Beyond sepsis: Staphylococcus epidermidis is an underestimated but significant contributor to neonatal morbidity

Abstract

Staphylococcus epidermidis accounts for the majority of cases of neonatal sepsis. Moreover, it has been demonstrated to be associated with neonatal morbidities, such as bronchopulmonary dysplasia (BPD), white matter injury (WMI), necrotizing enterocolitis (NEC) and retinopathy of prematurity (ROP), which affect short-term and long-term neonatal outcome. Imbalanced inflammation has been considered to be a major underlying mechanism of each entity. Conventionally regarded as a harmless commensal on human skin, S. epidermidis has received less attention than its more virulent relative Staphylococcus aureus. Particularities of neonatal innate immunity and nosocomial environmental factors, however, may contribute to the emergence of S. epidermidis as a significant nosocomial pathogen. Neonatal host response to S. epidermidis sepsis has not been fully elucidated. Evidence is emerging regarding the implication of S. epidermidis sepsis in the pathogenesis of neonatal inflammatory diseases. This review focuses on the interplay among S. epidermidis, neonatal innate immunity and inflammation-driven organ injury.

Keywords: Staphylococcus epidermidis; bronchopulmonary dysplasia; inflammatory disorders; innate immunity; necrotizing enterocolitis; neonatal sepsis; preterm infants; white matter injury.

Figure 1.

Putative mechanisms of Staphylococcus epidermidis-induced neonatal inflammatory response and consecutive organ injuries. PIA: polysaccharide intercellular adhesin; PSMs: phenol-soluble modulins; SCCmec: staphylococcal chromosome cassette mec; IS: insertion sequence; TNF-α: tumor necrosis factor-α; IL: interleukin; CNS: central nervous system; iNOS: inducible nitric oxide synthase; ICAM-1: intercellular adhesion molecule-1.