Clinical and clinicopathologic features of dogs that consumed foodborne hepatotoxic aflatoxins: 72 cases (2005-2006).
OBJECTIVE
To characterize clinical signs, clinicopathologic features, treatments, and survival in dogs with naturally acquired foodborne aflatoxicosis.


METHODS
Retrospective case series.


METHODS
72 dogs that consumed aflatoxin-contaminated commercial dog food.


METHODS
Medical records of affected dogs were reviewed. Between December 2005 and March 2006, dogs were identified as having foodborne aflatoxin hepatotoxicosis on the basis of the history of consumption of contaminated food or characteristic histopathologic lesions (subject dog or a recently deceased dog in the same household or kennel). Recorded information included signalment, clinical features, clinicopathologic test results, treatments, and survival. Data were analyzed by survival status.


RESULTS
Most dogs were of large breeds from breeding kennels. No significant differences were found in age or weight between 26 (36%) survivor dogs and 46 (64%) nonsurvivor dogs. Severity of clinical signs varied widely; 7 dogs died abruptly. In order of onset, clinical features included anorexia, lethargy, vomiting, jaundice, diarrhea (melena, hematochezia), abdominal effusion, peripheral edema, and terminal encephalopathy and hemorrhagic diathesis. Common clinicopathologic features included coagulopathic and electrolyte disturbances, hypoproteinemia, increased serum liver enzyme activities, hyperbilirubinemia, and hypocholesterolemia. Cytologic hepatocellular lipid vacuolation was confirmed in 11 dogs examined. In comparisons of clinicopathologic test results between survivor and nonsurvivor dogs, only granular cylindruria (7/21 dogs) consistently predicted death. Best early markers of aflatoxicosis were low plasma activities of anticoagulant proteins (protein C, antithrombin) and hypocholesterolemia. Despite aggressive treatment, many but not all severely affected dogs died.


CONCLUSIONS
Serum liver enzyme activities and bilirubin concentration were unreliable early markers of aflatoxin hepatotoxicosis in dogs. Hypocholesterolemia and decreased plasma protein C and antithrombin activities may function as exposure biomarkers.
Dereszynski
Diane M
DM
Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA.
Center
Sharon A
SA
Randolph
John F
JF
Brooks
Marjory B
MB
Hadden
Alice G
AG
Palyada
Kiran S
KS
McDonough
Sean P
SP
Messick
Joanne
J
Stokol
Tracy
T
Bischoff
Karyn L
KL
Gluckman
Stuart
S
Sanders
Sara Y
SY
D000348:Aflatoxins / Q000032:analysis; D000821:Animal Feed / Q000032:analysis; D000818:Animals; D000991:Antithrombins / Q000378:metabolism; D015415:Biomarkers / Q000097:blood; D002784:Cholesterol / Q000097:blood; D004283:Dog Diseases / Q000097:blood / Q000401:mortality / Q000473:pathology*; D004285:Dogs; D005260:Female; D005506:Food Contamination / Q000032:analysis; D005517:Foodborne Diseases / Q000097:blood / Q000401:mortality / Q000473:pathology / Q000662:veterinary*; D008099:Liver / Q000201:enzymology / Q000473:pathology*; D008297:Male; D011486:Protein C / Q000378:metabolism; D012189:Retrospective Studies; D016019:Survival Analysis; D000096702:Aflatoxin Poisoning
D000348:Aflatoxins; D000991:Antithrombins; D015415:Biomarkers; D011486:Protein C; D002784:Cholesterol