Squires and Naber (1993b) report a large incidence of blood spots in eggs from a vitamin A-deficient dietary treatment, which agrees with the results reported by Bearse et al. (1960). Gross and histologic examination of the reproductive tract of deficient hens verifies that the ovary is structurally changed by vitamin A-deficiency (Bermudez et al., 1993). Hens fed a vitamin A-deficient diet had increased numbers of atretic follicles on the ovary and these follicles had moderate to severe hemorrhage (Bermudez et al., 1993). In contrast, hens with low rates of egg production fed a vitamin A-supplemented diet did not have hemorrhaged ovarian follicles. Conversely, Squires and Naber (1993b) reported that hens fed vitamin A-deficient diets continued to produce eggs through 12 weeks of lay, presumably due to mobilization of liver stores of the vitamin. After this, the vitamin A content of yolks of the few eggs produced was similar to the yolk vitamin A content of supplemented hens. Yolk vitamin A content is thus a poor indicator of flock vitamin A status. Average survival times of the progeny fed a vitamin A-free diet increased in a linear fashion with the increasing levels of vitamin A in the maternal turkey diet (Jensen, 1965). Vitamin A level of the hen's diet is positively correlated with the growth of chicks and poults from that hen, and the level of vitamin A in the chick's and poult's diet is positively correlated with growth. Clearly a deficiency of vitamin A will produce a loss of appetite and a reduction in growth. A severe deficiency will produce ataxia and death if not corrected (Hill et al., 1961).
As vitamin A deficiency progresses in adult poultry, they become emaciated and weak and their feathers are ruffled. A marked decrease in egg production occurs and the length of time between clutches increases greatly. Hatchability is decreased and there is an increase in embryonic mortality in eggs from affected birds. A watery discharge from the nostrils and eyes is noted and eyelids are often stuck together.
When day-old chicks are given a vitamin A-free diet, clinical signs may appear at the end of the first week if the chicks are progeny of hens receiving a diet low in vitamin A. If chicks are progeny of hens receiving high levels of vitamin A, signs of deficiency may not appear until chicks are six or seven weeks of age even though they are receiving a diet completely devoid of vitamin A (Scott et al., 1982; West et al., 1992). Gross signs of vitamin A deficiency in chicks are characterized by anorexia, cessation of growth, drowsiness, weakness, incoordination, emaciation and ruffled plumage. The mucous epithelium is replaced by a stratified squamous, keratinizing epithelium. The mucous membranes of the nasal passage, mouth, esophagus and pharynx of poultry are affected and develop white pustules (Scott et al., 1982). The kidneys may be distended with uric acid deposits and the epithelium of the eye is affected, which produces exudates and eventually xerophthalmia. Severe vitamin A deficiency causes increased intestinal mucosal cell numbers (hyperplasia), reduced intestinal mucosal cell size, the loss of mucosal protein, reduced villus height and crypt depth, and diminished activities of gut disaccharidases, transpeptidase and alkaline phosphatase (Uni et al., 1998). It is clear that there is a breakdown of the epithelium of many systems in the body due to a vitamin A deficiency. Loss of membrane integrity, in turn, alters water retention (Lopez et al., 1973) and impairs the ability to withstand infection (Sijtsma et al., 1989a). Bacteria and other pathogenic microorganisms may invade tissues and enter the body, thereby producing infections that are secondary to original vitamin A deficiency signs.
Inadequate vitamin A also reduces the immune system's response to challenge and further contributes to disease susceptibility (Davis and Sell, 1989). Many experiments have revealed that increased morbidity is observed in chickens experimentally infected with Newcastle disease virus that were fed a diet marginally deficient in vitamin A (Sijtsma et al., 1989a, b). Low dietary vitamin A has been shown to cause reduced antibody production, defective T-cell responses, reduced phagocytosis and decreased resistance to infection by bacterial and viral pathogens and protozoan enteropathogens (Friedman and Sklan, 1997; Lessard et al., 1997; Coskun et al., 1998). Viral infections have been found to impair the vitamin A status of chickens (West et al., 1992).
Vitamin A deficiency can cause alterations in bone growth, which creates several areas of compression on the central nervous system that cause a loss in mobility (Howell and Thompson, 1967). Nockels (1988) reported that hypothyroidism is an early indication of vitamin A deficiency in chicks. Reductions in testis size, circulating testosterone and fertility have been reported during vitamin A deficiency in cockerels (Damjanou et al., 1980).
