Hepatic Lipidosis Associated with Cobalt De¢ciency in Omani Goats E.H. Johnson 1* , D.E. Muirhead 2 , K. Annamalai 1 , G.J. King 3 , R. Al-Busaidy 1 and M. Shahul Hameed 1 1 Sultan Qaboos University, College of Agriculture, Department of Animal and Veterinary Sciences, PO Box 34, Al-Khod 123, Muscat; 2 Department of Pathology, PO Box 33, Al- Khod 123, Muscat, Sultanate of Oman and 3 Diwan of Royal Court *Correspondence Johnson, E.H., Muirhead, D., Annamalai, K., King, G.J., Al-Busaidy, R. and Shahul Hameed, M., 1999. Hepatic lipidosis associated with cobalt de¢ciency in Omani goats. Veterinary Research Communications, 23(4), 215^221 ABSTRACT Livers from 36 of 684 (5.3%) apparently healthy goats examined at an abattoir in the greater Muscat area of Oman exhibited gross pathological ¢ndings characterized by extremely pale, friable, fatty livers encompassing the entire organ. Histopathologically, di¡use hepatic lipidosis and occasional bile duct proliferation were observed. Periodic acid^Schi¡-positive, diastase-resistant pigment was observed in the macrophages lining the sinusoids. These histopathological lesions were consistent with those characteristic of ovine white liver disease. Cobalt analysis revealed that normal livers had six times more cobalt and a 3-fold less fat content than those measured in the fatty livers. This is the ¢rst report of an association between cobalt de¢ciency and hepatic lipidosis in Omani goats. Keywords: cobalt de¢ciency, fat, goats, lipidosis, liver Abbreviations: dm, dry matter; ppm, parts per million INTRODUCTION The pathogenesis of hepatic lipidosis has been well characterized in large ruminants. It is generally associated with a negative energy balance induced by lactation, fetal growth, reduced feed intake, environmental chilling or disease. According to Pearson and Mass (1996), hepatic lipidosis occurs when the rate of hepatic triglyceride formation exceeds the rate of oxidation of fatty acids and the formation and release of very low-density lipoproteins into the peripheral circulation from the hepatocytes. In sheep, cobalt or vitamin B 12 de¢ciency may result in a clinical syndrome termed white liver disease that is characterized by severe ill-thrift, photodynamic dermatitis and hepatic lipidosis (Sutherland et al., 1979; Black et al ., 1988). Cobalt is an essential component of vitamin B 12 and its de¢ciency in sheep results in a variety of clinicopathological abnormalities that are closely associated with ine¤cient metabolism of propionate (Marston et al ., 1961). Propionate, produced in the rumen, is metabolized by the vitamin B 12 -dependent enzyme methylmalonyl-CoA mutase, via Veterinary Research Communications, 23 (1999) 215^221 # 1999 Kluwer Academic Publishers. Printed in the Netherlands 215