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PubMedDate not supplied

Evaluation of laboratory performance of the AOAC method for PSP toxin in shellfish.

Laboratory performance of the official AOAC method for paralytic shellfish poison (PSP) toxin in shellfish was evaluated. Two series of naturally toxic shellfish split samples were distributed (15 in 1979 and 19 in 1982) to state shellfish-monitoring laboratories which participate in the National Shellfish Sanitation Program. The laboratories performed bioassays on duplicate 100 g portions of each 220 g split sample. Bioassays were consistent among the laboratories and compared favorably with those of previous studies.

Animals↗
PubMed1987

Shellfish and fish poisoning related to the toxic dinoflagellates.

At least four different species of the toxic dinoflagellates cause shellfish and fish poisoning in the United States: Ptychodiscus brevis, neurotoxic shellfish poisoning; Protogonyaulax catenella and P tamarensis, paralytic shellfish poisoning; and Gambierdiscus toxicus, ciguatera fish poisoning. These three disorders have similar clinical manifestations, primarily neurologic and alimentary. A complete history is essential; confirmation, while dependent on specific laboratory analysis, is usually based on a history of ingestion of fish or shellfish previously associated with these types of poisonings. The principal toxins affect sodium channels; Ptychodiscus brevis toxins and ciguatoxin by stimulating these channels and saxitoxin by blocking them. Since no antidote is known, treatment is symptomatic. Public health measures and public education are necessary to prevent this form of poisoning.

Animals↗
PubMedDate not supplied

[A new pathophysiological explanation of ciguaterra (author's transl)].

After pointing out clinical, biochemical and biological similarities between paralytic shellfish poisoning and ciguaterra fish poisoning, the authors describe their recent discoveries in regard to ciguaterra origin. The causal agent searched without results since many years, might be a dinoflagellate, of the genus Diplopsalis.

Ciguatera Poisoning↗
PubMed1991

Poisonous marine morsels.

Consumption of seafood is increasing and physicians should know more about ichthyosarcotoxism, or fish-flesh poisoning. It appears in a variety of forms: poisoning, ciguatera, tetrodotoxin and scombroid poisoning. Ingestion of certain marine turtles and mammals also has been incriminated as the cause of illness. Paralytic shellfish poisoning can be deadly. In addition, red tide may cause respiratory problems.

Animals↗
PubMedDate not supplied

[Poisoning by paralytic molluscan toxins in Oaxaca].

Toxic Red Tides are caused by marine dinoflagellates which synthesize neurotoxins that accumulate in bivalve mollusks. Upon ingestion, these shellfish can cause paralysis and death. During the month of December, 1989, 99 cases of Paralytic Shellfish Poisoning in the areas of Salina Cruz and Huatulco, Oaxaca, were reported; three of which died. The majority of the cases involved the ingestion of oysters and clams. A short time later, the Red Tide was reported appearing. One hundred and fifteen seafood samples were analyzed through a biologic test in mice to determine the quantity of saxitoxin. Oysters and clams showed levels reaching 4 000 U.R. Laboratory analysis of seawater found very high quantities of Gimnodinium catenatum and Gonyaulax catenella. The control measures consisted of the prohibition of the harvest and sale of all bivalve mollusks as well as a public warning to avoid the consumption of such shellfish.

Animals↗
PubMed1986

Oliva vidua fulminans, a marine mollusc, responsible for five fatal cases of neurotoxic food poisoning in Sabah, Malaysia.

This is the first report in which a marine mollusc, Oliva vidua fulminans (olives), generally not known to be poisonous, was responsible for death in five children after consuming boiled olives with tamarind. The onset of symptoms was rapid 10 to 20 min after consumption of the olives. Signs and symptoms included nausea, vomiting, abdominal pain, tingling sensation around the lips, numbness around the mouth, drowsiness, lethargy and generalized weakness with paraesthesia in the limbs. The five deaths occurred within 3 to 4 hours after eating the poisoned olives and resulted from respiratory failure. Left-over olives from the affected household and freshly collected live olives had a toxicity of 14,200 mouse units (M.U.) and 15,000 M.U. per 100 g meat respectively. No other common chemical poison and organophosphorus insecticides were detected. The neurotoxic agent was acid and heat stable and was toxic at pH less than 4. Its action was similar to that of paralytic shellfish poisoning which was caused by toxins from certain dinoflagellates.

Adolescent↗
PubMed1975

Lack of secondary intoxification by red tide poison in the American lobster Homarus americanus.

Lobsters are able to feed on shellfish which are toxic with PSP (paralytic shellfish poisoning from Gonyaulax tamarensis) with no apparent harm to themselves, and no measurable assimilation of the poison into their tissues. Lobsters consumed food containing in excess of 1000 mug PSP. There was no impairment of respiration (oxygen consumption) measurable two to three hours after feeding, and no PSP measured in the meat of the claws and tail 48 to 120 hours after feeding. The only PSP was in the guts and contents which were measured 48 hours after feeding began.

Aging↗
PubMed1987

A theoretical discourse on the pharmacology of toxic marine ingestions.

The known and theoretical pharmacology of poisons involved in toxic marine ingestions has assisted in the development of specific therapeutics for these afflictions. The clinical manifestations of several toxic marine ingestions have suggested toxins/cogeners that may be involved in the poisoning process, providing direction for the development of diagnostic laboratory tests, including those for cyclic ethers. Future investigations should involve utilization of acetaminophen and indomethacin for chronic ciguatera fish poisoning, and the evaluation of the role of polycyclic ethers in the temperature sensation reversal phenomenon of both ciguatera and neurotropic shellfish poisoning.

Animals↗
PubMed1987

[Food-borne infections and poisonings].

A survey of the most common food borne infections (salmonellosis, tuberculosis, brucellosis, campylobacteriosis) is followed by a description of the most common food borne intoxications (botulism, staphylococcal intoxications, biogenic amines, toxic algae in mussels, i.e. "Paralytic Shellfish Poisoning").

Animals↗
PubMedDate not supplied

Comparison of paralytic toxins in aquaculture of purple clam in Taiwan.

Food poisoning incidents due to ingesting the cultured purple clam Soletellina diphos occurred in western Taiwan in February 1991. Clam specimens, sediment and the dinoflagellate Alexandrium tamarensis were collected and assayed for lethality as paralytic shellfish poison (PSP). The lethality of purple clam, wet sediment and phytoplankton was 1700 mouse units per specimen (MU/specimen), 0.05 MU/g and 3.6 x 10(-5) MU/cell, respectively. The toxins obtained from clam, sediment and phytoplankton consisted of gonyautoxins 1-4, along with trace amounts of neosaxitoxin.

Animals↗
PubMed1989

Domoic acid poisoning and mussel-associated intoxication: preliminary investigations into the response of mice and rats to toxic mussel extract.

Consumption of cultivated blue mussels from Prince Edward Island was recently associated with episodes of gastro-intestinal and neurological distress. Extracts of the toxic mussels, tested in the mouse bioassay for paralytic shellfish poison, caused an atypical response characterized by scratching, convulsions and death. The present investigation shows that the domoic acid present in toxic mussels can produce in mice and rats signs identical to those induced by mussel extracts. These studies, preliminary in nature by virtue of the scarcity of domoic acid, gave ip no-effect levels in mice of 0.59 mg/kg body weight based on the behavioural response (scratching) and 2.4 mg/kg for death. These levels correspond to levels of 24 and 94 ppm in mussels. When administered orally doses of between 35 and 70 mg domoic acid/kg body weight were required to produce toxicity in mice and rats. This reduced toxicity is consistent with a lack of absorption from the gastro-intestinal tract: faecal excretion accounted for 102 +/- 17% and 98 +/- 12% (mean +/- SE) of the domoic acid administered to mice and rats, respectively. Since human intoxication occurred at an estimated 1-5 mg domoic acid/kg body weight, susceptible individuals appear to be more sensitive than rodents to the oral toxicity of domoic acid.

Animals↗
PubMed1985

Occurrence of a water soluble toxin in a parrotfish (Ypsiscarus ovifrons) which is probably responsible for parrotfish liver poisoning.

The liver of the parrotfish Ypsiscarus ovifrons sometimes causes severe muscle pain, paralysis and dyspnea when ingested by humans. Individual livers, ovaries and digestive tracts and their contents were examined for lethal potency in mice. They were all toxic, except for livers obtained from April to June. Lethal potency ranged from 0.25 to 5.0 MU/g tissue. Livers were extracted with acidic aqueous ethanol and the extracts purified by charcoal treatment, gel filtration and partition and reversed phase column chromatography. Both the crude and partially purified toxin showed chemical and/or pharmacological properties different from those of tetrodotoxin or paralytic shellfish poisons.

Animals↗
PubMed1982

Gonyautoxin associated with RNA-containing fraction in the toxic scallop digestive gland.

A nontoxic high molecular substance associated with some paralytic shellfish poisons was separated by Sephadex G-50 gel filtration from the toxic digestive glands of the scallop Patinopecten yessoensis fed the causative plankton Protogonyaulax tamarensis. Unlike the corresponding fraction from the nontoxic digestive glands, the substance released gonyautoxins II and III on digestion with RNase T2, suggesting that it is associated with an RNA of P. tamarensis. It is possible that the toxification of scallop is partly due to the toxins already accumulated in Protogonyaulax cells, and partly due to incorporation of this precursor, which releases the toxins as a result of enzymic processes in the shellfish.

Animals↗
PubMed1975

Health hazards of bivalve-mollusk ingestion.

Bivalve mollusks (oysters, clans, and mussels) filter large quantities of water unselectively and thereby may concentrate a variety of aquatic contaminants pathogenic for man within edible shellfish viscera. The recognized bacterial disease associated with ingestion of contaminated bivalves include typhoid fever (not presently a public health problem), Vibrio parahemolyticus gastroenteritis, and Vibrio chloerae infection. The major known shellfish-associated viral diseases are viral hepatitis and possibly viral gastroenteritis. The ingestion of bivalves that have fed on the toxic species of dinoflagellates that produce red tides may be responsible for an uncommon and very rarely fatal illness, paralytic shellfish poisoning. Outbreaks of airborne respiratory irritation in populations exposed to red tides may be the most common public health problem associated with red tides. The health hazards resulting from industrial, agricultural, and oil pollution of bivalves in coastal waters and the hazard from improper handling of bacterially contaminated mollusks remain to be defined.

Animals↗
PubMed1990

Analysis of domoic acid and related compounds by mass spectrometry and gas chromatography/mass spectrometry as N-trifluoroacetyl-O-silyl derivatives.

A method is presented for the analysis of shellfish tissue for domoic acid, a neurotoxic amino acid responsible for cases of amnesic shellfish poisoning. Tissue extracts are first taken through a two-stage solid-phase extraction clean-up, using reversed-phase and strong cation exchange cartridges. A two-stage derivatization, using N-methyl-bis-trifluoroacetamide followed by either N-methyl-tert-butyldimethylsilyltrifluoroacetamide or N, O-bis-trimethylsilyltrifluoroacetamide, is then used to produce an N-trifluoroacetyl-O-silyl derivative which can be analyzed by mass spectrometry with introduction via direct inlet probe, moving-belt liquid chromatograph/mass spectrometer interface, or capillary column gas chromatography. The N-trifluoroacetyl-O-tert-butyldimethylsilyl derivative, which has good stability towards hydrolysis, provides a spectrum well suited to gas chromatography/mass spectrometry (GC/MS) using selected ion recording. GC/MS data for two related compounds, kainic acid and dihydrokainic acid, are also reported. The latter is used as an internal standard for quantification of domoic acid, although the method reported is intended primarily for confirmation of the toxin and related compounds in shellfish tissue.

Chromatography, Gas↗
PubMed1991

Light and scanning electron microscopic studies on effects of marine algal toxins toward freshly prepared hepatocytes.

Mussels exposed to dinoflagellates may represent a human health risk due to accumulation of a variety of algal toxins. In several parts of the world, algal toxins leading to diarrhea (diarrhetic shellfish poisons, DSP) are found in mussels for extended periods of the year. Routine monitoring of these toxins involves ip injections in mice. Chemical analytical methods have been developed for only some of the toxins in question, namely, those giving diarrhea. Other toxins in the DSP complex are not easily detected by analytical methods. In this report we show that freshly prepared hepatocytes from rats are a convenient means to differentiate between the toxins that give diarrhea and those that do not. Consequently, hepatocytes can be useful in both screening and as a tool in the process of developing analytical methods. Freshly prepared hepatocytes might be useful in combination either with the mouse bioassay or with chemical analytical methods.

Animals↗
PubMed1990

Gastrointestinal effects of contaminated mussels and putative antidotes thereof.

A recent outbreak of amnesic shellfish poisoning (ASP) in Atlantic Canada was characterized by severe gastrointestinal and central nervous system pathology. We examined the gastrointestinal effects of an acidic extract of blue mussels contaminated with domoic acid, the suspected toxin responsible for the ASP. We also tested the gastric effects pure domoic acid as well as a putative antagonist of neuroexcitant amino acid receptors, kynurenic acid. Mussel extract produced gastric (antral) ulcers, duodenal ulcers, gastric and duodenal hyperemia and bleeding, as well as peritoneal ascites. Kynurenic acid protected significantly against extract-induced gastropathy, particularly when given 60 or 75 minutes after extract. Pure domoic acid resulted in fatalities in all infant mice tested. These animals exhibited gastric bleeding and hemorrhage, especially at the higher doses employed. In otherwise untreated rats, kynurenic acid exerted significant anti-stress ulcer and anti-gastric secretory effects, but was less effective at blocking ethanol-induced gastric lesions. We suggest that there may be both peripheral as well as central effects of kynurenic acid in modulating normal and pathological gastric function.

Animals↗