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PubMedDate not supplied

[Paralytic shellfish poisoning (author's transl)].

Different diseases as viral or bacterian gastro-enteritis, Tiphoid, viral hepatitis can come from shellfishes. Less known is the shellfish poisoning although recent outbreaks took place in Spain, France, England, Morocco. Toxic poisoning is caused by a poison produced by dinoflagelates of plankton which get developped in shells and make them dangerous, even cooked, to be eaten. A respiratory failure can result from this neurotropic poison.

Adult↗
PubMed1990

[Paralytic shellfish poisoning by Spondylus calcifer contaminated with Pyrodinium bahamense, Costa Rica, 1989-1990].

This paper describes an outbreak of paralytic shellfish poisoning (PSP), affecting human populations on the Pacific Coast of Costa Rica in October 1989. Numbness in arms, face and legs occurred 30 to 45 minutes after ingestion of the large clam Spondylus calcifer. Paralysis of legs and respiratory symptoms followed, often persisting for one week. Large amounts of the dinoflagellate Pyrodinium bahamense were found in the intestine of the mollusk. A toxin was detected in crude or filtered and heated macerates of intestine, muscle, mantle and hepatopancreas of S. calcifer, and to a lesser extent Tagelus sp., by injection of its crude or diluted extracts in white mice. The effects in mice consisted in paralysis and asphyxia generally leading to death in less than 5 minutes, compatible with saxitoxin. Mice were killed by the toxin in macerates diluted 1:100 to 1:1000. No toxin was detected in Anadara tuberculosa (Bivalvia) or in peneids. Prevention rests on intersectoral actions between state and private sectors in charge of fishing, distribution and marketing of shellfish, as well as on education of the population at large.

Adult↗
PubMedDate not supplied

Liquid chromatographic determination of domoic acid in mussels, using AOAC paralytic shellfish poison extraction procedure: collaborative study.

A liquid chromatographic method using the AOAC paralytic shellfish poison (PSP) extraction procedure for domoic acid, a marine toxin, in mussel tissue was collaboratively studied in 10 laboratories. Domoic acid is extracted by boiling the homogenized tissue for 5 min with 0.1N HCl. The mixture is cooled, diluted to a known volume, and then centrifuged. An aliquot of the supernate is diluted, filtered, and analyzed by reverse-phase liquid chromatography with a mobile phase containing acetonitrile and water adjusted to about pH 2.5. Each collaborator received a prepared standard solution, a practice sample, and 7 randomly numbered unknown samples (1 blank mussel tissue, 1 spiked at 14.1 micrograms domoic acid/g, 1 spiked at 18.9 micrograms/g, and duplicate samples with naturally incurred domoic acid at 75 micrograms/g and at 186 micrograms/g). Five of the laboratories had little or no experience in domoic acid analysis. Ten of 11 laboratories completed the study and submitted results. Two individual values out of a total of 70 were found to be outliers. Mean recovery of domoic acid from the spiked extracts was 75%. Relative standard deviations between laboratories (RSDR) ranged from 7.5 to 19.4%; within-laboratory RSDs (RSDr) for the 2 blind duplicate pairs were 1.9 and 4.8%. The detection limit was about 1 microgram domoic acid/g. The method has been adopted official first action by AOAC.

Animals↗
PubMed1977

["Paralytic shellfish poisoning" (author's transl)].

In October 1976 an epidemic of 120 cases of paralytic shellfish poisoning was recorded in western Europe. Analysis of the 23 cases seen in Swizterland shows the following data; paresthesia of mouth and lips (100%); cerebellar syndrome (86%) with giddiness, ataxia, dysmetry and floating sensation; paresia or paralysis (62%); digestive symptoms (14%); no death. The mean incubation time is 3 hs 30 min; mean duration of the symptoms is 2 days. Half of the patients complain of asthenia and moderate memory disturbance lasting up to 3 weeks. The severity of the illness is in relation to the amount of ingested neurotoxin. The epidemiologic study shows that all European cases were due to consumption of mussels from the Atlantic coast of Spain.

Adult↗
PubMed1989

Liquid chromatographic determination of domoic acid in shellfish products using the paralytic shellfish poison extraction procedure of the association of official analytical chemists.

Domoic acid, the recently discovered toxic substance found in contaminated mussels from an area in eastern Prince Edward Island (Canada) was extracted from mussel tissue using the procedure of the Association of Official Analytical Chemists for paralytic shellfish poisons. This involved a 5-min boiling of the sample with 0.1 M hydrochloric acid then cooling and centrifuging. An aliquot of the supernatant was diluted ten to one-hundred times with water, filtered and analysed by reversed-phase liquid chromatography with a mobile phase consisting of acetonitrile-water (12:88) at pH 2.5 and an absorption wavelength of 242 nm. The detection limit was about 0.5 mg/kg domoic acid in seafood samples. The technique was successfully applied to a variety of commercially purchased shellfish and shellfish products.

Animals↗
PubMed1992

Detection of new 7-O-acyl derivatives of diarrhetic shellfish poisoning toxins by liquid chromatography-mass spectrometry.

A novel method for the detection of acylated diarrhetic shellfish poisoning toxins is reported. Direct determination of these compounds is possible using high performance liquid chromatography coupled with ion-spray mass spectrometry. An extract, purified from the digestive glands of toxic mussels (Mytilus edulis) contaminated with okadaic acid, dinophysistoxin-1, and a recently reported analog, dinophysistoxin-2, was also shown to contain small amounts of dinophysistoxin-3, a mixture of 7-O-acyl ester derivatives of dinophysistoxin-1. In addition, acyl ester derivatives of okadaic acid and dinophysistoxin-2 were also detected by direct LC-MS analysis and confirmed by analysis of their hydrolysis products. This is the first report of the detection of other naturally occurring 7-O-acyl esters similar to dinophysistoxin-3.

Acylation↗
PubMed1990

Paralytic shellfish poisoning: a case report and serial electrophysiologic observations.

We report serial electrophysiologic observations in a patient with acute bulbar and respiratory paralysis following ingestion of saxitoxin-contaminated clams. Prolonged distal motor and sensory latencies, slowed conduction velocities, and moderately diminished amplitudes were present at the outset. All values returned to normal over 5 days. These findings, the result of incomplete sodium channel blockade, distinguish paralytic shellfish poisoning from most other acute paralytic illnesses.

Animals↗
PubMed1992

Cross-reacting antigens in the butter clam (Saxidoma giganteus) and their relationship to total paralytic shellfish poison toxicity.

A specific protein with an apparent mol. wt of 23,000 was identified in foot homogenate derived from paralytic shellfish poisoning (PSP) contaminated butter clams and was found to cross-react with crab-saxitoxin-induced protein (SIP) antiserum. Antiserum, once cross-absorbed against non-toxic shellfish material, was incubated with tissue homogenate derived from 52 butter clams with varying total PSP toxicities in a prototype ELISA. A significant (r = 0.83; P less than 0.001) correlation existed between soluble clam antigen content in foot homogenate and total PSP toxicity; the latter measured by the mouse lethality bioassay. From the ELISA results, a soluble antigen threshold of 0.1% total protein was successfully used to distinguish between PSP toxic and non-toxic butter clams. It is proposed that this type of screening assay could be used in conjunction with the standard mouse bioassay to increase PSP monitoring and potentially reduce unnecessary animal testing.

Animals↗
PubMed1991

Clinical and epidemiological features of neurotoxic shellfish poisoning in North Carolina.

BACKGROUND: In October 1987, a red tide due to P. brevis affected the North Carolina coast for the first time. The purpose of our study was to describe the clinical and epidemiological features of neurotoxic shellfish poisoning (NSP), an illness caused by eating shellfish contaminated with the neurotoxins of P. brevis. METHODS: Active surveillance was established for cases of NSP. A descriptive study of the NSP cases was then completed. RESULTS: Forty-eight persons, who had eaten oysters at 20 meals, met the case definition. A variety of gastrointestinal tract and neurological symptoms were reported. The illnesses were generally mild and of short duration, and there were no deaths. Forty-one (85 percent) affected persons lived in five communities located within a 70-kilometer area along the coast. Cases occurred from October 27 to December 9; 27 (56 percent) of the cases occurred before the first closure of affected shellfish waters on November 2. There was a significant increase in the illness attack rate with an increase in the number of oysters eaten. CONCLUSIONS: Routine monitoring of coastal waters for P. brevis is needed to facilitate earlier recognition of red tides, closure of affected areas, and education of the public before substantial exposure to contaminated shellfish occurs.

Adolescent↗
PubMedDate not supplied

Zinc from oyster tissue as causative factor in mouse deaths in official bioassay for paralytic shellfish poison.

Toxicity (extreme weakness, body temperature drop, cyanosis, some slow deaths) in test mice, upon intraperitoneal injection of standard-method paralytic shellfish poison (PSP) extracts of some PSP-free oysters, is consistent with the relatively high levels of zinc in these extracts. As a rough guideline, the threshold for a toxic response corresponds to a drained tissue zinc level of over 900 micrograms/g. The identification of zinc as the substance responsible has been supported by inducing toxicity in control extracts by spiking with nontoxic levels of zinc, and by eliminating toxicity from toxic extracts by chemical removal (precipitation, ion exchange) of metals.

Animals↗
PubMed1989

Paralytic shellfish poisoning in northwest Spain: the toxicity of the dinoflagellate Gymnodinium catenatum.

The highly productive mussel fishery in the Rias Bajas region of northwest Spain has experienced several outbreaks of paralytic shellfish poisoning (PSP) beginning in 1976. In this study, similarities in the HPLC analyses of extracts from toxic shellfish, plankton tows and cultured dinoflagellates from the Rias Vigo and Pontevedra clearly indicate that Gymnodinium catenatum Graham is the organism responsible for recent PSP episodes. The toxin profile of the dinoflagellate contains an unusually high proportion of the low potency sulfocarbamoyl toxins (ca. 90-95 mole %), although a major portion of the overall toxicity is due to the more potent saxitoxin that is present at 5-10% of the total. Toxin profiles of shellfish showed approximately the same composition as that of the dinoflagellate, although the shellfish contained several carbamate toxins (GTX I, GTX II, GTX IV and NEO) that were not detected in G. catenatum culture extracts. The shellfish also contained decarbamoyl toxins (dc-GTX II and dc-GTX-III) at approximately 2% of the total profile. Since these were not detected in the dinoflagellate, their presence reflects either chemical or enzymatic conversion within the shellfish.

Animals↗
PubMed1991

Analysis of paralytic shellfish poisons by capillary electrophoresis.

A capillary electrophoresis (CE) method with UV detection is described for the separation and determination of underivatized toxins associated with paralytic shellfish poisoning (PSP). Confirmation of the electrophoretic peaks was facilitated by mass spectrometric (MS) detection using an ionspray CE-MS interface and by high-performance liquid chromatography with fluorescence detection. The determination of PSP toxins, such as saxitoxin and neosaxitoxin, in toxic dinoflagellates and scallops is demonstrated and comparisons are made with existing techniques.

Animals↗
PubMed1989

Serological cross-reactions between crab saxitoxin-induced protein and paralytic shellfish poison-contaminated shellfish.

A polyclonal antiserum generated against crab saxitoxin-induced protein was tested against paralytic shellfish poison (PSP)-contaminated crabs and shellfish. Antibody-reactive proteins in PSP-contaminated bivalve mollusc extracts were localized using SDS-PAGE and immunoblotting. PSP-contaminated clams and oysters possessed a higher degree of immunoreactivity to the saxitoxin-induced protein found in PSP-resistant crabs than their respective non-contaminated controls.

Animals↗
PubMed1992

Presence of paralytic shellfish poisoning toxins and soluble proteins in toxic butter clams (Saxidomus giganteus).

Butter clams obtained from a variety of locations along the northern British Columbia coast were assayed for the presence of individual paralytic shellfish poisoning toxins (PSPT) by HPLC and total PSPT toxicity using the mouse bioassay. Specific organs, namely the siphon, adductor muscle, foot and mantle were examined for soluble antigens that crossreacted with crab Saxitoxin-Induced Protein (SIP) using immunochemical (Western blotting) techniques. Butter clams containing high concentrations of PSPT also had several proteins that crossreacted with crab anti-SIP serum. In particular, soluble proteins with distinctly different molecular weights were found in the siphon and foot, respectively, in toxic shellfish. These proteins were absent in nontoxic butter clams. The concept of using PSPT-induced proteins in the butter clam as a screen for identifying toxic shellfish is introduced.

Animals↗
PubMed1992

Ionspray mass spectrometry of marine toxins. III. Analysis of paralytic shellfish poisoning toxins by flow-injection analysis, liquid chromatography/mass spectrometry and capillary electrophoresis/mass spectrometry.

Ionspray mass spectrometry has been used to monitor the purification of saxitoxin, the parent compound in the family of toxins responsible for paralytic shellfish poisoning (PSP), from a strain of the dinoflagellate Alexandrium excavatum. Quantitative results obtained by flow-injection analysis are compared to those obtained by high-performance liquid chromatography with post-column oxidation and fluorescence detection. The coupling of liquid chromatography and capillary electrophoresis with ionspray mass spectrometry is described for the separation of mixtures of PSP toxins and the highly potent pufferfish toxin tetrodotoxin. Tandem mass spectrometry is used to provide the structural information, and the ability to distinguish isomeric PSP toxins both chromatographically and mass spectrometrically is demonstrated.

Chromatography, High Pressure Liquid↗
PubMed1992

Ionspray mass spectrometry of marine toxins. IV. Determination of diarrhetic shellfish poisoning toxins in mussel tissue by liquid chromatography/mass spectrometry.

An improved liquid chromatographic/mass spectrometric (LC/MS) method utilizing gradient elution and ion-spray ionization is described for the sensitive determination of okadaic acid and dinophysistoxin-1, the principal toxins implicated in cases of diarrhetic shellfish poisoning. The method was used to confirm the presence of both toxins, together with a recently identified isomer of okadaic acid, dinophysistoxin-2, in various samples of cultivated blue mussels (Mytilus edulis) from Canadian and European waters. The method provided a mass detection limit of 0.4 ng for each toxin, thus allowing detection of 40 ng per g of whole mussel tissue (or approximately 10 ng/g if only the digestive glands were used in the assay). Quantitative results obtained by LC/MS were in good agreement with those obtained by derivatization and high-performance liquid chromatography with fluorescence detection.

Animals↗