What are Toxigenic Algae And Algal Food Poisoning?

• Toxigenic algae are algae (or algae-like microorganisms) that produce toxins under certain conditions, and “toxigenic” means toxin-making.
• In water bodies, when these algae multiply excessively, harmful blooms are formed, which may release those toxins into water.
• Some types of algae, for example cyanobacteria (blue-green algae), dinoflagellates, and certain diatoms, are known to be toxigenic.
• The toxins produced are called algal toxins or phycotoxins (or cyanotoxins if by cyanobacteria) and may harm humans, animals, aquatic life.
• Under favorable environment (warm temperature, excess nutrients, low water flow) toxigenic algae are more likely to form blooms.
• Exposure may occur via drinking contaminated water, eating seafood that bioaccumulates toxin, skin contact, or inhaling aerosols in rare cases.
• The term “toxigenic algae” is often used interchangeably with algae causing harmful algal blooms (HABs), though not all blooms are toxigenic.
• In early records (18th / 19th centuries) episodes of dense algal growth were noted in lakes/streams, especially as farming increased and nutrients washed into water, promoting blooms.
• It is believed that the oldest recorded toxic algal bloom occurred in Polish Lake Tuchomskie during the 17th century.
• European colonists in Florida (1500s) saw discoloration / blooms in coastal waters; these are among early documented harmful algal phenomena.
• In 1844 a “red tide” off the Florida Gulf Coast was possibly first formally observed, though no human deaths were clearly attributed then.
• In 1972, a harmful bloom of Alexandrium (formerly Gonyaulax tamarense) in New England caused shellfish poisoning via saxitoxin.
• The 1987 “Amnesic shellfish poisoning (ASP)” event in Prince Edward Island was due to domoic acid produced by a toxic diatom species; human fatalities / memory loss resulted.
• A very large cyanobacterial bloom in Australia’s Darling / Barwon Rivers in 1991 spanned over 1000 km, showing how big inland blooms may become.
• The “red tide” crisis in Chiloé (Chile, 2016) involved Alexandrium catenella and led to bans on seafood harvesting and heavy socioeconomic impacts.
• In marine waters, Heterosigma akashiwo has caused massive fish kills in Canada (British Columbia), affecting hundreds of thousands of salmon.
• Also, Aureoumbra lagunensis caused a 7-year “brown tide” (1990–1997) in Laguna Madre, Texas, severely reducing marine biodiversity in that area.
• In 2015 on U.S. West Coast, a harmful algal bloom with record toxin levels shut down Dungeness crab & razor clam fisheries temporarily.
• The largest / deadliest bloom in recent years was the 2018 event in Florida where hundreds of sea turtles, dolphins, manatees died due to toxic algae effects.

Toxins produced by some notable Algae

Dinoflagellates

Dinoflagellates produce potent neurotoxins, which affect nervous system of animals and humans, and are often implicated in shellfish poisoning.

Brevetoxins are made by Karenia brevis and bind to voltage-gated sodium channels, causing neurotoxic shellfish poisoning (NSP).

Saxitoxins (and related paralytic shellfish toxins, PSTs) are produced by Alexandrium and other dinoflagellates; they block sodium channels in nerve cells, leading to paralysis.

Pinnatoxins are generated by Vulcanodinium rugosum (a dinoflagellate); they block nicotinic acetylcholine receptors in nerves/muscles.

Karlotoxins are made by Karlodinium veneficum; they are hemolytic, ichthyotoxic, cytotoxic, and are implicated in fish kills.

Diatoms

Diatoms, though many are harmless, some species produce neurotoxins especially affecting shellfish and higher organisms.

Domoic acid is produced by diatoms like Pseudo-nitzschia; it causes amnesic shellfish poisoning (ASP) by overactivating glutamate receptors in nerve cells, leading to neurological damage.

Cyanobacteria

Cyanobacteria (blue-green algae) produce a wide variety of toxins, many of which harm liver, nerves, or multiple organs.

Microcystins are heptapeptide hepatotoxins produced by Microcystis, Planktothrix, Dolichospermum etc; they inhibit protein phosphatases in liver cells.

Cylindrospermopsin is made by Cylindrospermopsis, Aphanizomenon and others; it impairs protein synthesis, and damages liver, kidney, maybe other organs.

Anatoxin-a (and analogs) is a neurotoxin which binds to nicotinic acetylcholine receptors, causing rapid nerve overstimulation and paralysis.

Guanitoxin (also called anatoxin-a(S)) is an irreversible inhibitor of acetylcholinesterase, creating severe neurotoxic effect.

Nodularin is a cyclic peptide toxin, similar to microcystin, produced by Nodularia and sometimes Nostoc; it mainly affects the liver.

Lyngbyatoxin is an alkaloid produced by Lyngbya (a cyanobacterium); it causes dermatitis, and acts as a tumor promoter via protein kinase C pathways.

Here are examples of toxin-producing algae / algae-like organisms, grouped by water type (freshwater, marine / brackish) with some overlaps:

Freshwater & Brackish water toxin-producers

• Microcystis (cyanobacteria) — produces microcystins (hepatotoxins)
• Anabaena / Dolichospermum (cyanobacteria) — some strains produce anatoxin, saxitoxin, cylindrospermopsin
• Aphanizomenon (cyanobacteria) — may produce saxitoxin, cylindrospermopsin
• Planktothrix (cyanobacteria) — known for microcystin production
• Nodularia (cyanobacteria) — produces nodularin (a cyclic peptide toxin)

Marine / Brackish / Saltwater toxin-producers

• Karenia brevis (dinoflagellate) — produces brevetoxins, major in red tide events
• Alexandrium (dinoflagellate genus) — producers of saxitoxins (paralytic shellfish toxins)
• Gymnodinium / Pyrodinium (dinoflagellates) — implicated in saxitoxin production
• Dinophysis / Prorocentrum (dinoflagellates) — produce okadaic acid, dinophysistoxins, etc (causing diarrhetic shellfish poisoning)
• Pseudo-nitzschia (diatom genus) — produces domoic acid (neurotoxin)

What is the route of exposure to algal food poisoning?

The most common route is ingestion — eating or drinking food / water contaminated with algal toxins (for example shellfish, fish, or drinking water)

Through dermal contact — skin touches contaminated water, algae cells or scums, and toxins may penetrate or irritate skin.

By inhalation — breathing in aerosolized toxin particles or droplets (spray, mist) generated by wave / wind / bubbles.

Via eye contact — splash or aerosol can bring toxins into eyes, causing irritation or absorption.

By bioaccumulation in food chain — algae toxins accumulate in shellfish / fish, then humans are exposed when eating those animals.

In rare cases medical procedures (e.g. hemodialysis) may become unintended exposure route if contaminated water or circuits are used.

What are the toxicokinetics of algal toxins?

After ingestion, many algal toxins are poorly absorbed in intestine, so much remains in gut and is excreted via feces. For example microcystin shows low intestinal absorption.

The toxin that is absorbed is carried by bloodstream and is preferentially distributed to organs; often the liver is targeted because many toxins undergo hepatic uptake.

In the liver, biotransformation (metabolism) may occur — some toxins conjugated with glutathione or cysteine to less toxic forms.

Some portion of toxin or its metabolites is eliminated via urine and bile, or back into intestine, though excretion is often low / slow for many algal toxins.

For water-soluble toxins (those having carboxyl, sulfonic, amine groups), solubility helps distribution in body fluids (blood, interstitial fluid) and transport to tissues.

In cases like domoic acid (from diatoms), toxicokinetics includes rapid absorption, distribution into nervous tissues, and elimination; but details vary with species and dose.

Some toxins are resistant to degradation under physiological pH, temperature, or digestive enzymes, so they persist in body longer. For example, microcystins resist many proteases because of their cyclic structure.

Distribution to non-target organs (kidney, intestine, perhaps brain) occurs at lower levels, and residual toxin may accumulate in tissues.

In summary, absorption → distribution (especially liver) → metabolism (partial) → excretion (urine, bile, feces) is the general toxicokinetic path, but rates / extents depend on toxin’s chemical structure, dose, route, and organism.

Acute and chronic toxicity of Algal Toxins

• In acute toxicity, a large dose of algal toxin causes rapid onset of symptoms (hours to days), such as vomiting, diarrhea, liver failure, neurological signs (paralysis, seizures) which may lead to death.
• In acute cases, liver damage is often severe because many algal toxins are hepatotoxic (e.g. microcystins) and that damage can overwhelm detoxification mechanisms.
• Also in acute exposure, the toxin may cause bleeding, shock, cellular necrosis, and hemorrhage in organs.
• In chronic toxicity, repeated low-level exposure over weeks, months or years can lead to cumulative damage, even though symptoms may be subtle.
• Chronic exposure may produce liver fibrosis, tumors, organ degeneration, metabolic disruptions and increased cancer risk.
• For example, chronic microcystin-LR exposure in animals is linked to liver injury, tumor promotion, disturbances in insulin signaling and metabolic changes.
• In chronic cases, kidney, gastrointestinal tract, immune system may also suffer low-grade damage, especially with mixed toxins over time.
• With chronic exposure, subclinical or sublethal effects are more likely, so health may be impaired though overt poisoning is not obvious.
• The severity / type of acute or chronic effect depends on toxin type, dose, exposure route, frequency, and host susceptibility.

What are the strategies for the control and clinical management of Algal Food Poisoning?

• Prevention of algal food poisoning begins with controlling blooms: nutrients input must be reduced (less fertilizer runoff, better sewage treatment), and water bodies are monitored / tested.
• Physical / mechanical removal of algal cells or scums is used; flocculation (e.g. with clay) may aggregate cells so they sink, and thus reduce their numbers and toxin release.
• Chemical methods (e.g. hydrogen peroxide, or sometimes algaecides) have been tried to kill algae, but risk harming non-target organisms or releasing toxins.
• Biological control (parasites, predators) is proposed, but is largely experimental because of unknown ecological effects or unintended consequences.
• In case of human poisoning, supportive therapy is mainstay: fluids, electrolyte balance, symptomatic relief (antiemetics, pain relief), respiratory support if needed.
• For ingestion, if patient presents early (within ~1-2 hours), activated charcoal may be considered (unless contraindicated) to bind toxins in gut.
• In skin contact, remove contaminated clothing / jewelry, wash skin with soap and water for 10-15 min.
• Eye exposure: irrigate thoroughly (at least 15 min) with saline or water; remove contact lenses if worn; refer to ophthalmology if symptoms persist.
• In inhalation exposure, remove patient to clean air (away from toxin source), treat respiratory symptoms supportively.
• For marine toxin poisonings (e.g. shellfish toxins), no specific antidotes exist; management is symptomatic, including respiratory support (in paralytic shellfish poisoning) and supportive care
• In some cases (e.g. ciguatera poisoning), intravenous mannitol has been used (within 48-72 h), though evidence is variable.
• Monitoring of water and food (seafood) for toxin levels, issuing harvesting closures or consumption advisories, and public warnings are crucial in control.
• Public health measures (surveillance, risk communication, regulatory limits) must be enforced so that exposure risk is minimized.

How to spot Toxic Algae?

• On surface water, discoloration may be visible (green, blue-green, brown, red, white) which may hint at toxic algae presence.
• Scum, foam, mats, or “paint-like” streaks or floating clumps (on water / along shore) often accompany blooms which may be toxigenic.
• Reduced water clarity — water looks like “pea soup” or is very murky — is a common sign.
• Unusual odors (grassy, musty, rotten-plant) may be detected, especially as blooms age or decay.
• Dead fish, shellfish, or other aquatic animals visible on surface or at shoreline may indicate toxins and oxygen depletion.
• On shore, mats of dried algae / crusty layers may wash up, and these may still contain toxins.
• In rivers or streams, blooms may grow on bottom rocks or plants (benthic), and later detach and float to surface; these may be harder to see.
• Microscopic / lab testing is needed because you cannot know if algae are toxic just by appearance; toxins may be present before / after visible bloom.
• Inconsistently, some blooms don’t show strong surface signs, so caution is needed even when water looks “normal”.

Impact of Toxic Algae on Animals, plant and Human

• Animals (fish, birds, mammals) are harmed when toxins accumulate in their tissues; mass fish kills are often seen when blooms are intense.
• In marine mammals & birds, neurotoxic algae (e.g. producing domoic acid) cause seizures, disorientation, memory loss, even death.
• In livestock / pets, drinking contaminated water or grazing near blooms may lead to liver failure, paralysis, digestive distress, and sometimes death.
• In plants / aquatic vegetation, dense algal blooms reduce light penetration, so submerged plants get less sunlight and die or weaken.
• Also oxygen depletion (hypoxia) occurs when blooms die and decompose, and this suffocates aquatic animals and injures plant life.
• In humans, exposure via contaminated water, fish or shellfish leads to symptoms: vomiting, diarrhea, abdominal pain, neurological signs (numbness, confusion), liver damage sometimes.
• Skin contact causes irritation, rashes; eye contact may bring redness / pain.
• Inhalation of aerosolized toxins (spray, mist) can irritate respiratory tract, trigger asthma or breathing difficulty.
• Ecosystem balance is disturbed: food web alters, biodiversity loss is seen, habitat degradation happens.
• Human economic / social harm also arises: fisheries closures, drinking water contamination, loss of recreational use of water bodies.

What can algal toxins tell us about the condition of water?

• Presence of algal toxins in water suggests nutrient over-enrichment (especially phosphorus, nitrogen) which may have caused eutrophication.
• Elevated toxin levels often correlate with poor water exchange / stagnation, because when water moves slowly, toxic blooms are more likely to develop and persist.
• When toxins are detected, it implies that microbial / algal community structure is altered (dominance by toxigenic species rather than benign ones) — water ecology is stressed.
• Toxin presence can signal that water treatment capacity is strained: facilities may struggle to remove them, so water may taste / smell bad or remain unsafe.
• Algal toxins serve as early warning indicators that water quality is deteriorating before visible damage or mass death events occur.
• In source waters used for drinking, detection of toxins means public health risk is present and action/monitoring must be increased.
• Because many toxins resist degradation by usual processes, their detection implies persistent pollution stress rather than a one-time event.
• Overall, algal toxins give insight into water’s chemical, biological, and ecological state; they tell us that water is under stress, pollution is significant, and monitoring / management is urgently needed.

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