Leukocyte dysfunction in the bovine homologue of the Chediak-Higashi syndrome of humans.

The increased susceptibility to pyogenic infections noted in cattle with the Chediak-Higashi syndrome trait has been related to an impairment of leukocyte function at the cellular level. Investigations of the relationship of abnormal granule formation to increased susceptibility to infection, conducted with cell suspensions containing high concentrations of polymorphonuclear leukocytes, revealed a bactericidal defect that was associated with abnormal intracellular killing and not due to defective particle ingestion. The in vitro bactericidal defect was associated with a metabolic anomaly in the hexose monophosphate shunt, but not with an alteration in the capacity to reduce nitroblue tetrazolium dye. Ultrastructural histochemical studies of phagocytosis and phagolysosome formation in polymorphonuclear leukocytes suggest that the impairment in bactericidal capacity is correlated also with either a delay or failure of primary granules to degranulate.