Abstract
In an attempt to clarify the reported relationship between cobalt deficiency and the incidence of cerebrocortical necrosis (CCN), sheep were fed on a diet deficient in cobalt. High levels of thiaminase activity were found regularly in rumen and faeces samples from cobalt-deficient animals, and also from controls supplemented with cobalt or vitamin B12. There was a poor correlation between thiaminase activity and viable counts of the thiaminase-producing organisms Clostvidium spovogenes and Bacillus spp. Urinary excretion of thiamine appeared normal. When the sheep were killed, normal concentrations of thiamine were found in the liver. The sheep were deficient in vitamin B12, as judged by the concentrations in serum and liver, by urinary excretion of methylmalonic acid, and by clinical condition. Twitching and weakness were observed, but clinical signs of CCN did not develop.
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