Immunologic basis for increased susceptibility of the neonate to infection.

Neonatal infection with the GBS occurs in a small fraction of exposed infants who lack specific antibody. Diminished influx of PMNs to sites of infection as a result of abnormalities in chemotaxis, bone marrow exhaustion, and to a lesser degree relative complement deficiency and decreased microbicidal activity of PMNs may be additional predisposing factors. Infection with HSV occurs more often in infants born to mothers with primary rather than secondary infection; the lack of passively acquired antibody in such infants is a possible but unproved susceptibility factor. The failure of neonates to control HSV may also be related to decreased production of or response to interferon or to decreased activity of nonimmune and immune cellular cytotoxic mechanisms. Similarly, infection with Toxoplasma and intracellular bacterial pathogens, such as Listeria, may be more severe because of the decreased generation of lymphokines and interleukins, which attract macrophages to the site of infection and enable them to kill these organisms. Much of this analysis based on in vitro and animal studies summarizes current information in a rapidly changing field rather than stating established fact. The precise age at which most of the immune functions discussed reach maturity is unknown. However, the risk of severe infection with these pathogens appears to wane by 2 to 3 months of age. Although this may partly reflect decreased exposure, we might hypothesize that immune functions that are mature by this age are those most critical for protection. Future studies focusing on changes in immune function during the first months of life may provide useful insights into the immunobiology of these diseases and direct attention to the most fruitful areas for immunologic intervention.