Infection and Immunity: Neonatal Immunology

Each limb of the immune system is partially functional, partially non‐functional at the time of birth. Newborns are unusually susceptible to infection, and feeding practices, immunization schedules and certain congenital conditions are all affected by the state of the infants immune system. I shall review each of these systems. The granulocytes are slow to chemotax but can phagocytise well, and have only a modest reduction of bactericidal activity; however this latter ability may be compromised severely in the presence of stress or infection. The mononuclear phagocytes (monocytes) are also slow to chemotax, but their bactericidal and cytotoxic functions are normal. The fixed mononuclear cells may have diminished phagocytosis and killing capacity. The monocytes may also have a defect in antigen processing with decreased expression of DR antigen. Complement activity is about 25–50% of the maternal level but this is usually sufficient to prevent infection in the term infant. In the presence of prematurity complement components may be reduced sufficiently so as to produce a clinically significant opsonic deficiency. This can be corrected by plasma or gamma globulin. Certain Gram (‐) organisms need alternative complement pathway activation to affect opsonization the newborn may have decreased ability to activate this pathway. The antibody synthetic system is essentially inoperative at birth despite adequate B‐cells, as a result of intrinsic B‐cell inactivity and enhanced T‐cell suppression. Passive maternal IgG usually but not always, compensates for this deficit in the term infant. Local secretory IgA antibody synthesis is also absent for the first 6 to 8 weeks of life; this is compensated for in part by the ingestion of breast milk, The first antibody responses noted are IgA antibody responses, while IgG responses are initially sluggish and delayed. Poor IgG antibody responses to certain antigens, particularly polysaccharides, may persist for a prolonged period. Neonatal T‐cells show good recognition and proliferative responses but T‐cell cytotoxicity is compromised and certain lymphokines (e.g. MIF, immune interferon) are markedly deficient. Delayed cutaneous hypersensitivity is also deficient. Natural killer activity is also reduced. Thymus size and hormonalactivity is increased. Taken as a whole, the immature immune system does not have the capacity to fully respond to an invading organism, and the result is frequent, severe, and occasionally fatal infection.