Instrinsic defect of the polymorphonuclear leucocyte resulting in impaired chemotaxis and phagocytosis.

A patient is presented who has recurrent infections associated with a cellular defect of PMN chemotaxis and phagocytosis, as well as a sex-linked form of congenital agammaglobulinaemia. The impairments of PMN function were demonstrated in vitro by an inability of the patient's PMNs to respond to chemotactic factors, by an inability of the PMNs to phagocytize S. aureus, and by abnormal NBT tests. These abnormalities were not corrected by the addition of normal serum or plasma to the patient's PMNs. No evidence was obtained for a plasma inhibitor of PMN function.