Newer Insights in Etiology and Pathogenesis of Neonatal Sepsis

Neonatal sepsis is a pathophysiological response to the presence of microorganisms or their toxins in the blood during the first 28 days of life. Despite advances in neonatal intensive therapy and care, sepsis is still an important cause of morbidity and mortality in neonates, especially preterm and low birth weight neonates. Early neonatal sepsis manifests itself in the first 72 hours of life. The main risk factor for early neonatal sepsis is chorioamnionitis, and the most important causative are Streptococcus group B and Escherichia coli. Late neonatal sepsis manifests itself after 72 hours of life, and most often occurs in preterm neonates. Among the causative agents of late neonatal sepsis, coagulase-negative Staphylococcus dominates. The neonates are highly dependent of the innate immune system to defend against infection. In the pathophysiological response of the organism to infection, microcirculation, neutrophils and monocytes are first activated, and then the complement and the coagulation system. Also, mitochondrial dysfunction contributes to tissue damage in neonatal sepsis. The delayed response of adaptive immunity in the neonatal period is compensated by transplacental transfer of IgG antibodies originated from the mother, but also the IgA antibodies that the neonates receive from mother's milk. Compared to adults, the immune response have quantitative and qualitative differences, which contributes to their increased susceptibility to infection.