The thiamin content of most common feeds is sufficient to exceed thiamin requirements of most species by three to four times, based on normal feed intakes (Brent, 1985). Under normal feeding and management conditions, and in the absence of anti-metabolites, thiamin deficiency should theoretically not occur in either young or adult ruminants. Nevertheless, utilization of available thiamin in feedstuffs may be limited and may also be impaired by thiamin antagonists. Likewise, high sulfur intakes pose a risk for PEM. Thiamin supplementation should be considered for ruminant animals that may potentially develop PEM as a result of consuming high-concentrate diets or high-sulfate water. Grazing ruminants normally would not receive supplemental thiamin unless evidence is provided that consumed pastures contain antagonists. An example would be thiamin supplementation for livestock grazing potentially toxic tall fescue pastures during midsummer when toxicosis is likely to be severe. Thiamin may be supplied to cattle at the daily rate of 1 g per head (Lauriault et al., 1990; Dougherty et al., 1991). Johnson and Krautmann (1989) reported that feeding 500 mg of thiamin per head per day for the first 30 days that cattle are in the feedyard reduced the effects of thermal stress.
Although little information is available on the direct addition of thiamin to finishing cattle diets, Brethour (1972) reported that in two trials, a combination of thiamin and sodium carbonate supplement increased feed intake by 5% and daily gain by 8%. In a third trial, thiamin administered alone produced an intermediate response to calves immediately after weaning. Supplemental thiamin at 956 mg per day was not beneficial to stressed beef steers or heifers in two experiments (Silzell and Kegley, 1998). Goetsch and Owens (1987) reported that feeding 1,000 mg per day supplemental thiamin to steers markedly reduced rumen organic matter digestion and total tract digestion of starch and crude protein. Therefore, 1,000 mg per day may be excessive supplementation for cattle not suffering obvious thiamin deficiency symptoms.
Recently, a series of three experiments tested the effects of supplemental thiamin in lactating dairy cows (Shaver, 1999). Cows were fed rations with varying proportions of alfalfa silage and corn silage, supplemented with corn-soy or corn byproduct grain mixtures. Thiamin, as thiamin mononitrate, was fed at 150 mg per day in the first trial and 300 mg per day in the latter two trials. There was a significant trend toward increased milk production in the first two experiments, while in the third trial thiamin decreased milk fat percentage and yield. Thiamin status may be marginal under certain conditions in high producing dairy cows.
Subclinical deficiencies of thiamin can result in reduced synthesis of other B vitamins because certain rumen bacteria require thiamin for growth. Mathison (1986) reported a feedlot trial in which a significant response to supplemental thiamin was observed and transketolase activity was numerically reduced in the controls. Thiamin did not increase gain in two subsequent trials, although bloat apparently was reduced in one trial. In a concomitant field survey, conducted in Alberta, 2.7% of 645 beef cattle sampled were marginal in plasma thiamin pyrophosphate (TPP), the coenzyme for transketolase.
In acute PEM, 1,000 mg per day of injected thiamin is indicated until the animals resume eating, then 500 mg per day can be supplemented in the diet for 7 to 14 days (Mathison, 1986). Feeding 4 to 6 mg of thiamin per kg diet (1.8 to 2.7 mg per lb) has been suggested to help prevent subclinical thiamin deficiency in animals fed high-grain rations.
Animals with clinical signs of thiamin deficiency and (or) other indicators of insufficiency (i.e., reduced transketolase activity) should be rapidly treated with thiamin at therapeutic doses. Since thiamin deficiency causes anorexia, injection of the vitamin is preferred to the oral route in severe deficiency. Clinical signs in calves weighing less than 50 kg were prevented with 0.65 mg of thiamin hydrochloride per kg (0.30 mg per lb) of liquid diet fed at 10% of live weight (65 µg per kg or 29.5 µg per lb live weight) (Johnson et al., 1948). Treatment levels of thiamin for intravenous or intramuscular administration, for three-day periods, have been recommended for lambs and calves (100 to 400 mg per day) and for sheep and cattle (500 to 2,000 mg per day) (Zintzen, 1974).
For general maintenance following the treatment of mild cases of PEM, or as a prophylactic measure when a herd is at risk, 5 to 10 mg of thiamin should be added per kg of dry feed (2.3 to 4.5 mg per lb). Feeds should be supplemented with thiamin such that animals receive 100 to 500 mg daily. Likewise, roughage should be added to the daily diet at the rate of 1.5% of body weight. Smith (1979) has suggested an oral dose of 6.6 to 11 mg per kg body weight, repeated every six hours for 24 hours, for PEM therapy in goats.
The administration of thiamin to PEM animals generally produces rapid results, sometimes within hours. Where recognition of the disease has been delayed and irreversible necrosis has already developed in the brain, treatment with thiamin may be useless. The prognosis for recumbent animals is generally poor. Although treatment usually improves the condition of such animals, relapses and permanent damage are probable since irreversible changes will have occurred in the central nervous system.
Without doubt, PEM is the most important thiamin deficiency disease in ruminants. However, it is noteworthy that thiamin can also be used effectively as supportive treatment of the metabolic disorders rumen acidosis and ketosis (Harmeyer and Kollenkirchen, 1989). Even though treatment with thiamin can be therapeutically successful, it does not follow that a deficiency of thiamin contributes to the etiology of these two diseases (Zintzen, 1974).
Thiamin sources available for addition to feed are the hydrochloride and mononitrate salts. Because of its lower solubility in water, the mononitrate is preferred for addition to premixes. The mononitrate has somewhat better stability characteristics in dry products than the hydrochloride (Bauernfeind, 1969).
Stability of thiamin in premixes should be monitored. More than 50% of the thiamin was destroyed in vitamin-mineral premixes after one month at room temperature (Verbeeck, 1975). When thiamin was stored in premixes without minerals, no losses were encountered when kept at room temperature for six months. Choline in addition to trace minerals accelerates degradation of thiamin in premixes.
