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Poultry: Niacin
Deficiency

A deficiency of niacin is characterized by severe metabolic disorders in the skin and digestive organs. The first signs to appear are loss of appetite, retarded growth, weakness, digestive disorders and diarrhea (Illus. 1). The deficiency is found in both human and animal populations that are overly dependent on foods (particularly corn) low in available niacin and its precursor tryptophan. There is good evidence that poultry—even chick and turkey embryos—are able to synthesize niacin, but the rate of synthesis may be too slow for optimal growth.
Illustration 1

A. Chickens
Ruiz and Harms (1987) reported that broilers from three to seven weeks of age did not respond in terms of growth or feed utilization to niacin addition in a corn-soybean meal diet. Harms and Bootwalla (1992a) also concluded that White Leghorn pullets zero to six weeks consuming a corn-soybean meal diet do not respond to niacin. However, supplemental niacin is required for broilers from one to 21 days of age (Ruiz and Harms, 1990a, b). It has been claimed that before there can be a marked deficiency of niacin in the chicken, there must first be a deficiency of tryptophan. Chicks at hatch have considerable tryptophan contained in the protein of the yolk, thus a niacin deficiency will not readily occur unless the feed is low for both the amino acid and the vitamin (NRC, 1994).

Experiments using diets containing a limited amount of tryptophan have shown that the chick does require niacin and that a deficiency produces an enlargement of the tibiotarsal joint, a bowing of the legs, poor feathering, and a dermatitis(Illus. 2) on the feet and head (Scott et al., 1982). Oloyo (1997) noted that supplementing a niacin-deficient broiler diet with 15.0 mg of niacin per kg (6.8 mg per lb) prevented dermatitis, but 22.5 mg of niacin per kg (10.1 mg per lb) was required to prevent leg deformities. The main clinical sign of niacin deficiency in young chicks is an enlargement of the hock joint and bowing of the legs similar to perosis (Illus. 3). The main difference between this condition and the perosis of manganese or choline deficiency is that in niacin deficiency the Achilles' tendon rarely slips from its condyles.
Illustration 2
Illustration 3

Niacin deficiency in the chick is characterized by appetite loss and growth failure. The deficiency results in "black tongue," a condition characterized by inflammation of the tongue and mouth cavity. Beginning at about two weeks of age, the entire mouth cavity, as well as the esophagus, becomes distinctly inflamed, growth is retarded, and feed consumption is reduced. There is a weight loss and both egg production and hatchability are reduced in niacin deficiency of laying hens. Shell quality is improved with niacin supplementation (Leeson et al., 1991). Death loss can be affected. Jackson (1992) reported that 30 mg per kg (13.6 mg per lb) of dietary niacin significantly decreased mortality of layers, when compared to 10 mg per kg (4.5 mg per lb).

B. Turkeys and Other Poultry Species
Turkey poults, pheasant chicks, ducklings and goslings all expressed perosis (Illus. 4) as the primary niacin deficiency sign (NRC, 1994). Signs of niacin deficiency in turkeys and ducks, while similar to those in chickens, are much more severe. Compared to the chick, the turkey poult, duckling, pheasant chick and gosling have higher requirements for niacin. This higher requirement is related to the less efficient conversion of tryptophan to niacin by these species. Ducks receiving low-niacin diets show severely bowed legs and ultimately become so crippled and weak that they cannot walk. Niacin deficiency in the turkey is also characterized by a severe bowing of the legs and enlargement of the hock joint. Goslings on purified diets developed perosis and hock deformities that were prevented with nicotinic acid administration (Briggs et al., 1953).
Illustration 4
Rheinpfalz

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