Severe staphylococcal disease associated with allergic manifestations, hyperimmunoglobulinemia E, and defective neutrophil chemotaxis.

Neutrophil granulocyte function was determined in three patients with systemic staphylococcal infection, clinical manifestations of generalized allergic disease, and hyperimmunoglobulinemia E. Each of the patients had urticarial skin rashes before or at the time of development of staphylococcal suppurative lymphadenitis, pneumonia, or sepsis. Neutrophil chemotaxis, random migration, phagocytosis, and bactericidal capacity were assessed to determine if an abnormality in these functions might have contributed to the development of severe staphylococcal infections. Each of the three patients with generalized urticaria was found to have a marked defect in neutrophil chemotaxis. The mean chemotactic index of the patients was 12 +/- 4, whereas that of 20 controls was 72 +/- 11. Neutrophil random migration, phagocytosis, and bactericidal capacity were normal in each patient. The serum or plasma of the patients did not inhibit chemotaxis of control neutrophils and did not contain an increased concentration of the chemotactic-factor inactivator found in normal serum. Treatment of the neutrophils of these three patients with the competitive histamine H2 receptor blocking agent, burimamide, produced a significant increase in chemotactic responsiveness. These studies suggest the possibility of pharmacologic modification of neutrophil granulocyte function.