Difference between revisions of "Blue-Green Algae Toxicity"

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==Description==
 
==Description==
Blue-green algae is a type of phytoplankton found in ponds and other freshwater environments and toxic strains include ''Anacystis cyanea'', ''Microcystis aeruginosa''and ''Microcystis toxica''. The algae 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.
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Blue-green algae is a type of phytoplankton found in ponds and other freshwater environments and toxic species include ''Anabaena'' and ''Microcystis''. The algae 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==
 
==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.
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Based primarily on known ingestion, signs of poisioning or post mortem identification. Microscopic examination of the algae can be undertaken to confirm the presence of the toxigenic cyanobacteria. 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).
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Additionally a biochemistry profile  may suggest hepatotoxicity with raised Alanine transaminase (ALT), Aspartate transaminase (AST) and Alkaline phosphatase (ALP) values.
  
 
==History and Clinical Signs==
 
==History and Clinical Signs==
 
History of drinking from stagnant water source.
 
History of drinking from stagnant water source.
Some genera produce hepatotoxic peptides called microcytins whilst others especially Anabaena , can produce both neuro and hepatotoxins. If a toxic waterbloom contains both types of toxins, neurological signs will be seen first as these toxins act quicker than the hepatotoxins. 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.
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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.Some genera produce hepatotoxic peptides called microcytins whilst others especially ''Anabaena'' , can produce both neuro and hepatotoxins. If a toxic waterbloom contains both types of toxins, neurological signs will be seen first as these toxins act quicker than the hepatotoxins. Signs may include severe abdominal pain, vomiting and bloody diarrhoea, muscle tremors, convulsions, hyperaesthesia, staggering, dullness, recumbency, ataxia, flaccid paralysis.
  
 
==Pathology==
 
==Pathology==
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==Mechanism of toxicity==
 
==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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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, resulting in liver failure.  
 
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Neuro toixns produced by certain blue-green algae include Anatoxin-a which is a potent post-synaptic depolarizing neuromuscular blocker and Anatoxin-a which is a potent acetylcholinesterase inhibitor.   
Neurotoxins anatoxin-a and anatoxin-a(s) are prodcued by other blue-green algaeAnatoxin-a is a potent post-synaptic depolarizing neuromuscular blocker. Anatoxin-a(s) is a potent acetylcholinesterase inhibitor.   
 
  
  
 
==Treatment==
 
==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.
 
  
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Following known ingestion, affected animals should be placed out of the sunlight. Gastric decontamination can be performed unless there is evidence of impaired neurological status. Atropine and activated charcoal rcan be administered to reduce the muscarinic effects of the anticholinesterase anatoxin-a(s).
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Supportive treatment is required for other clinical signs which may include diarrhoea, dehydration, shock and hepatic insufficiency. To prevent toxicity animals should be kept away from infected water or algicides such as copper sulphate should be added to water soutces.
  
 
==Prognosis==
 
==Prognosis==
 
Poor. Dependent on the degree of liver damage and quantity ingested. Prompt treatment is essential.
 
Poor. Dependent on the degree of liver damage and quantity ingested. Prompt treatment is essential.
  
==Hepatotoxicity==
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Revision as of 13:11, 7 July 2010



Description

Blue-green algae is a type of phytoplankton found in ponds and other freshwater environments and toxic species include Anabaena and Microcystis. The algae 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

Based primarily on known ingestion, signs of poisioning or post mortem identification. Microscopic examination of the algae can be undertaken to confirm the presence of the toxigenic cyanobacteria. 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. Additionally a biochemistry profile may suggest hepatotoxicity with raised Alanine transaminase (ALT), Aspartate transaminase (AST) and Alkaline phosphatase (ALP) values.

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.Some genera produce hepatotoxic peptides called microcytins whilst others especially Anabaena , can produce both neuro and hepatotoxins. If a toxic waterbloom contains both types of toxins, neurological signs will be seen first as these toxins act quicker than the hepatotoxins. 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, resulting in liver failure. Neuro toixns produced by certain blue-green algae include Anatoxin-a which is a potent post-synaptic depolarizing neuromuscular blocker and Anatoxin-a which is a potent acetylcholinesterase inhibitor.


Treatment

Following known ingestion, affected animals should be placed out of the sunlight. Gastric decontamination can be performed unless there is evidence of impaired neurological status. Atropine and activated charcoal rcan be administered to reduce the muscarinic effects of the anticholinesterase anatoxin-a(s). Supportive treatment is required for other clinical signs which may include diarrhoea, dehydration, shock and hepatic insufficiency. To prevent toxicity animals should be kept away from infected water or algicides such as copper sulphate should be added to water soutces.

Prognosis

Poor. Dependent on the degree of liver damage and quantity ingested. Prompt treatment is essential.