29 05 2011





Aflatoxins are potent hepatotoxic and hepatocarcinogenic agents produced primarily by strains of the fungus Aspergillus.  Foodstuff may be contaminated with aflatoxins in the field or after harvest during storage and processing.


There have been many reports since the early 1960’s concerning aflatoxin toxicity in many species including dogs which have been found to be highly susceptible.


The vulnerability of dogs to acute and subacute licver disease in response to aflatoxins might reflect their inherently lower hepatocullurar concentration of glutathione (GSH), compared with other species, and perhaps their individual differences in activity of GSH-S-transferase.


Clinical signs in the dog include anorexia, lethargy, vomiting jaundice, diarrhea (melena, hematochezia), followed by abdominal effusion, peripheral edema, and terminal encephalopathy with hemorrhagic diathesis.  Approximately 10% of dogs died acutely with no recognized anticendent illness.


Common clinicopathologic features included coagulopathic and electrolyte disturbances, hypoproteinemia, increased serum liver enzyme activities, hyperbilirubinemia, and hypocholesterolemia.  Oncytology hepatocellular lipid vacuolation was evident.  Cylindruria consistently predicted death


The best early indicators of aflatoxicosis in the dog are low plasma activities of anticoagulant proteins (protein C, antithrombin) and hypocholesterolemia.


Treatment is directed at providing supportive care while the source of the toxin is eliminated.


To replenish systemic and hepatic GSH, hepatic supportive care with thiol donors was provided for 2 months following initial diagnosis.  N-acetylcysteine was given IV initially as the thiol donor, but changed to oral administration of s-adenosylmethionine when dogs could tolerate it.  Antiemetics were used to combat persistent vomiting or nausea.  Gastric atony may occur any does not respond to any form of antiemetic or prokinetic treatment.


Milk thistle (silybin) was administered because it is considered to be hepatic protective.  Blood-component treatment and vitamin K1 were administered to curtail concurrent coagulopathies.






“Diagnosis of Aflatoxicosis”.  Antech Diagnostics News. December 2008. P. 2.








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