Host defence to bacterial infection in the neonate

Host defence to bacterial infection is mainly determined by opsonins, i.e., IgG antibodies and complement, and phagocytic cells, which co-operate to remove bacterial invaders from host tissues. Various studies have clearly documented distinct defects in both arms of host defence in the newborn period. Chemotaxis, i.e., directed migration of polymorphonuclear leukocytes (PMN) is impaired in the neonate. Phagocytosis of bacteria by neonatal PMN is normal, but post-phagocytic events, particularly metabolic activation and bacterial killing are impaired, the latter defect apparently due to diminished generation of reactive oxygen species. Both classical and alternative pathway activity of complement are mildly diminished (50-80% of adult values) in the term newborn, but are more severely decreased in the premature infant (20-40% of adult values in 28 to 36 weeks prematures). Opsonic activity of transplacentally-derived IgG when compared to maternal IgG is strikingly deficient against staphylococci and group B streptococci (GBS), in the latter case depending on the GBS serotype. Since opsonization is a key process in antibacterial defence, it is speculated that these opsonic defects of IgG may be an essential determinant of the neonate's susceptibility to disease due to these bacteria.