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 studie d to determine the pattern of lesion development. All sheep developed lesions of HFC. Grossly, changes first began in the subcapsular hepati c parenchyma along the porta hepatis and spread peripherally until, in the final stages of the disease, approximately 80% of the liver was a ffected. Ascites, hydropericardium, and acquired hepatic vascular shun ts were present in sheep with severe HFC. Light microscopic lesions in itially appeared as accumulations of fine lipid droplets in the cytopl asm of periacinar hepatocytes but, with time, involved all hepatocytes of the lobule. The fat vacuoles in the periacinar hepatocytes coalesc ed to form larger vacuoles; and after rupture of adjacent fat-laden he patocytes, fatty cysts appeared. Fibrosis began in the periacinar zone associated with the ruptured fatty cysts and continued until there wa s widespread bridging periacinar fibrosis. Islands of regenerating hep atocytes were frequently sequestered within the bands of fibrous tissu e. Characteristically, the hepatic and posterior mediastinal lymph nod es, lung, and spleen contain ceroid. No lesions of hepatic encephalopa thy were found in any animal. HFC is a progressive, chronic disease of sheep, and the morphology of the hepatic lesions is similar to lipotr ope-deficient forms of nutritional cirrhosis. These findings are discu ssed in relation to similar nutritional deficiencies and toxicoses in sheep.