Marine Toxins

Primary reference(s)

WHO, no date. Marine biotoxins. World Health Organization (WHO). Accessed 12 October 2020.

Additional scientific description

Marine toxins are produced by algae or bacteria and are concentrated in contaminated fishery and aquaculture products. When people consume these contaminated products, depending on the toxin, the symptoms can be diarrheic, paralytic, amnesic, or neurologic, some of which result in high mortality and long-term morbidity (Sobel and Painter, 2005; WHO, no date).

Routine clinical diagnostic tests are not available for these toxins; diagnosis is based on clinical presentation and a history of eating fishery and aquaculture products in the preceding 24 hours (Sobel and Painter, 2005). There is no antidote for any of the marine toxins, and supportive care is the mainstay of treatment. Paralytic shellfish poisoning, and puffer fish poisoning can cause death within hours of consuming the toxins and may require immediate intensive care (Sobel and Painter, 2005).

A Joint FAO/IOC/WHO expert meeting classified the toxins into eight groups based on their chemical structure (FAO/WHO, 2016): the Azaspiracid (AZA) group, Brevetoxin group, Cyclic Imines group, Domoic Acid (DA) group, Okadaic Acid (OA) group, Pectenotoxin (PTX) group, Saxitoxin (STX) group, and Yessotoxin (YTX) group.

The Food and Agriculture Organization of the United Nations (FAO) reports that they can also be classified by the type of poisoning they cause (FAO, 2004):

Paralytic shellfish toxins causing paralytic shellfish poisoning (PSP): PSP poisoning in humans is caused by ingestion of shellfish containing PSP toxins. These PSP toxins are accumulated by shellfish grazing on algae producing these toxins. Symptoms of human PSP intoxication vary from a slight tingling or numbness to complete respiratory paralysis. In fatal cases, respiratory paralysis occurs within 2 to 12 hours of consuming the PSP-contaminated food. PSP toxins are produced mainly by dinoflagellates belonging to the genus Alexandrium, which may occur in both in the tropical and temperate climatic zones. Shellfish grazing on these algae can accumulate the toxins but the shellfish itself is rather resistant to the harmful effects of these toxins. PSP is well documented throughout the Southern Hemisphere in South Africa, Australia, India, Thailand, Brunei Darussalam, Sabah (Malaysia), the Philippines and Papua New Guinea (FAO, 2004).

Diarrhoeic shellfish toxins causing diarrhoeic shellfish poisoning (DSP). In humans, DSP poisoning is caused by the ingestion of contaminated bivalves such as mussels, scallops, oysters or clams. The fat-soluble DSP toxins accumulate in the fatty tissue of the bivalves. DSP symptoms include diarrhoea, nausea, vomiting and abdominal pain starting 30 minutes to a few hours after ingestion and complete recovery occurs within three days. DSP toxins can be divided into different groups depending on chemical structure. The first group, acidic toxins, includes okadaic acid and its derivatives named dynophysistoxins. The second group, neutral toxins, consists of polyether-lactones of the pectenotoxin group. The third group includes a sulphated polyether and its derivatives the yessotoxins (FAO, 2004).

Amnesic shellfish toxins causing amnesic shellfish poisoning (ASP). In humans, ASP is also known as domoic acid poisoning (DAP) because amnesia is not always present. It was first recognised in 1987 on Prince Edward Island, Canada. At this time, ASP caused three deaths and 105 cases of acute human poisoning following the consumption of blue mussels. The symptoms included abdominal cramps, vomiting, disorientation and memory loss (amnesia). The causative toxin (the excitatory amino acid domoic acid or DA) was produced by the diatom species Pseudo-nitzschia pungens f. multiseries (Nitzschia pungens f. multiseries) (FAO, 2004).

Neurotoxic shellfish toxins causing neurotoxic shellfish poisoning (NSP). NSP is caused by polyether brevetoxins produced by the unarmoured dinoflagellate Gymnodinium breve (also called Ptychodiscus breve, since 2000 called Karenia brevis). The brevetoxins are toxic to fish, marine mammals, birds and humans, but not to shellfish. Until 1992/1993, neurologic shellfish poisoning was considered to be endemic to the Gulf of Mexico and the east coast of Florida, where ‘red tides’ had been reported as early as 1844. An unusual feature of G. breve is the formation by wave action of toxic aerosols which can lead to asthma-like symptoms in humans. In 1987, a major Florida bloom event was dispersed by the Gulf Stream northward into North Carolina waters where it has since continued to be present. In early 1993, more than 180 human shellfish poisonings were reported from New Zealand caused by an organism similar to G. breve. Most likely, this was a member of the hidden plankton flora (previously present in low concentrations), which developed into bloom proportions triggered by unusual climatic conditions (higher than usual rainfall, lower than usual temperature) coincident with an El Niño event (FAO, 2004).

Azaspiracid shellfish toxins causing azaspiracid shellfish poisoning (AZP). In November 1995, at least eight people in the Netherlands became ill after eating mussels (Mytilus edulis) cultivated at Killary Harbour, Ireland. Although the symptoms resembled those of diarrhoeic shellfish poisoning (DSP), concentrations of the major DSP toxins were very low. The known organisms producing DSP toxins were not observed in water samples collected at that time. In addition, a slowly progressing paralysis was observed in the mouse assay using the mussel extracts. These neurotoxic symptoms were different from typical DSP toxicity. It was then that azaspiracid (formerly called Killary Toxin-3 or KT3) was identified and the new toxic syndrome was called azaspiracid poisoning (AZP) (FAO, 2004).

Ciguatoxins causing ciguatera poisoning: Ciguatera poisoning (CP) has been known for centuries. It was reported in the West Indies by Peter Martyr de Anghera in 1511, in islands of the Indian Ocean by Harmansen in 1601, and in the various archipelagos of the Pacific Ocean by De Quiros in 1606. Endemic areas are mainly the tropical and subtropical Pacific and Indian Ocean insular regions and the tropical Caribbean, but continental reef areas are also affected. The name ciguatera was given by Don Antonio Parra in Cuba in 1787 to intoxication following ingestion of the ‘cigua’, the Spanish trivial name of a univalve mollusc, Turbo pica, reputed to cause indigestion. The term cigua was somehow transferred to an intoxication caused by the ingestion of coral reef fish species. The causative toxins, the ciguatoxins, accumulate through the food chain, from small herbivorous fish grazing on the coral reefs to organs of the bigger carnivorous fish that feed on them (FAO, 2004).

Metrics and numeric limits

Not available.

Examples of drivers, outcomes and risk management

The substantial increase in the consumption of the fishery and aquaculture products in recent years, together with globalisation of trade, has increased the potential for human exposure to these marine biotoxins. Monitoring programmes for the toxins and their source organisms, and rapid notification of food safety issues by the authorities is essential to avoid foodborne intoxications. Extensive environmental monitoring and sometimes seasonal quarantine of a harvest are used to reduce risk of exposure (Sobel and Painter, 2005).

It is difficult to predict when a bloom will develop. Climatic and environmental conditions such as changes in salinity, rising water temperature, and increased nutrient levels and sunlight can influence population growth.

Control measures include the establishment of national monitoring programmes for marine biotoxins and their source organisms and their continuous update to include new and emerging toxins when necessary.