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Swine: Vitamin A
Deficiency

Rahman et al. (1996) recorded signs associated with hypovitaminosis A on a commercial hog farm and found agreement with observations reported by earlier workers (Hughes et al., 1928). Goodwin and Jennings (1958) and Palludan (1961) provided a comprehensive description of the congenital malformations associated with vitamin A deficiency in pregnant sows. In pigs, the absence of vitamin A results principally in nervous signs, such as unsteady gait, incoordination, trembling of the legs, spasms and paralysis (Hentges et al., 1952a) (Illus. 1). Eye lesions are less common. Reduced growth is a sign of vitamin A deficiency in all species. Insufficient vitamin A for rats reduces efficiency of the urea synthesis pathway, thus accounting for the increased amino nitrogen excretion seen with the deficiency (John and Sivakumar, 1989). An effect of vitamin A deficiency in swine on appetite or rate of gain often does not occur until eventual paralysis and weakness prohibit movement to the feeder (Cunha, 1977). Associated with vitamin A deficiency is increased cerobrospinal fluid (CSF) pressure. Nelson et al. (1962) reported that 8 to 16 mg of vitamin A per lb of body weight per day can produce lower CSF pressure. Nelson et al. (1964) reported CSF fluid pressure to be a very sensitive criterion for establishing vitamin A status of pigs fed vitamin A or vitamin A acid.

 
Illustration 1

Hjarde et al. (1961) reported that the influence of vitamin A deficiency depends on the age of the animal at the time of depletion. During reproduction and lactation, a vitamin A deficiency in the sow produces the following clinical signs: failure of estrus; resorption of young; wobbly gait; weaving and crossing of the hind legs while walking; dropping of the ears; curving with head down to one side; spasms; loss of control of hindquarters and forequarters, hence inability to stand up; and impaired vision (Cunha, 1977). Depending on degree of severity of vitamin A deficiency, fetuses were resorbed, born dead or carried to term. Fetuses carried to term showed a variety of defects, including various stages of arrested formation of the eyes (sometimes complete lack of eyeballs), harelips, cleft plate, misplaced kidneys, accessory ear-like growths, some with one eye, some with one large and one small eye and bilateral cryptorchidism (Guilbert et al., 1937; Cunha, 1977) (Illus. 2). Hjarde et al. (1961) reported that vitamin A deficiency at breeding age led to impaired spermiogenesis; metaplasia of oviduct, cervix and vagina; and compression of the brain.

 
Illustration 2

Vitamin A appears to improve reproductive performance of gilts by decreasing embryonic mortality, resulting in more pigs per litter (Brief and Chew, 1985). Weekly injections to supply 12,800 IU vitamin A and 32.6 mg beta-carotene per gilt daily resulted in elevated levels of plasma vitamin A and beta-carotene, reduced embryonic mortality and more and heavier pigs alive at birth and weaning. Coffey et al. (1989) indicated that injecting multiparous sows with beta-carotene at weaning increased litter size at the subsequent farrowing.

 
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