Potentially toxic species in NZ
Aphanizomenon flos aquae
blue green algae, cyanobacteria
Planktonic; trichromes solitary or united in spindle shaped bundles or parallel flakes forming a plate like thallus in some taxa. Trichromes narrow, more or less straight or slightly bend; sub symmetric structure; generally with gas vascuoles and without a gelatinous sheath
Other blue green algae.
Worldwide in natural or induced eutrophic (nutrient enriched/ stagnant) water bodies. Also found in still fresh waters, such as lakes, ponds, canals and reservoirs.
Aphanizonmenon sp. can produce the neurotoxins anatoxin a (a nicotinic depolarising alkaloid neurotoxin which is potent and fast acting), saxitoxins (which block nerve cell sodium channels) and the alkaloid hepatotoxin cylindrospermopsin.
There is no evidence of Aphanizonmenon sp. producing toxins in New Zealand
All mammals. Sickness and death has been reported in livestock, pets birds, and wildlife following ingestion .
Clinical signs depend on the quantity and type of toxin being produce by the Aphanizonmenon sp.. The range of clinical signs can be wide especially if more than one type of cyanotoxin is involved.
Anatoxin a mimics the effect of acetylcholine. 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.
There are no specific lesions in animals that die of cyanobacterial neurotoxicoses.
Saxitoxins block nerve cell sodium channels. They cause paralysis, respiratory depression and respiratory failure. In people incoordination, confused speech, nausea, vomiting, eye irritation, and respiratory distress may occur. In severe cases respiratory paralysis requires artificial respiration.
Cylindrospermopsin blocks protein synthesis with a major effect on liver cells. Effects include extended fibrosis and bile duct proliferation with isolated groups of hepatocytes remaining. Extensive subserosal haemorrhages of heart, and extended epicardial haemorrhages of the small intestine and omentum.
The liver is the main target organ of cylindrospermopsin toxicity with observed pathology being fatty vacuolation and hepatocyte necrosis. Investigation of mechanisms of toxicity indicates that while inhibition of protein synthesis is the dominant recognised effect of cylindrospermopsin, other mechanisms of toxicity are likely to be present.
Toxic signs may appear within 1hr, and death may occur in less than 24hrs after ingestion of the poisonous material. The most commonly reported sequence of events is rapid prostration, convulsions, and death. Abdominal pain, anorexia, vomiting, muscular tremors, dyspnea, cyanosis and salivation are common; less common are icterus, diarrhoea, and bloody faeces. Photosensitisation frequently occurs in animals that survive for several days.
Cyanobacteria may be found in the stomach and intestines, and there is often a greenish stain on the mouth, nose, legs and feet.
History, clinical signs and post mortem findings. Some laboratories are able to assay for the toxins, or microscopic examination may reveal the cyanobacteria.
Other toxicities causing liver failure or neurological signs.
Other toxicants which are inhibitors of cholinesterase (eg carbamate and organophosphate insecticides, Solanum species, etc), have nicotinic effects (eg nicotine sulphate, tobacco, hemlock, levamisole etc) or other hepatogenous photosensitisers (eg sporodesmin, pyrrolizidine alkaloid plants etc).
Animals are often found dead or die before treatment can be given if the neurotoxin is present. Decontamination (eg activated charcoal) is important and removal of animals from the contaminated water supply is essential. Affected animals should be placed out of direct sunlight in a protected area. There is as yet no therapeutic antagonist effective against anatoxin a or the saxitoxins. Treatment with the anticholinesterases edrophonium chloride and neostigmine were shown to have no apparent effect on the toxin induced neuromuscular blockade. Copper sulphate or other algicidal treatments may be added to the water in an attempt to control the cyanobacteria. In surviving animals, antibiotics, glucose, calcium and magnesium supplementation have been used.
To detoxify the water copper sulphate or calcium hypochlorite can be added at 12kg (70%) per 1000L, this is still safe for stock to drink, but toxin may persist after algae are killed. Care should be taken when applying management options such as algicides, as some techniques can results in the death of the cyanobacteria, causing a massive release of the cyanotoxins from the cells, thus escalating any potential risks.
Invariably fatal.
Avoid contaminated water.
Check water supplies regularly in the summer.
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Wood, S. (2001) Cyanobacteria an underestimated risk to animal health in New Zealand? Vetscript, December 2001, pp4 –5
Susan Wood