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Overview of Algal Poisoning


Wayne W. Carmichael

, PhD, Wright State University

Last full review/revision Dec 2013 | Content last modified Dec 2013
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Algal poisoning is an acute, often fatal condition caused by high concentrations of toxic blue-green algae (more commonly known as cyanobacteria—literally blue-green bacteria) in drinking water as well as in water used for agriculture, recreation, and aquaculture. Fatalities and severe illness of livestock, pets, wildlife, birds, and fish from heavy growths of cyanobacteria waterblooms occur in almost all countries of the world. Acute lethal poisonings have also been documented in people. Poisoning usually occurs during warm seasons when the waterblooms are more intense and of longer duration. Most poisonings occur among animals drinking cyanobacteria-infested freshwater, but aquatic animals, especially maricultured fish and shrimp, are also affected. The toxins of cyanobacteria comprise six distinct chemical classes collectively called cyanotoxins.

Etiology, Epidemiology, and Pathogenesis:

Although toxic strains within species of Anabaena, Aphanizomenon, Cylindrospermopsis, Microcystis, Nodularia, Nostoc, Oscillatoria, and Planktothrix are responsible for most cases of toxicity, there are >30 species of cyanobacteria that can be associated with toxic waterblooms. Neurotoxic alkaloids (called anatoxins) can be produced by Anabaena, Aphanizomenon, and Planktothrix, while saxitoxins (also called paralytic shellfish toxins) can be produced by Anabaena, Aphanizomenon, and Lyngbya. Hepatotoxic heptapeptides called microcystins can be produced by Anabaena, Microcystis, Nostoc, and Planktothrix. The brackish water genus Nodularia produces a hepatotoxic pentapeptide related, in both structure and function, to microcystins. Cylindrospermopsis, Anabaena, Aphanizomenon, Raphidiopsis, and Umezakia can produce a potent hepatotoxic alkaloid called cylindrospermopsin. Some genera, especially Anabaena, can produce both neuro- and hepatotoxins. If a toxic waterbloom contains both types of toxins, the neurotoxin signs are seen first, because their effects occur much sooner (minutes) than those of the hepatotoxins (1 to a few hours). Other noncyclic peptides and amino acids produced by cyanobacteria can also have biological activity. One recent amino acid with neurologic degenerative activity is BMAA (ß-methylamino alanine). BMAA has been implicated as the causative agent of amyotrophic lateral sclerosis or parkinsonism dementia.

Poisoning usually does not occur unless there is a heavy waterbloom that forms a dense surface scum. Factors that contribute to heavy waterblooms are nutrient-rich eutrophic to hypereutrophic water and warm, sunny weather. Evidence supports the observation that global climate change causes earlier, more intense, and longer-lasting warm weather that leads to more extensive waterblooms of cyanobacteria. Agriculture practices (eg, runoff of fertilizers and animal wastes) that promote nutrient enrichment also contribute to and intensify waterbloom formation. The problem is augmented by light winds or wind conditions that lead to areas of very high (scum) concentrations of cyanobacteria, especially leeward shoreline locations where livestock drink. Experiments with both toxin groups have revealed a steep dose-response curve, with as much as 90% of the lethal dose being ingested without measurable effect. Animal size and species sensitivity influence the degree of intoxication. Monogastric animals are less sensitive than ruminants and birds. Depending on waterbloom densities and toxin content, animals may need to ingest only a few ounces to be affected. However, if the waterbloom is less dense or cyanotoxin content is low, as much as several gallons may be needed to cause acute or lethal toxicity. Among domestic animals, dogs are most susceptible to a toxic waterbloom. This is due to their preference for swimming and drinking in dense waterblooms and a greater species sensitivity to the cyanotoxins, especially the neurotoxins.

Although the species sensitivity and signs of poisoning can vary depending on the type of exposure, the gross and histopathologic lesions are quite similar among species poisoned by the hepatotoxic peptides and neurotoxic alkaloids. Death from hepatotoxicosis induced by cyclic peptides is generally accepted as being the result of intrahepatic hemorrhage and hypovolemic shock. This conclusion is based on large increases in liver weight as well as in hepatic hemoglobin and iron content that account for blood loss sufficient to induce irreversible shock. In animals that live more than a few hours, hyperkalemia or hypoglycemia, or both, may lead to death from liver failure within a few days to a few weeks.

Neurotoxicosis, with death occurring in minutes to a few hours from respiratory arrest, may result from ingestion of the cyanobacteria that produce neurotoxic alkaloids. Species and strains of Anabaena, Aphanizomenon, Oscillatoria, and Planktothrix can produce a potent, postsynaptic cholinergic (nicotinic) agonist called anatoxin-a that causes a depolarizing neuromuscular blockade. Strains of Anabaena can produce an irreversible organophosphate anticholinesterase called anatoxin-a(s). Anabaena, Aphanizomenon, Cylindrospermopsis, and Lyngbya can produce the potent, presynaptic sodium channel blockers called saxitoxins.

Clinical Findings and Lesions:

One of the earliest effects (15–30 min) of microcystin poisoning is increased serum concentrations of bile acids, alkaline phosphatase, γ-glutamyltransferase, and AST. The WBC count and clotting times increase. Death may occur within a few hours (usually within 4–24 hr), up to a few days. Death may be preceded by coma, muscle tremors, paddling, and dyspnea. Watery or bloody diarrhea may also be seen. Gross lesions include hepatomegaly due mostly to intrahepatic hemorrhage. Intact clumps of greenish cyanobacteria can be found in the stomach and GI tract, and there is a greenish stain on the mouth, nose, legs, and feet. Hepatic necrosis begins centrilobularly and proceeds to the periportal regions. Hepatocytes are disassociated and rounded. After death, debris from disassociated hepatocytes can be found in the pulmonary vessels and kidneys. Clinical signs of neurotoxicosis progress from muscle fasciculations to decreased movement, abdominal breathing, cyanosis, convulsions, and death. Signs in birds are similar but include opisthotonos. In smaller animals, death is often preceded by leaping movements. Cattle and horses that survive acute poisoning may have signs of photosensitization in areas exposed to light (nose, ears, and back), followed by hair loss and sloughing of the skin.


Diagnosis is based primarily on history (recent contact with cyanobacteria waterbloom), signs of poisoning, and necropsy findings. Samples of the waterbloom should be taken as soon as possible for microscopic examination to confirm the presence of the toxigenic cyanobacteria and for cyanotoxin analysis. Although there are nontoxic and toxic strains of all the known toxic species, it is not possible to identify a toxic strain by visual examination. Cyanobacteria are detected by light microscopy, identified using morphologic characteristics, and counted per standard volume of water. Standard protocols to sample and monitor cyanobacteria as well as practical keys for the identification of toxic species are available.

Some laboratories can analyze for the cyanotoxins either by chemical or biologic assay. Animal bioassays (mouse tests) have traditionally been used to detect the presence of the entire range of cyanotoxins based on survival times and signs of poisoning. These tests provide a definitive indication of toxicity, although they cannot be used for precise quantification of compounds in water or to determine compliance with standards for environmental levels. A number of analytic techniques are available to determine microcystins in water. These techniques must provide for quantitative comparison to the guideline or regulatory value in terms of toxicity equivalents. The method most suitable in this regard is high-performance liquid chromatography (HPLC) or HPLC coupled with mass spectrometry. These methods still involve estimation of the concentration and therefore provide only an estimate of toxicity. This is largely due to the limited availability of certified reference standards for the cyanotoxins. Commercial reference materials, purified from laboratory cultures or waterbloom material, for some microcystins, nodularin, cylindrospermopsin, and saxitoxins are available. A synthetic reference material for anatoxin-a is also available. No known commercial reference material is available for anatoxin-a(s). Newer methods of immunoassay, for quantification purposes, are also available. These include commercial ELISA kits in both laboratory and field formats for microcystins/nodularin, cylindrospermopsin, and saxitoxins. Also available is a receptor-binding assay colorimetric plate kit for anatoxin-a.


After removal from the contaminated water supply, affected animals should be placed in a protected area out of direct sunlight. Ample quantities of water and good quality feed should be made available. Because the toxins have a steep dose-response curve, surviving animals have a good chance for recovery. Although therapies for cyanobacterial poisonings have not been investigated in detail, activated charcoal slurry is likely to be of benefit. In laboratory studies, an ion-exchange resin such as cholestyramine has proved useful to absorb the toxins from the GI tract, and certain bile acid transport blockers such as cyclosporin A, rifampin, and silymarin injected before dosing of microcystin have effectively prevented hepatotoxicity. No therapeutic antagonist has been found effective against anatoxin-a, cylindrospermopsin, or the saxitoxins, but atropine and activated charcoal reduce the muscarinic effects of the anticholinesterase anatoxin-a(s).


Removal of animals from the affected water supply is essential. If no other water supply is available, animals should be allowed to drink only from shore areas kept free (by prevailing winds) of dense surface scums of cyanobacteria. Some efforts have been made to erect surface barriers (logs or floating plastic booms) to keep shore areas free of surface scum, but these are not very successful. Cyanobacteria can be controlled by adding copper sulfate (CuSO4) or other copper-based algicidal treatments to the water. The usual treatment for CuSO4 is 0.2–0.4 ppm, equivalent to 0.65–1.3 oz/10,000 gal. of water or 1.4–2.8 lb/acre-foot of water. Livestock (especially sheep) should not be watered for at least 5 days after the last visible evidence of the cyanobacteria waterbloom. CuSO4 is best used to prevent waterbloom formation, and care should be taken to avoid water that has dead cyanobacteria cells, either from treatment with algicide or natural aging of the bloom, because most toxin is released in the water only after breakdown of the intact cyanobacteria cells. A chemical control method receiving attention are compounds to bind and remove phosphorus from eutrophic waters. This has the potential to minimize one of the more important nutrients responsible for cyanobacteria waterblooms. Common phosphorus treatments include lime, aluminum sulfate, ferric chloride, and some types of clay particles. These treatments also act as flocculating agents and form particulates with algae cells and other debris that settle out and remove the bloom from the water column. For example, when alum (potassium aluminum sulfate) is used in a water supply, a precipitate (floc) forms that carries algae cells, dirt, and bacteria to the bottom, but charged items such as phosphate and colloids are bound by the same precipitate through their charges. A newer, effective phosphorus-binding compound product available in the USA since 2010 uses a patented phosphorus-locking technology containing lanthanum (5%), a naturally occurring earth element, embedded inside a clay matrix (~95%).

Source water management techniques for control of cyanobacterial growth include flow maintenance in regulated rivers, water mixing techniques both to eliminate stratification and reduce nutrient release from sediments in reservoirs, and the use of algicides in dedicated water supply storages. Algicides disrupt cells and liberate intracellular toxins. Algicide use should be in accordance with local environment and chemical registration regulations. In situations where multiple offtakes are available, the selective withdrawal of water from different depths can minimize the intake of high surface accumulations of cyanobacterial cells.

Water treatment techniques can be highly effective to remove both cyanobacterial cells and cyanotoxins (especially microcystins) with the appropriate technology. Most cyanotoxins remain intracellular, unless the cells are lysed or damaged from age or stress from water conditions or chemical treatment. The one exception is cylindrospermopsin, which is actively secreted from even healthy cells. This makes it possible to remove cells and cyanotoxins (especially microcystins) by coagulation and filtration in a conventional treatment plant. Treatment of water containing cyanobacterial cells with oxidants such as chlorine or ozone, while killing cells, will result in the release of free cyanotoxin. Therefore, the practice of prechlorination or preozonation is not recommended without a subsequent step to remove dissolved cyanotoxins.

Microcystins are readily oxidized by a range of oxidants, including ozone and chlorine. Adequate contact time and pH control are needed to achieve optimal removal of these compounds, which is more difficult in the presence of whole cells. Microcystins, anatoxin-a, cylindrospermopsin, and some saxitoxins are also adsorbed from solution by both granular activated carbon and, less efficiently, by powdered activated carbon. The effectiveness of the process should be determined by monitoring cyanotoxin in the product water.

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