All filter-feeding molluscs accumulate and depurate paralytic shellfish toxins. Blue mussels become highly toxic within a few days of the onset of a red tide, but also lose their toxin load rapidly (Shumway, 1989). Mussels can become extremely toxic without apparent alert. For example, in Maine (August 1980) mussel toxin levels rose from the detection level to 8000+ ug/100g in 2 days (Shumway et al., 1988). Calculations based on laboratory feeding experiments suggest that during blooms of highly toxic dinoflagellates (ex. Alexandrium fundyense) the level of toxins in mussels can exceed acceptable levels in less than 1 hour (Bricelj et al, 1990). Soft-shell clams generally do not become as toxic as mussels. They require more time to accumulate high levels of toxins, and also require longer to cleanse themselves of toxins (White, 1988). Hard clams and oysters do not become as toxic as other molluscs (White, 1988). Mercenaria mercenaria exposed to P. tamarensis in the laboratory showed a pronounced valve closure (Shumway and Cucci, 1987). Briclej et al. (1990) demonstrated that M. mercenaria can ingest A. fundyense cells, although only when non-toxic cells are also present.
Scallops can become extremely toxic even during periods when blooms are not evident. However, scallops generally do not pose a threat of PSP since the adductor muscle, the only part of the scallop traditionally sold and consumed in Western society, does not accumulate toxins. Recently there has been pressure in the U.S. to market whole scallops. This practice is strongly advised against because of the high levels of toxins recorded in tissues other than the adductor muscle and the unpredictable nature of toxin levels in scallops.
In the past it was believed that toxic dinoflagellates did not harm or affect
shellfish. However, recent evidence has shown that in the presence of
Gonyaulax tamarensis, molluscs exhibit species specific responses that
include (Gainey and Shumway, 1988; Shumway et al., 1985): shell valve activity
alteration (Shumway and Cucci, 1987); oxygen consumption increase or decrease;
heart rates inhibited excited or unaffected; reduction of byssus production in
blue mussels and ribbed mussels (Shumway et al., 1987); filtration rate
decrease, increase or remain unchanged (Cucci et al., 1985; Shumway and Cucci,
Paralytic shellfish poisoning is a worldwide problem. Blooms have occurred in New England, Canada, Northwestern U.S., England, Norway, Brazil, Argentina, India, Thailand and Japan (Anderson, 1989; White, 1980).
Symptoms & Treatment
Symptoms usually begin within 30 minutes of consumption. The individual initially experiences a numbness, burning or tingling sensation of the lips and tongue, which spreads to the face and fingertips. This leads to general muscular incoordination of arms, legs and neck. Other less commonly reported symptoms include: weakness, dizziness, malaise, prostration, headache, salivation, rapid pulse, thirst, dysphagia, perspiration, impairment of vision or temporary blindness, ataxia with a "floating" sensation, incoherent speech or loss of voice, nausea, vomiting, diarrhea, feeling of loose teeth and convulsions. Severe cases of PSP can result in respiratory paralysis, and professional medical treatment should be sought. Although rare, PSP can be fatal. If the individual survives beyond 24 hours, total recovery with no lasting effects is expected (Hughes, 1979; Bryan, 1987; Concon, 1988).
Human susceptibility to paralytic shellfish toxins varies with weight, age and health of the individual. Mild cases of PSP have been reported in adults who have consumed 340 ug of the toxin, and ingestion of 1000 ug of the toxin has resulted in death. Due to the difficulty of determining toxin levels ingested by sick persons and the variability among individuals, these dosage levels should be considered rough estimates.
Between 1971 and 1977 there were 12 outbreaks of PSP, involving 68 individuals in the U.S. (Hughes, 1979). Only 2 of these outbreaks were attributed to commercially distributed shellfish (Hughes, 1979).
Detection & Prevention
The toxins cannot be destroyed by normal cooking, freezing or smoking. The best prevention of PSP is by detecting the toxins in shellfish and discarding them before they reach the market. The detection method used most often is the mouse bioassay. However, due to numerous disadvantages of this assay, alternate methods are being tested.
MOUSE BIOASSAY - To detect PSP, toxins are extracted from 25g of shellfish digestive gland and injected intraperitoneally into a 20g mouse. The mouse is then observed for 10 minutes for sign of toxicity and/or time of death. Aside from the general disadvantages of the mouse bioassay (see Ciguatera - Detection and Prevention) there are a number of additional problems in using this method for detecting PSP:
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