SIRS and group-B streptococcal sepsis in newborns: pathogenesis and perspectives in adjunctive therapy.

Clinical signs of systemic inflammation and suspected systemic infection are common in neonatal medicine. Yet, causative infectious organisms can only infrequently be isolated. In previously healthy infants at low risk of sepsis, group B streptococcus (GBS) is the most common isolate. In vitro and in vivo data suggest that immune cells from newborn infants have impaired antimicrobial properties against GBS. In contrast large amounts of inflammatory mediators are formed upon GBS challenge and Toll-like receptors (TLR) are critical host molecules in this context. Thus, the immune balance tilts towards inflammation, SIRS and sepsis. Adjunctive therapy of neonatal sepsis needs to adjust the inflammatory response without further impairing bacterial clearance. This article summarises the pathophysiological events leading to sepsis and suggests molecular targets for adjunctive therapy.