Clinico-pathological studies on thiamine deficiency, especially on experimental cerebrocortical necrosis in calves and sheep

Biochemical and pathological changes, and their relationship to clinical signs were observed in experimental cerebrocortical necrosis (CCN) and the spontaneous cases. Calves and sheep given with amprolium, a thiamine antagonist, showed abnormal electroencephalograms (EEG) and following neurological signs, and died. They were pathologically confirmed as CCN. Thiamine levels in blood and tissues were markedly reduced at death. Blood thiamine concentration and erythrocyte transketolase (ETK) activity decreased significantly before the onset of abnormal EEG. Thiamine concentrations in blood and tissues were reduced significantly in amprolium-treated sheep, which were killed at various clinical stages. Brain histopathological lesions became to be severe and extensive toward death. After a thiamine medication ETK activity, blood pyruvate and glucose level returned to the normal range within 6 hours in sheep affected with amprolium-induced CCN. Pathological lesions were severe in. the brain of sheep, in which the medication was done at late stage. Spontaneous CCN calves were confirmed as thiamine deficiency. High thiaminase activity was detected in feces of the CCN cases.