Four “miniature” piglets were fed a commercial complete combined diet to which had been added 0.55×0.60 ppm of aflatoxin B1 for 122 consecutive days. They showed transitory anorexia and discharge of hard feces, and a slight delay in growth. At autopsy, liver, spleen, and kidney increased in weight. The liver was enlarged and faded a little.Histopathologically, the liver was affected with early formation of pseudolobules, enlarged lobules, deposition of brownish yellow pigment in hepatic cells and sinusoids, central or fascicular necrosis of lobules, inequality in size of hepatic cells, appearance of cells with a large nucleus, thickening of interstitial tissue, septal formation, hyperplasia of bile ducts, and formation of pseudobile ducts. In addition, cells with a large nucleus appeared in the epithelia of uriniferous tubeles and ovarian follicles underwent cystic degeneration.From these results it was presumed that the present collective outbreak of hepatic cirrhosis in Saitama Prefecture might have been caused by feeding a diet containing aflatoxin produced by Astergillus flavus.