Several Dinophysis species produce diarrhoetic toxins (okadaic acid and dinophysistoxins) and pectenotoxins, and cause gastointestinal illness, Diarrhetic Shellfish Poisoning (DSP), even at low cell densities (<103 cells·L−1). They are the main threat, in terms of days of harvesting bans, to aquaculture in Northern Japan, Chile, and Europe. Toxicity and toxin profiles are very variable, more between strains than species. The distribution of DSP events mirrors that of shellfish production areas that have implemented toxin regulations, otherwise misinterpreted as bacterial or viral contamination. Field observations and laboratory experiments have shown that most of the toxins produced by Dinophysis are released into the medium, raising questions about the ecological role of extracelular toxins and their potential uptake by shellfish. Shellfish contamination results from a complex balance between food selection, adsorption, species-specific enzymatic transformations, and allometric processes. Highest risk areas are those combining Dinophysis strains with high cell content of okadaates, aquaculture with predominance of mytilids (good accumulators of toxins), and consumers who frequently include mussels in their diet. Regions including pectenotoxins in their regulated phycotoxins will suffer from much longer harvesting bans and from disloyal competition with production areas where these toxins have been deregulated.
The authors present evidence of the difficulties facing human taxonomists/ecologists in identifying marine dinoflagellates. This is especially important for work on harmful algal blooms in marine aquaculture. It is shown that it is difficult for people to categorise specimens from species with significant morphological variation, perhaps with morphologies overlapping with those of other species. Trained personnel can be expected to achieve 67 to 83% self-consistency and 43% consensus between people in an expert taxonomic labelling task. Experts who are routinely engaged in particular discriminations can return accuracies in the range of 84 to 95%. In general, neither human nor machine can be expected to give highly accurate or repeatable labelling of specimens. It is also shown that automation methods can perform as well as humans on these complex categorisations.
Two stralns of the paralytic shellfish tox~n (PST) producing dinoflagellate Alexandrium lninutum Halim (highly toxic ALlV and weakly toxic AL2V) were grown in batch culture with either nitrate or phosphate as the limiting nutrient. In comparison with cells of the strain ALlV, cells of AL2V grew at a similar C-specific rate, had a higher C/N ratio, and lower ratios of chl a/chl c2 and chl a/peridinin. Neither chlorophylls nor carotenoids could be used to estimate C-biomass, N-biomass or toxin content for this organism. The toxin profile for both strains was dominated (up to 95 %) by the gonyautoxin GTX4, with smaller proportions of GTX1. GTX2 and GTX3. The rate of toxin synthesis for both strains was greatest 1 to 2 d after the N-refeeding of N-deprived cells, with the net rate of toxin synthesis exceeding that of C-biomass and cell division by a factor of up to 4. Toxin synthesis was not enhanced by short-term P-stress. N-stress alone led to a decrease in toxin cell-', but P-stress followed by N-stress did not result in such a decline, implicating phosphorus in the regulation of toxin metabolism. Although arginine is a major precursor for PST synthesis, taurine, glycine, glutamine, and cell N showed similar relations to that observed for arginine with respect to toxin content. Furthermore, the mole ratio of arginine/toxin could vary by a factor of up to 5 between ALlV and AL2V at peak values of toxin cell-', and by more than 5 within a strain when growing under different conditions. These observations suggest that the relationship between free arginine content and toxin content is complex. No explanation for the higher toxin content of A L l V IS apparent, except that ALlV has a higher N-content per cell and this may be conducive to a higher rate of synthesis of the N-rich toxins.
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