HEPATIC-DYSFUNCTION AND PHOTODERMATITIS SECONDARY TO ALSIKE CLOVER POISONING

A 22-year-old Appaloosa mare was presented for evaluation of mild coli c of 2 days' duration and severe icterus. Marked icterus of the sclera and oral and vulvar mucous membranes as well as dermatitis of the muz zle and distal vulva were noted on physical examination. No signs of d epression or abnormal behavior were observed. Clinicopathologic data i ncluded a normal hemogram, increased serum hepatocellular and cholesta tic enzyme activity, hyperbilirubinemia (with increased direct- and in direct-reacting bilirubin), increased serum bile acids, and bilirubinu ria. Histopathology of liver biopsy demonstrated hepatocellular degene ration and necrosis, hepatocellular regeneration, bile duct proliferat ion, and periportal fibrosis. Treatment was instituted to support live r function and to prevent progression of the photodermatitis and devel opment of hepatoencephalopathy. Examination of the pasture grazed by t he horse demonstrated a luxuriant growth of alsike clover with little other edible vegetation. A diagnosis of alsike clover poisoning was ma de. Although the toxic principle of the disease is not yet determined, alsike clover poisoning is considered to be a specific disease entity that caused the observed hepatic dysfunction and photodermatitis.