plementation (53,000 IU vitamin A plus 400 mg ß-carotene) to dairy cows 6 weeks before dry off and 2 weeks after dry off influence the responsiveness of bovine neutrophils and lymphocytes (Tjoelker et al., 1988a,b).

Beef cattle requirements for vitamin A are 2,200 IU/kg dry feed for beef feedlot cattle; 2,800 IU/kg dry feed for pregnant beef heifers and cows; and 3,900 IU/kg dry feed for lactating cows and breeding bulls (Guilbert and Hart, 1935; Jones et al., 1938; Guilbert et al., 1940; Madsen et al., 1948; Church et al., 1956; Chapman et al., 1964; Cullison and Ward, 1965; Perry et al., 1965, 1968; Swanson et al., 1968; Kohlmeier and Burroughs, 1970; Meacham et al., 1970; Kirk et al., 1971; Eaton et al., 1972). These requirements are the same as those given in the sixth edition of this report (National Research Council, 1984); there has been no new research to determine requirements since then. An IU is defined as 0.300 µg of trans-vitamin A alcohol (retinol) or 0.550 µg of retinyl palmitate.

SIGNS OF VITAMIN-A DEFICIENCY

Vitamin-A deficiency results in tissue changes associated primarily with vision, bone development, and epithelial structure and maintenance. Signs of deficiency may be specific for vitamin-A deficiency or the clinical signs may be general.

Vitamin-A deficiency is most likely to occur when cattle are fed

  • high-concentrate diets;

  • bleached pasture or hay grown during drought conditions;

  • feeds that have received excess exposure to sunlight, air, and high temperature;

  • feeds that have been heavily processed or mixed with oxidizing materials such as minerals; and

  • feeds that have been stored for long periods of time.

Most susceptible are newborn calves deprived of colostrum and cattle unable to establish or maintain liver stores because of environmental or dietary stresses. Attempts to improve the vitamin-A status of the newborn calf by supplementing the dam’s diet have been successful, but very high levels of vitamin-A or carotene have been necessary (Branstetter et al., 1973). Deficiencies can be corrected by increasing carotene intake by adding to the diet fresh, leafy, high-quality forages, which contain large amounts of vitamin-A precursors and vitamin E, or by supplying vitamin-A supplements in the feed or by injection. Since inefficient conversion of carotene to vitamin A is often a part of the problem, administering preformed vitamin A is preferred when deficiencies are present. Injected vitamin A is more efficiently utilized than vitamin A provided in the diet (Perry et al., 1967; Schelling et al., 1975), possibly because of extensive destruction of the vitamin in the rumen and abomasum (Keating et al., 1964; Klatte et al., 1964; Mitchell et al., 1967).

Signs of vitamin-A deficiency include reduced feed intake, rough hair coat, edema of joints and brisket, lacrimation, xerophthalmia, night blindness, slow growth, diarrhea, convulsive seizures, improper bone growth, blindness, low conception rates, abortion, stillbirths, blind calves, abnormal semen, and other infections (Guilbert and Hart, 1935; Jones et al., 1938; Guilbert et al., 1940; Guilbert and Rochfort, 1940; Hart, 1940; Madsen and Earle, 1947; Madsen et al., 1948; Moore, 1957; Mitchell, 1967); however, only night blindness has proven unique to vitamin-A deficiency (Moore, 1939, 1941). Vitamin-A deficiency should be suspected when several of these symptoms are present. Clinical verification may include ophthalmoscopic examination, liver biopsy and assay, blood assay, testing spinal fluid pressure, conjunctival smears, and response to vitamin-A therapy.

SIGNS OF VITAMIN-A TOXICITY

Vitamin A has a wide margin of safety for use in ruminant animals. Ruminants appear to have a relatively high tolerance for vitamin A, presumably due in part to microbial degradation of vitamin A in the rumen (Rode et al., 1990). Extremely high concentrations of vitamin A can be toxic; however, toxicity is rarely a problem in livestock, unless unreasonably high concentrations are fed inadvertently (National Research Council, 1987).

Vitamin D

As a general term, vitamin D encompasses a group of closely related antirachitic compounds. There are two primary forms of vitamin D: ergocalciferol (vitamin D2), which is derived from the plant steroid, ergosterol; and cholecalciferol (vitamin D3), which is derived from the precursor 7-dehydrocholesterol and is found only in animal tissues or products.

Vitamin D is required for calcium and phosphorus absorption, normal mineralization of bone, and mobilization of calcium from bone. In addition, a regulatory role in immune cell function of vitamin D (1,25-dihydroxy D) has been suggested (Reinhardt and Hustmyer, 1987). Research in laboratory animals (DeLuca, 1974) indicates that before serving these functions, vitamin D must be metabolized to active forms.

Vitamin D is absorbed from the diet in the intestinal tract in association with lipids and the presence of bile salts. Once in the liver, one metabolite (25-hydroxy-vitamin-D3) is formed, which is about four times as active as vitamin D. This major circulating metabolite of vitamin D is then transported to the kidney, where another vitamin D metabolite (1,25-dihydroxy-vitamin-D3) is formed. This form is



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