Because it is a required cofactor in four key metabolic enzymes, biotin deficiency adversely affects many tissues, especially those with high rates of metabolic activity or cell division. Biotin is required for normal function of the thyroid and adrenal glands, reproductive and nervous systems. Its effect on the cutaneous system is most dramatic. The classic sign of biotin deficiency in animals and humans is a characteristic red, scaly dermatitis, especially around the eyes, nose and mouth. Metabolic changes include lactic acidosis, aciduria and increase in urinary excretion of 3-hydroxyisovaleric acid, a metabolite of leucine (Zempleni and Mock, 1999). The blockage in propionic acid metabolism results in accumulation of 3-hydroxypropionic acid in urine (Zempleni and Mock, 1999). Production of essential fatty acids is abnormal in biotin deficiency (Watkins, 1989), which may be the mechanism by which skin lesions are produced (Mock, 1991). Immune function is compromised by biotin deficiency, with reductions in plasma immunoglobulins and both T- and B-lymphocytes (Zempleni and Mock, 1999).
Biotin deficiency in calves is characterized by paralysis of the hind legs, generalized weakness and reduced urinary excretion of biotin (Wiese et al., 1946). The condition was corrected by parenteral administration of biotin. Flipse el al. (1948) reported a potassium-biotin interrelationship in calves, in which calves fed purified diets low in potassium and biotin developed progressive paralysis of the hind legs that spread to the forelegs, neck and respiratory system. Death resulted within 12 to 24 hours of the first symptoms; however, the condition could be cured by parenteral administration of either potassium salts or biotin.
A more recent study (Mulling et al., 1999) produced biotin deficiency in a calf for the purpose of studying its effects on hoof growth and keratinization. The calf displayed the classic biotin deficiency symptoms of dermatitis around the muzzle and eyes. The hoof epidermis displayed several specific abnormalities including a marked decrease in keratin production, a reduction in intracellular cementing substance, a very thin germinative cell layer and thin hoof sole with a brittle and crumbly consistency. The normal border of cornification between live and dead horn layers had completely disappeared in the biotin-deficient calf. The authors concluded, based on their observations, that biotin is clearly essential for normal keratinization and hoof horn quality ( Illus. 1).
