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Poultry: Folic Acid
Deficiency

Poultry are more susceptible to lack of folic acid than other farm livestock, as a deficiency can readily be produced by feeding a folic acid-deficient diet. Folic acid deficiency, as indicated by retarded growth and feed efficiency, could be produced in 15-day-old chicks fed corn-soybean meal diets (Pesti et al., 1991).

 

In folic acid deficiency megaloblastic arrest of erythrocyte formation in bone marrow causes severe macrocytic anemia as one of the first signs. Folic acid deficiency in chicks is also characterized by poor growth, very poor feathering, an anemic appearance, and perosis (Illus. 1 and 2). The chicks become lethargic, and feed intake declines. As anemia develops, the comb becomes waxy white and mucous membrane of the mouth becomes pale (Siddons, 1978). Turkey poults fed a folic acid-deficient diet show reduced growth rate and increased mortality (Illus. 3). The birds develop a spastic type of cervical paralysis in which the neck is stiff and extended but with only a moderate degree of anemia. Poults with cervical paralysis die within 2 days after the onset of these signs unless folic acid is administered immediately (Scott et al., 1982). Erythrocytes of deficient birds tend to be large in diameter, and their nuclei are less dense than those of birds receiving supplementary folic acid (Schweigert et al., 1948).
Illustration 1
Illustration 2
Illustration 3

Folic acid deficiency also results in poor feather development for chicks and turkeys, with the shafts weak and brittle. Folic acid, lysine, and iron are required for feather pigmentation, as depigmentation occurs in colored feathers during a deficiency of the vitamin.

 

It appears that egg production is less affected by folic acid deficiency than the development of the chick or poult. Egg and poult weights were significantly increased when turkey hens received higher dietary folic acid and when eggs were injected with folic acid (Robel, 1993b). Inadequate folic acid provided to the hen impairs the oviduct's response to estrogen and ability to form albumen (NRC, 1994). An inadequate intake of folic acid by breeding hens results in poor hatchability and a marked increase in embryonic mortality (Illus. 4), which occurs during the last days of incubation. A deformed beak and bending of the tibiotarsus are signs of the embryonic deficiency. Chicks that successfully emerge are stunted and have feathers that are poorly developed and abnormally pigmented (NRC, 1994).
Illustration 4

Folic acid deficiency has sometimes been associated with perosis, or slipped tendon. Pollard and Creek (1964) demonstrated histologically that the lesions of folic acid-deficient bones and cartilage are different from those produced by choline or manganese deficiencies. Abnormal structure of the hyaline cartilage is found in folic acid-deficient chicks, and ossification is retarded. These disorders are not found in chicks deficient in choline or manganese, although bone deformities and slipped tendons are found in both types of disorders. However, Bechtel (1964) claimed that choline is effective in preventing perosis only when sufficient folic acid is present in the diet. Dietary choline content has been shown to affect the chicks' requirement for folic acid. When the diet contained adequate choline, the folic acid requirement was 0.47 mg per kg (0.21 mg per lb) of diet, but this increased to 0.96 mg per kg (0.44 mg per lb) diet when the diet was choline deficient (Young et al., 1955). Increasing the protein content of the diet has also been shown to increase the incidence and severity of perosis in chicks receiving low levels of dietary folic acid. It is suggested that this increased requirement for folic acid in high-protein diets for poultry is a consequence of greater demand for folic acid in uric acid formation (Creek and Vasaitis, 1963).

 

Folic acid appears to be necessary for cell mitosis. In the absence of folic acid, oviduct growth is not increased in estrogen-treated chicks. The production of water-soluble proteins (particularly the albumen fraction) in the hormone-stimulated oviduct is also greatly reduced, and there is an alteration in the amino acid composition of these proteins. The percentages of arginine, leucine, serine and tryptophan are decreased and those of glycine and methionine, increased (Siddons, 1978).

 
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