Little is understood about why some species produce toxins and others do not. Scientists are trying to identify the genes involved in toxin production in order to elucidate the biosynthetic pathways, but this has thus far been a challenging task. In the meantime, scientists can only speculate about their function. Some possibilities are that they are:

• deterrents to grazers (the small animals or "zooplankton" that eat the algae);
• allelopathic compounds that restrict the growth of co-occurring algal species;
• storage products;
• secondary metabolites with no physiological function.

Fathom

Algal biotoxins are some of the most potent known to humans.

Humans are affected at the last stage of the food web. Toxic algae are first eaten by tiny zooplankton, or grazers, who are eaten by small fish, who are then eaten by larger fish higher in the food web. Some algal toxins are soluble in fat and thus they "biomagnify" in the food web. At each higher stage, the toxins that were produced by the algae get more concentrated in the bodies of the predators. In the case of shellfish, toxic algae are consumed as food by the filter feeders, and the biotoxins are concentrated and passed on to whoever consumes the affected shellfish.

There are a variety of toxins that come from various algal species. Some of the toxins are life threatening and all can temporarily incapacitate a person. The toxins are among the most potent natural toxins known to humanity, so only small concentrations can cause serious illness or even death. For a person weighing 165 lbs. (75 kg), a little more than half a gram of saxitoxin, which is responsible for paralytic shellfish poisoning, represents a minimum lethal dose.

The most significant public health problems caused by harmful algae are as follows:

Ciguatera Fish Poisoning (CFP)

	CFP
	causative organisms: Gambierdiscus toxicus, Prorocentrum spp., Ostreopsis spp., Coolia monotis toxins produced: ciguatoxin/maitotoxin symptoms: initially diarrhea, vomiting and abdominal pain, followed by neurological dysfunction, including reversal of temperature sensation, muscular aches, dizziness, anxiety, sweating and a numbness and tingling of the mouth and digits.

There is evidence that ciguatera is responsible for about half of all intoxications linked to consumption of fresh seafood. There is currently no easy way to tell if a seafood product has ciguatoxin or maitotoxin in it, either by smell or appearance, so the best prevention is to avoid eating tropical reef fish or large predator species of reef fish such as barracuda or moray eel. Grouper and red snapper should also be avoided. Although paralysis and death have been documented, symptoms are usually less severe although they can be debilitating. Recovery time can take weeks, months, or even years. Months after ciguatera poisoning, victims sometimes show sensitivity to certain foods, including any type of fish, ethanol, caffeine and nuts. No immunity is created against ciguatera--on the contrary, subsequent intoxications seem to be worse than the initial one. Treatment within 24 hours with IV mannitol is supposed to relieve some symptoms. There is no antidote and survivors eventually recover.

Amnesic Shellfish Poisoning (ASP)

	ASP
	causative organisms: multiple Pseudo-nitzschia spp. toxin produced: domoic acid symptoms: potentially fatal; within 24 hours of eating contaminated shellfish, nausea, vomiting, abdominal cramps and diarrhea develop. In severe cases, within 48 hours neurological symptoms appear such as dizziness, headache, seizures, disorientation, short-term memory loss, respiratory difficulty and coma.

In 1987, four people died and 153 cases of acute poisoning were reported following the consumption of toxic mussels from Prince Edward Island, Canada. Since these initial reportings, ASP toxins have also been detected in shellfish in California, Washington, Oregon, Maine and Massachusetts. Toxic organisms, but no toxic shellfish, have been reported in the northern Gulf of Mexico. Since 1987, Canadian and US authorities have monitored the water column for the presence of the causative diatom and checked shellfish for the presence of domoic acid. Shellfish beds are closed to harvesting when the domoic acid concentration reaches 20 µg/g for shellfish meat. The risk to human consumers and animals in the marine food web is more significant than previously believed because domoic acid can also accumulate in fish and crab viscera.

Paralytic Shellfish Poisoning (PSP)

	PSP
	causative organisms: Alexandrium spp., Gymnodinium catenatum, Pyrodinium bahamense toxins produced: saxitoxins symptoms: potentially fatal; death occurs within 24 hours in severe cases. In nonlethal cases, symptoms include tingling, numbness and burning of the perioral region, ataxia, giddiness, drowsiness, fever, rash and staggering.

The onset of PSP is rapid and, in very severe cases, can lead to respiratory arrest and death within 2 to 12 hours. According to one study, within 5 to 30 minutes of eating contaminated molluscs, a slight tingling sensation develops around the mouth, leading to numbness, which spreads to the face and neck in moderate cases. In severe cases, these symptoms spread to the extremities, with uncoordination and respiratory difficulty. In nonlethal cases, regardless of severity, victims start to recover after 12 hours and symptoms disappear completely within a few days. Humans, birds, fish and even marine mammals can all be affected by PSP, although there has only been one case reported of a human getting PSP from eating a bird, which occurred in Indonesia after the person ate all of the contaminated bird. People usually get PSP through eating raw or cooked shellfish, such as mussels, clams, oysters, scallops. PSP is best prevented by large-scale proactive monitoring programs and rapid closures to harvest of suspect or actual areas that contain the toxin.

Diarrhetic Shellfish Poisoning (DSP)

	DSP
	causative organisms: Dinophysis spp., Prorocentrum lima toxin produced: okadaic acid symptoms: within 30 minutes to a few hours of consumption incapacitating diarrhea, nausea, vomiting, abdominal cramps and chills.

DSP is found worldwide, with tens of thousands of cases being reported in Europe, Asia and South America since it was first discovered in the Netherlands in the 1960s. In the late 1970s it was reported in Japan, and since then 1,300 cases have been reported there, with the annual peak being from April to September. In 1981 over 5,000 cases were reported in Spain, with over 2,000 cases reported in France in 1984 and 1986. DSP is not fatal and victims recover within three days, with or without medical treatment.