Cerebrocortical necrosis in ruminants: Occurrence of thiaminase in the gut of normal and affected animals and its effect on thiamine status

Abstract

In 6 sheep affected with CCN, thiaminase activity was higher than 16 units in both faeces and rumen liquor. In 4 of 19 healthy sheep thiaminase activity was high in both faeces and rumen liquor. In healthy animals, faecal thiaminase activity was higher than 16 units in 10 out of 52 calves, 7 out of 26 steers and one out of 18 goats, Faecal thiaminase activity was relatively low in 25 horses and 14 cows. The faecal thiaminase activity of lambs at pasture fluctuated with time. There was a significant negative correlation between faecal thiaminase and thiamine status as assessed by blood transketolase apoenzyme and thiamine pyrophosphate (TPP) effect. It was confirmed that sheep affected with CCN had a thiamine deficiency as indicated by reduced blood transketolase holoenzyme and increased TPP effect. Four of 6 sheep with CCN recovered following thiamine treatment and whole blood transketolase activity returned to normal. Thiamine or TPP treatment also produced a decrease in blood transketolase apoenzyme and a decrease in TPP effect in normal healthy sheep. In vitro studies showed that thiaminase only caused rapid destruction of thiamine when a second substrate (co-substrate) was added. The fact that nicotinic acid is a co-substrate suggests that thiaminase can cause depletion of both these vitamins. A number of drugs commonly used as anthelmintics or tranquillizers were also found to be active as second substrates.