Biotransformations of Paralytic Shellfish Toxins by Bacteria Isolated from Bivalve Molluscs

Due to the possibility that bacteria could be involved in the clearance of paralytic shellfish toxins (PST) from bivalve molluscs, investigations into which, if any, bacteria were able to grow at the expense of PST focused on several common shellfish species. These species were blue mussels, oysters, razor fish, cockles, and queen and king scallops. Bacteria associated with these shellfish were isolated on marine agar 2216 and characterized by their carbon utilization profiles (BIOLOG). Selected isolates from groups demonstrating 90% similarity were screened for their ability to metabolize a range of PST (gonyautoxins 1 and 4 [GTX 1/4], GTX 2/3, GTX 5, saxitoxin, and neosaxitoxin) using a novel screening method and confirming its results by high-performance liquid chromatography. Results suggest that molluscan bacteria have different capacities to utilize and transform PST analogues. For example, isolates M12 and R65 were able to reductively transform GTX 1/4 with concomitant production of GTX 2/3, while isolate Q5 apparently degraded GTX 1/4 without the appearance of other GTXs. Other observed possible mechanisms of PST transformations include decarbamoylation by isolate M12 and sulfation of GTXs by isolates Q5, R65, M12, and C3. These findings raise questions as to the possible role of bacteria resident in the shellfish food transport system. Some researchers have suggested that the microflora play a role in supplying nutritional requirements of the host. This study demonstrates that bacteria may also be involved in PST transformation and elimination in molluscan species.     

Grazing on a toxic Alexandrium catenella bloom by the lobster krill Munida gregaria (Decapoda: Galatheoidea: Munididae)

Specimens of Munida gregaria were collected within and in the vicinity of a bloom of the toxic dinoflagellate Alexandrium catenella in Queen Charlotte Sound, New Zealand. The crustacean contained paralytic shellfish toxin (PST) with an analogue profile dominated by N-sulfocarbamoyl analogues (C1,2 and GTX5) and carbamate gonyautoxins (GTX1,4), similar to that of the dinoflagellate. A feeding experiment showed that M. gregaria is capable of actively grazing on A. catenella and it may play a role in controlling population growth of the dinoflagellate. This is the first account of the accumulation of PST by M. gregaria. When it is periodically abundant, M. gregaria is an important food item for fish, birds and other marine fauna and they are a vector by which PST may be transferred to higher trophic levels.     

Toxin content differs between life stages of Alexandrium fundyense (Dinophyceae)

Different life stages of two mating-compatible clones of the paralytic shellfish toxin (PST)-producing dinoflagellate Alexandrium fundyense Balech were separated using a combination of techniques; culturing and sampling methods were used to separate vegetative cells and gametes, and sorting flow cytometry was used to separate zygotes. PST profiles were significantly different between life stages; the two gonyautoxins GTX1 and 2 were present in vegetative and senescent cells, but disappeared from gametes and zygotes. Toxin-profile changes were shown to occur very quickly in both strains when pellicle cyst formation was induced by shaking (four minutes) followed by rinsing on a screen. These pellicle cysts produced from exponentially-growing, vegetative cells lost GTX1 and 2 completely. Rapid toxin epimerization of GTX1 to GTX4 and GTX2 to GTX3 is one possible explanation, although the biological advantage of this remains unclear. Another possible explanation is that during the mating phase of a bloom or when cells are disturbed, GTX1 and GTX2 are released into the surrounding water. It may be advantageous for a dinoflagellate bloom to be surrounded by free toxins in the water.     

Paralytic shellfish toxins in the chocolata clam, Megapitaria squalida (Bivalvia: Veneridae), in Bahía de La Paz, Gulf of California

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.     

PURIFICATION AND CHARACTERIZATION OF A SULFOTRANSFERASE SPECIFIC TO N-21 OF SAXITOXIN AND GONYAUTOXIN 2+3 FROM THE TOXIC DINOFLAGELLATE GYMNODINIUM CATENATUM (DINOPHYCEAE)

A sulfotransferase (ST) specific to N-21 of saxitoxin (STX) and gonyautoxin 2+3 (GTX2+3) designated as N-ST was purified to homogeneity from the cytosolic fraction of clonal-axenic vegetative cells of the toxic dinoflagellate Gymnodinium catenatum Graham GC21V, which causes paralytic shellfish poisoning. The enzyme transferred a sulfate group from 3'-phosphoadenosine 5'-phosphosulfate (PAPS) to N-21 in the carbamoyl group of STX and GTX2+3 to produce GTX5 and C1+2, respectively. The molecular mass of the purified enzyme was determined by SDS-PAGE to be 59 kDa. Gel filtration chromatography showed a native molecular mass of 65 kDa, indicating that the N-ST is a monomeric enzyme. The N-ST was specific to only N-21 of STX and GTX2+3, and O-22 sulfation was not observed. Moreover, the N-ST was not active toward neo STX and GTX1+4, which differed from STX and GTX2+3, respectively, in only N-1 hydroxylation. When various compounds previously reported to be substrates for STs in other organisms and paralytic shellfish poisoning toxins other than STX and GTX2+3 were added to the reaction mixture, N-ST activity was not decreased. The enzyme required PAPS as the sole source of sulfate. The enzyme was optimally active at pH 6.0 and 25° C, and its activity was enhanced by Mg^{2 +} and Co^{2 +} . The K_m values of the N-ST for STX and GTX2+3 were 16.1 μM and 29.8 μM, respectively.     

PRODUCTION OF PARALYTIC SHELLFISH TOXINS BY APHANIZOMENON SP. LMECYA 31 (CYANOBACTERIA)1

We examined intracellular and extracellular paralytic shellfish toxins (PST) in a strain of Aphanizomenon sp. (LMECYA31) isolated from a Portuguese freshwater reservoir throughout the growth cycle and under different conditions affected by temperature and nitrate and phosphate availability. PST concentrations and compositions were greatly influenced by cell density, growth stage, and temperature and nutrients conditions. On a per‐cell basis results showed (1) the enhancement of PST cell quota after the end of exponential growth phase in nutrient replete batch cultures, (2) the absence of a PST increment at late growth stages under phosphate limitation, (3) a rise in PST maximum cell quota under nitrate depletion, and (4) the enhancement of toxin production at higher temperatures. The relative proportion of the four toxins detected, neoSTX, dcSTX, STX and GTX5, also changed within and between culture settings. While growing under phosphate rich media cells produced mainly GTX5 and neoSTX, whereas under phosphate limitation the proportion of STX and dcSTX increased substantially with culture age. Large amounts of extracellular toxins were found in the culture medium, increasing during culture time. Extracellular toxin composition in each culture was fairly constant and always similar to the intracellular composition found at late stages of growth. This further supported other research that indicates that PSTs are released to the water through cell lysis, and a significant concentration of PST may be expected to remain in the water upon the collapse of a toxic bloom or after cells removal by water treatment.     

Intra-population clonal variability in allelochemical potency of the toxigenic dinoflagellate Alexandrium tamarense

Clonal variability in exponential growth rate and production of secondary metabolites was determined from clonal isolates of Alexandrium tamarense originating from a single geographical population from the east coast of Scotland. To assess variability in the selected phenotypic characteristics over a wide spectrum, 10 clones were chosen for experimentation from 67 clonal isolates pre-screened for their lytic capacity in a standardized bioassay with the cryptophyte Rhodomonas salina. Specific growth rates (μ) of the 10 clonal isolates ranged from 0.28 to 0.46 d⁻¹ and were significantly different among clones. Cell content (fmol cell⁻¹) and composition (mol%) of paralytic shellfish toxins (PSTs), analyzed by liquid chromatography with fluorescence detection (LC–FD), varied widely among these isolates, with total PST quotas ranging from 20 to 89 fmol cell⁻¹. Except for strain 3, the toxins C1/C2, neosaxitoxin (NEO), saxitoxin (STX), and gonyautoxins-1 and -4 (GTX1/GTX4), were consistently the most relatively abundant, with lesser amounts of GTX2/GTX3 evident among all isolates. Only clone 3 contained >20 mol% of toxin B1, with C1/C2, GTX2/GTX3 and NEO in almost equimolar ratios.Eight of the 10 clones caused cell lysis of both R. salina and the heterotrophic dinoflagellate Oxyrrhis marina, as quantified from the dose–response curves from short-term (24 h) co-incubation bioassays. For two clones, no significant mortality even at high Alexandrium cell concentrations (ca. 10⁴ mL⁻¹) was observed. Allelochemical activity expressed as EC₅₀ values, defined as the Alexandrium cell concentration causing lysis of 50% of target cells, varied by about an order of magnitude and was significantly different among clones. No correlation was observed between growth rate und allelochemical potency (as EC₅₀) indicating that at least under non-limiting growth conditions no obvious growth reducing costs are associated with the production of allelochemically active secondary metabolites.     

Growth and toxin production in batch cultures of a marine dinoflagellate Alexandrium tamarense HK9301 isolated from the South China Sea

Nutritional and environmental conditions were characterized for a batch culture of the marine dinoflagellate Alexandrium tamarense HK9301 isolated from the South China Sea for its growth (cells ml⁻¹), cellular toxin content (Qt in fmol cell⁻¹) and toxin composition (mol%). Under a nutrient replete condition, Qt increased with cell growth and peaked at the late stationary phase. Toxin content increased with the nitrate concentration in the culture while it reached a maximum at 5 μM phosphate. When nitrate was replaced with ammonia, Qt decreased by 4.5-fold. Salinity and light intensity were important factors affecting Qt. The latter increased two-fold over the range of salinity from 15 to 30‰, while decreased 38% as light intensity increased from 80 to 220 μE m⁻² s⁻¹. Toxin composition varied with growth phase and culture conditions. In nutrient replete cultures, toxin composition varied greatly in the early growth phase (first 3 days) and then C1/C2, C3/C4 and GTX1 remained relatively constant while GTX4 increased from 32 to 46% and GTX5 decreased from 28 to 15%. In general, the composition of GTXs was affected in a much greater extent than C toxins by changes in nutrient conditions, salinity and light intensity. This is especially true with GTX4 and GTX5. These data indicate that the cellular toxin content and toxin composition of A. tamarense HK9301 are not constant, but that they vary with growth phase and culture conditions. Use of toxin composition to identify a toxigenic marine dinoflagellate is not always valid. The data also reveal that high salinity and low light intensity, together with high nitrate and low phosphate concentrations, would favor toxin production by this species.     

Toxic Alexandrium minutum (Dinophyceae) from Vietnam with new gonyautoxin analogue

Clonal cultures of Alexandrium species collected from a shrimp pond on the northern coast of Vietnam were established and morphologically identified as Alexandrium minutum. Nucleotide sequences of domains 1 and 2 of the large subunit ribosomal (LSU) rRNA gene showed high sequence similarity to A. minutum isolates from Malaysia. Paralytic shellfish toxin profile of the clones was characterized by the dominance of GTX4, GTX1, and NEO. GTX3, GTX2, and dcSTX were also present in trace amount. Toxin content varied among the strains and growth stages, ranged from 3.0 to 12.5 fmol cell⁻¹. In addition to these known toxin components, a new gonyautoxin derivative was detected by HPLC, eluting between GTX4 and GTX1. The peak of this compound disappeared under non-oxidizing HPLC condition but unchanged either after treated with 0.05 M ammonium phosphate/10% mercaptoethanol or 0.1N HCl hydrolysis. LCMS ion scanning showed a parental ion of [M + H]⁺ at m/z 396, [M − SO₃]⁺ at m/z 316, and [M − SO₄]⁺ at m/z 298. Based on these results, the derivative was identified as deoxy-GTX4-12ol, and this represents the first report of this toxin analogue.     

中国东海和南海有害赤潮高发区麻痹性贝毒素研究

用小白鼠生物检测法和高效液相色谱法对采自浙江舟山和广东深圳海域贝类的麻痹性贝毒素进行了调查和分析,结果表明,舟山海域近岸的贝类毒素检出率为14％,染毒的贝类毒素含量不高,低于小白鼠生物检测法的测定范围;深圳近岸贝类毒素检出率为30％以上,华贵栉孔扇贝是主要的染毒贝类,有1个样品毒素含量达5．1Mu·g-1,超出安全食用标准．从深圳大亚湾华贵栉孔扇贝检测出10种麻痹性贝毒素成分,消化腺的主要毒素成分为GTXl+2和GTX5,Cl+2和GTX2+3,而剔除消化腺后其余贝组织的主要成分为neoSTX和GTX5．贝毒素主要积累在扇贝的消化腺内,消化腺含有的毒素是贝肉组织的8倍．     

Molecular phylogeny and toxin profiles of Alexandrium tamarense (Lebour) Balech (Dinophyceae) from the west coast of Greenland

Detection of paralytic shellfish poisoning (PSP) toxins in scallops from the west coast of Greenland exceeding the 800 μg toxin/kg shellfish limit led to an investigation with the aim of finding the responsible organism(s). Three strains of Alexandrium Halim were established from single cell isolations. Morphological identification of the strains and determination of their position within the genus by LSU rDNA sequences was carried out. Light microscopy revealed that the three strains was of the Alexandrium tamarense morphotype, and bayesian and neighbor-joining analyses of the LSU rDNA sequences placed them within Group I of the A. tamarense species complex. The toxicity and toxin profiles of the strains were measured by liquid chromatography fluorescence detection (LC-FD) and their identity was confirmed by liquid chromatography coupled with tandem mass spectrometry (LC–MS/MS). The three strains all turned out to be toxic and all produced large proportions (>60% total mol) of gonyautoxins 1 and 4 (GTX1/GTX4). This is the first record of saxitoxin producers from western Greenland. The toxin profiles were atypical for A. tamarense in their absence of N-sulfocarbanoyl C1/C2 or B1/B2 toxins. Rather the high molar percentage of GTX1/GTX4, the lesser amounts of only carbamoyl toxins and the absence of decarbamoyl derivatives are more characteristic features of A. minutum strains. This may indicate that the genetically determined toxin profiles in Alexandrium species are more complex than previously appreciated.     

Distribution of Vibrio vulnificus phage in oyster tissues and other estuarine habitats.

Phages lytic to Vibrio vulnificus were found in estuarine waters, sediments, plankton, crustacea, molluscan shellfish, and the intestines of finfish of the U.S. Gulf Coast, but no apparent relationship between densities of V. vulnificus and its phages was observed. Phage diversity and abundance in molluscan shellfish were much greater than in other habitats. V. vulnificus phages isolated from oysters did not lyse other mesophilic bacteria also isolated from oysters. Both V. vulnificus and its phages were found in a variety of oyster tissues and fluids with lowest densities in the hemolymph and mantle fluid. These findings suggest a close ecological relationship between V. vulnificus phages and molluscan shellfish.     

IDENTIFICATION AND TOXICITY OF ALEXANDRIUM TAMARENSE (DINOPHYCEAE) IN SCOTTISH WATERS1

Contamination of shellfish with paralytic shellfish poisoning (PSP) toxins produced by Alexandrium species poses a potential threat to the sustainability of the Scottish aquaculture industry. Routine LM analysis of water samples from around the Scottish coast has previously identified Alexandrium (Dinophyceae) as a regular part of the spring and summer phytoplankton communities in Scottish coastal waters. In this study, Alexandrium tamarense (M. Lebour) Balech isolated from sediment and water samples was established in laboratory culture. Species identification of these isolates was confirmed using thecal plate dissections and by molecular characterization based on their LSU and, in some cases, ITS rDNA sequence. Molecular characterization and phylogenetic analysis showed the presence of two ribotypes of A. tamarense: Group I (North American ribotype) and Group III (Western European ribotype). Assessment of PSP toxin production using hydrophilic interaction liquid chromatography–tandem mass spectrometry (HILIC–MS/MS) showed that A. tamarense Group I produced a complex array of toxins (～2,000 fg STX equivalents · cell^?1) with the major toxins being C2, neosaxitoxin (NEO), saxitoxin (STX), gonyautoxin‐4 (GTX‐4), and GTX‐3, while A. tamarense Group III did not produce toxins. Historically, it was considered that all Alexandrium species occurring in Scottish waters produce potent PSP toxins. This study has highlighted the presence of both PSP toxin‐producing and benign species of A. tamarense and questions the ecological significance of this finding.     

Reevaluation of Production of Paralytic Shellfish Toxin by Bacteria Associated with Dinoflagellates of the Portuguese Coast

Paralytic shellfish toxins (PSTs) are potent neurotoxins produced by certain dinoflagellate and cyanobacterial species. The autonomous production of PSTs by bacteria remains controversial. In this study, PST production by two bacterial strains, isolated previously from toxic dinoflagellates, was evaluated using biological and analytical methods. Analyses were performed under conditions determined previously to be optimal for toxin production and detection. Our data are inconsistent with autonomous bacterial PST production under these conditions, thereby challenging previous findings for the same strains.     

Reevaluation of production of paralytic shellfish toxin by bacteria associated with dinoflagellates of the Portuguese coast

Paralytic shellfish toxins (PSTs) are potent neurotoxins produced by certain dinoflagellate and cyanobacterial species. The autonomous production of PSTs by bacteria remains controversial. In this study, PST production by two bacterial strains, isolated previously from toxic dinoflagellates, was evaluated using biological and analytical methods. Analyses were performed under conditions determined previously to be optimal for toxin production and detection. Our data are inconsistent with autonomous bacterial PST production under these conditions, thereby challenging previous findings for the same strains.     

Human intoxication with paralytic shellfish toxins: clinical parameters and toxin analysis in plasma and urine

This study reports the data recorded from four patients intoxicated with shellfish during the summer 2002, after consuming ribbed mussels (Aulacomya ater) with paralytic shellfish toxin contents of 8,066 +/- 61.37 microg/100 gr of tissue. Data associated with clinical variables and paralytic shellfish toxins analysis in plasma and urine of the intoxicated patients are shown. For this purpose, the evolution of respiratory frequency, arterial blood pressure and heart rate of the poisoned patients were followed and recorded. The clinical treatment to reach a clinically stable condition and return to normal physiological parameters was a combination of hydration with saline solution supplemented with Dobutamine (vasoactive drug), Furosemide (diuretic) and Ranitidine (inhibitor of acid secretion). The physiological condition of patients began to improve after four hours of clinical treatment, and a stable condition was reached between 12 to 24 hours. The HPLC-FLD analysis showed only the GTX3/GTX2 epimers in the blood and urine samples. Also, these epimers were the only paralytic shellfish toxins found in the shellfish extract sample.     

Toxin profile of Alexandrium catenella from the Chilean coast as determined by liquid chromatography with fluorescence detection and liquid chromatography coupled with tandem mass spectrometry

The profile of tetrahydropurine neurotoxins associated with paralytic shellfish poisoning (PSP) was determined from a Chilean strain of the marine dinoflagellate Alexandrium catenella. The toxin composition was compared with that of toxic shellfish, presumably contaminated by natural blooms of A. catenella from the same region in southern Chile. Ion pair-liquid chromatography with post-column derivatization and fluorescence detection (LC-FD) was employed for relative quantitative analysis of the toxin components, whereas unambiguous identification of the toxins was confirmed by tandem mass spectrometry (LC–MS/MS). In the dinoflagellate strain from Chile, the N-sulfocarbamoyl derivatives (C1/C2, B1) and the carbamoyl gonyautoxins GTX1/GTX4 comprise >90% of the total PSP toxin content on a molar basis. This toxin composition is consistent with that determined for A. catenella populations from the Pacific coast in the northern hemisphere. The characteristic toxin profile is also reflected in the shellfish, but with evidence of epimerization and metabolic transformations of C1 and C2 to GTX2 and GTX3, respectively. This work represents the first unequivocal identification and confirmation of such PSP toxin components from the Chilean coast.     

The toxigenic marine dinoflagellate Alexandrium tamarense as the probable cause of mortality of caged salmon in Nova Scotia

The toxins associated with paralytic shellfish poisoning (PSP) are potent neurotoxins produced by natural populations of the marine dinoflagellate Alexandrium tamarense. In early June 2000, a massive bloom (>7×10⁵ cells l⁻¹) of this dinoflagellate coincided with an unusually high mortality of farmed salmon in sea cages in southeastern Nova Scotia. Conditions in the water column in the harbour were characterised by the establishment of a sharp pycnocline after salinity stratification due to abundant freshwater runoff. In situ fluorescence revealed a high sub-surface (2–4 m depth) chlorophyll peak related to the plankton bloom. The intense bloom was virtually monospecific and toxicity was clearly related to the concentration of Alexandrium cells in plankton size fractions. Cultured clonal isolates of A. tamarense from the aquaculture sites were very toxic on a per cell basis and yielded a diversity of PSP toxin profiles, some of which were similar to those from plankton concentrates from the natural bloom population. The toxin profile of plankton concentrates from the 21–56 μm size fraction was complex, dominated by the N-sulfocarbamoyl derivative C2, with levels of other PSP toxins GTX4, NEO, GTX5 (=B1), GTX3, GTX1, STX, C1, and GTX2, in decreasing order of relative abundance. Although no PSP toxin was found systemically in the fish tissues (liver, digestive tract) from this salmon kill event, the detection of Alexandrium cells and low levels of PSP toxins in salmon gills provide evidence that the enhanced mortalities were caused by direct exposure to toxic Alexandrium cells and/or to soluble toxins released during the bloom.     

Pseudoalteromonas Bacteria Are Capable of Degrading Paralytic Shellfish Toxins

Marine bacterial isolates cultured from the digestive tracts of blue mussels (Mytilus edulis) contaminated with paralytic shellfish toxins (PSTs) were screened for the ability to reduce the toxicity of a PST mixture. Seven isolates reduced the overall toxicity of the algal extract by ≥90% within 3 days. These isolates shared at least 99% 16S rRNA gene sequence similarity with five Pseudoalteromonas spp. Phenotypic tests suggested that all are novel strains of Pseudoalteromonas haloplanktis.Among the marine algal biotoxins identified to date; paralytic shellfish toxins (PSTs) constitute the most serious threat to the safety of the food supply, mainly due to their high acute toxicities and the absence of antidotes or effective medical treatments (8). Paralytic shellfish poisoning is caused by ingestion of one or more of the chemically related PSTs (see Fig. S1 in the supplemental material). PSTs are mainly produced by marine dinoflagellates, including Alexandrium spp., Gymnodinium catenatum, and Pyrodinium bahamense var. compresssum (16). Since bivalve molluscs filter-feed on marine algae, they tend to concentrate PSTs largely, but not exclusively, in their digestive organs (7, 9, 10, 29). Not affected by commercial sterilization (14, 18) or cooking, PSTs present significant risks to the food supply, particularly during periods of toxic algal blooms. Practical methods for PST detoxification of living shellfish do not exist (5).Transformations of PSTs by bacteria have been reported in the literature (23-25, 31, 35, 36, 38); early studies focused on the conversion of hydroxysulfate carbamate derivatives (gonyautoxins 1 and 4) to the more highly toxic saxitoxin (STX) (23-25). In addition, several reports have noted the high capacity of the digestive gland for PST transformation (12, 28, 32, 39), suggesting the presence of toxin-transforming enzymes and/or microorganisms in bivalve molluscs. The partial degradation of gonyautoxins 1 and 4 and C1/C2 by marine bacteria has also been reported (38). In addition, Stewart et al. (37) discovered the bacterial degradation of domoic acid (another marine toxin that causes amnesic shellfish poisoning), collectively suggesting that bacteria might play a role in the elimination of marine toxins from toxic bivalve molluscs. The capacity to catabolize domoic acid is greater in cultures isolated from blue mussels that rapidly eliminate domoic acid than in bacterial isolates from bivalves known to retain the toxin for longer time periods (e.g., scallops), suggesting these bacteria play a role in the elimination of marine toxins.Recently, we reported the kinetics of PST destruction for a group of marine bacteria isolated from toxic blue mussels (11). Here we report the phenotypic and taxonomic characterization of these unique marine bacteria.