The Cooking Inn : Seafood Safety

Seafood Safety

Contaminated Species

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, 1987).

Geographic Area

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.

Statistics

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:

This assay is significantly limited in its minimum detection level of approximately 37ug/100g meat, which is close to the maximum allowed level of 80ug/100g meat (Yang et al., 1987).
Schantz "salt effect" may cause an underestimate of the toxin concentration by as much as a factor of 3, especially at low toxin levels (Schantz et al., 1958, as cited in Sullivan, 1988).
Accuracy can be 20% (Sullivan and Wekell, 1987).
A high concentration of free fatty acids can cause false positives (Hamano et al., 1985).

HPLC (Sullivan and Wekell, 1987; Sullivan et al., 1985) - The high performance liquid chromatography method is based on the oxidation of toxins to fluorescent products. Depending on the toxins present, the limit of detection can be as low as 10-30 ug STX/100g, and accuracy can be +/-10%. When toxin levels are approximately 200ug or below by the mouse bioassay, the HPLC method may indicate significantly higher total toxin levels, possibly resulting in false positives (Hurst et al, 1985).

AUTOANALYZER (Sullivan et al., 1985; Jonas-Davis et al., 184) - This technique may be useful for prescreening shellfish since it is rapid and easy. The results of the autoanalyzer would divide shellfish samples into low (<61ug/100g), medium (61-250 ug/100g) and high groups (>250 ug/100g), with only the medium group being subject to a more time consuming and accurate assay.

RADIOIMMUNOASSAY (Yang et al., 1987) - The radioimmunoassay is a competitive assay in which radiolabeled, anti-saxitoxin serum is added to a sample of shellfish tissue extract. Excess antibody is removed and the samples are analyzed with a scintillation counter. If saxitoxin is present in the shellfish, the DPM will be high. If the shellfish is free of toxin the DPM will be low. This technique is very sensitive to saxitoxin. A complete standard curve is mandatory for each run.

COMPETITIVE DISPLACEMENT ASSAY (Davio and Fontelo, 1984; Hall et al., 1985) - Saxitoxin acts by binding to sodium channels in nerve cell membranes. The competitive displacement assay detects saxitoxin by measuring the amount of radiolabeled saxitoxin displaced from a rat brain membrane preparation. This assay is extremely sensitive and selective for saxitoxin.

FLY BIOASSAY (Ross et al., 1985; Hall et al., 1985) - Toxins are extracted from shellfish and injected into a house fly. The fly is then observed for time of death. This method is more sensitive than the mouse bioassay, since flies are not affected by the "Schantz salt effect".

Amnesic Shellfish Poisoning

Description

Shellfish can become toxic to humans by consuming large quantities of the diatom, Nitzschia pungens (Bird and Wright, 1989; Duerden, 1989). N. pungens is a common coastal water alga of the Atlantic, Pacific and Indian Oceans and ranges between 62N and 41S latitude (Bird and Wright, 1989). It has a broad thermal tolerance and can thrive in the low salinities of estuaries. N. pungens was considered an innocuous alga until 1987, when a bloom off the coast of Prince Edward Island produced the toxin, domoic acid (also called acidic amino acid). Observations of natural N. pungens populations show that appreciable quantities of domoic acid are only produced when the alga is present at high densities. This is confirmed by laboratory cultures which only produce the toxin once the culture has reached the stationary phase. It is also possible that not all forms of N. pungens are capable of producing domoic acid (Bird and Wright, 1989).

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