The lesions of hepatic fatty cirrhosis in sheep

During a natural outbreak of hepatic fatty cirrhosis (HFC) in western Texas, 500 2-6-year-old Rambouillet ewe sheep were sequentially studied to determine the pattern of lesion development. All sheep developed lesions of HFC. Grossly, changes first began in the subcapsular hepatic parenchyma along the porta hepatis and spread peripherally until, in the final stages of the disease, approximately 80% of the liver was affected. Ascites, hydropericardium, and acquired hepatic vascular shunts were present in sheep with severe HFC. Light microscopic lesions initially appeared as accumulations of fine lipid droplets in the cytoplasm of periacinar hepatocytes but, with time, involved all hepatocytes of the lobule. The fat vacuoles in the periacinar hepatocytes coalesced to form larger vacuoles; and after rupture of adjacent fat-laden hepatocytes, fatty cysts appeared. Fibrosis began in the periacinar zone associated with the ruptured fatty cysts and continued until there was widespread bridging periacinar fibrosis. Islands of regenerating hepatocytes were frequently sequestered within the bands of fibrous tissue. Characteristically, the hepatic and posterior mediastinal lymph nodes, lung, and spleen contain ceroid. No lesions of hepatic encephalopathy were found in any animal. HFC is a progressive, chronic disease of sheep, and the morphology of the hepatic lesions is similar to lipotrope-deficient forms of nutritional cirrhosis. These findings are discussed in relation to similar nutritional deficiencies and toxicoses in sheep.