Mollusks And Man - A Medical Perspective

     The occurrence of intermittent "blooms" of planktonic micro-organisms has been chronicled since biblical times. The well-known passage in Exodus (chap. 7, verses 20-21): "And all the waters that were in the river turned to blood. And all the fish that was [sic] in the river died; and the river stank, and the Egyptians could not drink of the river and there was blood throughout all the land of Egypt," can arguably be attributed to the occurrence of a red tide. Such periodic changes in water tint are now known to result from natural but catastrophic increases in the concentration of unicellular organisms - for instance, red-pigmented dinoflagellates (Protozoa) such as Gymnodinium breve, which occurs in the Gulf of Mexico. Classical references to the red tide phenomenon include the Iliad, the works of Tacitus (A.D. ca. 55 - ca. 120) and logs of the earliest European explorers. There is reason to believe that the Red Sea derives its name from this phenomenon. Ancient Talmudic law prohibiting certain foods such as pork may have had a solid foundation in the principles of public health as we have learned many centuries later in the case of trichinosis. Perhaps the proscription against shellfish (Leviticus) was similarly grounded in scientific observation? We shall probably never know, but it is an attractive hypothesis.

     Millennia later, in 1689, the Renaissance scholar, Christian Mentzel (1622-1701), known principally for his Chinese-Latin dictionary and a natural history of Brazil, reported the case of a young German girl "who had eaten too well of mussels" (translation of Latin) suffering acutely from nausea, redness of the skin, shortness of breath, and convulsive movements. Vomiting was induced with a feather and produced a partially digested meal of mussels (no doubt Mytilus edulis) and was followed by prompt improvement and eventual recovery. A century later (June, 1793; reported in 1798), members of the crew of Captain (H.M.S.) George Vancouver's crew became ill within one to two hours after consuming "muscles" (again Mytilus edulis) collected fresh in Fitzhugh Sound, British Columbia. The symptoms were quite uniform: nausea, numbness of the face and extremities, and generalized weakness. All but one man recovered; this unfortunate died peacefully 4 1/2 hours after the lethal breakfast - too weak to swallow (and, presumably, to breathe).

     By 1965 about a hundred more outbreaks of this kind of shellfish poisoning had been recorded world-wide involving over 1,000 cases and a fatality rate of 8.5% or more. The most disastrous occurrence of this kind was in 1799 at Peril Way, near Sitka, Alaska, when over 100 men died less than two hours after consuming - you guessed it, Mytilus edulis, our old acquaintance, the circumboreal Blue Mussel. Although the mussel accounts for the majority of outbreaks, dozens of marine bivalves, notably Saxidomus species and Crassostrea gigas (Pacific Northwest), and Mya arenaria in the Northwest Atlantic have been incriminated. Outbreaks are clustered geographically in Northern Hemispheric cold-temperature waters, but are also known from similar zones in the Southern Hemisphere (Chile, South Africa, New Zealand). Occurrences in tropical and sub-tropical regions are quite uncommon but are reported from the Gulf of Mexico, especially West Florida.

     In cooler waters, virtually all cases have occurred in the summer months, producing the signature of a biorhythm and support for the proverbial "R" month culinary endorsement. However, a caveat for many readers: winter months are actually MORE risky for this paralytic shellfish poisoning (P.S.P.) in warmer climes such as West Florida.

     Let us return to the red tides as we retrace our understanding of the biological processes which produce P.S.P. Excepting the Talmudic hypothesis (see above), the first evidence of a public health policy relating to dinoflagellate comes from the Amerindians of our Pacific coast before the European immigration, who warned against shellfish consumption when coastal waters were luminescent at night. We now know that the aptly-dubbed dinoflagellate Noctiluca scintillans accounts for the episodic phenomenon in California summers and keeps company with Gonyaulax (see below).

     During the nineteenth century, a number of biomedical scientists (including some prominent names in the history of medicine) addressed the problem of P.S.P. and a number of hypotheses as to its causation were put forth: putrefaction and copper intoxication of the bivalve flesh were the most popular. Perhaps fortuitously, if only in a public health sense, in the early 1930's a fearsome series of P.S.P. outbreaks in the San Francisco area impelled K. F. Meyer and Hermann Sommer of the University of California's George Williams Hooper Foundation (of which this writer, by mere coincidence, is an alumnus) to study how toxic Mytilus californianus became tainted. Using mussels, laboratory mice, and fresh and filtered seawater coincident with a P.S.P. outbreak in the summer of 1935, they elegantly demonstrated that the concentration of the dinoflagellate Gonyaulax catenella in seawater was proportional to the toxicity of the mussels exposed to it in the laboratory. Furthermore, they obtained a toxin from the dinoflagellate with essentially identical properties to that of the exposed mussels. Thus the mussels were demonstrated to be the "transvectors" of the poisonous plankton toxin - in one sense innocent bystanders poised in the middle of the food chain, but in another, seductive co-conspirators. A year later (1939) Koch reported a similar incrimination of Pyrodiniun phoneus, another dinoflagellate, in the Belgian outbreaks of P.S.P. transvected by Mytilus edulis. These two protozoans and Gonyaulax tamarensis in the Northwest Atlantic account for a overwhelming majority of recent and historical P.S.P. cases. Gymnodinium breve is cause of both the red tide and P.S.P. in the Gulf of Mexico.

     Biochemists and toxicologists have studied P.S.P. toxin and determined that it amounts to about seven percent of the dinoflagellate's dry weight. It is a potent neurotoxin, almost 100 times stronger than strychnine and curare, 300 times more potent than nerve gas, somewhat weaker than cobra neurotoxin, and considerably less toxic than tetanus and botulism toxins. It is relatively thermostable, which, unlike the case with Hepatitis A virus and Vibrio species, allows the flesh of bivalves to remain hazardous despite cooking.

     Red tide alerts (or the equivalent warning for Gonyaulax, which are not so colorful) are to be taken seriously by harvesters as they are the mainstay in the control of P.S.P. Cooking is of some value in reducing risk, but it is certainly not foolproof. Severe cases should be treated in hospital with induced vomiting and/or stomach pumping, and, when available and necessary, ventilator support. The latter would probably have saved a great majority of the historic fatalities if that form of care had been available.

     There are other toxic mollusks of far lesser significance: Neptunea whelks in England and Japan; Haliotis viscera In Japan; Muricids, especially Bolinus brandaris whose purple (hypobranchial) gland has a neurotoxin, murexine, but rarely if ever, affects man; Cittarium pica, eaten in the West Indies, but capable of producing illness (it is noteworthy that Cubans call this species 'cigua", and it is, however inaccurately, the linguistic root of the term "ciguatera," an illness of greater importance caused by a dinoflagellate neurotoxin transvected by marine food fish, not by the snail); Aplysia (sea hares) were known to the ancients as early as Pliny (A.D.29-79) for their toxicity, but are sufficiently unappetizing in appearance to account for a total absence of reported human illness since the fall of the Roman Empire.

Adapted from The Junonia, newsletter of the Sanibel-Captiva Shell Club, September, 1995; published in the Shell-O-Gram, January-February, 1996.