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==Description==
 
==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.
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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 associated with high levels of phosphate and nitrate in the water. These algae can be extremely toxic and can poison livestock, birds and sometimes dogs.
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==History and Clinical Signs==
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History of drinking from stagnant water source.
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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 [[Icterus|jaundice]] and [[Photosensitisation|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.
    
==Diagnosis==
 
==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.
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Based primarily on known ingestion, signs of poisoning 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.
 
Additionally a biochemistry profile  may suggest hepatotoxicity with raised Alanine transaminase (ALT), Aspartate transaminase (AST) and Alkaline phosphatase (ALP) values.
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==History and Clinical Signs==
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History of drinking from stagnant water source.
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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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Inflammed and congested liver, with areas of massive or periacinar hepatic necrosis. The lungs, mesenteric vessels lymph nodes and gall bladder may show congestion.  
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Inflamed and congested liver, with areas of massive or periacinar hepatic necrosis. The lungs, mesenteric vessels lymph nodes and gall bladder may show congestion.  
 
Inflammatory and congestive changes as well as the presence of clumps of algae may be present in the gastrointestinal tract.
 
Inflammatory and congestive changes as well as the presence of clumps of algae may be present in the gastrointestinal tract.
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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.  
 
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.   
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Neuro toxins 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==
 
==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 can be administered to reduce the muscarinic effects of the anticholinesterase anatoxin-a(s).
 
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 can 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.  
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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 sources.  
    
==Prognosis==
 
==Prognosis==
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==References==
 
==References==
Andrews., A.H, Humphreys., D.J (1982) Poisoning in Veterinary Practice. NOAH
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Andrews., A.H, Humphreys., D.J (1982) '''Poisoning in Veterinary Practice'''. NOAH
    
3rd Year BVetMed,Alimentary Module,Toxicology (2007).p 22 RVC lecture notes
 
3rd Year BVetMed,Alimentary Module,Toxicology (2007).p 22 RVC lecture notes
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[[Category:Hepatotoxicity, Acute]]
 
[[Category:Hepatotoxicity, Acute]]
    
[[Category:To_Do_-_Caz]]
 
[[Category:To_Do_-_Caz]]
 
[[Category:Dog]][[Category:Cattle]][[Category:Birds]]
 
[[Category:Dog]][[Category:Cattle]][[Category:Birds]]
[[Category:To_Do_-_Review]]
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[[Category:Expert_Review]]
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