blue-green algae (BGA) toxins in waterways

see also:

• toxinology
• Victorian BGA bloom outbreaks updates online
• https://www.cdc.gov/habs/materials/factsheet-cyanobacterial-habs.html
• dinoflagellate blooms can also produce toxins
  • Karenia mikimotoi, Karenia cristata and other Karenia sp brown blooms can cause coughing, eye irritation, etc to humans on beaches or swimming as well as death to sea life
    • toxins include brevetoxins, gymnocin A and B
    • eg. March 2025 bloom on the coast of the Fleurieu Peninsula in South Australia

• waterways often become impacted by large blooms of blue green algae (BGA) which are capable of producing toxins
• water treatments such as chemical sterilisation, boiling, filtration and UV sterilisation will NOT decontaminate the water of the toxins and thus the water cannot be readily made potable
• also called cyanobacterial harmful algal bloom (cHAB)
• it is becoming increasingly recognised as a potential issue in reservoirs supplying drinking water:
  • the most likely risk to consumers of drinking water are from the hepatotoxins
  • the three main reservoirs supplying Brisbane in Australia all carry substantial populations of the toxic Cylindrospermopsis raciborskii. This cyanobacterium forms dense layers 5–10m below the surface, so that the first indication of the proliferation of the organism may be the blocking of filters in the drinking water treatment plant.
• Not all algal blooms are harmful
• examples of such species include:
  • Aphanizomenonaceae Family
  • Microcystis sp
  • Chrysosporum ovalisporum
• certain BGA species can produce cyanotoxins which have additional effects
  • there are a number of different potential toxins including:
    • microcystin
      • peptide hepatotoxin produced by Microcystis, Planktothrix and Anabaena
        • Microcystis is the most abundant cyanobacterium forming toxic blooms, with toxin concentrations sufficient to poison domestic animals.
      • highly stable in water and are resistant to boiling
      • resistant to digestion in the gastrointestinal tract of eukaryotes, as peptide bonds linking to the D-amino acids are not susceptible to normal hydrolytic enzymes
      • toxins are concentrated into the liver by an active transport system, similar to the bile acid transporter
      • specifically inhibit protein phosphatases 1 and 2A, which have a vital role in cell control and in intracellular structure
      • acute poisoning is through destruction of the liver architecture, leading to blood loss into the liver and hemorrhagic shock, and later death is through liver failure with massive destruction of hepatocytes.
      • chronic exposure to these toxins in drinking water led to ongoing active liver injury in mice and there is a suggestion they may increase risk of hepatocellular carcinoma
    • nodularin
    • cylindrospermopsin
      • an alkaloid cytotoxic compound produced by Cylindrospermopsis raciborskii, Aphanizomenon ovalisporum, and Umezakia natans and is likely to occur widely in freshwater sources
      • is a potent inhibitor of protein synthesis and has marked genotoxicity, probable mutagenicity, and is a potential carcinogen
      • alkaloid cytotoxins that were relatively recently discovered, following the widespread human poisoning at Palm Island, Australia due to contamination of the water supply
    • anatoxin-a
      • neurotoxin produced by Anabaena, Aphanizomenon and Planktothrix;
      • an alkaloid which closely resembles an organophosphorus insecticide, and acts as an anticholinesterase and can cause death by respiratory paralysis;
      • stable in the environment but unlikely to persist in water supplies
      • rapidly excreted if ingested
    • anatoin-a(s) - neurotoxin
    • lyngbyatoxin
      • produced by Lyngbya cyanobacteria and can cause “seaweed dermatitis”, a contact dermatitis
      • ingestion may be fatal (eg. ingesting fish which have fed on it) as it can cause an illness similar to ciguatera poisoning
      • eg. mainly in tropical waters such as Moreton Bay area in Qld
    • saxitoxin
      • neurotoxin - alkaloid blocks sodium conduction in axons preventing nerve impulse transmission, leading to paralysis
      • well known as the cause of paralytic shellfish poisonings, which have resulted in many hundreds of human deaths worldwide
      • not limited to marine waters, and also occur in freshwater cyanobacteria such as Anabaena, Aphanizomenon and Lyngbya - The massive waterbloom of Anabaena circinalis on 1,000km of the Darling River in Australia in 1991 killed a large number of sheep and cattle, and also resulted in detectable neurotoxicity in town water supplies.
      • heat-stable molecules, which are not easily removed in conventional water treatments unless pH and chlorine residuals are carefully controlled, but can be effectively removed by ozone or activated carbon
      • oral LD50 in mice is about 260μg/kg bodyweight
      • acute poisoning in humans is unlikely to occur from contaminated water supplies, as the human body can tolerate about 100μg of saxitoxin without ill effect
      • no cumulative effects have been demonstrated
    • beta-methylamino-L-alanine (BMAA)
      • this neurotoxic amino acid has been implicated in contributing to motor neurone disease (MND) ¹⁾
      • some areas of Australia have higher rates of MND such as the Riverina, an agricultural region of New South Wales (Lake Wyangan, a reservoir that frequently has outbreaks of cyanobacteria), which has between 5-7x the national incidence of MND.
• live cyanobacteria are unable to invade, colonize, and grow in humans or animals
• one toxin (microcystin LR) has been classified by the International Agency for Research on Cancer (IARC) as a possible carcinogen (classification 2B). The clinical significance in humans with chronic exposure is not clear

• during blooms, do NOT:
  • swim in the water
  • drink the water
  • inhale droplets (eg. by water skiiing)
  • eat fish, molluscs, etc which eat the toxins
    • shell fish such as mussels can concentrate toxins, including saxitoxin, a neurotoxin which if eaten may result in paralytic shell fish poisoning
  • have contact with surface scum along shores
• children and animals are particularly at risk

• these are dose-related and dependent on type of toxin and route of exposure:
• skin / eye exposure
  • skin and eye irritation / conjunctivitis / photophobia
  • peri-oral blisters
  • dermatitis
• inhalation
  • mild respiratory tract effects, sore throat
  • hay fever-like symptoms
  • may cause pneumonitis
• ingestion
  • nausea, vomiting and diarrhoea
  • can also cause electrolyte imbalances, headache, malaise, and muscle weakness/ pain in joints and limbs
  • onset is usually 3–5 hours and symptoms can last 1–2 days
  • moderate effects may include the addition of abdominal pain, hypotension, headache, malaise and myalgia
  • large ingestions may cause multi-organ failure and death
  • the various toxins have differing properties but as a group, cyanotoxins can cause a range of effects including hepatotoxicity, cytotoxicity (affecting liver, kidney, heart, lungs, and stomach) and neurotoxicity
• inadvertent use of toxin contaminated water for dialysis
  • severe illness is likely with hepatic failure and death - 50 patients died in 1 week from such exposure in a Brazil dialysis clinic in 1996 ²⁾

• gastroenteritis
• drug overdose - especially paracetamol
• agricultural chemicals and industrial pollutants such as heavy metals
  • organophosphate poisoning
• mushroom poisoning
• plant intoxication

• remove exposure
• supportive care
• Rx skin irritation as for contact dermatitis
  • remove contaminated clothing and jewelry
  • wash skin with soap and water for 10–15 minutes
  • antihistamines and steroids can be used.
• Rx eye irritation as for usual eye irritation - permanent harm is unlikely
  • remove contact lenses.
  • irrigate the eyes with normal saline for at least 15 minutes
  • slit lamp examination if ongoing pain
  • consider referral to an ophthalmologist if eye symptoms persist after copious irrigation.
• Rx of inhalations:
  • supportive care
  • consider CXR
• Rx of ingestions:
  • activated charcoal can be considered if the patient arrives within 1–2 hours after a toxic ingestion, assuming no contraindications.
  • FBE, U&E, LFTs
  • IV fluids as indicated
  • there are no effective antidotes
  • there are no specific lab. tests to diagnose toxicity although specialist laboratories can do tests on faeces, urine, stomach contents (if available), tissues, serum, and water specimens.

• effects seem to be more serious in animals than in humans especially dogs
• effects are mainly gastrointestinal, such as vomiting and foaming at the mouth.
• exposure can also cause lethargy and neurologic symptoms, including stumbling, behavior changes, spastic twitching, loss of coordination, ataxia, violent tremors, partial paralysis, respiratory paralysis, hepatoenteritis, toxic liver injury, hepatic lesions with necrosis, petechial hemorrhages of the heart, and death.
• exposure has caused death in fish, dogs, cattle, and birds.