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The human neuropathology of encephalopathic mussel toxin poisoning.
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Acute manifestations of domoic acid poisoning: case presentations.
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[Clostridium perfringens. An outbreak of food poisoning in a military camp].
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Post-mortem analysis of samples from a human victim of a fatal poisoning caused by the xanthid crab, Zosimus aeneus.
After ingestion of a specimen of the crab Zosimus aeneus (Xanthidae), an East Timorese adult male died within several hours. Xanthid crabs are known to harbour paralytic shellfish toxins (PSTs), tetrodotoxin and palytoxin. A post-mortem examination did not find any obvious pathological abnormalities. This absence of pathologies is more often associated with PSTs and tetrodotoxin intoxication. A second, yet uneaten specimen of Z. aeneus from the same meal, contained a significant amount of PSTs and these same toxins were identified in the gut contents, blood, liver and urine of the victim. Metabolism of the PSTs occurred with the ingested crab harbouring gonyautoxin 2, gonyautoxin 3 and saxitoxin (STX) whereas neoSTX, decarbamoylSTX and STX dominated the PSTs in the victim's urine. The PST composition in the gut contents, in both their identity and proportion, was intermediate between the eaten crab and the urine suggesting that toxin conversion commenced in the victim's gut. The dose consumed by the victim was calculated to be between 1 and 2 microg STX equivalents/kg based upon the concentration in the remains of the cooked crab. The victim's meal did not consist solely of the toxic crab eaten and the possibility of other food items acting in a synergistic manner with the consumed PSTs cannot be discounted.
[Paralytic poisoning caused by mollusks].
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[Mytilic or paralytic seafood poisoning].
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Neurotoxic fish poisoning in the Solomon Islands.
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[Paralysing shell fish poisoning].
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[A case report of tetrodotoxin poisoning following ingestion of a trumpet shell "Boshubora"].
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[Food poisoning caused by Zeus siquijorensis frequently occurring in China].
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Yessotoxin, a shellfish biotoxin, is a potent inducer of the permeability transition in isolated mitochondria and intact cells.
The diarrhetic poisoning by bivalve molluscs, diarrhetic shellfish poisoning, is due to consumption of mussels containing biotoxins produced by some Dinoflagellate species. Toxic effects of yessotoxin (YTX) include morphological alterations of mitochondria from heart and liver but the biochemical basis for these alterations is completely unknown. This paper demonstrates that YTX is a very powerful compound that opens the permeability transition pore (PTP) of the inner mitochondrial membrane of rat liver mitochondria at nanomolar concentrations. The effect requires the presence of a permissive level of calcium, by itself incapable of opening the pore. The direct effect of YTX on PTP is further confirmed by the inhibition exerted by cyclosporin A (CsA) that is known as a powerful inhibitor of PTP opening. Moreover, YTX induces membrane depolarization as shown by the quenching of tetramethylrhodamine methyl ester (TMRM), also prevented by the addition of CsA. YTX caused PTP opening in Morris Hepatoma 1C1 cells, as shown by the occurrence of CsA-sensitive depolarization within minutes of the addition of submicromolar concentrations of the toxin. These results provide a biochemical basis for the mitochondrial alterations observed in the course of intoxication with YTX, offering the first clue into the pathogenesis of diseases caused by YTX, and providing a novel tool to study the PTP in situ.
Food poisoning associated with biotoxins in fish and shellfish.
PURPOSE OF REVIEW: In recent times the number of blooms of algae that produce toxins has increased in frequency, intensity and geographical distribution. This review describes some of the illnesses caused by fish and shellfish contaminated with toxins produced by marine algae and by bacteria. RECENT FINDINGS: The increase in toxic algal blooms may be a result of increased awareness, aquaculture, eutrophication, or transport of cysts in ship ballast. Improved chemical methods for the detection of algal toxins are now being developed, and so the number of toxins recognized is increasing. Toxicological data on some of these algal toxins are lacking. Despite the increase in occurrence of algal toxins, scombrotoxic poisoning remains the most common cause of food poisoning associated with the consumption of fish and shellfish. This may be real or it may be a reflection of lack of suitable tests for algal toxins or under-recognition by workers in health care. SUMMARY: The major problem worldwide in this field is the lack of pure toxins for use in developing and standardizing chemical methods for toxin detection. Such methods would permit increased testing of both food and clinical specimens, and hence would prevent the entry of toxic food into the food chain and increase laboratory confirmation of incidents of illness.
Infectious and toxic syndromes from fish and shellfish consumption. A review.
Primary care physicians care for large numbers of patients presenting with "food poisoning" or gastroenteritis. When a patient who presents with acute gastrointestinal illness, especially in conjunction with neurologic or cutaneous symptoms, is evaluated, the history should focus on past seafood consumption (particularly raw or undercooked seafood). The infectious syndromes are generally self-limited and respond to supportive care; exceptions are those caused by Vibrio cholerae and Vibrio vulnificus, which may be fatal in severe cases. The toxic syndromes are uncommon and fall into two categories: the histaminelike syndrome of scombroid poisoning and the neurotoxic syndromes, including ciguatera, paralytic shellfish poisoning, and puffer fish poisoning. Recognition of these clinical entities may lead to more appropriate management and preventive measures.
Water-related disease in Florida: continuing threats require vigilance.
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Neuropathology of experimental domoic acid poisoning in non-human primates and rats.
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Dose-response in an outbreak of non-bacterial food poisoning traced to a mixed seafood cocktail.
An outbreak of non-bacterial food poisoning presumed due to small round, structured viruses (SRSV) occurred at a national conference. A detailed postal survey of all conference attenders was carried out to ascertain the cause of the outbreak and 355 questionnaires were returned. Univariate analysis showed that mussels in the seafood cocktail were the likely vehicle of infection. A dose-response relationship between the amount of seafood cocktail consumed and the risk of illness was demonstrated. Dose-response has not previously been documented in a food-borne outbreak due to small round structured virus. Detailed quantitative food histories can be useful in eliciting dose-response relationships and may be crucial in establishing the vehicle of infection when investigating food poisoning following consumption of a set-menu meal. Their use should be considered in other outbreak situations.
Depuration kinetics and persistence of the cyanobacterial toxin microcystin-LR in the freshwater bivalve Unio douglasiae.
We carried out uptake and depuration experiments in the laboratory to investigate the effects of temperature (15 degrees C and 25 degrees C) on the depuration kinetics and persistence of a cyanobacterial toxin, microcystin-LR (MCYST-LR), in a freshwater bivalve, Unio douglasiae. Bivalves were fed toxic Microcystis cells in the 15-day uptake experiment and nontoxic diatoms in the following 15-day depuration experiment. Each bivalve's hepatopancreas was lyophilized and extracted with a butanol:methanol:water solution for analysis of MCYST-LR by high-performance liquid chromatography. The toxin in the organ accumulated rapidly after the beginning of the uptake experiment and reached approximately steady-state conditions on day 5 at concentrations of 130 +/- 11 microg g(-1) dry weight at 15 degrees C and 250 +/- 40 microg g(-1) at 25 degrees C. In the depuration experiments MCYST-LR was eliminated asymptotically from the tissue. The values of the depuration rate constant (k(d)), calculated with a first-order one-compartment model, were found to be 0.142 +/- 0.044 day(-1) at 15 degrees C and 0.226 +/- 0.046 day(-1) at 25 degrees C. The depuration Q(10) value from 15 degrees C to 25 degrees C equaled 1.6. This study was the first to reveal the kinetics of depuration for MCYST-LR in a bivalve. The results show that MCYST-LR may be eliminated slowly in autumn and winter and persist in the tissue until spring. Thus, in terms of toxicokinetics, the risk to people of being poisoned by bivalves would increase if toxic blooms occur in autumn.