Difference between revisions of "Blue-Green Algae Toxicity"
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==Diagnosis== | ==Diagnosis== | ||
| − | + | It is possible to test water for the presence of blue-green algae. This can be done by fixing fresh samples in a 1:10 dilution of formalin or frozen water samples can be evaluated for lethality using a mouse bioassay. | |
A biochemistry profile may suggest hepatotoxicity with increases in Alanine transaminase (ALT), Aspartate transaminase (AST) and Alkaline phosphatase (ALP). | A biochemistry profile may suggest hepatotoxicity with increases in Alanine transaminase (ALT), Aspartate transaminase (AST) and Alkaline phosphatase (ALP). | ||
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==Pathology== | ==Pathology== | ||
| − | Inflammed and congested liver, with areas of necrosis. The lungs mesenteric vessels and lymph nodes and gall bladder may show congestion. | + | Inflammed and congested liver, with areas of massive or periacinar hepatic necrosis. The lungs, mesenteric vessels and lymph nodes and gall bladder may show congestion. |
Inflammatory and congestive changes in the gastrointestinal tract may also be present. | Inflammatory and congestive changes in the gastrointestinal tract may also be present. | ||
| + | ==Mechanism of toxicity== | ||
| + | |||
| + | Blue green algae causes toxicity by metabolism into the cyclic peptide, microcystin. This causes dysfunctional phosphorylation of cellular keratins, leading to disruption of the normal cytoskeleton. This in turn leads to a "rounding up" effect of the hepatocytes, disruption of the hepatic sinusoids, separation of hepatocytes and excessive apoptosis, which all will result in liver failure. | ||
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| + | Neurotoxins anatoxin-a and anatoxin-a(s) are prodcued by other blue-green algae. Anatoxin-a is a potent post-synaptic depolarizing neuromuscular blocker. Anatoxin-a(s) is a potent acetylcholinesterase inhibitor. | ||
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There is no specific anti-dote. | There is no specific anti-dote. | ||
| − | Following known ingestion, gastric decontamination can be performed unless there is evidence of impaired neurological status. | + | Following known ingestion, gastric decontamination can be performed unless there is evidence of impaired neurological status.Intravenous injection of a mixture of sodium nitrite and sodium thiosulphate |
Supportive treatment is required for other clinical signs which may include diarrhoea, dehydration, shock and hepatic insufficiency. To prevent toxicity keep animals away from infected water or use algicides such as copper sulphate to water soutces. | Supportive treatment is required for other clinical signs which may include diarrhoea, dehydration, shock and hepatic insufficiency. To prevent toxicity keep animals away from infected water or use algicides such as copper sulphate to water soutces. | ||
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Revision as of 12:37, 7 July 2010
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This article is still under construction. |
Description
Blue-green algae (Microcystis aeruginosa) is a type of phytoplankton that is found in ponds and other freshwater environments. They arise following long spells of hot dry weather and hence bloom in the summer but are also assosiated with high levels of phosphate and nitrate in the water. These algae can be extremely toxic and can poision livestock, birds and sometimes dogs.
Diagnosis
It is possible to test water for the presence of blue-green algae. This can be done by fixing fresh samples in a 1:10 dilution of formalin or frozen water samples can be evaluated for lethality using a mouse bioassay. A biochemistry profile may suggest hepatotoxicity with increases in Alanine transaminase (ALT), Aspartate transaminase (AST) and Alkaline phosphatase (ALP).
History and Clinical Signs
History of drinking from stagnant water source. Clinical signs can be variable but in acute cases death can occur within a few hours. In less severe cases liver damage causing jaundice and photosensitisation may lead to death. Generalised signs may include severe abdominal pain, vomiting and bloody diarrhoea, muscle tremors, convulsions, hyperaesthesia, staggering, dullness, recumbency, ataxia, flaccid paralysis.
Pathology
Inflammed and congested liver, with areas of massive or periacinar hepatic necrosis. The lungs, mesenteric vessels and lymph nodes and gall bladder may show congestion. Inflammatory and congestive changes in the gastrointestinal tract may also be present.
Mechanism of toxicity
Blue green algae causes toxicity by metabolism into the cyclic peptide, microcystin. This causes dysfunctional phosphorylation of cellular keratins, leading to disruption of the normal cytoskeleton. This in turn leads to a "rounding up" effect of the hepatocytes, disruption of the hepatic sinusoids, separation of hepatocytes and excessive apoptosis, which all will result in liver failure.
Neurotoxins anatoxin-a and anatoxin-a(s) are prodcued by other blue-green algae. Anatoxin-a is a potent post-synaptic depolarizing neuromuscular blocker. Anatoxin-a(s) is a potent acetylcholinesterase inhibitor.
Treatment
There is no specific anti-dote.
Following known ingestion, gastric decontamination can be performed unless there is evidence of impaired neurological status.Intravenous injection of a mixture of sodium nitrite and sodium thiosulphate Supportive treatment is required for other clinical signs which may include diarrhoea, dehydration, shock and hepatic insufficiency. To prevent toxicity keep animals away from infected water or use algicides such as copper sulphate to water soutces.
Prognosis
Poor. Dependent on the degree of liver damage and quantity ingested. Prompt treatment is essential.