Of some 60 or so species that cause red tides, only a handful is known to be toxic. Dominant dinoflagellate HAB genera include Alexandrium, Karenia, and Pfiesteria. The diatom genus most commonly associated with HABs is Pseudo-nitzschia. Each of these genera produces a different toxin and thus has a different role on organisms further up the food chain. Next, we discuss some of the HAB species in detail.
Alexandrium spp. is the dominant taxon in coastal regions of New England and eastern Canada but it is also found from California to Alaska.
It is a heterotropic dinoflagellate that produces a saxitoxin, one of the most powerful known types of neurotoxins. These toxins destroy the function of nerve cells and can thereby cause paralysis. Saxitoxins are most effectively concentrated by shellfish such as clams, quahogs, mussels, scallops and oysters that filter large volumes of sea water to acquire their nutrition. Although the saxitoxin does not harm these shellfish, even in small quantities, the toxin can be extremely dangerous for humans, resulting in a serious illness known as paralytic shellfish poisoning (PSP). The saxitoxin attacks the human nervous system within 30 minutes of ingestion with symptoms that may include numbness, tingling, weakness, partial paralysis, incoherent speech, and nausea. In severe cases, the toxin can lead to respiratory failure and death within a few hours. Alexandrium spp. toxins have also been harmful to whales, sea otters and birds.
The following videos describe the causes and impacts of red tides as well as possible antidotes for shellfish poisoning.
Video: Red Tide - Death Comes to Gasparilla Island Florida (5:59)
Video: Prized Science Episode 4: Taming the Red Tides (4:28)
Karenia is the dominant taxon causing red tides in Florida and Texas, but rarely species of Karenia have also been found up the east coast in North Carolina.
Examples of Karenia
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It produces a toxin known as a brevetoxin (named after a species of Karenia, K. brevis). Like saxitoxins, brevetoxins damage nerve cells, leading to disruption of normal neurological processes and causing neurotoxic shellfish poisoning (NSP). In humans, gastrointestinal symptoms and a variety of neurological ailments result, but there are no known fatalities. However, in fish, the brevetoxins attack the central nervous system and cause respiratory failure. Karenia dinoflagellates are responsible for massive fish and bird kills in the Gulf of Mexico. The brevetoxins are colorless, odorless, and heat and acid stable, thus they survive food preparation.
The genus Gambierdiscus lives in tropical waters, usually in reefs, and produces a toxin known as Ciguatoxin that causes gastrointestinal problems followed by mild neurological symptoms. This syndrome is known as Ciguatera fish poisoning. Because the toxin is fat soluble, it gets concentrated up the food chain by bioaccumulation from seaweed to smaller fish than to larger fish. The larger fish, which are the most dangerous to eat because they have the highest toxin concentrations, include commercially available seafood such as grouper, snapper, and barracuda. Ciguatera is responsible for more human illnesses—estimated between 10,000 to 50,000 cases annually—than any other HAB toxin.
Pseudo-nitzschia and the species Nitzschia navis-varingica are common diatom genera in Californian red tides. These taxa produce domoic acid, which is concentrated by filter-feeding shellfish. This neurotoxin can also bioaccumulate in fish such as anchovies that feed directly on the diatoms. Domoic acid causes a variety of gastrointestinal ailments, memory loss and brain damage in humans and is hence referred to as amnesic shellfish poisoning. Rarely, the neurotoxin can be fatal. It can also affect marine mammals, causing seizures.
The species Pfiesteria piscicida and P. shumwayae have been the most common dinoflagellate species in red tides in estuaries and bays along the east coast of the US from Delaware to Florida. The species occur in environments where freshwater and saltwater mix and have not been reported from freshwater environments or the open ocean. Pfiesteria blooms are restricted to summer months. Species have been associated with massive kills of menhaden and other estuarine fish in the Chesapeake Bay and the Tar-Pamlico and Neuse River Estuaries in North Carolina. The fish in contact with Pfiesteria rapidly develop bleeding lesions and have skin actively flake off them, and it has been proposed that the presence of live fish stimulates the production of toxin in the dinoflagellate. Ultimately the open lesions may destroy gill function and lead to death. Nevertheless, the connection between fish mortality and Pfiesteria is still doubted by some scientists. In fact, the effects of Pfiesteria on fish and human health has been one of the largest and nastiest controversies in marine science over the last 25 years and it does not appear that the conflict is anywhere near over.
The following video explains some of the research on Pfiesteria.
Video: Pfiesteria Update: An Enduring Debate (4:57)
At least part of the debate has been fueled by the popular press, who have focused attention on the organism after studies suggested that it was carnivorous. These studies indicated that Pfiesteria species ingested the skin of fish after it flaked off. In fact, lab studies have shown that when fish were left in tanks with Pfiesteria, the fish died within hours. For this to occur, however, the dinoflagellate and fish must be in direct contact. Without contact, the same studies show that fish suffered no ill effects. Some scientists alternatively point to water molds or fungi including the species Aphanomyces invadans as the pathogen cause of the ulcerative lesions, skin loss, and damage to gills. A. invadans and other fungi are universally present in fish with ulcers and skin loss. Also weakening the case for Pfiesteria, this genus is still known to exist in North Carolina estuaries, but fish kills have become less frequent recently. Moreover, where lesions on the fish menhaden were observed, nearby fish including catfish, perch, and carp were unaffected. These disparities have cast some doubt on whether Pfiesteria is harmful to fish at all. In fact, great differences exist among public health professionals, and warnings from different state agencies are in conflict.
Examples of Pfiesteria
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The health impact of Pfiesteria on humans is also uncertain, as is the method of transmission of the potential toxin. Scientists working with Pfiesteria in the laboratory have suffered from long-term neurological symptoms, such as memory loss, fatigue, and dermatological problems, and fisherman in contact with Pfiesteria-related fish kills have also suffered from similar ailments. However, other groups of fishermen who have come in close contact with lesion-covered fish have not reported adverse effects. There are reports that the hypothetical Pfiesteria toxin is transmitted via aerosols.
Until recently, the missing link in the Pfiesteria conundrum is that the toxin produced by this organism has been elusive. However, in 2007 scientists in a government lab claimed the first positive identification of a toxin associated with Pfiesteria. Even with this identification, questions remain; for one the toxin is unstable in the natural environment, and second, it is not been proven to have adverse health effects. Thus, the controversy about Pfiesteria is far from over. In all reality, a number of factors may result in the fish kills; in particular, the fish in estuaries may have already been under great stress from other biological agents (bacteria, viruses, fungi, parasites), exposure to chemicals (pollutants, toxins), suboptimal water quality and rapid water temperature change, that have the potential to cause lesions to form.
Far less controversial than the relationship of Pfiesteria with fish kills are studies that directly relate fish kills to low oxygen levels caused by algal blooms. In a number of estuaries along the eastern US, warmer waters in summer combined with increased production by algae, as a result of increased runoff and eutrophication, lead to severely decreased oxygen levels and major fish kills without the involvement of a toxin.