Potentially toxic species known to occur in New Zealand
Anabaena circinalis
Anabaena flos-aquae
Anabaena lemmermanii
Anabaena spiroides
Anabaena planktonica
Anabaena smithii
Anabaena affinis
Anabaena aphanizomanioides
Anabaena oscillariodies
Other Anabaena sp?
Blue-green algae
Planktonic or attached to moist substrates. Trichromes solitary or aggregated in floccose masses or united in a thin mucilaginous stratum; straight, flexuous, circinate, spirally coiled or irregulary twisted.
Anabaena species often form thick, wind-concentrated surface blooms or scums especially during summer months when there is warm, sunny weather and if the water is nutrient rich..
Other cyanobacteria.
In the North Island Anabaena blooms have been reported in lakes in the Rotorua area including Rotorua, Roitoiti, Rotoehu, Okaro, Opuri, Ngahewa. Blloms have occurred on Lake Taupo, Lake Waitawa, Lake Maraetai, Kimihia (Waikato) and the Waikato River, Lake Orakai (Napier), Lake Henely (Masterton), Karori Reservior (Wgtn)
In the South Island blooms have been reported on Lakes Roundabout, Lake Hayes, Lake Johston, Lake Wakatipu, Lake Waihola, Butchers Dam, Woods Dam and Tomahawk Lagoon.
Anabaena sp. can produce the hepatotoxic cyclic peptide microcycystin and the neurotoxins anatoxin-a (a nicotinic depolarising alkaloid neurotoxin which is potent and fast-acting), anatoxin-a(S) (an organophosphorus cholinesterase inhibitor, responsible for the voluminous salivation sometimes observed) and saxitoxins.
Anabaena species that produce neurotoxin may kill within 1 to 2 minutes of ingestion. One study estimates the oral minimum lethal dose to be 420 mg/kg body weight.
Sensitivity and animal size influence the toxicity, with monogastric animals being less sensitive than ruminants and birds. There are be both toxic and non-toxic strains within the species.
Anabaena sp. in New Zealand are believed to produce microcystins. Further work is currently underway at Massey & Victoria University, ESR and Agresearch to establish whether anatoxins and saxitoxins are produced by Anabaena species in New Zealand.
Cattle, sheep, dogs and other pets, honey bees, laboratory mice and rats, chickens, ducks, pheasants, goldfish, wildfowl, humans
Clinical signs depend on the quantity and type of toxin being produce by the Anabaena 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. Anatoxin ?a (S) is an anticholinesterase, and has not been recorded in New Zealand. Exposure causes an increase in salivation, lacrimation, ataxia, diarrhoea, dyspnoea and death within an hour. Signs similar to anatoxin-a may also occur.
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. Hepatotoxins (eg microcystins, nodularin) cause intrahepatic haemorrhage and liver damage. Sometimes convulsions, paralysis or muscle tremors precede death. Depending on the amount of toxin ingested signs can be acute or chronic. The liver may appear normal, but is usually enlarged and dark red from congestion and intrahepatic haemorrhage. Histologically, a widespread centrilobular to midzonal necrosis is observed.
In animals that live for a few hours death from liver failure caused by hyperkalaemia or hypoglycaemia may occur within a few days.
Cyanobacteria may be found in the stomach and intestines, and there is often a greenish stain on the mouth, nose, legs and feet. Liver damage may be exhibited as a pale tan liver with focal, subcapsular haemorrhagic plaques, or as diffuse reddening. Hepatomegaly is mostly due to intrahepatic haemorrhage. Hepatocytes may show vacuolation and swelling, there is narrowing of sinusoids and loss of tubular arrangements. Necrosis in the liver begins around the centrilobular vein and proceeds to the periportal regions. The kidneys may show severe tubular degeneration and intratubular eosinophilic casts. Debris from disassociated hepatocytes may be found in the pulmonary vessels and kidneys. Pronounced haemorrhage from small vessels under the skin.
History, clinical signs and post mortem findings. Some laboratories are able to assay for the toxins, or microscopic examination may reveal the cyanobacteria.
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. Atropine may be administered in an attempt to negate the effects of anatoxin-a (s), and artificial respiration may prolong life. 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. There is no specific treatment for hepatotoxins. Symptomatic treatment may be of use, eg intravenous fluids may help prevent dehydration. Copper sulphate or other algicidal treatments may be added to the water in an attempt to control the cyanobacteria. 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.
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