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PubMed2004

Amnesic shellfish poison.

Amnesic shellfish poisoning (ASP) is caused by consumption of shellfish that have accumulated domoic acid, a neurotoxin produced by some strains of phytoplankton. The neurotoxic properties of domoic acid result in neuronal degeneration and necrosis in specific regions of the hippocampus. A serious outbreak of ASP occurred in Canada in 1987 and involved 150 reported cases, 19 hospitalisations and 4 deaths after consumption of contaminated mussels. Symptoms ranged from gastrointestinal disturbances, to neurotoxic effects such as hallucinations, memory loss and coma. Monitoring programmes are in place in numerous countries worldwide and closures of shellfish harvesting areas occur when domoic acid concentrations exceed regulatory limits. This paper reviews the chemistry, sources, metabolism and toxicology of domoic acid as well as human case reports of ASP and discusses a possible mechanism of toxicity.

Amnesia↗
PubMed2006

Consumption of viscera as the most important risk factor in the largest outbreak of shellfish poisoning in Hong Kong, 2005.

Poisoning from shellfish toxins is associated with significant morbidity worldwide. During 10-15 March 2005, 36 clusters of shellfish poisoning related to consumption of fresh scallops (Atrina vexillum) were reported to the Center for Health Protection, Department of Health Hong Kong. We conducted a case-control study to identify the risk factors associated with shellfish poisoning. Detailed demographic, clinical, shellfish consumption data of these subjects were collected using standardized questionnaires. Fifty-eight cases and 44 controls were identified. The mean age for the cases was 37.5 years (range 10-81 years); 45% (n=26) were male. Ninety-five percent had onset of symptoms within 12 hours of consumption of scallops (range: 10 minutes to 30 hours, median: 45 minutes). Dizziness (87.9%) and blurred vision (53.4%) were the predominant symptoms. The mean number of pieces of scallop meat and viscera taken by the cases were 3.7 and 3.6, respectively, significantly higher than that for the controls, which were 1.6 (p<0.001) and 0.5 (p<0.001), respectively. Forty-two percent (n=22) and 19% (n=7) of cases and controls, respectively, took soup/sauce from the same dish that was cooked with the scallops (p=0.02). Consumption of scallop viscera was identified as the only significant risk factor (Adjusted OR=9.93, p=0.001) after adjusting for other risk factors. The result show that consumption of scallop viscera is an important risk factor for shellfish poisoning. The public should be warned specifically in health education messages to avoid eating viscera of scallops.

Adolescent↗
PubMed1997

Comparison of a protein phosphatase inhibition assay, HPLC assay and enzyme-linked immunosorbent assay with the mouse bioassay for the detection of diarrhetic shellfish poisoning toxins in European shellfish.

Consumption of shellfish contaminated with algal toxins produced by marine dinoflagellates can lead to diarrhetic shellfish poisoning (DSP). UK legislation necessitates toxin detection by mouse bioassay but this method is non-specific and lacks sensitivity. As an alternative method, an HPLC technique has been optimized, with detection limits of 0.26 micrograms of toxin/g of shellfish hepatopancreas for both Okadaic Acid (OA) and Dinophysistoxin-1 (DTX-1). A colorimetric protein phosphatase inhibition (PPI) assay has also been optimized. This assay detects inhibition of protein phosphatase 1 (PPI gamma) by OA and DTX-1 with detection limits of 1.5 ng of total toxin/g of hepatopancreas. Contaminated shellfish from several European sources, the UK monitoring programmes and mussels associated with an outbreak of DSP poisoning in the UK, have been analyzed and assessed using the two alternative methods and a commercially available enzyme-linked immunosorbent assay (ELISA) kit. The results indicate that both the HPLC and PPI assays correlate well with each other and with the UK standard mouse bioassay. In contrast, and not withstanding its advantages of rapidity and ease, the ELISA kit did not accurately and consistently detect low toxin concentrations, although it may be useful as a screening tool.

Animals↗
PubMed2002

Detection of paralytic shellfish poisoning (PSP) toxins in shellfish tissue using MIST Alert, a new rapid test, in parallel with the regulatory AOAC mouse bioassay.

In parallel trials with the mouse bioassay, MIST Alert for Paralytic Shellfish Poisoning (PSP), a rapid diagnostic test for PSP, detected 100% of the toxic extracts in over 2100 regulatory samples. Toxic extracts contained at least 80 microg saxitoxin equivalents (STX equiv.) in 100 g of shellfish tissue, or more, as measured by the regulatory AOAC mouse bioassay. Only one potentially toxic sample, which contained 78 and 86 microg STX equiv./100 g shellfish tissue in two different mouse bioassays, was recorded as negative in one replicate of MIST Alert. All other toxic extracts among more than 2100 regulatory shellfish tissue samples were detected by MIST Alert for PSP. The MIST Alert for PSP also detected the majority of extracts containing PSP toxin greater than 32 microg STX equiv./100 g, which is the mouse bioassay detection limit. The MIST Alert for PSP gave a false positive result compared to the mouse bioassay at an average rate of about 14% over all sites, although some differences were seen between sites. Further analysis by high performance liquid chromatography (HPLC) of the (false positive) extracts showed that many contained PSP toxicity in the range of 20-40 microg STX equiv./100 g, below the level detectable by the mouse bioassay. The MIST Alert for PSP gave false positive results from extracts containing less than 20 microg STX equiv./100 g shellfish tissue only about 6% of the time. The PSP family of toxin analogues can occur in any combination in naturally contaminated shellfish tissue and the antibody mixture in the MIST Alert tests detect each of the different PSP toxin analogues with different efficacy. It is therefore impossible to provide an exact detection limit for the MIST Alert that would be applicable for all possible toxin profiles. Through the experience of comparison testing with the regulatory mouse bioassay in many parts of the world, with over 2100 different samples, the MIST Alert for PSP has proven its ability to detect all types of profiles of the PSP toxin analogues. The detection limit for MIST Alert for PSP was about 40 microg STX equiv./100 g for the 'average' profile of PSP toxin analogues. Since the detection limit depends on the toxin profile in the individual extract, it will also vary depending on the profile of analogues most commonly found at each geographic location. This was observed in our study. Over all sites in the trials, approximately 5% of samples below 40 microg STX equiv./100 g were positive, and 5% of samples between 40-80 microg STX equiv./100 g were negative. This is a reflection of the different analogue profiles found in naturally contaminated extracts, even after acid hydrolysis using the AOAC extraction method.

Animals↗
PubMed1999

Detection of diarrhetic shellfish poisoning toxins from tropical shellfish using liquid chromatography-selected reaction monitoring mass spectrometry.

A negative mode liquid chromatography-selected reaction monitoring mass spectrometry (LC-SRM MS) method was developed to detect low concentrations of the diarrhetic shellfish poisoning (DSP) toxins okadaic acid and dinophysistoxin-1 (DTX-1). Detection relies upon monitoring the transition of negative precursor ions [M - H]- to a common fragment ion of m/z 255. Our limit of detection for okadaic acid with this method is 0.5 pg on column. LC-SRM MS has allowed us to detect persistent, low concentrations of DSP toxins from Singapore shellfish.

Animals↗
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

Determination and confirmation of the amnesic shellfish poisoning toxin, domoic acid, in shellfish from Scotland by liquid chromatography and mass spectrometry.

During 1998 and early 1999, shellfish samples from sites in Scotland were found to contain the amnesic shellfish poisoning toxin, domoic acid (DA). Two different techniques, liquid chromatography (LC) with UV diode-array detection and LC with mass spectrometric (MS) detection, were used to detect and confirm DA in shellfish extracts. The LC/UV method was validated for routine monitoring by recovery experiments on spiked mussel and scallop tissues with a certified mussel tissue used as reference material. Crude extracts of selected samples as well as extracts cleaned with strong anion exchange (SAX) were analyzed by both LC/UV and LC/MS. Good correlation (linear regression r2 = 0.996, slope = 0.93) between the 2 methods was found for cleaned extracts. Analyses of crude extracts by LC/UV produced false-positive results in 2 crab samples, whereas LC/MS analyses gave accurate results. It was concluded that LC/UV is a valid approach for routine monitoring of DA in shellfish when cleanup is performed with a SAX cartridge to prevent false positives. A variety of shellfish species were surveyed for DA content, including Pecten maximus (king scallops), Chlamys opercularis (queen scallop), Mytilus edulis (blue mussels), Cancer pugaris (crab), and Ensis ensis (razor fish). The highest concentration of DA was 105 microg/g in Pecten maximus.

Amnesia↗
PubMed2001

Study of paralytic shellfish poisoning toxin profile in shellfish from the Mediterranean shore of Morocco.

Since 1992, a monitoring program for bivalve molluscs contaminated by algal toxins was established at different stations along the Mediterranean Moroccan shores. The monitored stations were tested every 2 weeks. The presence of toxicity was determined using the mouse bioassay method. Toxin profile was carried out by HPLC/FD in selected contaminated tissues. According to the outcomes of this surveillance from 1994 to 1999, reliable information on toxicity of shellfish was obtained. They indicate that PSP is a recurrent toxicity in molluscs along the Mediterranean shore of Morocco. It has been noted a difference of PSP accumulation among individual shellfish. The cockle (Achanthocardia tuberculatum) presents toxicity throughout the year, while other specimens from the same area such as clam (Callista chione), warty venus (Venus gallina) and marine beans (Donax trunculus) accumulate it seasonally from January to April, after which they depurate the toxin. Moreover, the study of toxin profiles among individual shellfish was undertaken. It was found that shellfish presented a complex profile pointing to contamination by Gymnodinium catenatum.

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↗
PubMed1995

Paralytic shellfish poisoning in Alaska: a 20-year retrospective analysis.

Outbreaks of paralytic shellfish poisoning have occurred worldwide. The authors reviewed records at the Alaska Division of Public Health to determine the epidemiologic characteristics of this disease. To assess risk factors for illness, the authors conducted a case-control study. A case was defined as illness compatible with paralytic shellfish poisoning within 12 hours of the consumption of shellfish, and a control was defined as a non-ill participant at a meal in which at least one case occurred. The authors documented 54 outbreaks of paralytic shellfish poisoning involving 117 ill persons from 1973 to 1992. One person died, four (3%) required intubation, and 29 (25%) required an emergency flight to a hospital. Outbreaks occurred with multiple shellfish species, during all four seasons, and at many locations. During the case-control study, illness was not associated with the shellfish toxin level, method of preparation, dose, race, sex, or age; alcohol consumption was associated with a reduced risk of illness (odds ratio = 0.05; p = 0.03). Although paralytic shellfish poisoning causes significant illness, the authors could not identify risk factors with clear implications for prevention strategies. This suggests that shellfish from uncertified beaches should not be eaten. Alcohol may protect against the adverse effects of paralytic shellfish poison.

Adolescent↗
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↗
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↗
PubMed1994

Isolation and purification procedures for the preparation of paralytic shellfish poisoning toxin standards.

Paralytic shellfish poisoning (PSP) is caused by mixtures of saxitoxin analogs of which more than eighteen are known. Reliable and sensitive analytical methods and assays for these toxins are essential to protect the consumer and the shellfish industry, but research has been restricted by a shortage of the pure compounds. Only saxitoxin has so far been generally available as a PSP toxin standard, yet sulfated analogs usually occur in higher concentrations than saxitoxin in toxic marine algae and shellfish. Methods are described for the purification of some of the common PSP toxins, in quantities sufficient for the preparation of PSP standards from the dinoflagellate Alexandrium excavatum, the giant sea scallop (Placopecten megallanicus) hepatopancreas, and the cyanobacterium Aphanizomenon flos-aquae. Purity was monitored by high performance liquid chromatography with fluorescence detection (HPLC-FD), ionspray mass spectrometry (ISP-MS), capillary electrophoresis (CE), and proton NMR spectroscopy.

Animals↗