Toxin production in cyanobacteria varies with species, time of year,
cell concentration and other environmental and physiological factors.
Exposure to cyanobacterial toxins can occur via skin contact, drinking,
inhalation and haemodialysis. The symptoms below are generally extreme
examples, and high exposure to the toxins would be required to produce
An amine alkaloid neurotoxin.
Postsynaptic cholinergic nicotine agonist and neuromuscular-blocking agent. Causes calcium ion influx to muscle tissue.
The onset of clinical signs is abrupt (within 60 minutes). Signs include lethargy, muscle tremors, hyperpnoea, cyanosis, paralysis, hyperaesthesis, convulsions and death within 30 minutes after signs appear as a result of respiratory arrest.
A neurotoxic, cyclic N-hydroxyguanidine alkaloid phosphate ester.
Exposure to anatoxin-a (s) causes an increase in salivation, lacrimation, ataxia, diarrhoea, dyspnoea and death within an hour. Signs similar to anatoxin-a may also occur. This toxin has not currently been recorded in New Zealand (Wood & Parton, 2003).
An alkyl phenol.
Is currently researched in context of causing cancer.
Extreme inflammatory agent causing severe skin dermatitis, diarrhoea, burning sensation in throat and mouth, lethargy and muscle contractions (in mice) (Nagai et al. 1996).
A cyclic guanidine alkaloid, included in the cyanobacterial hepatoxin group
Blocks protein synthesis with a major effect on liver cells.
Causes damage to the kidneys, spleen, intestine, thymus, liver and heart in vertebrates (Codd et al., 1999).
A lipopolysaccharide endotoxin.
Less toxic than Salmonella LPS. But requires further
investigation, as it may be fatal when present in high concentrations
(Codd et al., 1999).
A cyclic peptide, included in the cyanobacterial hepatoxin group.
Inhibits eukaryotic protein phosphatases. In eukaryotes these protein phosphatases regulate a wide range of developmental, metabolic and physiological processes, which may be inhibited or disrupted by the presence of high concentrations of microcystins and nodularians. Disrupts vertebrate liver structure and function.
Weakness, recumbency, pallor, cold extremities, laboured breathing, vomiting and diarrhoea. Respiratory arrest. Haemorrhaging into the liver. Microcystins have caused tumour growth in animal studies and may be linked with liver cancer. These toxins have also been associated with skin irritation including dermatitis, conjunctival and allergic reactions occurring due to skin contact (Codd et al., 1999).
A group of at least 19 carbamate alkaloid neurotoxins. Saxitoxins are also produced by marine dinoflagellates.
Inhibits neurotransmission by blocking sodium channels.
They cause paralysis, respiratory depression and respiratory failure. In people incoordination, confused speech, nausea, vomiting, eye irritation, and respiratory distress may occur.
Bernard, C., Harvey, M., Briand, J.F., Bire, R., Krys, S. and Fontaine, J.J. (2003). Toxicological Comparison of Diverse Cylindrospermopsis raciborskii Strains: Evidence of Liver Damage Caused by a French C. raciborskii Strain. Environmental Toxicology, 18: 176-186.
Clifford, M.N., Walker, R., Ijomah, P., Wright, J., Murray, C.K. and Hardy, R. (1992). Do Saxitoxin-like substances have a role in scombrotoxicosis. Food Additives and Contaminants, 9: 657-667.
Codd, G.A., Bell, S.G., Kunimitsu, K., Ward, C.J., Beattie, K.A. and Metcalf, J.S. (1999). Cyanobacterial toxins, exposure routes and human health. European Journal of Phycology, 34: 405-415.
Nagai, H., Yasumoto, T. and Hokama, Y. (1996). Aplysiatoxin and debromoaplysiatoxin as the causative agents of a red alga Gracilaria coronopifolia poisoning in Hawaii. Toxicon, 37: 753-761.
Steffenson, D., Burch, M., Nicholson, B., Drikas, M. and Baker, P. (1999). Management of toxic blue-green algae (cyanobacteria) in Australia. Environmental Toxicology, 14: 183-185.
Wood, S.A. and Parton, K. (2003). Livestock poisoning by blue-green algae. VETscript, March 2003