Thiamin requirements are difficult to establish in ruminants because of rumen and likely, intestinal synthesis. However, synthesis in the intestine may not be important, as most of it apparently occurs in the lower intestinal tract where absorption of thiamin is limited.
Animals with a functional rumen are generally considered to have no dietary thiamin requirement because of rumen microbial synthesis. However, thiamin deficiency can be produced in lambs and calves and other young ruminants that do not have a functional rumen. Thiamin-responsive polioencephalomalacia occurs in cattle and sheep with functional rumens. Acute thiamin deficiency has been produced in calves and lambs by feeding a thiamin-free diet (Drapper and Johnson, 1951; Benevenga et al. 1966). The estimated requirement for the dairy calf is 65 µg per kg (29.5 µg per lb) of body weight or 6.5 mg per kg (3.0 mg per lb) of milk replacer powder (NRC, 1989).
Thiamin deficiency in the young ruminant can be produced as late as the sixth week of life. Gastrointestinal (GI) synthesis of thiamin becomes significant in calves from about the sixth week of life on, but this synthesis is still relatively poor from weaning tip to five months of age (Zintzen, 1974). The GI-synthesis of thiamin is enhanced by readily fermentable carbohydrates and by nitrogen sources such as urea. Concentration of thiamin in the gastrointestinal tract, especially in the rumen, is more uniform than in feed. Thiamin synthesis appears to vary inversely with feed thiamin concentration, suggesting some type of feedback regulation of rumen thiamin synthesis (Zintzen, 1974).
In steers, Miller et al.(1986a, b) reported little effect of either ration concentrate level, antibiotic or ionophore feeding on thiamin synthesis or absorption. Duodenal thiamin concentration increased with increasing thiamin intake. There was also an increase in rumen disappearance of thiamin with increasing intake.
Thiamin requirement rises as consumption of carbohydrate does (Benevenga et al., 1966). When dietary thiamin is deficient, body reserves are depleted more rapidly in animals fed a high carbohydrate diet than in those fed a diet high in fat and protein. The "thiamin-sparing" effect of fat and protein has long been known. Inadequate nitrogen in the ration of lactating cows may decrease thiamin synthesis in the rumen and the amount of thiamin entering the duodenum (Breves et al., 1984).
Metabolic body size, genetics and metabolic state can affect the thiamin requirements. Infectious and parasitic diseases also increase thiamin requirements. When dietary thiamin is marginal, typical deficiency signs of thiamin are more likely to develop in infected animals than in normal animals. Endoparasites, such as strongylids and coccidia, compete with the host for thiamin contained in feed. In poultry blood, thiamin is reduced in experimentally produced coccidiosis. Blood thiamin concentrations were inversely correlated to the severity of infection (McManus and Judith, 1972). Therefore circumstantial evidence suggests that young ruminants heavily infested with coccidia and being treated with amprolium should receive supplemental thiamin as a precautionary measure.
Thiamin requirements are increased if the diet contains thiaminase activity. Spoiled and moldy feeds may contain thiaminases. Fusarium molds produce thiaminase (Fritz et al., 1973). High dietary intakes of sulfur (Gooneratne et al., 1989; Kandylis, 1984), especially combined with low copper status (Olkowski et al., 1991), as well as substances in tall fescue (Festuca arundinacea) (Edwin et al., 1968; Lauriault et al., 1990) are antagonistic to thiamin, resulting in higher dietary requirements. These conditions are discussed further in the section on thiamin deficiencies.
