A study of the pathogenesis of the peripheral neuropathy associated with riboflavin deficiency in the chicken

Vita.The pathogenesis of the peripheral neuropathy associated with riboflavin deficiency was studied in the young rapidly growing chicken using histologic, ultrastructural and histochemical techniques. Ninety-six one-day-old chickens were divided into 5 groups. Two groups were fed a balanced control diet for 52 days which contained a level of riboflavin (11.65 mg/kg) similar to that in commercial diets. One of the 2 control groups was fed the diet ad libitum and the other group was pair-fed receiving the amount of feed consumed by an equal number of chickens receiving the most severely riboflavin-deficient diet. Three other groups were fed riboflavin deficient diets. Two of these groups received a diet markedly deficient in riboflavin (1.65 mg/kg) but differed in that one group received the diet continuously for the 52 days of the experiment while the other group received the diet until clinical signs of riboflavin deficiency were present in almost all chickens in the group (19 days) when they were fed the control diet until the affected chickens had recovered. The third group receiving a riboflavin deficient diet was fed a diet for 52 days which contained a marginally deficient level of the vitamin (3.65 mg/kg) for the line of chickens used (estimated daily requirements of riboflavin range from 3.67 - 6.00 mg/kg). Clinical signs of riboflavin deficiency were not seen in any of the chickens fed the control diet, either ad libitum or pair-fed. Clinical signs of riboflavin deficiency were detected in both groups fed the diet most deficient in riboflavin (1.65 mg/kg) and were characterized by partial or complete paralysis.