Characteristics of vitamin B6 deficiency in most species are retarded growth, dermatitis, epileptic-like convulsions, anemia and partial alopecia. Due to the predominate role of vitamin B6 in amino acid metabolism, a deficiency is characterized by reduced protein utilization and nitrogen retention and impairment of tryptophan and niacin metabolism.
Due to rumen microbial synthesis, vitamin B6 deficiency in ruminants with a functioning rumen has not been reported in the literature. Vitamin B6 has been shown to be essential for the young calf when selected experimental diets are used. Calves that were reared on a "milk substitute" lost appetite within two to four weeks, their growth was impaired, and they progressively showed apathy, diarrhea, anorexia and incoordination. In the last stages convulsions were soon followed by death (Johnson et al., 1947). The convulsions included thrashing of the legs and head and grinding of the teeth (Johnson et al., 1950).
Postmortem examination of vitamin B6 -deficient calves revealed hemorrhages in the epicardium and in the kidneys, demyelination of the peripheral nerves, proliferation of Schwann cells, desquamation of the intestinal mucosa and pneumonia (Johnson et al., 1950). Analyses of the urine from the vitamin B6 -deficient calves showed greatly reduced excretion of pyridoxine, pyridoxal, pyridoxamine and pyridoxic acid (the major excretory metabolite). In the early stages of a vitamin B6 deficiency in calves, animals fully recovered after an oral dose of 100 mg of vitamin B6 (Johnson et al., 1950). However, if this treatment was delayed until the occurrence of convulsive seizures, it was no longer possible to save the calf, even when the vitamin was administered by injection, indicating that irreparable damage had occurred.
