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PubMedDate not supplied

Evaluation of a postcolumn electrochemical reactor for oxidation of paralytic shellfish poison toxins.

A liquid chromatographic method using a postcolumn electrochemical reactor that oxidizes paralytic shellfish poison toxins to fluorescent derivatives has been developed. Several experimental parameters, including pH and oxidation potential, were investigated. For nonhydroxylated toxins, the sensitivity improved with increasing pH and voltage. At optimum operating conditions, the sensitivity for saxitoxin and gonyautoxins 2 and 3 was an order of magnitude greater than that for neosaxitoxin and B1 and 2 orders of magnitude greater than that for B2. The limit of detection for saxitoxin was 0.10 ng (signal-to-noise ratio, 3:1). Electrochemical oxidation products were similar to those formed in the prechromatographic periodate oxidation method. Shellfish and plankton extracts were analyzed with the electrochemical system, and results agreed well with those obtained with established methods. Shellfish samples contaminated at the regulatory limit of 0.8 microgram/g were readily analyzed by the method.

Animals↗
PubMedDate not supplied

Iron milk medium method for recovering Clostridium perfringens from shellfish: collaborative study.

Eleven laboratories participated in a collaborative study analyzing shellfish (oysters, Crassostrea gigas) for the detection and enumeration of Clostridium perfringens by the iron milk medium (IMM) method. The IMM method was compared to AOAC Official Method 976.30. Shellfish were artificially inoculated with C. perfringens cells (vegetative and spores) at low (1 x 10(3) colony forming units [cfu]/g), medium (1 x 10(4) cfu/g), and high (1 x 10(6) cfu/g) levels. Negative controls (zero level) were analyzed by each laboratory. C. perfringens FD-1, the strain involved in a foodborne illness, was used. Blind duplicates of each inoculum level were analyzed, giving a total of 16 samples per laboratory. The selectivity of IMM relies solely on the rapid growth of C. perfringens at 45 degrees C indicated by stormy fermentation reaction within 18 h. C. perfringens is detected and enumerated using the most probable number technique. A statistical evaluation of the data found no significant differences between the estimates from the 2 methods. The IMM method for detection of C. perfringens from shellfish has been adopted first action by AOAC INTERNATIONAL.

Animals↗
PubMed1993

[Poisoning by the consumption of shellfish contaminated with paralytic venom in the XII Region, Chile. Anatomopathological study].

The necropsy findings of ten subjects died as a consequence of paralytic shellfish intoxication are presented. These deaths occurred between march 1991 and january 1992, affected to seamen and occurred within 72 hours of contaminated shellfish ingestion. Necropsies were performed within 24 hours of death. The most outstanding necropsy findings were the presence of pink lividities, mydriasis and isocoria, airway obstruction with gastric contents, severe brain, lung liver and spleen swelling and edema, and digestive and respiratory mucosal congestion and friability. The toxicological study of urine, gastric content and organ samples revealed the presence of shellfish paralytic poison.

Adolescent↗
PubMedDate not supplied

Determination of diarrheic shellfish toxins in mussels by microliquid chromatography-tandem mass spectrometry.

A fast, sensitive, and specific procedure for determining toxins that cause diarrheic shellfish poisoning (DSP) using microliquid chromatography coupled with tandem mass spectrometry (micro-LC-MS-MS) is reported. The lipophylic polyether acidic toxins okadaic acid (OA), its isomer dinophysistoxin-2 (DTX-2), the 35-methylokadaic acid dinophysistoxin-1 (DTX-1), and the novel toxin dinophysistoxin-1B (DTX-2B; recently isolated from Irish mussels) were extracted from shellfish tissues with acetone and chromatographed by isocratic elution at 10 microL/min with CH3 CN-H2O, 80 + 20 (v/v), containing 0.1% trifluoroacetic acid, through a C18 reversed-phase column (1.0 mm id). The chromatograph is coupled via an ion spray interface to an atmospheric pressure ionization source. Collision-induced-dissociation (CID) ion mass spectra of the protonated molecule, [M + H]+, at m/z 805 for OA, DTX-2, and DTX-2B and at m/z 819 for DTX-1, were obtained in MS-MS experiments to identify 2 diagnostic fragment ions for each analyte that could be used for selected-reaction-monitoring (SRM) micro-LC-MS-MS analysis. The CID spectrum of DTX-2B confirmed it to be a new OA isomer, like DTX-2. Standard curves obtained by SRM micro-LC-MS-MS were linear (r2 > or = 0.9992) over the range 0.05-1.00 micrograms/mL (i.e., 0.10-2.00 micrograms toxin/g hepatopancreas), and a detection limit of 15 pg/injection was obtained for each DSP toxin. Average recoveries ranged from 95 to 101%, and coefficients of variation ranged from 1.8 to 3.4%. This novel SRM micro-LC-MS-MS method was used to confirm acidic DSP toxins in Irish and Italian toxic mussels. It offers a high degree of specificity because analyte confirmation is based on retention time, molecular weight, structural information obtained from the presence of 2 diagnostic fragments for each analyte, and ion ratios. OA was found in both Irish (< or = 0.7 micrograms/g hepatopancreas) and Italian (< or = 1.5 micrograms/g hepatopancreas) mussels. DTX-1 was found only in Italian mussels (< or = 0.3 micrograms/g hepatopancreas). DTX-2 (< or = 6.1 micrograms/g hepatopancreas) and DTX-2B (< or = 0.08 micrograms/hepatopancreas) were unique to Irish shellfish.

Animals↗
PubMed1997

Fish- and shellfish--borne trematode infections in Canada.

Food-borne trematode infections are endemic in various parts of the world, particularly Southeast Asia. Despite the high prevalence, morbidity and total costs of these infections, they remain poorly recognized by public health authorities and consumers. Factors such as poor sanitation and traditional methods of food preparation hasten the spread of food-borne trematode infections in endemic regions and must be carefully examined in order to develop effective control strategies. There is also a growing risk to consumers in non-endemic countries as a result of international trade. A considerable quantity of freshwater fish and shellfish is imported into Canada from endemic countries in Southeast Asia. Some of these products are imported fresh or processed in such a way that the infective metacercariae may not be destroyed. Further, current inspection procedures in Canada may not detect the presence of all parasites in imported fish products. Therefore, there may be a risk of infection if the fish or shellfish is consumed raw or lightly cooked. Many of the cases of infection in Canada involve recent immigrants from endemic regions who have become infected either before arriving or through the consumption of traditional or ethnic dishes prepared from imported products. International travel and the increasing availability and interest in ethnic foods also contribute to the risk of infection in all Canadians. In addition to these imported trematodes, a number of species are found in freshwater fishes and shellfish in North America and have also caused illness in humans. Although the prevalence of infection remains relatively low in Canada, the need for an increased general awareness of food-borne trematode infections and their causes is indicated.

Animals↗
PubMed1999

Winter accumulation of paralytic shellfish toxins in digestive glands of mussels from Arcachon and Toulon (France) without detectable toxic plankton species revealed by interference in the mouse bioassay for lipophilic toxins.

Since January 1993, neurological symptoms and rapid deaths (5 to 10 min) were typically observed in the mouse bioassay of acetone extracts of digestive glands from Arcachon and Toulon (France) during the winter season. It was assumed initially that a new lipophilic toxin was present because tests using the AOAC mouse bioassay for paralytic shellfish toxins on acid extracts of whole shellfish meat were negative, no known lipophilic toxins were detected and no toxic phytoplankton species were observed in the area during the poisoning events. In this study, however, preparative isolation of the toxic factor from toxic mussel digestive glands has revealed the presence of paralytic shellfish toxins, the principal ones being gonyautoxins-2 and -3 at Arcachon and gonyautoxins-1, -4, -2 and -3 at Toulon. The toxin concentrations recorded were below levels harmful to consumers and therefore represent a false positive in the mouse bioassay for lipophilic toxins based upon acetone extraction. The origin of the toxins remains to be determined.

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↗
PubMed1996

Isolation of dinophysistoxin-2 and the high-performance liquid chromatographic analysis of diarrhetic shellfish toxins using derivatisation with 1-bromoacetylpyrene.

The rare diarrhetic shellfish toxin, dinophysistoxin-2 (DTX-2), was isolated from the digestive glands of mussels (Mytilus edulis). This was achieved by chromatography on silica and Sephadex LH-20 followed by reversed-phase solid phase extraction and semi-preparative high-performance liquid chromatography (HPLC) with an Ultremex C18 column. Using 1-bromoacetylpyrene (BAP), as a precolumn derivatisation reagent, the diarrhetic shellfish toxins, okadaic acid (OA), dinophysistoxin-1 (DTX-1) and DTX-2, were determined by HPLC with fluorimetric detection. Derivatisation using BAP was compared with 9-anthryldiazomethane (ADAM) and, although the latter exhibited a four-fold better sensitivity, the BAP method gave fewer artefact peaks from reagent decomposition. The limits of detection of OA and DTX-2 were 0.4 ng on-column using BAP, which permits this method to be used for the regulatory control of these toxins in shellfish.

Animals↗
PubMed1982

The distribution of Vibrio parahaemolyticus serotypes in Kenyan seafish, shellfish, marine water and sediment.

Vibrio parahaemolyticus was recovered from 74 of 912 marine samples screened for the organism. Of 74 isolates of V. parahaemolyticus obtained from marine fish, crustacean shellfish (prawns, lobster, crabs), and molluscan shellfish (oysters), and from water and sediment collected off the coast of Kenya, only 33 were positively identified. The isolates were only from seafish and shellfish. The main serotypes were 0,3:K37; 0,3:K40; 0,8:39; 0,10:23; 0,10:K52; and 0,11:K40. All the serotypes were Kanagawa-negative. The rest of the samples, mainly marine sediment and water, revealed what was described as untypable Vibrios. This is the first report of the organism in this part of the world where no clinical disease is reported.

Animals↗
PubMed1991

Liquid chromatography-linked protein phosphatase bioassay; a highly sensitive marine bioscreen for okadaic acid and related diarrhetic shellfish toxins.

Okadaic acid and dinophysistoxin-1 were resolved by liquid chromatography, then identified and quantitated by specific inhibition of both protein phosphatase-1 and -2A (PP1/PP2A) catalytic subunits in a 32P-phosphorylase a phosphatase radioassay. Based on the IC50 for PP2A inhibition (0.2 nM), the procedure has a detection sensitivity of less than 10 pg okadaic acid. Confirmative identification by PP1 inhibition (IC50 = 19 nM) requires 500 pg okadaic acid. Analyses of methanolic extracts from control, "okadaic acid spiked" and suspected diarrhetic mussels showed the bioscreen to be accurate, reproducible and identified okadaic acid/dinophysistoxin-1 in Canadian shellfish for the first time. In addition, a protein phosphatase inhibitor distinct from okadaic acid/dinophysistoxin-1 was identified in diarrhetic mussels with a potency equivalent to 900 ng okadaic acid/g digestive tract. Protein phosphatase inhibition probably underlies the biological activity of okadaic acid as a diarrhetic shellfish toxin and tumour promoter (Cohen, P., Holmes, C. F. B. and Tsukitani, Y. (1990), TIBS 15, 98-102). The liquid chromatography-linked protein phosphatase bioscreen should therefore facilitate identification of novel toxins comprising diarrhetic profiles in infested shellfish.

Animals↗
PubMed1990

Incidence of Vibrio vulnificus in northern New England water and shellfish.

Vibrio vulnificus, an autochthonous inhabitant of the estuarine environment, was detected in water and oysters from the Great Bay Estuary System of New Hampshire and Maine. Previously, it had not been detected north of Boston Harbor on the east coast of the United States. V. vulnificus was detected in water and shellfish samples at five out of ten sites, and only in areas that were not open to recreational shellfishing. Although samples were collected from May into December, V. vulnificus was only detected in shellfish in July and August. Water sampling began in August, and V. vulnificus persisted at one site into October.

Animals↗
PubMed1997

The toxin of diarrheic shellfish poisoning, okadaic acid, increases intestinal epithelial paracellular permeability.

BACKGROUND & AIMS: Diarrhea associated with shellfish poisoning is poorly understood. The responsible toxin, dinophysistoxin 1, has been identified as okadaic acid, a potent phosphatase inhibitor, but its effects on intestinal epithelia have not been examined. The aim of this study was to investigate the effect of okadaic acid on intestinal epithelial function, both Cl- secretion and barrier function. METHODS: Cultured human intestinal epithelial T84 cell monolayers were used. The effect of okadaic acid on these monolayers was assessed by measuring electrophysiological parameters, lactate dehydrogenase release, and 22Na+ and [3H]mannitol flux rates. Protein phosphorylation studies were performed to identify potentially involved proteins. RESULTS: Okadaic acid does not directly stimulate Cl- secretion from intestinal epithelial cells. On the contrary, the response to well-characterized secretagogues is attenuated by okadaic acid. However, it does decrease transepithelial electrical resistance in a polarized fashion without inducing cytotoxicity. Sodium-mannitol flux studies suggest that the observed decrease in resistance is attributable to an increase in paracellular permeability. CONCLUSIONS: Okadaic acid, the toxin responsible for diarrheic shellfish poisoning, does not stimulate Cl- secretion but increases the paracellular permeability of intestinal epithelia. This alteration in intestinal epithelial physiology may contribute to the diarrhea of shellfish poisoning.

Cell Membrane Permeability↗
PubMed2000

Development of a method for the identification of azaspiracid in shellfish by liquid chromatography-tandem mass spectrometry.

Azaspiracid is the main toxin responsible for a number of recent human intoxications in Europe resulting from shellfish consumption. The first micro liquid chromatography-tandem mass spectrometry (micro-LC-MS-MS) method was developed for the determination of this novel shellfish poisoning toxin in mussels. The analyte was extracted from whole mussel meat with acetone and chromatographed on a C18 reversed-phase column (1.0 mm I.D.) by isocratic elution at 30 microl/min with acetonitrile-water (85:15, v/v), containing 0.03% trifluoroacetic acid. The toxin was ionised in an ionspray interface operating in the positive ion mode, where only the intact protonated molecule, [M+H]+, was generated at m/z 842. This served as precursor ion for collision-induced dissociation and three product ions, [M+H-nH2O]- with n=1-3, were identified for the unambiguous toxin confirmation by selected reaction monitoring LC-MS-MS analysis. A detection limit of 20 pg, based on a 3:1 signal-to-noise ratio, was achieved for the analyte. This LC-MS-MS method was successfully applied to determine azaspiracid in toxic cultivated shellfish from two regions of Ireland.

Animals↗
PubMed1997

Hypertension and identification of toxin in human urine and serum following a cluster of mussel-associated paralytic shellfish poisoning outbreaks.

Following four outbreaks of paralytic shellfish poisoning on Kodiak Island, Alaska, during 1994, medical records of ill persons were reviewed and interviews were conducted. Urine and serum specimens were analyzed at three independent laboratories using four different saxitoxin binding assays. High-performance liquid chromatography was used to determine the presence of specific toxin congeners. Among 11 ill persons, three required mechanical ventilation and one died. Mean peak systolic and diastolic blood pressure measurements were 172 (range 128-247) and 102 (range 78-165) mmHg, respectively, and blood pressure measurements corresponded with ingested toxin dose. All four different laboratory methodologies detected toxin in serum at 2.8-47 nM during acute illness and toxin in urine at 65-372 nM after acute symptom resolution. The composition of specific paralytic shellfish poisons differed between mussels and human biological specimens, suggesting that human metabolism of toxins had occurred. The results of this study indicate that saxitoxin analogues may cause severe hypertension. In addition, we demonstrate that saxitoxins can be detected in human biological specimens, that nanomolar serum toxin levels may cause serious illness and that human metabolism of toxin may occur. Clearance of paralytic shellfish poisons from serum was evident within 24 hr and urine was identified as a major route of toxin excretion in humans.

Adolescent↗
PubMed1998

Development of a bioassay employing the desert locust (Schistocerca gregaria) for the detection of saxitoxin and related compounds in cyanobacteria and shellfish.

Monitoring paralytic shellfish toxins (PST) in shellfish and freshwater cyanobacteria is largely dependent on the mouse bioassay. An alternative assay was devised using the desert locust Schistocerca gregaria. The bioassay successfully identified the optimum extraction procedure for PST from cyanobacterial cells and was also suitable for screening acid extracts of shellfish flesh. These results demonstrate the potential of the locust bioassay for the routine screening of PST in a range of sample matrices.

Animals↗
PubMed1998

Comparative analyses by HPLC and the sodium channel and saxiphilin 3H-saxitoxin receptor assays for paralytic shellfish toxins in crustaceans and molluscs from tropical North West Australia.

The increased frequency and distribution of red tides requires the development of high-throughput detection methods for paralytic shellfish toxins (PST). Community ethics also requires that there be a reduced reliance upon the standard mouse bioassay. A biomolecular assay such as the sodium channel 3H-saxitoxin binding assay can satisfy both of these requirements but may be compromised by cross-reactivity with the structurally unrelated tetrodotoxins (TTX). This study utilised the sodium channel assay but also an alternative 3H-saxitoxin binding assay based upon a saxiphilin isoform from the centipede Ethmostigmus rubripes to screen for PSTs. Saxiphilin is a novel transferrin which binds saxitoxin (STX) but differs from the sodium channel in not having any measurable affinity for TTX. A detailed analysis of toxin composition was achieved by high performance liquid chromatography (HPLC). Various crustaceans and molluscs accumulate PSTs and TTX, thus proving useful biomarkers for these toxins in their immediate environment and an ideal challenge to the detection and analysis of PSTs in this presumptive screening program. Also, there has been little investigation of PSTs in invertebrates from the Indian Ocean so this region was selected to extend our knowledge of the distribution of these toxins. 190 crabs and shellfish encompassing 31 species were collected from reefs along the North-West Australian coast and tested for PSTs and TTX by sodium channel and saxiphilin bioassays as well as HPLC. PSTs were detected in 18 species of crabs and shellfish of the 31 species tested. Eight of these species have not been previously described as toxic, these being the crabs Euzanthus exsculptus, Lophozozymus octodentatus, Metopograpsus frontalis, Pilumnus pulcher, Platypodia pseudogranulosa and Portunus pelagicus, and the molluscs Tectus fenestratus and Trochus hanleyanus. By HPLC, only one or both of STX and decarbamoyl-STX was detected in any extract. Some extracts markedly inhibited 3H-saxitoxin binding by the sodium channel but not by saxiphilin. The close agreement between toxin quantification by the PST specific methods of HPLC and the saxiphilin bioassay is indicative that the additional toxicity detected by the sodium channel assay is TTX.

Amphibian Proteins↗
PubMed1996

Chlordane contamination in selected estuarine and coastal marine finfish and shellfish of New Jersey, USA.

Analysis of chlordane contamination in selected finfish and shellfish species from estuarine and coastal marine waters of New Jersey, USA, indicates consistently highest organochlorine pesticide levels in samples from the north and northeast regions of the state. Gas chromatographic analysis of tissue samples from four finfish species (American eel, Anguilla rostrata; bluefish, Pomatomus saltatrix; striped bass, Morone saxatilis; and weakfish, Cynoscion regalis) and one shellfish species (blue crab, Callinectes sapidus) collected at 28 stations throughout the state during the 1986-1987 sampling period and 42 stations during the 1988-1991 sampling period revealed chlordane concentrations ranging from 5 to 2150 ppb wet weight (wet wt). Highest mean concentrations of chlordane (300 ppb wet wt) occurred in American eel from the Camden region, with secondary maxima (100 ppb wet wt) observed in the northeast region. Lower mean concentrations of chlordane (< 100 ppb wet wt) were recorded in tissue samples of other species collected elsewhere in the state. In general, the lowest levels of chlordane contamination (mean < 50 ppb wet wt) were found in samples from the south coast and Delaware regions. A major conclusion of this study is that some commercially and recreationally important finfish and shellfish species in New Jersey waters, especially those which are lipid-rich, have continued to accumulate chlordane from the environment long after restrictive regulations were first placed on its use in the US. The greatest impact of chlordane contamination is nearby metropolitan centers of the state (i.e., New York, Newark, Camden), although the total concentrations of chlordane in tissue samples from these areas are currently far less than the US Food and Drug Administration action level of 300 ppb wet wt.

Journal Article↗
PubMed2002

Toxic equivalency factors for PAH and their applicability in shellfish pollution monitoring studies.

Fish and shellfish are exposed to a wide range of polycyclic aromatic hydrocarbons (PAH) following oil spills at sea, and can become contaminated as a result. Finfish have a more effective mixed-function oxidase enzyme system than shellfish, and are therefore able to metabolise and excrete PAH more effectively than the invertebrates. Thus, contamination by high-molecular weight PAH, including those with carcinogenic potential and so of concern with regard to human consumers, is therefore usually observed in shellfish, and particularly in bivalve molluscs. Oil spills are not the sole source of PAH, however, as parent compounds are also generated by a wide range of combustion processes. In this paper, consideration is given to monitoring data gathered following recent oil spills (both of crude oil and diesel fuel), alongside data from other studies. These include studies conducted around a former gasworks site and downstream of an aluminium smelter in the UK, and from mussel monitoring studies undertaken in the UK and the USA (including the Exxon Valdez oil spill and the National Status and Trends programme), and in other countries in Europe. For comparative purposes the PAH concentrations are summed and also expressed as benzo[a]pyrene equivalents, their relative concentrations being weighted in relation to the carcinogenic potential of individual PAH compounds using toxic equivalency factors (TEF). Our aim was to assess the utility of this approach in fishery resource monitoring and control following oil spills. Certainly this approach seems useful from the data assessed in this study. and the relative ranking of the various studies seems to reflect the relative degree of concern for human consumers due to the differing contamination sources. As a simple tool for control purposes it is equally applicable to PAH derived from oil spills, and from industrial and combustion sources.

Animals↗