The thiamin content of most common feeds should be three to four times greater than requirements for most species (Brent, 1985). However, this would not be true for cats, mink, fox, and other carnivores, which have a higher requirement for the vitamin. Under normal feeding and management conditions, and in the absence of antimetabolites, thiamin deficiency should theoretically not occur in either dogs or cats. Nevertheless, utilization of available thiamin in feedstuffs may be limited and may also be impaired by thiamin antagonists.
Clinical cases of thiamin deficiency in cats and dogs have been associated with feeding of either canned commercial foods or raw fish. With cats, it should be borne in mind that cats like fish and that tinned cat foods often contain fish. The quantity of thiaminase may be sufficient to destroy even thiamin added to the food as a supplement (Br”unlich and Zintzen, 1976). Five cases of thiamin deficiency in cats prompted a Canadian group of researchers (Loew et al., 1970) to investigate tinned cat foods bought on the open market. They found that not only fish-based foods but also foods based on liver, beef and poultry meat contained extremely low concentrations of thiamin and were responsible for the occurrence of the thiamin deficiency signs.
Thiamin is readily destroyed by heat, especially under neutral or alkaline conditions, and extensive losses may occur in canned cat and dog foods during processing and storage (Baggs et al., 1978). Losses of 74% of thiamin have been reported for some canned dog foods due to retorting and storage for 14 days (Hoffmann-La Roche, 1981). Since naturally occurring clinical cases of thiamin deficiency in dogs and cats attributed to thermal destruction of thiamin in meat have been reported, intake of thiamin should, therefore, be calculated from analyses of diets taken at the time of consumption.
This destruction of thiamin has important implications in the feeding of cats and dogs, as sulfur dioxide-treated meat can induce a thiamin-deficient state when fed alone or mixed with thiamin-replete commercial pet foods. Although legislation in many countries prohibits the use of sulfur dioxide in human foods, nutritionists and producers should be aware of the health risks that these treated meats pose to cats and dogs (Studdert and Labuc, 1991).
For pet foods, thiamin is a particularly important vitamin from the aspect of dietary formulation because it is progressively destroyed by cooking and various antagonists, particularly thiaminases, which are found in a number of foods, particularly raw fish. Thiaminases are themselves inactivated by heat so the maintenance of an adequate thiamin intake must take all of these various factors into consideration. For commercially prepared dog and cat foods, the normal practice is to supplement with a large enough quantity before processing so that even if particularly serious losses occur, the amount remaining in the finished product will still meet or exceed the dietary recommendations.
Treatment of dogs and cats with thiamin deficiency includes elimination of raw fish or other antagonists from the diet, feeding a well-balanced, commercial pet food, and thiamin therapy. Thiamin should be administered intravenously or subcutaneously at a dose of 75 to 100 mg twice daily until neurological signs subside (Loew et al., 1970; Case et al., 1995). Oral thiamin supplementation should also be administered for several months following the initial clinical episode (Houston and Hulland, 1988). In most affected pets, these clinical signs will decrease within several days. However, if severe neurological damage has occurred, the pet may never make a full recovery. A permanent intolerance of physical exercise and some degree of persistent ataxia occasionally occur in animals that have recovered from thiamin deficiency (Case et al., 1995).
Most commercial therapeutic diets designed for animals with cardiac disease contain increased levels of water-soluble vitamins to offset potential urinary losses. For example, dogs and cats receiving furosemide have increased urinary loss of water-soluble vitamins. Humans treated with furosemide have developed thiamin deficiency (Freeman et al., 1998).
Stability of thiamin in feed premixes can be a problem. More than 50% of the thiamin was destroyed in premixes after one month at room temperature (Verbeeck, 1975). When thiamin was observed in premixes without minerals, no losses were encountered when kept at room temperature for six months. When the minerals were supplied as sulfates, the losses of thiamin were greatly increased. After six months, only 27% of the activity of thiamin hydrochloride remained in a vitamin premix that also contained choline and trace minerals (Gadient, 1986).
