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==History and Clinical Signs==
 
==History and Clinical Signs==
 
History of drinking from stagnant water source.
 
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.
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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 and lymph nodes and gall bladder may show congestion.  
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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.  
Inflammatory and congestive changes in the gastrointestinal tract may also be present.
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Inflammatory and congestive changes as well as the presence of clumps of algae may be present in the gastrointestinal tract.
    
==Mechanism of toxicity==
 
==Mechanism of toxicity==
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==Treatment==
 
==Treatment==
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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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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.  
 
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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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.
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==References==
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Andrews., A.H, Humphreys., D.J (1982) Poisoning in Veterinary Practice. NOAH
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3rd YEAR BVetMed,Alimentary Module,Toxicology (2007).p 22 RVC lecture notes
     
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