Host Defense against Infection in the Newborn

Prof. Richard B. Johnston, Jr., MD, March of Dimes Birth Defects Foundation, National Office, 1275 Mamaronock Avenue, White Plains, N.Y. (USA) It has long been recognized that newborn infants exhibit a predispostion to infection by a variety of microorganisms. Infection remains one of the major threats to the neonate even today. In some cases, infection might be explained by massive exposure to the infecting organism in utero or during the birth process, e.g., syphilis, group B streptococcus, and herpes simplex virus. In general, however, it appears likely that newborn infants carry an undue susceptibility to infection because they cannot mount normal host defense. A large number of studies have been conducted in an attempt to discover specific abnormalities. Many of these have detected subnormal function of various aspects of the newborn’s inflammatory response, yet no single defect can explain why newborns sustain serious infection so commonly. The barrier function of skin and mucous membranes is clearly important in the neonatal period, but the function of antimicrobial peptides such as magainins and defensins has not been described in the human newborn. The maternal dowry of antibodies in the IgG class reflects the mother’s experience with infection except in preterm babies, especially those born at less than about 32-34 weeks of gestation, who start at antibody deficit. The active antibody response by the baby to new polysaccharide antigens is blunted, and the baby lacks memory lymphocytes that expedite a rapid response to familiar microbial products. This problem undoubtedly plays a role in the predisposition of the newborn to bacterial infections, but to date prophylactic infusion of immunoglobulin had not been shown conclusively to reduce the threat of infection. Complement, to other key system involved in opsonization, is clearly deficient in newborns, and the deficiency is more pronounced in pre-term babies. The alternative pathway, which allows complement activation in the absence of specific antibody, is relatively more defective than the classical pathway. Thus, the effect of antibody deficiency is compounded by defective function of the complement system. Newborns generally begin life with normal or increased numbers of circulating phagocytes (neutrophils and monocytes), as well as lymphocytes. However, the reserve supply of