential ciguatoxic patients who reported fish consumption, 43 had values within the range of normal volunteers, and 9 had concentrations in the nondiagnostic range (73.9-100 ng). Thirty-four patients (40%) had concentrations 3 standard deviations above asymptomatic negative controls (>100 ng PbTx-1 equiv/mL). They had a mean concentration of 1,074 +/- 244.5 ng PbTx-1 equiv/mL (range 101-7,056ng).. Preliminary findings of elevated PbTx-1 equivalents in 40% of the patients with both ciguatera symptomatology and fish consumption in a geographical area where ciguatera is common suggest that the neuroblastoma bioassay may be a potential diagnostic tool for acute ciguatera intoxication.

Topics: Acute Disease; Adolescent; Adult; Aged; Aged, 80 and over; Animals; Biological Assay; Child; Child, Preschool; Ciguatera Poisoning; Ciguatoxins; Dose-Response Relationship, Drug; Female; Foodborne Diseases; Gastrointestinal Diseases; Humans; Infant; Male; Marine Toxins; Middle Aged; Neurotoxins; Oxocins; Pilot Projects; Puerto Rico; Tropical Climate

Clinical reports and descriptions of chronic fatigue syndrome (CFS) and chronic ciguatera fish poisoning (CCFP) show great similarities in clinical symptomology. These similarities in the literature suggested the exploration of lipids in sera of CFS, CCFP, and other diseases with the membrane immunobead assay (MIA), which is typically used for screening ciguateric ocean fish. Sera from patients with other diseases, including hepatitis B, cancer, and diabetes, were included to assess the degree of specificity involved. Sera were treated with acetone in a ratio of 1 part serum to 4 parts acetone. The suspension was centrifuged, and the acetone layer was evaporated. The residue was weighed and redissolved in 1.0 mL methanol and tested by the MIA, undiluted and titered to 1:160. The undiluted acetone fraction of the 37 normal showed +/- activity to +activity with 16 no titer, 15 with 1:5 titer and two with 1:10 titer, and four with > or =1:40 titers. One hundred fifteen CFS sera showed 1 with 1+ and 114 with 2+ activity in the undiluted samples, 1 with 1:10 titer, 3 with 1:20 titer, 31 with 1:40 titer, 50 with 1:80 titer, and 30 with 160 titer. Thus 95.6% of the samples had > or =1:40 titer. Eight hepatitis B sera samples had > or =1:40 titers. Four CCFP samples had > or =1:40 titers. Three of 16 cancer samples had 1:40 titer. These data are summarized in Fig. 1. As shown in Table 1, a significant increase (P<0.001) in the chronic phase lipids (CPLs) was shown relative to the normal group. A preliminary chemical study in C18 octadecylsilyl columns showed all fractions (100% chloroform, 9:1 chloroform : methanol, 1:1 chloroform : methanol, and 100% methanol) to contain lipids reactive to MAb-CTX with different intensities. Prostaglandins were shown in 100% methanol fraction. Competitive MIA with crude fish ciguatoxin and CFS with synthetic JKLM ciguatoxin epitope suggested similarities in structure with ciguatoxin. This was compatible with the neuroblastoma assay demonstrated in the C(18) column fractions 9:1 and 1:1, chloroform : methanol solvents.

Topics: Acute Disease; Animals; Antibodies, Monoclonal; Cell Line, Tumor; Cell Survival; Chronic Disease; Ciguatera Poisoning; Ciguatoxins; Epitopes; Fatigue Syndrome, Chronic; Female; Hepatitis B; Humans; Lipids; Male; Mice; Neoplasms; Neuroblastoma

A young male presented with acute cervico-facial swelling and loss of consciousness, following ingestion of barracuda flesh. He recovered after administration of anti-histamines and steroids. Toxicity associated with barracuda is discussed.

Topics: Acute Disease; Adult; Animals; Ciguatoxins; Edema; Face; Fishes; Foodborne Diseases; Histamine H1 Antagonists; Humans; Male; Neck; Unconsciousness