Ulvund M.J.: Ovine white-liver disease (OWLD) . Pathology. Acta vet. scand. 1990, 31, 309-324. -Microscopic liver changes could earliest be found after I month on OWLD pasture, and included extensive fatty change with large spherical vacuoles in hepatocytes, varying size of hepatocytes and nuclei, and formation of Councilman bodies. Later came ceroid deposits, biliary hyperplasia and mesenchymal proliferation . Changes occurred in all lambs which died or were killed due to OWLD, and altogether 83070 of the lambs grazing OWLD pastures showed typicalor suspect changes. Widespread haemosiderosis of the spleen was common. In severely affected lambs, sclerosis of the Peyer's patches and of the germinative centres of the intestinal lymph nodes were seen, as were neuronal atrophy and patchy microcavitation of areas in the brain stem. Four had polyvasculitis. Cobalt/vitamin B Il supplemented lambs showed no specific changes. Lambs which grew well on other pastures (H lambs), but which were subclinicallyCO/B I2 deficient some years, showed no fulminant hepatic OWLD, but 15% developed some features seen in OWLD. They showed no extensive fatty change. Results indicate that OWLD is a manifestation of B Il deficiency worsened by factors triggering early hepatic fatty change resulting in a more severe liver damage with loss of intracellular homeostasis rendering the hepatocytes vulnerable to other elements, like copper. sheep; cobalt/vitamin BI2 deficiency.