Complement deficiency and neutrophil dysfunction as risk factors for bacterial infection in newborns and the role of granulocyte transfusion in therapy

Abstract

The similarity in the susceptibility to bacterial infections of newborns and older patients with complement deficiencies, neutropenia, or neutrophil function defects has suggested that neutrophils and/or complement might also be defective in newborns. Although no individual element of the phagocytic host defense system is severely deficient, several partial deficiencies have been identified. These involve important amplification pathways of complement and neutrophil activation and may combine to cause significant decreases in phagocyte activity at sites of infection. Because of decreased specific antibody, initial activation of the classical complement pathway is decreased. Low levels of C3 and factor B decrease amplification by the alternative pathway and result in marked decreases in opsonization and generation of chemotactic activity from C5. There are also quantitative and qualitative neutrophil defects. The recent observations that newborns' neutrophils are relatively deficient in membrane expression of their major adherence protein/C3bi receptor help explain the decreased mobility and phagocytic activity of these cells. Thus, several partial deficiencies combine to cause severe impairments in delivery of neutrophils to sites of infection and contribute to the increased susceptibility of the newborn to infection.