In growing chicks, turkey poults and quail, vitamin B12 reduces body weight gain, feed intake, and feed conversion. Vitamin B12 deficiency in growing chicks and turkeys may result in a nervous disorder and defective feathering. It has also been related to leg weakness and perosis; however, this appears to be a secondary effect. Perosis may occur in vitamin B12-deficient chicks or poults when the diet lacks choline, methionine, or betaine as a source of methyl groups. Addition of B12 may prevent perosis under these conditions because of its effect on synthesis of methyl groups. Additional clinical signs in B12 deficiency include anemia, gizzard erosion, and fatty deposits in the heart, liver, and kidneys. Poor feathering and mortality are the most obvious signs of a vitamin B12 deficiency, and gizzard erosions may also appear (NRC, 1994).
In hens, body weight and egg production are maintained despite a deficiency, but B12 has an important influence on egg size (Scott et al., 1982). However, Squires and Naber (1992) reported that both egg production and hen weight increased with vitamin B12 supplementation, as did hatchability and egg weight.
Hatchability of incubated eggs may be severely reduced if the breeder diet contains inadequate vitamin B12 (Squires and Naber, 1992; Zhang et al., 1994). Changes that manifest themselves in vitamin B12-deficient chick embryos (Olcese et al., 1950) may be summarized as: (1) general hemorrhagic condition; (2) fatty liver in varying degrees; (3) heart often enlarged and irregular in shape; (4) kidneys pale or yellow, sometimes hemorrhagic; (5) incidence of perosis; (6) myoatrophy of the leg; (7) fewer myelinated fibers in the spinal cord; and (8) high incidence of embryonic malpositions. Hypertrophy of the thyroid gland has also been repeatedly observed (Ferguson and Couch, 1954).
The most obvious change in B12 -deficient embryos is myoatrophy of the leg, a condition characterized by atrophy of thigh muscles (Olcese et al., 1950). Two to five months may be needed to deplete hens of vitamin B12 stores to such an extent that progeny will hatch with low vitamin B12 reserves. The rate of depletion is most rapid when hens are fed high-protein diets (Scott et al., 1982). Chicks that do hatch without adequate carryover of vitamin B12 from the dam have a high rate of mortality. Vitamin B12-deficient embryos die at about day 17.
