Difference between revisions of "Blue-Green Algae Toxicity"

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Also know as: '''''Cyanobacteria toxicity
 
  
==Introduction==
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==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 [[Algal Bloom|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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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.
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==Signalment==
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==Diagnosis==
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Test water for 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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Althouh non-specific, a biochemical profile suggests hepatotoxicity with increases in ALT, AST and ALKP.
  
 
==History and Clinical Signs==
 
==History and Clinical Signs==
History of drinking from stagnant water source.
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History of drinking from stagnant water.
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.
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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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==Pathology==
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Petechiae in the heart.
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Congestion of the lungs, liver, mesenteric vessels and lymph nodes.
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Inflammatory and congestive changes in the gastrointestinal tract.
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Swollen liver, centrilobular necrosis and oedema of the gallbladder.
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Confirmatory tests:
 +
 
 +
==Treatment==
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There is no specific anti-dote.
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With a history of recent ingestion, gastric decontamination can be performed unless there is evidence of impaired neurological status.
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Detoxifixation and supportive treatment for the diarrhoea, dehydration, shock and hepatic insufficiency.
 +
Keep animals away from infected water.
 +
Add algicides such as copper sulphate to the water.
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Prognosis:
 +
 
 +
 
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==Prognosis==
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Poor. Dependent on the degree of liver damage and quantity ingested. Prompt treatment is essential.
 +
 
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==Hepatotoxicity==
  
==Diagnosis==
 
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.
 
  
==Pathology==
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====Clinical====
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*prostration and death
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*perhaps convulsions
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*gastroenteritis in lesser cases
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====Gross====
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*haemorrhagic gastroenteritis
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*massive or periacinar hepatic necrosis
  
Inflamed 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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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==
  
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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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.  
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==
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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. 
  
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 sources.
 
  
==Prognosis==
 
Poor. Dependent on the degree of liver damage and quantity ingested. Prompt treatment is essential.
 
  
{{Learning
 
|literature search = [http://www.cabdirect.org/search.html?q=%28title%3A%28%22Blue+green+algae%22+%29+OR+title%3A%28cyanobacteria%29%29+AND+ab%3A%28toxicity%29 Blue-green algae toxicity]
 
|full text = [http://www.cabi.org/cabdirect/FullTextPDF/2007/20073098746.pdf '''Harmful cyanotoxins: hepatotoxic effects of microcystin in mammalian animals.''' Bownik, A.; Skowron´ski, T.; Polskiego Towarzystwa Nauk Weterynaryjnych, Lublin, Poland, Medycyna Weterynaryjna, 2007, 63, 5, pp 522-524, 30 ref. - '''Full Text Review''']
 
}}
 
  
== References ==
 
  
Andrews., A.H, Humphreys., D.J (1982) '''Poisoning in Veterinary Practice'''.'' NOAH ''
 
  
3rd Year BVetMed, Alimentary Module, Toxicology (2007). p 22 RVC lecture notes
 
  
  
{{review}}
 
  
{{OpenPages}}
 
  
[[Category:Hepatotoxicity,_Acute]] [[Category:Liver_Diseases_-_Dog]] [[Category:Liver_Diseases_-_Cattle]] [[Category:Alimentary Diseases - Birds]] [[Category:Expert_Review - Small Animal]][[Category:Expert Review - Farm Animal]]
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[[Category:Hepatotoxicity, Acute]]
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[[Category:To_Do_-_Clinical]]
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[[Category:To_Do_-_Caz]]
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[[Category:Dog]][[Category:Cattle]][[Category:Birds]]

Revision as of 12:11, 7 July 2010



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.

Signalment

Diagnosis

Test water for 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. Althouh non-specific, a biochemical profile suggests hepatotoxicity with increases in ALT, AST and ALKP.

History and Clinical Signs

History of drinking from stagnant water. 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

Petechiae in the heart. Congestion of the lungs, liver, mesenteric vessels and lymph nodes. Inflammatory and congestive changes in the gastrointestinal tract. Swollen liver, centrilobular necrosis and oedema of the gallbladder. Confirmatory tests:

Treatment

There is no specific anti-dote.

With a history of recent ingestion, gastric decontamination can be performed unless there is evidence of impaired neurological status. Detoxifixation and supportive treatment for the diarrhoea, dehydration, shock and hepatic insufficiency. Keep animals away from infected water. Add algicides such as copper sulphate to the water. Prognosis:


Prognosis

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

Hepatotoxicity

Clinical

  • prostration and death
  • perhaps convulsions
  • gastroenteritis in lesser cases

Gross

  • haemorrhagic gastroenteritis
  • massive or periacinar hepatic necrosis


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.