Toxigenic Algae And Algal Food Poisoning- An Overview

Toxigenic algae are the major concern of algal poisoning for aquatic animals, amphibians, reptiles, birds, mammals as well as humans and are found in marine, brackish and freshwater habitats.
Some of the algal toxins are potent to cause poisoning cases in humans after consumption and death cases are also reported.
Toxins produced by algae and cyanobacteria are referred to as phytotoxins which mean organic poisonous substances that produce various potent toxic compounds.
The ability to produce the potent toxic compounds might be during the course of evolution to avoid predation which is not been reported to date.

Marine algae (dinoflagellates), yellow-brown algae (diatoms), and blue-green algae (cyanobacteria) produce phycotoxins like saxitoxin, gonyautoxin, okadaic toxin, brevetoxin, ciguatoxin, domoic toxin, palytoxin, and tetrodotoxin.
These toxins are toxic to humans causing gastrointestinal disorders causing algal pollution and killing many aquatic animals.
The death of fishes is caused by inadequate oxygen supply under shallow water caused by the decomposition of large masses of algae.
Algae such as Prymnesium parvum and dinoflagellates Gymnodinium veneficum, Gymnodinium brevis and Gonyaulax monitala are poisonous to fishes.
Human shellfish poisoning is caused by the dinoflagellates Gonyaulax tamarensis and Gonyaulax catenella.
Many fishes are non-poisonous but become poisonous when these toxic algae are consumed by them and the chain goes by the human consumption of herbivorous fish and shellfish.
These toxic algae also contaminate drinking water used for food and feed preparation and cause poisoning to humans and animals when directly consumed.
Different food poisoning is caused by different sources and types of toxicity likewise azaspiracid shellfish poisoning (ASP) is caused by 12 azaspiracid analogs, neurotoxic shellfish poisoning (NSP) by brevetoxins, ciguatera fish poisoning (CFP or Ciguatera) by ciguatoxin, gambiertoxin and maitotoxin.
Others are paralytic shellfish poisoning (PSP), amnesic shellfish poisoning (ASP), and diarrhetic shellfish poisoning (DSP) caused by saxitoxins, DA derivatives, okadaic acid, and dinophysistoxins.
Golden algal toxins, karlotoxins, Pfiesteria toxins, pectenotoxins, and yessotoxins are less-characterized toxins.
Harmful algal blooms (HAB), dinoflagellate blooms, cyanotoxins are phycotoxins responsible for causing red tides.

Table of Contents

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Toxins produced by Dinoflagellates

The dinoflagellate cells contain chlorophylls a and c with two lipid-soluble toxins (hemolytic and neurotoxin) that affect the lives of fresh and marine water animals.
Gonyaulax is red dinoflagellate and appears red in the water as they go through rapid multiplication producing pigment that changes color from brown to red.
The toxins produced by dinoflagellates cause gastrointestinal problems and respiratory paralysis.
The brevetoxin causes a neurological problem that occurs in most cases of seafood poisoning.

Toxins produced by Diatoms

Yellow-brown algae belong to the diatoms also known as phytoflagellates that are found in brackish ponds and estuarine water.
Prymnesium parvum is a yellow-brown alga that contains chlorophylls a, c and e with a toxin that inhibits the transfer of oxygen on the fish gill membrane.
This toxin is thermolabile and contains a potent hemolytic agent causing seafood poisoning, and gastrointestinal and respiratory problems in humans.
This toxicity of fish has caused a great problem and economic losses for commercial farms in many countries.

Toxins produced by Cyanobacteria

Cyanobacteria are also known as blue-green algae and the species Nodularia spumigena is involved in toxin production causing food poisoning in humans.
Nodularia spumigena and Microcystis aeruginosa are found in brackish and freshwater and are responsible for causing livestock poisoning.
Anabaena circinalis and Anabaena flos-aquae are common species that produce heat-stable neurotoxin and anatoxin-a which is toxic to many animals.
The clinical symptoms of these toxins are leaping movements, abdominal breathing, convulsions, lacrimation, salivation, urination, and diarrhea.
Other toxin-producing cyanobacteria species are Aphanizomenon spp, Anabaena spp, Cylindrospermopsis spp, Lyngbya spp, Caulerpa spp, Schizothrix spp, and Planktothrix spp.

Some toxins originated from bacteria associated with algae that contaminate fishes and become poisonous to the fish itself and to the animals who consume it. The bacteria is present inside the fish body and produce toxins from their feed that may be associated with algae.

Route of exposure to Algal Food Poisoning

The major route of exposure is through the consumption of contaminated seafood products such as contaminated clams, mussels, scallops, oysters, and other shellfish.
Ciguatera is caused by the large reef fish, barracuda and grouper whereas saxitoxin is caused by the consumption of pufferfish.
Airborne toxins are also known to occur by the inhalation of brevetoxin produced by Karenia brevis.
This airborne toxin causes respiratory irritation to people living in nearby areas which can be avoided by the use of particle filter masks.
Ciguateratoxins and maitotoxins are transmitted through sexual contact and also cause acute health problems in the fetus and newborn babies.
These toxins can be transferred vertically through the placenta and during breast milk transmission from mother to infant.
Some toxins produced by cyanobacteria can infect humans through direct skin contact or by drinking contaminated water.
Fishermen and boatmen are the high-risk possible group for contamination.

Toxicokinetics of Algal Toxins

The metabolism of algal toxins occurs rapidly from the gastrointestinal and respiratory tracts where the lipophilic and hydrophilic algal toxins are absorbed.
The acute inhalation of the brevetoxin toxicokinetics starts within 7 days of exposure and gets absorbed in the lungs and gets distributed throughout the body via blood circulation.
The toxins get accumulated in the skeletal muscle, intestine, and liver whereas only a low amount of toxins are present in the blood, brain, and fat.
About 20% of toxins remain in the lung, liver, and kidney for up to a week and slowly get disseminated.
Similarly, domoic acid is absorbed orally and gets distributed to the blood to other body parts but cannot penetrate the blood-brain carrier.
This toxin may cause impaired renal function with increased blood serum concentration and risks.
Saxitoxin is metabolized through glucuronidation in humans which is a detoxification pathway that converts xenobiotics to water-soluble metabolites.
After the saxitoxin metabolism, the toxins are excreted in the urine, and feces and remain in the blood, bile, cerebrospinal fluid, stomach, spleen, liver, heart, brain, adrenal glands, thyroid glands, and pancreas.
The cyanobacterial toxins are absorbed from the gastrointestinal tract where the microcystins are transported into the liver from the blood.
Microcystins remain in the liver for up to 6 days whereas in the kidney they remain for about 24 hours.

Acute and chronic toxicity

The gastrointestinal signs and symptoms start within minutes to 24 hours after the consumption of contaminated seafood.
The symptoms include difficulty breathing, numbness and tingling in the peripheral nervous system, hallucination, memory loss, fluctuating blood pressure, and cardiac arrhythmia.
The illness may last from hours to months depending upon the particular disease and dose concentration.
Chronic toxicity affects the cells and tissues of the organs but its exposure has not been studied in detail.

Control and clinical management of Algal Food Poisoning

Medical treatment must be provided within 3 days of illness that helps to resolve acute symptoms and also prevents chronic symptoms.
If symptoms reoccur, repeated treatment must be given with the use of activated charcoal or dilute bicarbonate solution for gut emptying and decontamination to prevent vomiting and diarrhea.
Atropine and Amitriptyline are recommended for relieving symptoms such as fatigue and paresthesias.
Fluid therapy and bed rest is recommended and hospitalization is not required if the symptoms are mild.
Ventilatory support and artificial respiration treatment are most effective for the saxitoxin treatment.
The US Food and Drug Administration (FDA) has established action levels to implement the HACCP plan for the prevention of unsafe products from reaching the customer.

References

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