Vitamin A deficiency would not be expected for dogs or cats in the wild because they are carnivorous and usually consume sufficiently large quantities of the vitamin from organ meats (particularly liver), which can be stored during periods of inadequate consumption.
Generally domesticated cats and dogs are not deficient in vitamin A. However, storage or reserves may be low in cases such as steatorrhea, chronic liver disease or chronic enteritis, where absorption is depressed while turnover of intestinal epithelium is increased. On the other hand, they must start as pups or kittens without any stores, since placental transport is low, and steadily accumulate these reserves without appreciable interruption to have an adequate supply for brief episodes of stress or for pregnancy and lactation (Ralston Purina, 1987). An early, rich source of vitamin A is colostrum. Thus, orphaned kittens and pups should be supplemented until they can consume an adequate supply in their diet.
Vitamin A assimilation is decreased, and its utilization is increased, by infection (Nockels, 1988). Aflatoxin ingestion has also been reported to reduce vitamin A stores in the liver and induce its deficiency. Chickens evidenced decreased tissue accumulation of oxycarotenoid pigments when fed aflatoxin. It is therefore important that pets that are sick or are receiving vitamin A antagonists receive diets that are fortified with the vitamin.
Supplementation of pet foods would be particularly essential if vitamin A-rich organ meats (particularly liver and kidney) were not part of the diets. For cats, fish by-products (e.g., fish liver oils) could be an important source of vitamin A. Lacking the capability to convert carotene to vitamin A, cats need preformed vitamin A (vitamin A from commercial synthesis or animal origin) to meet their requirement (Gershoff et al., 1957a).
Several factors can influence the loss of vitamin A from feedstuffs during storage. Stabilized vitamin A (e.g., beadlets) is not easily destroyed in a vitamin mix, but there is only a 58% retention when the vitamin premix also contains choline and trace minerals (Coelho, 1991). The trace minerals in feeds and supplements, particularly copper, are detrimental to vitamin A stability. Dash and Mitchell (1976) reported the vitamin A content of 1,293 commercial feeds over a three-year period. The loss of vitamin A was over 50% in one year's time. Vitamin A loss in commercial feeds was evident even if the commercial feeds contained stabilized vitamin A supplements.
Vitamin A and carotene destruction also occurs from processing of feeds with steam and pressure. Pelleting effects on vitamin A in feed are caused by die thickness and hole size, which produce frictional heat and a shearing effect that can break supplemental vitamin A beadlets and expose the vitamin. In addition, steam application exposes feed to heat and moisture. Running fines back through the pellet mill exposes vitamin A to the same factors a second time. Between 30% and 40% of vitamin A present at mixing may be destroyed during pelleting (Shields et al., 1982).
Most supplemental vitamin A used today for animals is administered orally in a product form that blends uniformly in dry feed. However, in a time of need, an intramuscular injection of the vitamin is probably the surest route of administration, especially if food consumption is depressed or the animal suffers from malabsorption.
Because of the poor stability of vitamin A, particularly when exposed to oxygen, trace minerals, pelleting, feed storage and other factors, the feed industry has readily accepted the dry, stabilized forms of the vitamin. The stability of vitamin A in pet foods has been improved in recent years by chemical stabilization as an ester and by physical protection using antioxidants, emulsifying agents and stabilized materials, including gelatin, crosslinked gelatin and sugar in spray-dried beadlet, or prilled products (Bauernfeind and DeRitter, 1972; Shields et al., 1982). Stabilized and protectively coated (or beaded) forms of vitamin A slow destruction of the vitamin but for highest potency fresh supplies of the mixture should be available on a regular basis. Practical considerations that affect vitamin A stability are listed in Table 1. The gelatin beadlet in which the vitamin A ester (palmitate or acetate) is emulsified into a gelatin-plasticizer-antioxidant viscous liquid formulation and spray-dried onto discrete dry particles results in products with good chemical stability, good physical stability and excellent biological availability (Bauernfeind and DeRitter, 1972).
