Biochemical Aspects of Cobalt Deficiency in Sheep with Special Reference to Vitamin Status and a Possible Involvement in the Aetiology of Cerebrocortical Necrosis

Abstract

SUMMARY The development of cobalt deficiency in sheep was best indicated by low plasma vitamin B12 levels, loss of appetite and elevated blood pyruvate. The susceptibility of cobalt-deficient animals to infection was attributed to an induced vitamin C deficiency and evidence was obtained of thiamine deficiency in the advanced cobalt-deficient state despite faecal thiaminase not usually being detected until near the terminal stages of cerebrocortical necrosis. Faecal thiaminase activity was inversely related to erythrocyte transketolase activity. Cobalt supplementation was effective in preventing the development of these vitamin deficiencies and of cerebrocortical necrosis.