Caprine hepatic lipidosis induced through the intake of low levels of dietary cobalt Eugene H. Johnson a, * , Khalid Al-Habsi a , Evelyn Kaplan b , Anandarajah Srikandakumar a , Isam T. Kadim a , Kanthi Annamalai a , Rashid Al-Busaidy a , Osman Mahgoub a a Department of Animal and Veterinary Sciences, College of Agricultural and Marine Sciences, P.O. Box 34, Al-Khod 123, Muscat, Sultanate of Oman b Department of Pathology, College of Medicine and Health Sciences, P.O. Box 35, Al-Khod 123, Muscat, Sultanate of Oman Accepted 3 October 2003 Abstract Forty-one, 10-week-old newly weaned goats were randomly allocated into two groups, namely control (n ¼ 22) and treated (n ¼ 19). Kids in both groups were fed Rhodegrass hay ad libitum that contained <0.1 mg/kg DM cobalt and 150 g/day of a commercially prepared ruminant concentrate that contained approximately 0.12 mg/kg DM cobalt. This diet provided the minimum daily requirement of cobalt as specified for sheep. The treated goats were supplemented with bi-monthly subcutaneous injections of 2000 lg of hydroxycobalamin. All goats were weighed and blood samples collected monthly for haematological, clinical biochemical and serum vitamin B 12 analysis. After a 10-month experimental period the goats were slaughtered. The control animals exhibited significantly (P < 0:05) lower weight gains, and had dry scruffy hair coats. In addition, there was a decline in erythrocyte counts, mean haemoglobin, packed cell volume, mean corpuscular volume, mean corpuscular haemoglobin and mean corpuscular haemoglobin concentration. Controls also exhibited significantly (P < 0:05) lower levels of total serum proteins and elevated levels of serum alkaline phosphatase compared to treated goats. Fourteen (63.6%) of the control goats de- veloped pathology consistent with reported field cases of hepatic lipidosis associated with low liver levels of cobalt. Only one (5.3%) of the treated goats developed hepatic lipidosis. Contrary to previous reports that suggested that goats are less sensitive to low levels of dietary cobalt than sheep, it is apparent that this is not the case with Omani goats. This is the first report of the induction of hepatic lipidosis in goats due to feeding low levels of cobalt in their diet. Ó 2003 Elsevier Ltd. All rights reserved. Keywords: Goats; Liver; Hepatic lipidosis; Cobalt; Vitamin B 12 1. Introduction Cobalt is an essential component of vitamin B 12 . Consequently, diets containing inadequate amounts of cobalt result in vitamin B 12 deficiencies. In sheep, vita- min B 12 deficiencies result clinically in signs of anaemia, weight loss, poor production, and photosensitivity (Ulvund and Pestalozzi, 1990). In addition, diets defi- cient in cobalt have been described in sheep to cause fatty hepatic degeneration that has been termed ovine white liver disease (OWLD) (Sutherland et al., 1979; Mitchell et al., 1982; Mcloughlin et al., 1984; Richards and Harrison, 1981; Ulvund, 1990a). Classically, these livers are described grossly as being pale and friable and histopathologically as having accumulation of lipid droplets and lipofucsin in hepatocytes, hepatocyte ne- crosis and biliary hyperplasia (Kennedy et al., 1994). Goats, for unknown reasons have been described as being less sensitive to low levels of dietary cobalt (Clark et al., 1986; Mburu et al., 1993). Consequently, there is little information available pertaining to the clinical and pathological consequences of vitamin B 12 deficiencies in this species. In Oman, hepatic lipidosis has been described as the most commonly occurring liver pathology in goats The Veterinary Journal 168 (2004) 174–179 The Veterinary Journal www.elsevier.com/locate/tvjl * Corresponding author. Tel.: +968-515-234; fax: +968-513-418. E-mail address: ejohnson@squ.edu.om (E.H. Johnson). 1090-0233/$ - see front matter Ó 2003 Elsevier Ltd. All rights reserved. doi:10.1016/j.tvjl.2003.10.012