Abstract
Newborn immunity, microbial colonization and infection Newborns in nurseries and neonatal intensive care units (NICU) are at risk for nosocomial infections due to an environment, which is dramatically different from the sterile environment of the uterus. Invasive devices and frequent use of antimicrobial substances represent particular risks.1 Many of the newborn’s defence mechanisms are not fully developed: for example phagocytic activity, immunoglobulin synthesis or T-lymphocyte function.2 The immune deficiency is age-related, i.e. the earlier during gestation the infant is born, the higher is the susceptibility to infection. During the intrauterine period no immunologic significant stimuli are present to prime protective immune reactions. The infant therefore depends on passively acquired maternal antibodies, which are transmitted via the placenta starting from 24 to 26 weeks of gestation. Prematurely born infants demonstrate significantly lower IgG antibody levels than full term infants.3 However, these passively acquired antibodies represent the mother’s prior exposure which certainly was different to the antigenic challenges of a NICU. Due to the sterile intrauterine environment the newborn lacks any normal microbial flora. In healthy newborns colonization of mucous membranes and skin develops rapidly by transmission of microbes from the infant’s mother and other family members. Neonates starting life in a NICU acquire their flora from their contacts with doctors and nurses and the environmental of the ward, possibly resulting in early colonization with antibiotic resistant bacteria. Skin and mucous membranes of premature children are markedly permeable to exogenic antigens thus increasing the risk for microbial invasion of tissues and the vascular system.4 Vertical and horizontal transmission Besides human and inanimate sources of infection, neonates acquire microorganisms from the maternal birth canal, which may cause infection (Table 1).
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