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At least 19 recordsLinked to original sources
PubMedDate not supplied

Liquid chromatographic determination of paralytic shellfish poisons in shellfish after prechromatographic oxidation.

A liquid chromatographic method for quantitating paralytic shellfish poison toxins in shellfish has been developed in which the toxins are converted to fluorescent purines by prechromatographic oxidation under mildly basic conditions with hydrogen peroxide or periodate. The addition of ammonium formate to the periodate oxidation reaction greatly improved the yield of fluorescent derivatives for neosaxitoxin, gonyautoxin-1, B-2, and C-3 compared to the same reaction without ammonium formate. As little as 3-6 ng of each of the nonhydroxylated toxins and 7-12 ng of the hydroxylated compounds per gram of shellfish could be detected. Reversed-phase chromatography using ammonium formate in the mobile phase improved the chromatography of neosaxitoxin and B-2 compared to results obtained earlier. Because the oxidation products of neosaxitoxin and B-2 could not be separated, parent compounds were separated before oxidation by using an SPE-COOH ion exchange cartridge. The repeatability coefficient of variation for the oxidation reactions ranged from 3 to 8% for the peroxide reaction, and from 4 to 11% for the periodate reaction, depending upon the individual toxin determined and its concentration in the extract (0.04-0.55 micrograms/g). The method was compared to the mouse bioassay and the postcolumn oxidation method. In most cases, results were comparable.

Chromatography, Liquid↗
PubMedDate not supplied

Comparison evaluation of liquid chromatographic and bioassay methods of analysis for determination of paralytic shellfish poisons in shellfish tissues.

A liquid chromatographic (LC) method was compared with the AOAC mouse bioassay method (18.086-18.092) for determination of paralytic shellfish toxins in shellfish tissues. Shellfish samples were collected from Massachusetts coastal waters as part of a state surveillance program, and extracts of shellfish meat were analyzed for toxins by using both analytical methods. Overall correlation of the LC and bioassay methods is good (r = 0.943), but for samples with toxicities less than 100 micrograms saxitoxin/100 g shellfish meat, the correlation is significantly less (r = 0.531). Limits of detection are 10 micrograms saxitoxin/100 g shellfish meat and 40 micrograms saxitoxin/100 g shellfish meat for the LC and bioassay methods, respectively. Analytical capacity of the LC method is limited to 12 samples/person-day compared with 30 samples/person-day for the bioassay. Sampling capacity of the LC method could be increased by using a fluorescence detector with a wider response range, which would eliminate the need for dilution of concentrated samples.

Animals↗
PubMed1985

A combination fluorescence assay and Folin-Ciocalteau phenol reagent assay for the detection of paralytic shellfish poisons.

Paralytic shellfish poison (PSP) profiles of crude shellfish extracts were determined by linear gradient elution from a Bio-Rad AG-50-X4 strong cation-exchange resin mini-column. STX, GTX2 and GTX3 were detected by fluorescence assay. NeoSTX and GTX1/GTX4 were detected with a Folin-Ciocalteau phenol reagent assay. The major toxicity associated with extracts of Mytilus edulis and Mya arenaria collected during a 1972 red tide off Hampton, New Hampshire, was due to the presence of GTX1/GTX4, with some activity associated with neoSTX, GTX2 and GTX3. STX was also present. Correlations to mouse toxicity are provided.

Amino Acids↗
PubMed1978

Paralytic shellfish poisoning.

Two cases of paralytic shellfish poisoning after ingestion of mussels occurred in October 1977 in Nova Scotia. The incidence of this type of poisoning is relatively high among persons living on the coast of the Bay of Fundy and the estuary of the St. Lawrence River. The causative organism, Gonyaulax tamarensis, elaborates an endotoxin, saxitoxin, that blocks neuromuscular transmission in the motor axon and muscle membrane while leaving the end-plate unaffected; it also suppresses conduction in the atrioventricular node and inhibits the respiratory centre. The clinical manifestations are unique and include numbness of the lips, tongue and fingertips within minutes of ingestion of the poisoned shellfish, then numbness of the legs, arms and neck, with general muscular incoordination, and finally respiratory distress and muscular paralysis. Treatment is symptomatic and prevention can only occur by public education.

Bivalvia↗
PubMed1977

Paralytic shellfish poisoning: a review.

Paralytic shellfish poisoning (PSP) in man results from the consumption of mussels, clams, and oysters that have fed on toxic dinoflagellates. Motile, marine protozoa of the dinoflagellate group often produce "blooms," i.e., red tides, which color the sea. Not all genera or species are toxic to fish and mammals, nor are the toxic principles the same in all poisonous protozoa. At least 5 of the group are known to cause poisonings in man. Shellfish poisonings other than PSP are also recognized. The PSP toxin, saxitoxin, is concentrated in the viscera and occasionally in the mantle and syphon of marine bivalves. Cooking does not completely destroy the low molecular weight poisonous factor. Reported mortality ranges from 8.5 to 23.2%. The disease is of significant public health concern in some localities of the world from May to November.

Disease Outbreaks↗
PubMed1986

Paralytic shellfish poisoning in Singapore.

Paralytic shellfish poisoning is caused by the ingestion of shellfish meat rendered toxic by exposure to a high level of toxic dinoflagellates during the phenomenon of "red tide". This paper reports the first outbreak of paralytic shellfish poisoning from green mussels in Singapore which resulted in two deaths. Analysis of the mussel meat by a standardised mouse bioassay confirmed the presence of the toxin. An attempt was also made to extend the bioassay to an analysis of the gastrointestinal contents. The clinical features of the condition are presented.

Animals↗
PubMedDate not supplied

Variability of mouse bioassay for determination of paralytic shellfish poisoning toxins.

Toxic shellfish extracts and paralytic shellfish poison (PSP) standard solutions, tested over a range of pH levels, storage conditions, and temperatures, were monitored for toxin concentration, using the mouse bioassay and thin layer chromatography (TLC). A comparison of PSP toxin concentrations in toxic shellfish extracts and PSP standard solutions when dilution was varied suggests that other factors in the shellfish extracts contribute to the toxicity in mice; the closet agreement was at the death time range of 5-8 min. The toxicities of PSP standard solutions at pH levels ranging from 2 to 6 and held at 4 degrees C for various times were relatively constant; however, there was a gradual decrease in toxicity with pH 6 solutions. Also, standard solutions (pH 6) held at 4 degrees C for 28 days showed a 50% decrease in toxicity when the pH was adjusted to 2. TLC analyses of PSP standard solutions and toxic shellfish extracts revealed multiple spots at the Rf ranges of saxitoxin/neosaxitoxin and gonyaulax toxins I-IV. PSP standard solutions usually had a single spot in the saxitoxin/neosaxitoxin area. No attempt was made to confirm the identity of these compounds. Previously tested toxic shellfish extracts with subsequent pH adjustment to 1.5 and additional heat treatment (100 degrees C for 5 min) showed no appreciable difference in mouse toxicity. The use of antifoaming agents during the acid extraction step did not affect the final amounts of PSP obtained.

Animals↗
PubMed1991

Creatine kinase MB elevation in paralytic shellfish poisoning.

An outbreak of paralytic shellfish poisoning occurred in southern Taiwan, affecting 116 persons who had consumed purple clams. Two victims died within four hours. Gonyautoxins were identified as causative toxins. During the outbreak, five patients with paralytic shellfish poisoning were seen in our hospital. All recovered following supportive treatments. Serum creatine kinase concentration was elevated in three of the five patients. The levels of the enzyme did not seem to correlate with the severity of poisoning. The most significant finding was the previously unreported observation of elevation of the creatine kinase MB level. In all four patients who had creatine kinase MB value determined, it was elevated.

Adult↗
PubMed1975

Paralytic shellfish poisoning in Papua New Guinea.

Paralytic shellfish poisoning is differentiated from other forms of poisioning from marine animals. An outbreak in a village near Port Moresby is described, and the clinical picture seen in that and subsequent cases (25 plus 3 fatalities) is discussed. The clinical manifestations of almost pure cerebellar incoordination, without other constant neurological signs, is emphasized and the name Ataxic Shellfish Poisoning is suggested. The aetiology whereby toxic marine plakton organisms are siphoned and filtered from the water and accumulate in shellfish is described.

Adult↗
PubMed1990

Lethal paralytic shellfish poisoning in Guatemala.

An outbreak of paralytic shellfish poisoning occurred in Champerico, on the Pacific coast of Guatemala, July-August 1987. Of 187 people affected with characteristic neurologic symptoms, 26 died. A case study implicated a species of clam, Amphichaena kindermani, harvested from local beaches as the vehicle of the neurotoxins (saxitoxins). Children less than 6 years old had a higher fatality rate (50%) than people greater than 18 years of age (7%). The minimum lethal dose for 1 child was estimated to have been 140 mouse units of toxin/kg body weight; thus children may be more sensitive to the saxitoxins than are adults. This is the first large outbreak of paralytic shellfish poisoning recognized in Guatemala.

Adolescent↗
PubMed1991

Paralytic shellfish poisoning--Massachusetts and Alaska, 1990.

Paralytic shellfish poisoning (PSP) is a foodborne illness caused by consumption of shellfish or broth from cooked shellfish that contain either concentrated saxitoxin, an alkaloid neurotoxin, or related compounds. This report summarizes outbreaks of PSP that occurred in Massachusetts and Alaska in June 1990.

Adult↗
PubMed1987

Intoxications from the seas: ciguatera, scombroid, and paralytic shellfish poisoning.

Sporadic cases and outbreaks of intoxications borne by fish and shellfish have increased in frequency during recent years. Ciguatera, scombroid, and paralytic shellfish poisoning account for nearly 16 per cent of all reported foodborne outbreaks of disease in the United States. Fishborne ciguatera and paralytic shellfish poisoning are characterized by gastrointestinal and neuromuscular manifestations attributable to toxins of dinoflagellates. These toxins impair sodium transport in cell membranes. Treatment is primarily supportive. Scombroid fish intoxication resembles histamine poisoning and may be treated effectively with antihistamines or cimetidine. Prevention of these intoxications at present depends upon avoidance of potential vectors.

Animals↗
PubMedDate not supplied

Measurements of paralytic shellfish poisons. A review of biological and chemical procedures.

Paralytic shellfish poisons (PSP) are derivatives of a tetrahydropurine base, which includes saxitoxin, 1-hydroxy saxitoxin, and 11-hydroxy saxitoxin sulfate. These compounds are produced by Gonyaulax catenella and other dinoflagellate species, and the algal toxins (phycotoxins) contaminate shellfish during the filter-feeding process performed by the bivalve molluscs. Increased incidence of algal blooms and outbreaks of PSP food poisonings have been encountered in recent years, resulting in a demand for closely monitoring of shellfish for these toxins. The existing biological and chemical procedures for analysis are reviewed. The mouse bioassay is commonly used in routine analysis, but is nonspecific. Several of the chemical procedures are specific and more sensitive than the mouse bioassay. The disadvantage, however, seems to be that not all known PSP compounds can be quantitiatively measured by any single chemical procedure.

Animals↗
PubMed1986

Paralytic shellfish poisons produced by the freshwater cyanobacterium Aphanizomenon flos-aquae NH-5.

A single filament clonal isolate of Aphanizomenon flos-aquae was made from a water bloom sample taken at a small pond near Durham, New Hampshire, in 1980. When batch cultured the strain was toxic to mice and had an i.p. LD50 of about 5.0 mg/kg. Using an extraction procedure originally designed for paralytic shellfish poisons and other neurotoxins of freshwater cyanobacteria, a purification method was developed. The procedure involved acidified water/ethanol extraction of the cells followed by ultrafiltration, gel filtration, use of C18 cartridges to remove pigments, ion-exchange and high performance liquid chromatography using u.v. detection at 220 or 240 nm. Thin-layer chromatography and high performance liquid chromatography results indicate that Aphanizomenon flos-aquae NH-5 may produce paralytic shellfish poisons, mainly neo-saxitoxin and saxitoxin. Three labile toxins were also detected which were not similar to any of the known paralytic shellfish poisons.

Animals↗
PubMed1988

Resistance of nerves from certain toxic crabs to paralytic shellfish poison and tetrodotoxin.

The inhibitory effect of paralytic shellfish poison and tetrodotoxin on nerves from toxic and nontoxic crabs was examined. The toxins at concentrations of 10(-3) - 10(-4) M partially or completely inhibited the action potential of nerves isolated from the legs of toxic crab species (Zosimus aeneus, Atergatis floridus and Platypodia granulosa), but had no effect at 10(-6) M, the concentration at which the action potential of nerves from a nontoxic crab (Plagusia dentipes) was inhibited completely. A xanthid crab Daira perlata was intermediate in respect to the resistance to toxins. These results agree with the previous results obtained by i.p. administration of both toxins into those crabs.

Action Potentials↗
PubMed1990

A toxin profile for shellfish involved in an outbreak of paralytic shellfish poisoning in India.

Toxin profiles of clams and oysters involved in the outbreak of paralytic shellfish poisoning in India in 1983 were studied by a liquid chromatographic technique. Gonyautoxins 1, 2, 3, 4 and 8, and 11-epigonyautoxin 8 appeared to be the major toxins along with small amounts of saxitoxin, neosaxitoxin, decarbamoylsaxitoxin, decarbamoylgonyautoxins 2 and 3, C3 and C4. Toxin profile suggests the involvement of Alexandrium spp. in this outbreak.

Animals↗
PubMed1979

Paralytic shellfish poisoning. A report of 17 cases in Cape Town.

An outbreak of 17 cases of paralytic shellfish poisoning in humans occurred in Cape Town during May 1978. The clinical features were typical and no deaths occurred. Efforts to correlate the severity of disease with the amount of toxin ingested, to demonstrate a protective effect of alcohol, and to demonstrate the immunogenicity of the toxin proved unsuccessful. The regional ecological effects are described. Continued monitoring for the presence of toxic dinoflagellates must be conducted, and the dangers of the consumption of mussels from the Cape west coast should be widely publicized.

Bivalvia↗