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Poultry: Riboflavin

Deficiency

A decreased rate of growth and lower feed efficiency are common signs of riboflavin deficiency in all species affected. Typical clinical signs often involve the eye, skin and nervous system. The most critical requirements for riboflavin are those exhibited by the young chick and the breeder hen. The characteristic sign of riboflavin deficiency in the chick is "curled-toe" paralysis. It does not develop, however, in a total riboflavin-free diet or when the deficiency is very marked, because the chicks die before it appears. Chicks are first noted to be walking on their hocks with their toes curled inward (Illus. 1 and 2). Deficient chicks do not move about, except when forced to do so, and their toes are curled inward both when walking and when resting on their hocks (Scott et al., 1982). Legs become paralyzed, but the birds may otherwise appear normal. Approximately 10% incidence of curled-toe paralysis was observed among birds fed a diet with no added riboflavin (1.5 mg per kg or 0.68 mg per lb) (Bootwalla and Harms, 1990).

Illustration 1
Illustration 2

Changes in the sciatic nerves produce the curled-toe paralysis in growing chicks. There is a marked enlargement of sciatic and brachial nerve sheaths with sciatic nerves reaching a diameter four to six times normal size. Histologic examinations of affected nerves show definite degenerative changes in myelin sheaths, which when severe may pinch the nerve, producing a permanent stimulus that causes the curled-toe paralysis (Scott et al., 1982). When the curled-toe deformity is long standing, irreparable damage has occurred in the sciatic nerve and administration of riboflavin no longer cures the condition. Retarded growth, splay and hock-resting postures and leg paralysis, rather than curled-toe paralysis, have been reported in some studies as the predominant signs of riboflavin deficiency in chicks (Ruiz and Harms, 1988; Chung and Baker, 1990).

Turkey poults and pheasants exhibit clinical signs similar to those of the chick, whereas ducks and geese are more likely to have a bowing of the legs in conjunction with perosis (NRC, 1994). In the poult, a dermatitis appears in about eight days; the vent becomes encrusted, inflamed and excoriated; growth is retarded or completely stopped by about the seventeenth day; and deaths begin to occur about the twenty-first day. However, when poults were fed a corn-soy diet analyzed to contain 2.7 mg per kg (1.2 mg per lb) of naturally occurring riboflavin, the only signs exhibited by poults were a paralysis of one or both legs, poor feathering, poor growth and, finally, mortality (Ruiz and Harms, 1989). In the duckling, diarrhea and cessation of growth are generally associated with riboflavin deficiency. Other signs of riboflavin deficiency are retardation of growth (Illus. 3 and 4), diarrhea after eight to 10 days, and high mortality after about three weeks. When chicks are fed a diet deficient in riboflavin, their appetite is fairly good but they grow very slowly and become weak and emaciated. There is no apparent impairment of feather growth; on the contrary, main wing feathers often appear to be disproportionally long. Increased hematocrit, increased mean corpuscular volume, decreased mean hemoglobin concentration and a marked heterophil leucocytosis appeared in the chick prior to neurological manifestations (NRC, 1994).

Illustration 3
Illustration 4

In laying poultry, hatchability of incubated eggs is first reduced and subsequently egg production is decreased, roughly in proportion to degree of deficiency. Embryonic mortality has two typical peaks (the fourth and twentieth days of incubation) and often an intermediate peak on the fourteenth day. Embryos that fail to hatch from eggs of hens receiving low-riboflavin diets are dwarfed and exhibit pronounced micromelia; some embryos are edematous. The down fails to emerge properly, thus resulting in a typical abnormality termed "clubbed down," which is most common in neck areas and around the vent. The nervous systems of these embryos show degenerative changes much like those described in thiamin-deficient chicks. When dietary riboflavin provided to breeder hens was decreased from 9.7 to 1.7 mg per kg (4.4 to 0.77 mg per lb) embryo mortality increased to 83.3% and hatchability to 3.1%; however, decreasing riboflavin from 9.7 to 7.0 or 4.4 mg per kg (4.4 to 3.2 or 2.0 mg per lb) had no effect on these variables (Flores-Garcia and Scholtyssek, 1992).

Naber and Squires (1993b) reported that the riboflavin of egg albumen is a sensitive measurement to determine if riboflavin had been added to the diet of laying chickens. Hens fed a riboflavin-deficient diet laid eggs with low concentrations of the vitamin within four days. Therefore, the correlation between egg albumen riboflavin content and feed riboflavin content is high.

Chicks fed a diet only marginally deficient in riboflavin often recover spontaneously. The condition is curable in the early stages, but in its acute stage it is irreversible (NRC, 1994). There is increasing evidence that vigor and livability of the baby chicks are directly tied to amount of riboflavin in the hen’s diet (Hoffmann-La Roche, 1969). Ruiz and Harms (1988) observed that riboflavin deficiency is more severe in modern strains of chicks and poults than in those used 40 to 50 years ago, perhaps due to the faster growth rate and improved feed conversion of the modern broiler.

 

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