A Note on Zinc and Immunocompetence

Abstract

In Prasad’s initial description of the extraordinarily complex syndrome produced by profound zinc deficiency in humans, evidence of increased susceptibility to infection was one manifestation of this nutritional deficiency (Prasad et al. 1961). Holstein—Friesian cattle bearing the highly lethal A46 mutation also have severe zinc deficiency that is attributable to failure to absorb zinc normally from the gastrointestinal tract. These cattle have a profound immune deficiency disease and frequently die from infections. Their immunodeficiency disease is characterized by failure of development of normal T cell-mediated immunities, defective delayed hypersensitivity reactions, feeble allograft immunity, failure of normal development of the thymus, deficiencies of T lymphocytes in blood and thymus-dependent regions of the lymphoid tissues and defective defences against viruses, fungi and bacteria. In addition, these genetically defective cattle exhibit striking malfunctions of the gastrointestinal tract, and a pleurioroficial dermatitis characterized by parakeratoses. All of these manifestations, including all of the immunodeficiencies which occur in these zinc-deficient cattle, are corrected by administration of zinc orally or parenterally (Brummerstedt et al. 1971; Andresen et al. 1974).