Diarrhetic Shellfish Poisoning
This information is courtesy of Lora E. Fleming, NIEHS Marine and Freshwater Biomedical Sciences Center
DSP is a gastrointestinal illness without neurologic manifestations reported worldwide (ILO 1984, Halstead 1988, Aune & Yndstad 1993). It is caused by the consumption of contaminated shellfish (Halstead 1988).
The first reported cases of DSP were in the Netherlands in the 1960s, followed by similar reports in the late 1970s from Japan (Aune & Yndstad 1993). Since then, more than 1300 cases have been reported from Japan, with the peak season from April to September. Other outbreaks have been reported in Europe and South America as well as the Far East. In Spain, over 5000 cases were reported in 1981; In France in 1984 and 1986, over 2000 cases were reported each year and over 300 cases were reported in Scandinavia in 1984 (Asomata et al, 1978, Yasumoto et al, 1980, Viviani 1992, Aune & Yndstad 1993). Mussels exported from Denmark to France caused DSP poisoning in over 400 people in 1990 (Hald et al, 1991). Finally in 1991 DSP was reported in over 100 people in Chile; in 1992, DSP was detected in toxic concentrations in shellfish beds in Uruguay (Lembeye et al, 1993, Mendez 1992, Aune & Yndstand 1993). Although DSP is reported worldwide, the most highly affected areas appear to be Europe and Japan (Aune & Yndstad 1993).
The causative organisms are the marine dinoflagellates Dinophysis, although there is an uneven distribution among species and location of toxin production. These dinoflagellates are widely distributed, but do not always form red tides. The associated toxins produced by the Dinophysis dinoflagellates are okadaic acid and its derivatives; there are at least 9 total toxins produced by these dinoflagellates. (Asomata et al, 1978, Yasumoto et al, 1980, ILO 1984, Lee 1989).
Diarrhea was the most commonly reported symptom (92%), closely followed by nausea (80%) and vomiting (79%), with onset 30 minutes to 12 hours from ingestion. Complete clinical recovery is seen even in severe cases within 3 days (Asomata et al, 1978, Viviani 1992, Aune & Yndstad 1993).
A mouse bioassay using an intraperitoneal injection of toxin extracts with a 24 hour waiting period is used in Japan and shellfish with DSP toxin levels greater than 50 MU/kg are banned; similar surveillance systems have been established in the European countries (ILO 1984, Viviani 1992, Aune & Yndstad 1993). An HPLC method for detection of DSP toxins is available and used in Sweden for monitoring purposes (Lee et al, 1987).
Treatment is symptomatic and supportive with regards to short-term diarrhea and accompanying fluid and electrolyte losses. In general, hospitalization is not necessary; fluid and electrolytes can usually be replaced orally. Other diarrhetic illnesses associated with shellfish consumption, such as bacterial or viral contamination should be ruled out (Aune & Yndstad 1993).
As with many of the marine toxin induced diseases, the initial or index case(s) are often the tip of the iceberg. Therefore any suspected cases of DSP should be reported to the appropriate public health authorities for follow up to ascertain other cases and to prevent further spread. And every effort should be made to obtain contaminated materials and their source.
D. fortii at levels of 200 cell/litre in mussels and scallops becomes toxic for humans; the minimal amount of DSP toxins required to induce disease in humans was 12 MU.
Okadaic acid, dinophysiotoxin 1 and 3 are acidic, while there is another neutral group of toxins which are polyether lactones named pectonotoxins and yessotoxin. Diarrhea is caused in mice when the acidic component of okadaic acid is injected interperitoneally. Pectonotoxin 1 causes liver damage in mice under similar circumstances. Both the pectenotoxins and yessotoxin are lethal in mice with ip injection.
Okadaic acid is lipophilic. It is a potent inhibitor of protein phosphorylase phosphatase 1 and 2A in the cytosol of the mammalian cells that dephosphorylate serine and threonine. It probably causes diarrhea by stimulating the phosphorylation that controls sodium secretion by intestinal cells similar to Vibrio cholerae, although by a different mechanism. Okadaic Acid also acts through the variations of cellular concentration of the Ca2+ second messenger. It strongly increases the Ltype inward Ca2+ current in isolated guinea pig cardiac myocytes. Finally, okadaic acid functions not only as a tumor promotor (promoter of skin tumor in the mouse using DMBA as the initiator), but it is also capable of reversing cell transformation in some oncogenes.
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Last updated: February 2, 2016