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Swine: Vitamin B6

Deficiency

Characteristics of vitamin B6 deficiency in most species are retarded growth, dermatitis, epileptic-like convulsion, anemia and partial alopecia (Illus. 1). Due to the predominant function of the vitamin in protein metabolism, in vitamin B6 deficiency a fall in nitrogen retention is observed, feed protein is not well utilized, nitrogen excretion is excessive and impaired tryptophan metabolism may result.

 

Illustration 1

An indication of a vitamin B6 deficiency is elevated urinary levels of xanthurenic acid and kynurenic acid, indicating incomplete conversion of tryptophan. For status evaluation, Driskell (1984) concluded that the best assessment parameter for vitamin B6 status in clinical cases is measurement of either the coenzyme stimulation of erythrocyte alanine aminotransferase activity or PLP level.

In growing pigs, clinical signs of vitamin B6 deficiency include a poor appetite, slow growth (Illus. 2), microcytic hypochromic anemia, epileptic-like fits or convulsions (Illus. 3), fatty infiltration of the liver, diarrhea, rough hair coat, scaly skin, a brown exudate around the eyes, demyelination of peripheral nerves and subcutaneous edema (Bauernfeind, 1974; Braunlich, 1974; Cunha, 1977). Hughes and Squibb (1942) reported many of these deficiency symptoms and also an unsteady gait in pyridoxine-deficient pigs. Almost identical symptoms of B6 deficiency were reported in baby pigs (Lehrer et al., 1951). Follis and Wintrobe (1945) reported specifically on the effects of pyridoxine deficiency on the nervous tissues. Myelin degeneration of the peripheral portion of the sensory nerve was observed to be the initial neural change in pyridoxine-deficient animals. Based on morphologic data the preliminary site of injury in pyridoxine-deficient animals is in the myelin sheath and axon. Like some other vitamins, vitamin B6 deficiency reduces the immune responses of the pig (Harmon et al., 1963). The first and most conspicuous sign in baby pigs that vitamin B6 is insufficient is a loss of appetite that may appear in less than two weeks if the deficiency is severe. This is accompanied by reduced growth, vomiting, diarrhea, and a peculiar compulsion to lick.

 

Illustration 2
Illustration 3

When deficiency of vitamin B6 reaches an advanced stage (probably due to degeneration of the peripheral nerves), disordered movement and ataxia appear. Finally, convulsions develop at irregular intervals but are apparently stimulated by excitement, as they are most often observed at feeding time. Between these convulsions, pigs lie down and are apathetic and unresponsive (Braunlich, 1974). Braunlich (1974) suggested that a vitamin B6 deficiency may go unnoticed in swine because of a lack of visible signs associated specifically with the deficiency. Metabolic disorders may be revealed only by poor appetite, slow growth, and inefficient feed utilization. In some experiments with vitamin B6, protein retention by pigs deficient in the vitamin was reduced to less than half of that shown in animals receiving sufficient amounts of the vitamin.

During reproduction and lactation, sows fed a corn-sorghum-soybean meal diet responded to vitamin B6 supplementation of 4.4 mg per kg (2 mg per lb) of feed (Adams et al., 1967). Vitamin B6 supplementation of 11 mg per kg (5 mg per lb) of feed produced a slightly superior daily gain in weight, more piglets born alive, and a smaller number of resorbed fetuses as compared with control sows that received only 1 mg per kg (0.45 mg per lb) of vitamin B6 (Ritchie et al., 1960). Knights et al. (1998) observed a tendency for reduced weaning-to-estrus interval and increased nitrogen retention in Yorkshire and Hampshire sows. These researchers also observed an increased litter size in Yorkshire sows following feeding of 16 ppm pyridoxine daily to sows from weaning through the next gestation. In rats, Roth-Maier et al. (1996) concluded that adequate levels of B6 during lactation did not compensate for a lack of B6 during gestation and vice versa, as a high dose of B6 during gestation was unable to alleviate all effects of a suboptimal supply of B6 during lactation. These conclusions were based on data assessing rat liver B6 status.

 

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