Swine: Riboflavin

Deficiency

Typical swine diets based largely on grains are often borderline to deficient in riboflavin. A decreased rate of growth and lower feed efficiency are common signs of riboflavin deficiency in all species affected. Reduced feed intake was demonstrated in gilts given a lactation diet containing 1.3 mg per kg (0.6 mg per lb) riboflavin. These gilts consumed 30% less feed than those gilts that received diets with 2.3 to 5.3 mg per kg (1.0 to 2.4 mg per lb) riboflavin (Frank et al., 1988). Typical clinical signs often involve the eye, skin and nervous system.

Signs of riboflavin deficiency in the young growing pig include anorexia, slow growth (Illus. 1 ), rough hair coat, dermatitis, alopecia, abnormal stiffness, unsteady gait, scours, ulcerative colitis, inflammation of anal mucosa, vomiting, cataracts, light sensitivity and eye lens opacities (Hughes, 1940; Lehrer and Wiese, 1952; Cunha, 1977; NRC, 1998). In severe riboflavin deficiency of pigs, researchers have observed increased blood neutrophil granulocytes, decreased immune response, discolored liver and kidney tissue, fatty liver, collapsed follicles, degenerating ova and degenerating myelin of the sciatic and brachial nerves (NRC, 1998). Lehrer and Wiese (1952) indicated that the external deficiency symptoms observed in their study could be reversed by supplementation of 1 to 1.5 mg of riboflavin per day for 16 days. However, the internal tissue changes were not corrected during this supplementation interval.

Miller and Ellis (1951) and Miller et al. (1953) reported that riboflavin deficiency seriously impaired reproduction in pigs. Sows receiving 0.55 mg riboflavin per kg (0.25 mg per lb) of feed failed to reproduce or experienced death. Offspring from riboflavin-deficient sows are shown in (Illus. 2). Cunha (1977) summarized the clinical signs for gilts fed a riboflavin-deficient diet during reproduction and lactation as follows: (1) erratic or, at times, complete loss of appetite; (2) poor gains; (3) parturition four to 16 days prematurely; (4) one case of death of fetus in advanced stage with resorption in evidence; (5) all pigs either were dead at birth or died within 48 hours thereafter; (6) enlarged front legs in some pigs, due to gelatinous edema in the connective tissue and generalized edema in many others; and (7) two hairless litters. The longer the period on riboflavin-deficient diets, the more severe the deficiency signs became. Christensen (1980) likewise reported resorption of fetuses and premature farrowing for riboflavin-deficient sows.

Riboflavin deficiency has led to anestrus (Esch et al., 1981). Deficiency of riboflavin in post-pubertal gilts has led to a cessation of ovarian cyclicity without overt signs of deficiency. Gilts fed a riboflavin-deficient diet had a progressively longer average time interval between consecutive estrus periods until becoming anestrus 63 days after the beginning of the study. Teratogenic effects have been observed, including skeletal abnormalities, shortened bones and fusions between ribs (Zintzen, 1975).

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