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Characteristics of vitamin B6 deficiency are retarded growth, dermatitis, epileptic-like convulsions, anemia and partial alopecia. Due to the predominant function of the vitamin in protein metabolism, in vitamin B6 deficiency, a reduction in nitrogen retention is observed, feed protein is not well utilized, nitrogen excretion is excessive and impaired tryptophan metabolism may result. Also, lipid metabolism is affected; desaturation and elongation of fatty acids is impaired in growing chickens (An et al., 1995). Chicks fed a vitamin B6-deficient diet have little appetite and grow slowly, with plumage failing to develop fully (Illus. 1). Chicks receiving a B6-deficient diet exhibited general weakness after a few days of deprivation. The birds squat in a characteristic posture (Illus. 2), with wings slightly spread and head resting on the ground (Bräunlich, 1974). Miller (1963) observed high proportions of pendulous crops in vitamin B6-deficient chicks.
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A more specific sign of B6 deficiency is the nature of the nervous condition that develops. Deficient chicks are abnormally excitable. As deprivation continues, nervous disorders become increasingly severe (Bräunlich, 1974). There is trembling and vibration of the tip of the tail, with movement stiff and jerky. Chicks run aimlessly about with lowered head and drooping wings (Illus. 3). Finally, convulsions develop, during which chicks fall on their side or back, with the legs scrabbling. Violent convulsions cause complete exhaustion and may lead to death. These clinical signs may be distinguished from those of encephalomalacia by the greater intensity of activity during a B6 deficiency seizure, which results in complete exhaustion and often death (Scott et al., 1982).
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Blood alterations are also typical of a vitamin B6 inadequacy in chicks. An extreme deficiency leads to microcytic, polychromatic, hypochromic anemia in conjunction with atrophy of the spleen and thymus (Asmar et al., 1968). Marginal deficiencies provoke microcytic, normochromic polycythemia (Blalock and Thaxton, 1984), and deficient chicks show a decreased immunoglobulin M and immunoglobulin G response to antibody challenge (Blalock et al., 1984).
Similar signs of a vitamin B6 deficiency have been observed in turkey poults: loss of appetite, poor growth (Illus. 4), oversensitivity, cramps and eventually death. Ducklings not receiving enough vitamin B6 grow slowly, and development of plumage is poor. At five days of age, ducklings showed retarded growth (Yang and Jeng, 1989). Clinical signs, which were first observed at 7 days of age, were characterized by decreased appetite, extreme weakness, hyperexcitability, convulsions and death. Hematologic examination at three weeks of age indicated that vitamin B6 deficiency in ducklings resulted in microcytic, hypochromic anemia.
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Signs of B6 deficiency in chicks appear very rapidly after introduction of a B6-deficient feed. Fuller and Kifer (1959) reported that signs of a deficiency appeared on the eighth day. Chronic borderline B6 deficiency produces perosis; usually one leg is severely crippled, and one or both of the middle toes may be bent inward at the first joint (Gries and Scott, 1972). Vitamin B6 deficiency in growing chicks affected biomechanical properties of tibial bone, with reduced dry weight and cortical thickness (Masse et al., 1994; 1996). A marked increase in gizzard erosion was found in vitamin B6-deficient chicks (Daghir and Haddad, 1981).
For adult poultry, vitamin B6 deficiency results in reduced egg production and hatchability as well as decreased feed consumption, weight loss and death. A severe deficiency [levels of vitamin B6 below 0.5 mg per kg (0.23 mg per lb)] of diet causes rapid involution of the ovary, oviduct, comb and wattles in mature laying hens. Involution of testes, comb and wattles occurs in vitamin B6-deficient adult cockerels (Scott et al., 1982).
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