Infection determinants at extremes of age

Abstract

The immune defence of the full-term neonate is compromised in several ways. Although adequate numbers of B lymphocytes are present, antibody production may be delayed compared with the adult. Decreased levels of complement components contribute to the impaired opsonization potential of newborn sera and in turn, to impaired chemotactic responses of neonatal polymorphonuclear leucocytes (PMN). Multiple abnormalities in neonatal PMN function, coupled with deficient bone marrow supplies during stress, contribute greatly to the increased vulnerability to infection of neonates. Infection is a major problem for infants born before 28 weeks. Their serum IgG antibody levels are extremely low and the deficiencies in complement levels and PMN chemotatic responses noted in full-term neonates are even more marked and persist for longer. Opsonic activity decreases with decreasing gestational age and septicaemic pre-term infants are liable to develop neutrophil storage pool exhaustion. In contrast to neonates, the effect of ageing on the immune response is more variable but the changes in cell-mediated immunity have the greatest clinical impact. This decline in T cell function alters the balance between the immune system and intracellular organisms and leads to reactivation of previously controlled infections. Impaired function of immunoregulatory cells contributes to the poor and unsustained antibody responses of the elderly to primary and booster immunizations. Immunosenescence contributes to the morbidity and mortality of old age by several mechanisms, but mainly through an increased susceptibility to infection.