Abstract
Ovine hepatic fatty cirrhosis (HFC) was found to be a noninfectious chronic progressive disease of the liver, characterized macroscopically by various amounts of fatty degeneration, cirrhosis and compensatory hypertrophy. The disease occurred in five West Texas counties and was clinically characterized by a long subclinical course, gradual weight loss, ascites, emaciation, debilitation and hepatic coma. Microscopically, the affected hepatocytes underwent a sequence of pathological changes described as follows: cytoplasmic distension with small lipid droplets, coalescence of the small lipid droplets to form large lipid spherules, rupture of cytoplasmic septa between contiguous hepatocytes by intracellular pressures apparently due to enlarging lipid spherules, formation of fatty cysts around large lipid spherules, dissolution of fatty cysts, condensation of hepatic reticulin and proliferation of fibrous connective tissue. Ceroid was found in the liver, lung, spleen and the hepatic and posterior mediastinal lymph nodes. The fundamental lesion of HFC was an abnormal accumulation of intrahepatocytic lipid with fibrosis apparently occurring only when the amount of accumulated lipid was enough to rupture hepatocytes and form fatty cysts. The relationship between the pathological lesions of HFC and nutritional cirrhosis was revolved. ...
Adams, Leslie Garry (1968). A morphological and biochemical study of the pathogenesis of ovine hepatic fatty cirrhosis. Texas A&M University. Texas A&M University. Libraries. Available electronically from
https : / /hdl .handle .net /1969 .1 /DISSERTATIONS -171487.