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Vitamin A is required for normal visual function, maintenance of healthy epithelial tissues and mucous membranes, normal bone development and functional immunity in animals. Vitamin A deficiency signs observed in ruminants vary, but most relate to degenerative changes in these tissues. Numerous studies have demonstrated increased frequency and severity of infection in vitamin A-deficient animals. Low vitamin A status reduces antibody production and impairs cell-mediated immune response against pathogens (Davis and Sell, 1983). Vitamin A is required for production of leukocytes and other cells of the immune system.
Clinical signs of vitamin A deficiency may be specific or nonspecific. General signs observed include loss of appetite, loss of weight, unthrifty appearance, thick nasal discharge and reduced fertility. The normal epithelia of the body are progressively replaced by stratified, keratinized tissue. This effect has been noted in the respiratory, alimentary, reproductive and genitourinary tracts as well as in the eye. This keratinization reduces the effectiveness of the epithelial tissues as a barrier to the entrance of infectious organisms. Thus, respiratory and upper respiratory diseases tend to be more severe in animals with vitamin A deficiency.
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In cattle, signs of vitamin A deficiency include reduced feed intake and growth rate; rough hair coat; edema of the joints and brisket; diarrhea; lacrimation; xerophthalmia; night blindness; blindness from corneal opacity; convulsive seizures; abnormal bone growth; low conception rates; abortion; stillbirths; weak, blind or stillborn calves; abnormal sperm and reduced libido in bulls; and increased susceptibility to respiratory and other infections ( Illus. 1, 2, 3, 4 and 5) (NRC, 1996, McDowell, 2000). Cattle with marginal vitamin A status may be more susceptible to pinkeye or other diseases affecting the mucous membranes. Animals in advanced stages of deficiency may exhibit a staggering gait, convulsive seizures ("fainting" in feedlot cattle) and papilledema of the eye, resulting from elevated cerebrospinal fluid pressure (Illus. 6).
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Vitamin A is critical for successful reproduction. Vitamin A deficiency lowers reproductive efficiency in both males and females. Reduced libido and sterility in bulls with degeneration of seminiferous tubules has been reported (Larkin and Yates, 1964). Spermatozoa decrease in number and motility, and numbers of abnormal sperm increase markedly. In cows, key indications of deficiency are reduced conception rate (Table 1), shortened pregnancies, increased incidence of abortions, high incidence of retained placenta and birth of dead, weak, uncoordinated or blind calves. Blindness in newborn calves is caused by malformation and closure of the optic foramen, constricting the optic nerve (Miller, 1979). If born alive, calves have trouble gaining their balance and lack the instinct to nurse. Vitamin A-deficient newborn calves may show a very severe, often fatal diarrhea. In young calves, signs of vitamin A deficiency also include watery eyes, nasal discharge, muscular incoordination, staggering gait and convulsive seizures (McDowell, 2000). Elevated cerebrospinal fluid (CSF) pressure is the earliest change specific for vitamin A deficiency in the calf and is a precursor to most of the severe neurologic symptoms described.
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The classic sign of vitamin A deficiency in ruminants is night blindness, due to the loss of activity of the rod cells in the retina, which are active in dim light. As vitamin A deficiency develops, the adaptation to dim light and darkness is reduced, eventually resulting in night blindness. This condition is readily detected when animals encounter obstacles in dim light. Night blindness and blindness may be the first noticeable sign of vitamin A deficiency in rapidly growing cattle fed high-concentrate rations. In severe vitamin A deficiency, characteristic changes occur in the eye, including excessive lacrimation (tearing), keratitis, softening and clouding of the cornea, and development of xerophthalmia, characterized by drying of the conjunctiva. In cattle, copious lacrimation (rather than xeropthalmia) is the most prominent clinical sign of vitamin A deficiency (Maynard et al., 1979). The degenerative changes in the eye in vitamin A deficiency are shown in Illus. 4. Blindness can result from either epithelial degeneration or secondary to eye infections caused by the deficiency.
In finishing cattle, generalized edema can occur, with signs of lameness in the hock and knee joints and swelling in the brisket area (NRC, 1996). Booth et al. (1987) reported feedlot cattle with low serum vitamin A concentration, apparent blindness, fixed dilated pupils, severe ataxia and poor weight gains. Feedlot cattle with mild vitamin A deficiency exhibit reduced feed intake and weight gains. Reduced feed intake may result in deficiencies of other nutrients, particularly when the diet is marginal in those nutrients.
Because vitamin A is involved in normal bone development, the long bones of deficient animals are altered in shape during growth. Teeth are also affected. Failure of the spine and other bones to develop normally causes increased pressure on and degeneration of the nerves. For example, blindness in calves results from constriction of the optic nerve caused by a narrowing of the bone canal through which it passes, the optic foreman (Maynard et al., 1979). Bone abnormalities in the spine and pelvis may be responsible for muscular incoordination and other neurologic symptoms exhibited by vitamin A-deficient cattle.
Vitamin A is required for normal development, maintenance and function of the immune system. Feeding rations with low vitamin A activity has been shown to increase the incidence and severity of bovine mastitis (Chew, 1987, 1993). Adequate intake of vitamin A and beta-carotene is necessary for protection against mastitis. Vitamin A helps maintain epithelial integrity and normal immune cell function, while the antioxidant activity of beta-carotene increases the bactericidal activity of blood and milk polymorphonuclear neutrophils (PMNs) against Staph. aureus (Daniel et al., 1991a, b). In addition, some studies have shown that beta-carotene has a favorable effect on fertility (Table 2) of heifers and lactating cows (Lotthammer, 1979; Bonsembiante et al., 1986), while others (Oldham et al., 1991; Akordor et al., 1986) have shown no effect of beta-carotene on reproductive performance or incidence mastitis. Additional studies are needed to clarify the physiologic role of beta-carotene as differences in results may relate to variations in body stores of beta-carotene and (or) vitamin A in experimental animals.
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In the 1950s, it was discovered that cattle developed signs of vitamin A deficiency, originally referred to as X-disease (hyperkeratosis), from consuming feeds that contained a chlorinated naphthalene found in lubricating oil. The depressed vitamin A levels in blood plasma led investigators to conclude that the toxic substance interfered with the conversion of carotene to vitamin A (Maynard et al., 1979). Removal of naphthalenes from oils eliminated X-disease.
Studies have shown that vitamin A-deficient cattle lack heat tolerance. Deficient cattle stand panting, and daily feed consumption is reduced (Perry, 1980), whereas vitamin A supplemented cattle show improved hot weather tolerance and spend more time ruminating.
Vitamin A deficiency signs can result indirectly from deficiencies of zinc, iodine, phosphorus, protein or vitamin E, because these nutrients are required for the normal utilization and metabolism of vitamin A.
Zinc deficiency interferes with the synthesis in the liver of retinol binding protein (RBP) which carries vitamin A (retinol) in plasma. Thus, in zinc deficiency decreased liver RBP levels may cause low plasma vitamin A concentrations. Zinc-deficient goats have been observed to have low serum vitamin A despite adequate dietary vitamin A (Chhabra et al., 1980). In calves, serum vitamin A was significantly higher for animals supplemented with 50 mg per kg (22.7 mg per lb) of zinc (Chhabra and Arora, 1987). Cattle from tropical Northern Australia showed a 12% annual mortality in part because of a slow release of liver vitamin A (Guerin, 1981). Apparently, high calcium and low zinc concentrations in native forages contributed to this slow liver vitamin A release. Since tropical forages have often been shown to be low in zinc (McDowell et al., 1984), conditioned vitamin A deficiencies may be resulting even though liver vitamin A values indicate adequate concentrations of this vitamin. This points out the importance of balanced vitamin-mineral nutrition for grazing livestock.
Deficiencies of phosphorus, iodine, protein or vitamin E reduce vitamin A utilization and may cause vitamin A deficiency signs. Retinyl phosphate is an intermediary in retinol metabolism. Transthyretin, a thyroid hormone binding protein, forms a complex with retinol binding protein in plasma (Olson, 1991). Therefore iodine status and thyroid activity can influence retinol transport and uptake. Protein deficiency can limit synthesis of RBP, and vitamin E enhances vitamin A stability and utilization.
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Clinical signs of vitamin A deficiency in sheep (Illus. 7 and 8) are similar to those of cattle. Night blindness is the common means of determining the deficiency, although severe vitamin A deficiency in feedlot lambs may progress to total blindness (NRC, 1985). Vitamin A deficiency results in keratinization of the respiratory, alimentary, reproductive, urinary and ocular epithelia. Keratinization of these tissues reduces their resistance to infection (Weber, 1983). Bruns and Webb (1990) found that vitamin A- deficient lambs had depressed humoral immune response to ovalbumin. Adrenal function is compromised by vitamin A deficiency (Webb et al., 1968). Additional clinical deficiency signs include growth retardation, bone malformation, degeneration of the reproductive organs and elevated pressure in cerebrospinal fluid. Deficiency interferes with normal development of bone, which may contribute to muscular incoordination and nervous signs. Also, deficiency of the vitamin can result in lambs born weak, malformed or dead (Illus. 10). Retained placenta also occurs in vitamin A-deficient ewes.
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Vitamin A deficiency has resulted in low semen quality in rams (Lindley et al., 1949). Vitamin A deficiency has detrimental effects on wool production and characteristics, including shortened wool fibers and decreases in fiber thickness, strength, and elongation (Faird and Ghanem, 1982).
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Vitamin A deficiency in goats may first appear as a nonspecific rough, dull hair coat. Goats deficient in vitamin A exhibit keratinization of the epithelium of the respiratory, alimentary, reproductive and urinary tracts, and of the eye (NRC, 1981). Signs include increased susceptibility to multiple infections; especially respiratory infection; poor bone development; birth of abnormal offspring; and visual impairment. Night-blindness is the classic deficiency sign. Experimentally produced signs of vitamin A deficiency in goats include loss of appetite, loss of weight, unthrifty appearance, night blindness and a thick nasal discharge (Schmidt, 1941).
In India, limited work with goats suggests that vitamin A deficiency leads to development of urinary calculi (Majumdar and Gupta, 1960). Vitamin A deficiency impairs fertility, either temporarily or permanently. Metritis may be caused by damage to the integrity of the uterine mucosa (Guss, 1977). In adult goats, reduced fertility is a common clinical sign. Doe goats show poor conception rates and shortened or delayed estrus, and bucks exhibit reduced semen quality.
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