Shellfish, food toxins

Various shellfish-associated toxins, in Foodborne Pathogenic Microrganisms and Natural Toxins Handbook The Bad Bug Book. US Food and Drug Administration Center for Food Safety and Applied Nutrition, Washington, DC. Last update 28 January, 2004. http //www.cfsan.fda.gov/ mow/chap37.html. Accessed 8 July, 2005. 

Chn, E.S. et al.. Screening of paralytic shellfish poisoning toxins in natnraUy occnrring samples with three different direct competitive enzyme-finked immnnosorbent assays, Agric. Food Chem., 44,4043, 1996. 

Maneiro, 1. et al.. Zooplankton as a potential transmission vector of diarrhetic shellfish poisoning toxins through the food web. Mar. Ecol. Prog. Sen, 201, 155, 2000. 

Oikawa, H., Fujita, T., Saito, K., Watabe, S., Satomi, M., and Yano, Y. (2004) Comparison of paralytic shellfish poisoning toxin between carnivorous crabs (Telmessus acutidens and Charybdis japonica) and their prey mussel Mytilus galloprovincialis) in an inshore food chain. Toxicon, 43, 713-719. 

The use of high performance liquid chromatography (HPLC) for the study of paralytic shellfish poisoning (PSP) has facilitated a greater understanding of the biochemistry and chemistry of the toxins involved. HPLC enables the determination of the type and quantity of the PSP toxins present in biological samples. An overview of the HPLC method is presented that outlines the conditions for both separation and detection of the PSP toxins. Examples of the use of the HPLC method in toxin research are reviewed, including its use in the determination of the enzymatic conversion of the toxins and studies on the movement of the toxins up the marine food chain. 

By utilizing the HPLC method, it is possible to determine the level of each individual toxin in sample solutions. This provides a "toxin profile" that can be very useful in PSP toxin research studies. The ability to examine relative changes in toxin concentration and profile has greatly facilitated studies relating to toxin production by dinoflagellates, metabolism of toxins in shellfish, and movement of toxins up the food chain. Since the HPLC method is easily automated and requires only very small sample sizes (< 1 g tissue), it has clear advantages over other analytical procedures for the toxins in many research situations. Two examples of the utilization of HPLC for the study of the PSP toxins follow. 

Acute poisoning of humans by freshwater cyanobacteria as occurs with paralytic shellfish poisoning, while reported, has never been confirmed. Humans are probably just as susceptible as pets, livestock, or wildlife but people naturally avoid contact with heavy waterblooms of cyanobacteria. In addition, there are no known vectors, like shellfish, to concentrate toxins from cyanobacteria into the human food chain. Susceptibility of humans to cyanobacteria toxins is supported mostly by indirect evidence. In many of these cases, however, if a more thorough epidemiological study had been possible these cases probably would have shown direct evidence for toxicity. 

Phycotoxins accumulate in fish and shellfish because of the natural feeding habits of the respective organisms, rather than because of food handling or processing practices. The toxins causing the diseases discussed in this chapter are heat stable (Australia New Zealand Food Authority, 2001 Committee on Evaluation of the Safety of Fishery Products, 1991). Complete inactivation of saxitoxin (associated with PSP) requires at least ten minutes of exposure to 260°C dry heat. Brevetoxins (associated with NSP) were inactivated (i.e., to levels below the limit of assay detection using Japanese medaka [Oryzias latipes]) by exposure to 500°C heat for 10 to 15 minutes (Poli, 1988). Complete inactivation required 10 minutes exposure to 2760°C dry heat (Wannamacher, 2000). 

This nonsystematic approach to monitoring has proven inadequate for protecting the U.S. food supply. In response, the FDA enacted the Hazard Analysis and Critical Control Points (HACCP) program of 1997 (U.S. Food and Drug Administration, 1995, 2001). In the U.S., the FDA has established action levels in suspect seafood for the toxins causing some of the shellfish poisonings (see Table 7.3). When an action level is reached, the HACCP plan must be followed to prevent unsafe product from reaching consumers. 

U.S. Food and Drug Administration (FDA) action levels in seafood for the toxins associated with shellfish poisonings. 

Aune, T. and Yndestad, M., Diarrhetic shellfish poisoning, in Falconer, I.R., ed.. Algal Toxins in Seafood and Drinking Water, Academic Press, San Diego, 1993. Australia New Zealand Food Authority, Shellfish Toxins in Food, A Toxicological Review and Risk Assessment, Australia New Zealand Food Authority, Canberra, 2001. 

Red tides (and some with other colors as well) occur with some regularity in certain coastal waters of New England, Alaska, California, and several other areas. If it is the type of tide that can produce PSP or other toxins, public health officials typically quarantine affected areas to prevent harvesting of shellfish. In some areas of the Gulf of Alaska, large reservoirs of shellfish cannot be used as food because of a persistent PSP problem. 

While the sulfamates themselves probably have low HOP, they can hydrolyze at low rates to the more toxic carbamates under conditions of food storage, preparation, or digestion. From the work of Sullivan ( ), it appears that latent sulfamate toxicity can also be potentiated through enzymatic conversion in some shellfish to the corresponding decarbamoyl toxins. The value needed for public health protection is therefore the potential human oral potency, the HOP that product might attain under a worst-case scenario of conversions. 

Since 1976, when a herring kill was caused by paralytic shellfish toxins in the Bay of Fundy, our laboratory has been investigating the effects of the toxins on fish and the food web routes through which the toxins reach fish. 

Table V. Amounts of Foods Necessary to Supply a Potential Lethal Dose of Paralytic Shellfish Toxins to a 100-g Fish...

Fish Products. As explained earlier, it is unlikely that paralytic shellfish toxins have an impact on the utilization of fish products from the point of view of the suitability of fish as food, except perhaps in cases where whole fish are eaten with little processing. Fish simply are unable to accumulate the toxins in their muscle tissues. But the toxins do appear to have an impact on the marketing of fish products, related to consumer wariness of seafood products in general during red tide and PSP incidents. The media blitz surrounding these incidents often leaves consumers unaware of which particular seafood items to be cautious. Consequently, finfish as well as shellfish products have been avoided during these episodes (25). 

Government regulatory agencies monitor some toxins as potential food contaminants. For example, agencies routinely monitor shellfish for several toxins and when necessary issue restrictions on harvesting. Many of the naturally occurring toxins are unregulated and the consumer must be aware of the potential hazards. It is really... 

Azaspiracids [azaspiracid-1 (18)] are another class of highly unusual polyketide polyethers originally isolated from Irish mussels that caused azaspiracid shellfish poisoning (5). They are produced by the dinoflagellate Protoperidinium crassipes. A similar class of polyether toxins named pinnatoxins [pinnatoxin A (19)] were reported from the bivalve Pinna pectinata a closely related species P. attenuata is known to cause food poisoning in China. Pinnatoxins are likely of dinoflagellate origin and activate Ca channels (15). 

Most species contributing to algal blooms are harmless however, some of the toxins produced by certain species are highly toxic. Often, the algae and the shellfish that consume them are unaffected. However, further up the food chain, these toxins can be fatal. Man, dolphins, manatees, and reptiles are potentially exposed to aerosolized toxins. Brevetoxins are potent ichthyotoxins and have been responsible for the death of billions of fish over the years. Brevetoxin is absorbed directly across the gill membranes of fish or through ingestion of K. brevis cells. Some of these toxicity differences will depend on the differential susceptibility of fish species to exposure to K. brevis strains involved, toxic components and concentration, stability of extracellular toxins, and exposure routes. Mortality typically occurs at cell concentrations of 2.5 x 10 K. brevis cells per liter, which is often considered to be a lethal concentration. 

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