saxitoxin and Paralysis

Saxitoxins (STX) and tetrodotoxins (TTX) are a group of chemical compounds produced by certain species of marine algae and fish. Lethal dose for a human is about 0.5-2.0 mg when the toxin enters the body via food, and 0.05 mg of poisoning at the time of injection. In the case of aerosol the lethal dose for human being is 5 mg/min/m(3). STX and TTX poisoning cause mostly symptoms from the nervous system in the form of: paresthesia around the lips, tongue, gums, distal segments of the limbs, headache, dysphonia, astigmatism, floating feeling, muscle weakness, paralysis of cranial and peripheral nerves. There is no specific antidote for STX and TTX. It is recommended supportive treatment.

Topics: Administration, Inhalation; Administration, Oral; Aerosols; Animals; Astigmatism; Biological Warfare Agents; Dysphonia; Headache; Humans; Lethal Dose 50; Muscle Weakness; Paralysis; Paresthesia; Saxitoxin; Tetrodotoxin

Paralytic shellfish poisoning (PSP), due to saxitoxin and related compounds, typically results from the consumption of filter-feeding molluscan shellfish that concentrate toxins from marine dinoflagellates. In addition to these microalgal sources, saxitoxin and related compounds, referred to in this review as STXs, are also produced in freshwater cyanobacteria and have been associated with calcareous red macroalgae. STXs are transferred and bioaccumulate throughout aquatic food webs, and can be vectored to terrestrial biota, including humans. Fisheries closures and human intoxications due to STXs have been documented in several non-traditional (i.e. non-filter-feeding) vectors. These include, but are not limited to, marine gastropods, both carnivorous and grazing, crustacea, and fish that acquire STXs through toxin transfer. Often due to spatial, temporal, or a species disconnection from the primary source of STXs (bloom forming dinoflagellates), monitoring and management of such non-traditional PSP vectors has been challenging. A brief literature review is provided for filter feeding (traditional) and non-filter feeding (non-traditional) vectors of STXs with specific reference to human effects. We include several case studies pertaining to management actions to prevent PSP, as well as food poisoning incidents from STX(s) accumulation in non-traditional PSP vectors.

Topics: Animals; Eutrophication; Food Chain; Humans; Paralysis; Public Health; Saxitoxin; Seafood; Shellfish Poisoning

Topics: Animals; Bacterial Toxins; Biotransformation; Dinoflagellida; Electromyography; Female; Foodborne Diseases; Marine Toxins; Paralysis; Saxitoxin; Shellfish; Shellfish Poisoning

Topics: Action Potentials; Animals; Humans; Marine Toxins; Mice; Paralysis; Saxitoxin; Shellfish

Paralytic shellfish toxins (PST) traditionally have been analyzed by liquid chromatography with either pre- or post-column derivatization and always with a silica-based stationary phase. This technique resulted in different methods that need more than one run to analyze the toxins. Furthermore, tetrodotoxin (TTX) was recently found in bivalves of northward locations in Europe due to climate change, so it is important to analyze it along with PST because their signs of toxicity are similar in the bioassay. The methods described here detail a new approach to eliminate different runs, by using a new porous graphitic carbon stationary phase. Firstly we describe the separation of 13 PST that belong to different groups, taking into account the side-chains of substituents, in one single run of less than 30 min with good reproducibility. The method was assayed in four shellfish matrices: mussel (Mytillus galloprovincialis), clam (Pecten maximus), scallop (Ruditapes decussatus) and oyster (Ostrea edulis). The results for all of the parameters studied are provided, and the detection limits for the majority of toxins were improved with regard to previous liquid chromatography methods: the lowest values were those for decarbamoyl-gonyautoxin 2 (dcGTX2) and gonyautoxin 2 (GTX2) in mussel (0.0001 mg saxitoxin (STX)·diHCl kg(-1) for each toxin), decarbamoyl-saxitoxin (dcSTX) in clam (0.0003 mg STX·diHCl kg(-1)), N-sulfocarbamoyl-gonyautoxins 2 and 3 (C1 and C2) in scallop (0.0001 mg STX·diHCl kg(-1) for each toxin) and dcSTX (0.0003 mg STX·diHCl kg(-1) ) in oyster; gonyautoxin 2 (GTX2) showed the highest limit of detection in oyster (0.0366 mg STX·diHCl kg(-1)). Secondly, we propose a modification of the method for the simultaneous analysis of PST and TTX, with some minor changes in the solvent gradient, although the detection limit for TTX does not allow its use nowadays for regulatory purposes.

Topics: Animals; Bivalvia; Chromatography, High Pressure Liquid; Fluorometry; Food Contamination; Graphite; Limit of Detection; Mytilus; Ostrea; Oxidation-Reduction; Paralysis; Pecten; Pectinidae; Porosity; Reproducibility of Results; Saxitoxin; Seafood; Shellfish Poisoning; Tetrodotoxin

Topics: Analgesia; Anesthesia, Local; Animals; Liposomes; Paralysis; Saxitoxin; Shellfish; Time Factors

Paralytic shellfish poisoning (PSP) and diarrhetic shellfish poisoning (DSP) in 7 species of economical shellfishes were analyzed for 1 year, which collected from Huangsha seafood market of Guangzhou from Apr, 2004 to Mar, 2005.. The levels of PSP and DSP in bivalves were determined with mouse bioassay of AOAC. The risk assessment of PSP and DSP in bivalves was conducted according to FAO and Chinese Administration Organization of Fish Culture and Seaport.. PSP was detected in 2 species of the shellfishes assayed and DSP was found out in 6 species. The content of PSP was lower than 4MU/g tissue, whereas the level of PSP in glands was higher than in muscles. DSP toxin was detected in 36 samples of 6 species, what is more, DSP level in 10 samples exceeded the safety threshold. The levels in PSP and DSP of bivalves were all higher in spring and winter with some characteristic of season.. The results suggested that PSP in economical shellfish in Guangzhou market was lower, and shellfish was safe to eat in term of the PSP level if glands were discarded, but DSP contamination in bivalves was severe. It is essential to detect and assess the risk of DSP and PSP in bivalves from seafood market in the future.

Topics: Animals; Bivalvia; Diarrhea; Food Contamination; Marine Toxins; Mice; Paralysis; Saxitoxin; Shellfish; Shellfish Poisoning

Bivalve molluscs, the primary vectors of paralytic shellfish poisoning (PSP) in humans, show marked inter-species variation in their capacity to accumulate PSP toxins (PSTs) which has a neural basis. PSTs cause human fatalities by blocking sodium conductance in nerve fibres. Here we identify a molecular basis for inter-population variation in PSP resistance within a species, consistent with genetic adaptation to PSTs. Softshell clams (Mya arenaria) from areas exposed to 'red tides' are more resistant to PSTs, as demonstrated by whole-nerve assays, and accumulate toxins at greater rates than sensitive clams from unexposed areas. PSTs lead to selective mortality of sensitive clams. Resistance is caused by natural mutation of a single amino acid residue, which causes a 1,000-fold decrease in affinity at the saxitoxin-binding site in the sodium channel pore of resistant, but not sensitive, clams. Thus PSTs might act as potent natural selection agents, leading to greater toxin resistance in clam populations and increased risk of PSP in humans. Furthermore, global expansion of PSP to previously unaffected coastal areas might result in long-term changes to communities and ecosystems.

Topics: Amino Acid Sequence; Animals; Bivalvia; Cell Line; Ciguatera Poisoning; Drug Resistance; Electric Conductivity; Humans; Molecular Sequence Data; Mutation; Paralysis; Risk; Saxitoxin; Selection, Genetic; Sodium; Sodium Channel Blockers; Sodium Channels; Tetrodotoxin

This paper reports the results of investigations of shellfish toxin contamination of products obtained from Shanghai seafood markets. From May to October 2003, 66 samples were collected from several major seafood markets. Paralytic shellfish poisoning (PSP) and diarrhetic shellfish poisoning (DSP) toxins in shellfish samples were monitored primarily by a mouse bioassay, then analysed by HPLC for the chemical contents of the toxins. According to the mouse bioassay, eight samples were detected to be contaminated by PSP toxins and seven samples were contaminated by DSP toxins. Subsequent HPLC analysis indicated that the concentrations of the PSP toxins ranged from 0.2 to 1.9 microg/100 g tissues and the main components were gonyautoxins 2/3 (GTX2/3). As for DSP, okadaic acid was detected in three samples, and its concentration ranged from 3.2 to 17.5 microg/100 g tissues. Beside okadaic acid, its analogues, dinophysistoxins (DTX1), were found in one sample. According to the results, gastropod (Neverita didyma) and scallop (Argopecten irradians) were more likely contaminated with PSP and DSP toxins, and most of the contaminated samples were collected from Tongchuan and Fuxi markets. In addition, the contaminated samples were always found in May, June and July. Therefore, consumers should be cautious about eating the potential toxic shellfish during this specific period.

Topics: Animals; Biological Assay; China; Chromatography, High Pressure Liquid; Diarrhea; Enzyme Inhibitors; Food Contamination; Marine Toxins; Mice; Okadaic Acid; Paralysis; Saxitoxin; Shellfish

The dietary uptake of one suite of dinoflagellate-produced neurotoxins, that are commonly called paralytic shellfish poisoning (PSP) toxins, is known to cause acute fish kills. However, little is known about the effects of dissolved phase exposure and the potential sublethal effects of this route of exposure on early developmental stages of fish. Toxin exposure during early development is of particular concern because the embryos and larvae of some marine fish species may be unable to actively avoid the dissolved toxins that algal cells release into the water column during harmful algal blooms. Here we use the zebrafish (Danio rerio) as a model experimental system to explore the sublethal effects of a dissolved PSP toxin, saxitoxin (STX), on early development in fish, including sensorimotor function, morphology, and long-term growth and survival. Aqueous phase exposures of 229 +/- 7 microg STX eq. l(-1) caused reductions in sensorimotor function as early as 48 h postfertilization (hpf) and paralysis in all larvae by 4 days postfertilization (dpf). Rohon-Beard mechanosensory neurons appeared to be more sensitive to STX than dorsal root ganglion neurons at this dose. Additionally, exposure to 481 +/- 40 microg STX eq. l(-1) resulted in severe edema of the eye, pericardium, and yolk sac in all exposed larvae by 6 dpf. The onset of paralysis in STX-exposed larvae was stage-specific, with older larvae becoming paralyzed more quickly than younger larvae (5 h at 6 dpf as compared to 8 and 46 h for 4 and 2 dpf larvae, respectively). When transferred to clean water, many larvae recovered from the morphological and sensorimotor effects of STX. Thus, the sublethal effects of the toxin on larval morphology and behavior were reversible. However, zebrafish exposed to STX transiently during larval development (from 2 to 4 dpf) had significantly reduced growth and survival at 18 and 30 days of age. Collectively, these data show that (1) dissolved phase STX is bioavailable to fish embryos and larvae, (2) the toxin is a paralytic with potencies that are stage-specific for fish larvae, (3) the observed toxicological effects of STX exposure are reversible, and (4) a short-term toxin exposure can negatively impact the survival of fish several weeks later. Dissolved algal toxins may therefore have important sublethal effects on vulnerable species of fish.

Topics: Animals; Biological Availability; Eye; Larva; Motor Activity; Paralysis; Pericardium; Saxitoxin; Toxicity Tests; Yolk Sac; Zebrafish

Occurrence and toxic profiles of paralytic shellfish toxins (PST) in the chocolata clam Megapitaria squalida were investigated. From December 2001 to December 2002, 25 clams were obtained monthly from Bahia de La Paz, Gulf of California. Additionally, net (20 microm) and bottle phytoplankton samples were also collected to identify toxic species. Toxins were analyzed by HPLC with post-column oxidation and fluorescence detection. Toxicity in the clam was low and varied from 0.14 to 5.46 microg/STXeq/100 g. Toxicity was detected in December, March, April, June, and August. Toxin profile was composed mainly by STX, GTX2, GTX3, dcGTX2, dcGTX3, C2, dcSTX and B1. Gymnodinium catenatum was the only PST-producing dinoflagellate identified in the phytoplankton samples throughout the study period. G. catenatum was observed mainly in net samples from December 2001 to December 2002; however, in bottle samples, G. catenatum was only observed in five months. Highest abundance (2600 cells l(-1)) was observed in March and the lowest (160 cells l(-1)) in June. G. catenatum mainly formed two-cell chains and rarely four or eight. The presence of PST in net phytoplankton samples support the fact that G. catenatum is the main source of PST in the clams. This study represents the first report of PST toxins in the chocolata clam from Bahia de La Paz.

Topics: Animals; Bivalvia; Dinoflagellida; Mexico; Paralysis; Phytoplankton; Population Density; Population Dynamics; Saxitoxin; Shellfish; Shellfish Poisoning; Time Factors

Paralytic shellfish poisoning is one of the most severe forms of food poisoning. The toxins responsible for this type of poisoning are metabolic products of dinoflagellates, which block neuronal transmission by binding to the voltage-gated Na(+) channel. Accumulation of paralytic toxins in shellfish is an unpredictable phenomenon that necessitates the implementation of a widespread and thorough monitoring program for mollusk toxicity. All of these programs require periodical collection and analysis of a wide range of shellfish. Therefore, development of accurate analytical protocols for the rapid determination of toxicity levels would streamline this process. Our laboratory has developed a fluorimetric microplate bioassay that rapidly and specifically determines the presence of paralytic shellfish toxins in many seafood samples. This method is based on the pharmacological activity of toxins and involves several steps: (i) Incubation of excitable cells in 96 well microtiter plates with the fluorescent dye, bis-oxonol, the distribution of which across the membrane is potential-dependent. (ii) Cell depolarization with veratridine, a sodium channel-activating toxin. (iii) Dose-dependent inhibition of depolarization with saxitoxin or natural samples containing paralytic shellfish toxins. Measuring toxin-induced changes in membrane potential allowed for quantification and estimation of the toxic potency of the samples. This new approach offers significant advantages over classical methods and can be easily automated.

Topics: Animals; Biological Assay; Bivalvia; Dinoflagellida; Fluorometry; Food Contamination; Gramicidin; Humans; Male; Marine Toxins; Membrane Potentials; Mice; Paralysis; Reproducibility of Results; Saxitoxin; Sensitivity and Specificity; Shellfish; Shellfish Poisoning; Sodium Channels; Time Factors; Tumor Cells, Cultured; Veratridine

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

Topics: Animals; Biological Assay; False Positive Reactions; Mice; Mollusca; Paralysis; Reagent Strips; Reproducibility of Results; Saxitoxin; Sensitivity and Specificity; Shellfish

We determined the seasonal distribution of paralytic shellfish toxins (PSTs) and PST producing bacteria in > 15, 5-15, and 0.22-5 microm size fractions in the St Lawrence. We also measured PSTs in a local population of Mytilus edulis. PST concentrations were determined in each size fraction and in laboratory incubations of sub-samples by high performance liquid chromatography (HPLC), including the rigorous elimination of suspected toxin 'imposter' peaks. Mussel toxin levels were determined by mouse bioassay and HPLC. PSTs were detected in all size fractions during the summer sampling season, with 47% of the water column toxin levels associated with particles smaller than Alexandrium tamarense (< 15 microm). Even in the > 15 microm size fraction, we estimated that as much as 92% of PSTs could be associated with particles other than A. tamarense. Our results stress the importance of taking into account the potential presence of PSTs in size fractions other than that containing the known algal producer when attempting to model shellfish intoxication, especially during years of low cell abundance. Finally, our HPLC results confirmed the presence of bacteria capable of autonomous PST production in the St Lawrence as well as demonstrating their regular presence and apparent diversity in the plankton.

Topics: Animals; Bacterial Toxins; Biological Assay; Bivalvia; Chemical Fractionation; Chromatography, High Pressure Liquid; Mice; Paralysis; Particle Size; Quebec; Saxitoxin; Seasons; Seawater; Shellfish; Shellfish Poisoning

Saxitoxin (STX) and its derivatives are highly toxic natural compounds produced by dinoflagellates commonly present in marine phytoplankton. During algal blooms ("red tides"), shellfish accumulate saxitoxins leading to paralytic shellfish poisoning (PSP) in human consumers. PSP is a consequence of the high-affinity block of voltage-dependent Na channels in neuronal and muscle cells. PSP poses a significant public health threat and an enormous economic challenge to the shellfish industry worldwide. The standard screening method for marine toxins is the mouse mortality bioassay that is ethically problematic, costly and time-consuming. We report here an alternative, functional assay based on electrical recordings in cultured cells stably expressing a PSP target molecule, the STX-sensitive skeletal muscle Na channel. STX-equivalent concentration in the extracts was calibrated by comparison with purified STX, yielding a highly significant correlation (R=0.95; N=30) between electrophysiological determinations and the values obtained by conventional methods. This simple, economical, and reproducible assay obviates the need to sacrifice millions of animals in mandatory paralytic shellfish toxin screening programs.

Topics: Animals; Binding, Competitive; Cell Line; Electrophysiology; Humans; Marine Toxins; Mice; Paralysis; Patch-Clamp Techniques; Recombinant Proteins; Reproducibility of Results; Saxitoxin; Shellfish; Sodium Channel Blockers; Sodium Channels

Topics: Animals; Calibration; Cell Survival; Chromatography, High Pressure Liquid; Colorimetry; Diarrhea; Fluorescent Dyes; Marine Toxins; Mass Spectrometry; Mice; Morocco; Okadaic Acid; Paralysis; Phosphoprotein Phosphatases; Saxitoxin; Shellfish

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.

Topics: Animals; Biological Assay; Bivalvia; Digestive System; Foodborne Diseases; France; Lipid Metabolism; Lipids; Marine Toxins; Mice; Paralysis; Plankton; Saxitoxin; Seasons

A rapid qualitative screening method was developed for the fractionation of paralytic shellfish poisoning toxins. Periodic acid, t-butyl hydroperoxide, and hydrogen peroxide were tested as oxidants for the fluorometric detection of paralytic shellfish toxins. Hydrogen peroxide was found to be the most convenient and efficient oxidant since the fluorescence can be detected after the incubation of toxins at 100 degrees C for 3-5 min. In addition to the structure of the compound, the incubation temperature and time, the amount of acid, and the peroxide concentration affect the fluorescence reaction. This method was more efficient than the previously published peroxidation methods which involved lengthy incubation periods or time-consuming pH adjustment. Also, far greater sensitivity was achieved with the new method with levels of 0.027, 0.054, 0.023, 0.003, 0.0002, and 0.0006 pmol being easily detected for saxitoxin, neosaxitoxin, gonyautoxin 1 and 4, gonyautoxin 2 and 3, C toxins, and B toxins, respectively. The method is particularly valuable for the screening of fractions separated by column chromatography.

Topics: Acetic Acid; Animals; Chromatography, High Pressure Liquid; Fluorescent Dyes; Hydrogen Peroxide; Hydrogen-Ion Concentration; Marine Toxins; Mollusca; Oxidants; Oxidation-Reduction; Paralysis; Periodic Acid; Saxitoxin; Sensitivity and Specificity; Shellfish; Shellfish Poisoning; Temperature; tert-Butylhydroperoxide; Time Factors

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.

Topics: Adolescent; Adult; Alaska; Animals; Bivalvia; Chromatography, High Pressure Liquid; Disease Outbreaks; Female; Humans; Hypertension; Male; Middle Aged; Paralysis; Poisoning; Saxitoxin; Sodium Channel Blockers; Sodium Channels

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.

Topics: Adolescent; Adult; Aged; Alaska; Animals; Child; Child, Preschool; Disease Outbreaks; Female; Foodborne Diseases; Humans; Logistic Models; Male; Marine Toxins; Middle Aged; Mollusca; Paralysis; Paresthesia; Retrospective Studies; Risk Factors; Saxitoxin; Shellfish Poisoning

Topics: Child, Preschool; Female; Humans; Neurotoxins; Paralysis; Saxitoxin; Shellfish

Paralytic toxicity was detected by tetrodotoxin (TTX) bioassay in all 15 specimens of the xanthid crab Lophozozymus pictor collected from northern Taiwan in 1993. The average toxicity of crab specimens was 921 +/- 231 (mean +/- S.E.) mouse units. The toxin of crab was partially purified and then identified. It was found that the crab toxin contained TTX and gonyautoxin. The ratio of TTX to gonyautoxin for crab toxin was about 9:1.

Topics: Animals; Brachyura; Chromatography, High Pressure Liquid; Dinoflagellida; Electrophoresis, Polyacrylamide Gel; Fish Venoms; Food Contamination; Foodborne Diseases; Gas Chromatography-Mass Spectrometry; Marine Toxins; Paralysis; Saxitoxin; Shellfish; Tetrodotoxin

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.

Topics: Adolescent; Adult; Aged; Child; Chile; Female; Humans; Male; Middle Aged; Paralysis; Saxitoxin; Shellfish Poisoning; Time Factors

Topics: Adult; Animals; Autopsy; Chile; Dinoflagellida; Female; Food Contamination; Foodborne Diseases; Humans; Male; Paralysis; Saxitoxin; Shellfish Poisoning

Sodium channels obtained from rat brain membrane preparations were coated onto microtiter plates and used to develop a direct solid-phase binding assay. The tritiated sodium channel blocker saxitoxin ([3H]-saxitoxin; STX) was used to detect toxins in paralytic shellfish poisoning (PSP) by measuring the competitive displacement of other toxins. With this assay the amount of STX and tetrodotoxin needed to displace 50% of bound [3H]STX was 1.7 and 1.76 ng/ml for buffer samples, respectively. In the direct solid-phase binding assays, the PSP toxins were effectively bound to the rat brain membranes. The IC50 of this assay for different PSP toxin solutions obtained from mussels contaminated in red tides ranged from 0.03 to 0.30 ng/ml. Therefore, this assay represents a potentially useful method for the detection of toxin-contaminated mussels.

Topics: Animals; Binding, Competitive; Bivalvia; Female; In Vitro Techniques; Marine Toxins; Neurotoxins; Paralysis; Radioligand Assay; Rats; Rats, Sprague-Dawley; Saxitoxin; Sensitivity and Specificity; Sodium Channels

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.

Topics: Animals; Biological Assay; Bivalvia; Brachyura; Cross Reactions; Foodborne Diseases; Immunoblotting; Mice; Mollusk Venoms; Muscle Proteins; Muscles; Paralysis; Saxitoxin

Topics: Adult; Alaska; Animals; Bivalvia; Disease Outbreaks; Humans; Male; Massachusetts; Middle Aged; Paralysis; Saxitoxin; Shellfish Poisoning

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.

Topics: Adult; Alaska; Animals; Bivalvia; Disease Outbreaks; Foodborne Diseases; Humans; Male; Massachusetts; Middle Aged; Paralysis; Saxitoxin; Shellfish Poisoning

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.

Topics: Adolescent; Adult; Age Factors; Aged; Aged, 80 and over; Animals; Bivalvia; Case-Control Studies; Child; Child, Preschool; Disease Outbreaks; Female; Guatemala; Humans; Infant; Male; Middle Aged; Paralysis; Saxitoxin; Shellfish Poisoning

A bacterium Moraxella sp. isolated from Protogonyaulax tamarensis was cultured in various conditions. Changes of toxicity and toxin components of the cells during culture were analyzed by bioassay and HPLC-fluorometric analysis. Toxin productivity of Moraxella sp. increased when it was cultured in nutrition-deficient environments. The main toxins produced by Moraxella sp. in these conditions were gonyautoxins (GTXs), mainly GTX 1 and 4 which are major toxins of P. tamarensis.

Topics: Animals; Bacterial Toxins; Culture Media; Dinoflagellida; Marine Toxins; Moraxella; Paralysis; Saxitoxin

Mutations in the enhancer of seizure (e(sei] locus have been isolated on the basis of their ability to cause temperature-induced paralysis of alleles at the seizure (sei) locus at temperatures at which these mutations ordinarily do not paralyze. This enhancer is specific to the seizure locus and is without effect on other temperature-sensitive paralytic mutants including para, nap, tip-E and shi. This suggests that the enhancer responds specifically to the mechanism of paralysis mediated by the seizure mutations. The e(sei) is a recessive mutation which maps to 39.0 on the left arm of chromosome 3. Deficiency mapping has placed it at 69A4-B5 on the salivary gland polytene chromosome map. When a new enhancer allele was isolated following P-M hybrid dysgenesis, there was a concomitant P-element insertion at 69B. In the absence of seizure mutations, the enhancer mutation causes non-temperature dependent hyperactivity when agitated and interferes with the climbing response. Electrophysiological studies examined the effects of increasing temperature on electrical activity in the adult giant fiber/flight muscle system. Neuronal hyperactivity was seen in both e(sei) and sei single mutant homozygotes, but not in wild type. The hyperactivity was more severe in the sei;e(sei) double mutants. The correlation between the physiological effects and the mutant behavior suggests that both sei and e(sei) cause membrane excitability defects. Since previous work has shown that seizure mutants affect [3H]saxitoxin binding to the voltage-sensitive sodium channel, e(sei) may code for a gene product which interacts with this channel.

Topics: Alleles; Animals; Chromosome Mapping; DNA Transposable Elements; Drosophila melanogaster; Electrophysiology; Genes; Ion Channels; Motor Neurons; Muscles; Paralysis; Saxitoxin; Seizures; Temperature

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.

Topics: Animals; Biological Assay; Bivalvia; Dinoflagellida; Humans; Mice; Paralysis; Saxitoxin; Shellfish; Shellfish Poisoning; Singapore

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.

Topics: Amino Acids; Animals; Bivalvia; Indicators and Reagents; Marine Toxins; Mice; Molybdenum; Paralysis; Saxitoxin; Shellfish; Spectrometry, Fluorescence; Spectrophotometry, Infrared; Tungsten; Tungsten Compounds

Samples of Saxidomus nuttali and Mytilus californianus collected during the 1981 dinoflagellate bloom at Bodega Bay, California, were analyzed for the presence of paralytic toxins. Neck tissue of S. nuttali contained saxitoxin (STX) and neoSTX (95% of the total toxicity), whereas the bodies contained neoSTX and a mixture of the gonyautoxins. In a sample of M. californianus the presence of neoSTX and the gonyautoxins was demonstrated, whereas a second sample, collected at a different site, contained almost exclusively neoSTX.

Topics: Animals; Bivalvia; California; Chromatography, Thin Layer; Dinoflagellida; Male; Marine Toxins; Mice; Mice, Inbred ICR; Mollusca; Paralysis; Saxitoxin

Topics: Animals; Cross-Sectional Studies; Diagnosis, Differential; Dinoflagellida; Europe; Humans; International Cooperation; Japan; Mice; Paralysis; Risk; Saxitoxin; Shellfish Poisoning; United States

Topics: Animals; Bivalvia; Dinoflagellida; Foodborne Diseases; Humans; Mollusca; Paralysis; Saxitoxin; Shellfish Poisoning

Topics: Aged; Animals; Bivalvia; Canada; Disease Outbreaks; Female; Foodborne Diseases; Humans; Male; Mice; Middle Aged; Paralysis; Paresthesia; Saxitoxin; Shellfish; Shellfish Poisoning

Topics: Humans; Male; Paralysis; Saxitoxin; Shellfish Poisoning

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.

Topics: Bivalvia; Classification; Dinoflagellida; Ethanol; Female; Humans; Male; Paralysis; Saxitoxin; Seasons; Shellfish Poisoning; South Africa

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.

Topics: Bivalvia; Critical Care; Dinoflagellida; Humans; Male; Middle Aged; Nova Scotia; Paralysis; Saxitoxin; Shellfish Poisoning

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.

Topics: Disease Outbreaks; Humans; Paralysis; Saxitoxin; Shellfish Poisoning

Topics: Alaska; History, 18th Century; Humans; Paralysis; Saxitoxin; Shellfish Poisoning