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Sample Paper on Algal Toxin

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Sample Paper on Algal Toxin


Different kinds of algae blooms including dinoflagellates, true algae and cyanobacteria occur naturally in marine and freshwater resources. Most algal blooms are harmless but some algae species such as cyanobacteria release toxins that can kill fish, wildlife, livestock and humans. Toxic marine algae blooms and cyanobacteria have increased significantly in recent years due to increased pollution of marine and freshwater sources (Krahl 2009, p. 129). Algal toxins affect humans when they eat contaminated seafood, and drink or wash with contaminated water. The increased prevalence of toxic algae is thus a growing health and safety concern needing public attention. The present study discusses the frequency of occurrence of algal toxins, its risk status, diagnosis and control.

Algal Toxins

The most common types of algal toxins include brevetoxins, demoic acid, saxitoxins and ciguatoxins (Krahl 2009, p. 130). Brevetoxins are caused by Ptychodiscus brevis, a dinoflagellate that forms red blooms. Brevetoxins are polyether compounds with the molecular formula of C­­50 H70 O14 (Miller 1990, p. 59). Scientists have extracted at least six brevetoxins but brevetoxin B is the most abundant. Brevetoxins cause hemolytic symptoms and neuromascular blockage in humans by activating the Na+ channels. Other symptoms of brevetoxin poisoning in humans include acute apnea, diarrhea, cardiac arrhythmias and sensory problems. Saxitoxins are caused by A. cantenella and A. tamarense dinoflagellates (Faber 2012, p. 1). Saxitoxins cause paralytic shellfish poisoning in humans upon consuming infected fish and other marine foods. Saxitoxins inhibit neuromascular function by interfering with the flow of sodium ions. Domoic acid is a toxin produced by Pseudo-nitzschia and Chondria armata. It enters the human food chain through ingestion by marine organisms especially shellfish. Domoic acid is a tricarboxylic acid with relatively lower toxicity to animals and humans than other algal saxitoxins and brevetoxins because of its poor absorption in the digestive system, short half-life and limited ability to penetrate the blood barrier (Pulido 2008, p. 181). Ciguatoxins are produced by Gambierdiscus toxicus (Wang 2008, p. 351). The primary mode of transmission of ciguatoxins into the human body is through the consumption of infected coral reef fish. These toxins are lipid soluble, heat-stable and oxygenated. Once in the body of animals, ciguatoxins cause calcium and sodium fluxes in cells resulting in many neurological, gastrointestinal and cardiovascular symptoms. Ciguatoxins bind to receptors in the sodium pathway leading to the loss of neuromascular functioning (Wang, 2008, p. 358).


Outbreaks of waterborne diseases caused by algal toxins have been reported in various parts of the world. For example, outbreaks caused by saxitoxins have been reported in North America, Europe, South Africa and Japan (Faber 2012, p. 2). Each year, about 1600 people suffer from saxitoxin poisoning and up to 10 percent of these cases are fatal. Out of the 905 cases of saxitoxin poisoning reported between 1969 and 1983, 24 resulted in death (Faber 2012, p. 3). An infected person can die within 12 hours of ingesting the saxitoxin. The lethal dose of saxitoxins is 500-12400 µg/kg body weight for humans and varies with age and other factors such as availability of emergency care. Children are the most vulnerable. Ingesting saxitoxin at high concentrations results in numbness and tingling of the areas around the mouth and legs as well as respiratory problems within one hour of ingestion. The likelihood of death drops significantly after 12 hours but the body needs at least 24 hours to excrete the toxin (Faber 2012, p. 2). Domoic acid poisoning was reported in 1987 in Canada where more than 200 people were affected (Pulido 2008, p. 182). Symptoms of domoic intoxication occurred within 24-48 hours and included vomiting, nausea, diarrhea, coma, memory loss and neurological dysfunction. Ten percent of the cases were severe and 4 of these were fatal. Domoic acid damages the brain by causing neural shrinkage, edema, cell death and vacuolization of the cytoplasm (Pulido 2008, p. 184). Domoic acid acts as an excitatory compound targeting glutamate receptors (Pulido 2008, p.194). Other effects of domoic acid poisoning include retinal damage, sensory problems due to damage to the spinal cord as well as cardiac diseases.

An algal toxin outbreak occurred in Europe in 1989 where blue-green algae poisoning killed more than 30 animals near Rutland (Reynolds 2010, p. 29). Two soldiers undergoing training at Staffordshire recreational reservoir fell seriously ill due to algal toxins from Microcystis aphanizomenon and Anabaena species present in the water. The analysis of the contaminated water revealed that three main categories of toxins were present in the water: neurotoxins, hepatotoxins and lipolysaccharides. Neurotoxins are alkaloids that attack the neuromascular system causing blockage. Examples of neurotoxins include saxitoxins, yessotoxins, ciguatoxins, and maitotoxins (Wang, 2008, p. 354). Hepatotoxins are complex proteins that cause vomiting, fatigue, acute liver damage and diarrhea. Lipopolysaccharides cause skin irritation. However, the symptom analysis of the affected soldiers showed that the most likely cause of poisoning was hepatotoxins. The lethal dose of hepatotoxins produced by blue green algae is 30-300‌µg/kg of bodyweight (Reynolds, 2010, p. 30). Algal blooms are also toxic to birds and cause deaths in some cases. For example, domoic acid caused by Pseudo-nitzschia has been associated with the die-offs of brown pelicans of central California (Oregon State University, 2003, p. 1). Brevetoxins produced by Gymnodinium breve have been associated with the death of fish and birds in Florida. For example, 149 West Indian Manatees and numerous bottlenose dolphins died of K. brevis poisoning in Florida in 1998-1999 (Bourdelais et al. 2002, p. 465).  

Hazard levels

The hazard levels of algal toxins vary with the type of toxin and the effectiveness of risk response strategies. For example, the risk of brevetoxin poisoning is quite low. Although outbreaks of brevetoxin have been reported in the Gulf of Mexico, Florida and New Zealand, these cases are rare because of intensive prevention efforts especially by the governments of the respective regions (Watkins et al. 2008, p. 438). For example, the government of Florida monitors brevetoxin levels in its marine reserves and provides special medical response to victims of brevetoxin poisoning. Similarly, the risk of saxitoxin poisoning in humans is quite low although some cases have been fatal (Mulvenna et al. 2012, p. 816). The low level of saxitoxin threat has been maintained over the last five decades by ensuring the level of saxitoxins in commercially distributed seafood remains below 0.8 mg/kg. The risk of ciguatera poisoning is medium. About 400 million people are exposed to ciguatera worldwide through the consumption of contaminated fish (Caillaud et al. 2010, p. 1841). However, the mortality rate of ciguatera poisoning is very low (less than 0.1%).  Generally, the risk of algal toxin outbreaks is quite low because algal blooms proliferate under specific environmental conditions. Harmful algae multiply slowly in lakes and water bodies with insufficient nutrients (Reynolds 2010, p. 34). For example, the toxic blue-green algae do not exceed 10µg/L when phosphorous levels in marine water are low. In addition, harmful blue-green algae do not do well in winter. During winter, harmless algae such as Asterionella and Cyclotella multiply rapidly and consume much of the available phosphorus in freshwater. If phosphorous levels remain significantly low, harmful algae will not spread even during summer when the temperatures are favorable (Reynolds 2010, p. 34). However, water reservoirs that have sufficient residue phosphorous especially those that receive additional nutrients from agricultural runoffs and sewage have sufficient food to support the growth of harmful algae during summer. Britain has experienced warmer, drier winters and sunny summers in the last several years, which may explain the observed increase in harmful algae populations. The increase in world population and the resulting increase in generation of animal waste, sewage, and fertilizer runoff explain the rising population of cyanobacteria and other toxic algae blooms (Brand 2009, p. 92).

Toxin Detection Methods

Toxin detection has been traditionally conducted using animal bioassay, which involves administering samples of seafood to laboratory mice or other animals to identify symptoms if any and fatalities (Vilariho et al 2010, p. 1673). For example, mouse bioassay was the main method of detecting okadaic acid in shellfish and other seafood. Okadaic acid is a toxin produced by Prorocentrum and Dinophysis (Pravda, Kreuzer & Guilbault 2002, p. 6). It causes diarrhea in humans upon ingestion. However, animal bioassay tests have low specificity and thus low reliability. The current method of detecting okadaic acid is high performance liquid chromatography (HPLC) (Vilariho et al 2010, p. 1673). Enzyme immunoassays are used to detect tetrodotoxin, a toxin found mainly in puffer-fish. Initially, tetrodotoxin was detected using animal bioassays until the more sensitive enzyme immunoassay techniques such as TTX ELISA were developed. HPLC is also used to detect domoic acid but other methods such as ELISA and capillary electrophoresis with UV detection are equally effective (Pravda, Kreuzer & Guilbault 2002, p. 8). Researchers are currently searching for new ways of assessing algal toxins and other marine toxins. Assessment methods may be either analytical or non-analytical. Analytical methods are capable of identifying and quantifying the toxins while non-analytical methods can quantify but not identify the toxins. Examples of analytical toxin detection methods are high HPLC with fluorimetric detection, HPLC with ultraviolet detection, liquid chromatography (LC) with mass spectrometry and LC with tandem-mass spectrometry. These methods can detect most algal toxins including brevetoxins, saxitoxin, okadaic acid, ciguatoxins and domoic acid (Vilariho et al 2010, p. 1673). The non-analytical methods used to detect algal toxins are called biosensors because they utilize biological elements to detect toxins. Immune-based biosensors employ structural features of toxins to detect the toxins while receptor-based biosensors utilize the action pathways of toxins for detection. Biosensors utilize a similar detection mechanism that involves the use of a biologically recognizable component attached to a transducer that translates the biosignal into a digital signal.

The detection and identification of algal toxins, especially those produced by cyanobacteria, is difficult and tedious because over 70 types of these toxins have been detected (Weller 2013, p. 15087). Analytical bioassay techniques known for their high sensitivity and power such as the LC-mass spectrometry may fail to detect many of the variants of cyanobacteria toxins. Better technologies need to be developed to enable the detection of many of the variants of nodularins and microcystis. One of the most promising technologies suggested is Adda-selective antibody-based biosensors (Weller 2013, p. 15087). However, the technology is still in its early stages of development. Although mass-spectrometry with high resolution is now considered a reliable assessment technique for algal toxins, it does not produce reliable quantification solutions partly due to the lack of standards for generating and interpreting results. Contextual factors may affect the reliability of any bioassay technique. Algal toxins usually cause time-bound hazards because toxic algal blooms proliferate at certain periods especially in summer. This means that periodical sampling and laboratory analysis is not a reliable method of predicting toxin outbreaks. Worse still, frequent laboratory-based bioassays are too costly to undertake, meaning that the chances of detecting and preventing toxin outbreaks are very low. Even when samples are collected for testing, it takes a long time to analyze the product and determine its toxicity (Weller 2013, p. 15087). The water production plants may not have the facilities and the capacity to hold water until the bioassay results are out and still meet the customers’ water requirements.

Monitoring Algal Toxins in Seafood

The monitoring of algal toxins requires thorough understanding of algae life history, survival factors, actual abundance, and ecological vulnerabilities and reactions. These measures may be local, national or regional. For example, efforts to monitor ciguatera poisoning in Europe involve identifying the areas prone to ciguatera and controlling the sale and consumptions of fish from such areas (Caillaud et al. 2010, p. 1877). To ensure consumer safety, the European Union (EU) regulates ciguatoxin levels in commercially produced seafood. The EU regulation prohibits the sale of foods containing harmful levels of ciguatoxins and other toxins (Caillaud et al. 2010, p. 1880).  Food plants are not allowed to manufacture fish products derived from certain fish such as Molidae, Tetraodontidae and Diodontidae because these fish families are poisonous. The EU sets standards of hygiene and levels of toxins in seafood that food manufacturers must meet for their products to be allowed into the market. Furthermore, the EU specifies the methods that must be used to detect algal toxins in shellfish—immunosorbant assay, HPLC and mouse bioassay. Some EU countries such as France have implemented legislations to ensure fish products from ciguatera endemic areas meet the EU toxin standards (Caillaud et al. 2010, p. 1881).

 Local methods of preventing the spread of algae blooms include the use of algaecides such as copper sulfate (Knauert & Knauer 2008, p. 312). However, both organic and inorganic algaecides lack proven effectiveness in eliminating algae blooms. In addition, algaecides are used under close monitoring and regulation because of their potential toxicity to water reservoirs (Reynolds 2010, p. 34). Some have suggested the use of straw bales to kill green algae in streams and canals, but the effective dose of straw bales for use in large reservoirs and lakes is unknown considering straw bales have a high oxygen demand (Reynolds 2010, p. 34). Periodic emptying of a water reservoir to kill blue-green algae before they mature may be effective for slow growing species. Unfortunately, this method does not support the goal of most water reservoirs, which is to conserve ecological systems. Applying chemicals to water to remove nutrients such as phosphorous and nitrogen may be helpful to prevent proliferation of toxic algae. However, chemical use is ineffective in reservoirs with significant algal toxin abundance.

The methods used to manage algal toxins include mitigation, prevention and control. The purpose of mitigation efforts is to reduce the adverse effects of an existing algal bloom. Over 50 countries worldwide engage in routine monitoring of the levels of toxins in shellfish with the view of limiting the consumption and sale of infected fish (Anderson 2009, p. 344). Prevention efforts include strategies to keep algal blooms from thriving especially by controlling nutrient supply. They include reduction of sewage discharge and regulation of fertilizer application. However, efforts to prevent the influx of nutrients into oceans and freshwater sources have not been effective. Controlling algae blooms involves suppressing or destroying existing blooms through chemical, biological and ecological means. For example, the fish farmers in Korea and the United States use sedimentation to remove algae cells from water in fish ponds (Anderson 2009, p. 345). Biological and chemical methods of bloom control are still underdeveloped because most biological and chemical agents have negative long term impact on the environment such as causing the death of some plant and animal species (Anderson 2009, p. 347).


Algal toxins are a potentially serious threat to public health because of the unpredictable nature of outbreaks and the serious consequences such outbreaks can have on humans including illness and death. The risk of toxin outbreaks related to algae blooms is likely to continue growing in the next several decades considering the increasing levels of nutrients in water sources caused by increased use of agricultural fertilizers, waste disposal and industrial pollution. In addition, the warmer global climate caused by the gradual depletion of ozone layer favors the proliferation of toxic algae species most of which thrive in warmer climates. Furthermore, the lack of effective techniques and measures to detect and control hazards associated with algal toxins renders public health care systems incapable of responding to algal outbreaks effectively. This scenario calls for increased attention to and support for efforts to generate deeper understanding of algal toxicity as a health concern in order to accelerate the progress towards a lasting solution to the problem.








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