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Shellfish Poisoning (shellfish + poisoning)
Selected AbstractsDecimal reduction times of Pyrodinium bahamense var. compressum and Escherichia coli in chlorine- and ultraviolet-treated seawaterLETTERS IN APPLIED MICROBIOLOGY, Issue 5 2001M.P.V. Azanza Aims:,Decimal reduction times (D -values) of the vegetative cells of Pyrodinium bahamense var. compressum and Escherichia coli in ultraviolet- and chlorine-treated seawater were established. Methods and Results:,The cells of the test organisms were exposed to ultraviolet- and chlorine-treated seawater and maintained at 20,35 ppt salinity and 20 to 35°C. The dinoflagellate cells which cause Paralytic Shellfish Poisoning (PSP) were found to be more resilient than the bacterial cells. Ultraviolet treatment was found to be more effective than chlorine to both test organisms. Irreversible morphological changes in the treated dinoflagellate cells were noted, including protoplast discoloration, cellular membrane leakage and damage to the thecal armour. Conclusions:,The vegetative cells of both test organisms in seawater were more sensitive to ultraviolet treatment than to chlorine exposure. Generally, the dinoflagellate cells were less susceptible than bacterial cells to both disinfection treatments. Significance and Impact of the Study:,Results of this study may have significant implications in depuration procedures for molluscs and cleaning protocols for ballast waters of ships. [source] DOMOIC ACID PRODUCTION By PSEUDO-NITZSCHIA SERIATA (BACILLARIOPHYCEAE) IN SCOTTISH WATERS,JOURNAL OF PHYCOLOGY, Issue 4 2004Johanna Fehling In 1999, a 49,000 km2 area in western Scottish waters was closed to shellfish harvesting due to the amnesic shellfish poisoning (ASP) toxin domoic acid (DA). The only previously confirmed DA producer identified had been Pseudo-nitzschia australis Frenguelli. The toxin has appeared every year since and has led to more harvesting closures. We isolated and cultured two strains of Pseudo-nitzschia seriata f. seriata (P. T. Cleve) H. Peragallo from western Scottish waters in 2001 and 2002. They were identified using TEM analysis of their morphological fine structure and sequencing of the internal transcribed spacer (ITS)1, 5.8S, ITS2, and partial large subunit (LSU) rDNA. The morphology of the Scottish P. seriata f. seriata strains differed slightly, for example, in the number of poroid rows, from descriptions in identification keys. Comparison of P. seriata sequences with those of two co-occurring Pseudo-nitzschia australis isolates showed an overall divergence of only 0.012. Sequence divergence between both species was highest in the ITS1 region (0.036). Combined morphological and genetic approaches are needed to identify closely related Pseudo-nitzschia species. The P. seriata strains grew successfully at 15°C, suggesting that although seen as a psychrophilic species, it may also occur at higher water temperatures. All isolates produced DA in stationary phase (measured on day 25): 0.16,0.23 pg DA·cell,1 in P. seriata and 0.15,1.68 pg DA·cell,1 in P. australis. Our study is the first to identify P. seriata f. seriata as a DA producer in Scottish waters and indicates that at least it and P. australis can be responsible for ASP toxicity in that region. [source] 41 Incidence of paralytic shellfish toxin in bivalve mollusc tissue from the oregon coastJOURNAL OF PHYCOLOGY, Issue 2003R. C. Everroad Saxitoxin and domoic acid sequestration by bivalve molluscs occurs periodically along the Oregon coast, presumably as a result of harmful algal blooms (HABs). Since 1958 and more continuously since 1979, the Oregon Shellfish Program (OSP) has assayed toxin levels in these molluscs as part of a monitoring program for paralytic (PSP) and amnesic (ASP) shellfish poisoning. We have created a working data base for all PSP sampling by the OSP between 1958 and 2001 and have examined the data for spatial and temporal trends in the appearance of toxin in shellfish, amount of toxin, and apparent duration of toxic events. In this report, we examine the data from the five stations with the longest record of continuous sampling (1979,2000) for evidence of correlation with El Niño events, upwelling, and/or a pattern of increasing frequency or intensity of toxic events. We also compare the pattern of appearance of toxin at open coast stations with the timing of first appearance of toxin in shellfish at adjacent estuarine stations. This is an important analysis because, in Oregon, shellfish closures due to PSP occur frequently in mussel beds on the open coast and the source of toxin-producing organisms is unknown. [source] THE CYANOTOXINS-BIOACTIVE METABOLITES OF CYANOBACTERIA: OCCURRENCE, ECOLOGICAL ROLE, TAXONOMIC CONCERNS AND EFFECTS ON HUMANSJOURNAL OF PHYCOLOGY, Issue 2001Article first published online: 24 SEP 200 Carmichael, W. W. Department of Biological Sciences, Wright State University, Dayton, Ohio 45435 USA Cyanobacteria toxins (cyanotoxins) include cytotoxins and biotoxins with cytotoxins including about 60 compounds ranging from phytoalexins to animicrobials to enzyme inhibitors to compounds that can reverse multidrug resistance. Producer organisms include marine/brackish water Cystoseira, Hormothamnin, Lyngbya, Nodularia and Synechocystis, and the freshwater/terrestrial genera Anabaena, Dichotrix, Fischerella, Hapalosiphon, Lyngbya, Microcystis, Nostoc, Oscillatoria, Planktothrix, Phormidium, Schizothrix, Scytonema, Spirulina, Stigonema and Symploca. Since many of these compounds have been identified, not during ecological studies, but during drug discovery investigations, their ecological role is only speculative. Biotoxins are responsible for acute lethal, acute, chronic and sub-chronic poisonings of wild/domestic animals and humans. They include the neurotoxins; anatoxin-a, anatoxin-a(s) and saxitoxins plus the hepatotoxins; microcystins, nodularins and cylindrospermopsin. These compounds are included when referencing harmful algal blooms (HAB's) such as the more predominate marine PSP (paralytic shellfish poisoning), DSP (diarrhetic shellfish poisoning), NSP (neurotoxic shellfish poisoning), ASP (amnesic shellfish poisoning) and EAS (estuary associated syndrome). The CTP (cyanobacteria toxin poisoning) organisms occur in freshwater lakes, ponds, rivers and reservoirs throughout the world. Organisms responsible for CTP's are Anabaena, Aphanizomenon, Cylindrosperm- opsis, Microcystis, Nodularia, Nostoc Oscillatoria (Planktothrix), Trichodesmium and certain picoplanktic genera. Concern for animal and human health impairments arises from animal poisonings, associated with cyanobacteria waterblooms, beginning with the later part of the 1800's. It was not until the 1950's that we began to understand that cyanobacteria could indeed produce highly toxic compounds. A recent 1998 compilation of all available information on toxic cyanobacteria was published by the World Health Organization. This increasing focus on the role of cyanobacteria metabolites in chemical ecology, drug discovery and toxinology has placed new importance on using correct taxonomy for communication of responsible organisms. [source] Oxidative metabolism by Thalassiosira weissflogii (Bacillariophyceae) of a diol-ester of okadaic acid, the diarrhetic shellfish poisoningJOURNAL OF PHYCOLOGY, Issue 2 2000Anthony J. Windust Previous investigations into the comparative toxicity of the diarrhetic shellfish poisoning (DSP) toxins to Thalassiosira weissflogii (Grun.) Fryxell et Hasle found that this diatom oxidatively metabolized okadaic acid diol-ester (OA diol-ester) to a more water-soluble product. This oxidative transformation of OA diol-ester by the diatom is significant for two reasons. First, it is known that dinophysistoxin-4 (DTX-4), the primary DSP toxin produced by the dinoflagellate Exuviaella lima (Ehr.) Butschli, will be hydrolyzed to the diol-ester following cell rupture (e.g. ingestion by a predator). Second, it implies that the ester, an uncharged, lipophilic intermediate, can easily enter cells and therefore may play an important role in the uptake and transfer of DSP toxins through the food web. It has been suggested that the water soluble DTX-4 may also be the form in which DSP toxins are excreted from the producing cell. Therefore, the stability of DTX-4 was examined when incubated either in fresh seawater medium into which washed cells of E. lima were introduced or in seawater medium conditioned by E. lima cells. Rapid hydrolysis of DTX-4 to the diol-ester took place in both cases. Thus, regardless of the route by which DTX-4 is liberated from the cell, either by cell disruption or excretion, the diol-ester will be the dominant form of the toxin to challenge associated organisms. To examine the metabolism of OA diol-ester by T. weissflogii in more detail, serial cultures of the diatom were challenged with OA diol-ester at a concentration of 2.0 ,g·mL,1. The metabolism and fate of the diol-ester in both cellular and medium fractions were monitored over 3 days using liquid chromatography with either ultraviolet (LC-UV) or mass spectrometric (LC-MS) detection. During the course of the experiment, all of the diol-ester was metabolized. LC-MS analysis revealed the presence of multiple oxidative products of OA diol-ester in the medium fraction, including a carboxylic acid derivative. The major metabolites were isolated in sufficient quantity to permit structural elucidation by NMR and MS. All the metabolites identified resulted from oxidation of the diol-ester side chain with the primary sites of attack at the terminal, subterminal, and unsaturated carbons. OA was found in both cellular and medium fractions, and its production was directly correlated with the metabolism of the diol-ester. The relative partitioning of both OA diol-ester and its oxidation products between cells and medium supports the contention that OA diol-ester can readily enter cells, be metabolized, and then excreted in more water-soluble forms. [source] | ||||||||||