The role of infection in necrotising enterocolitis

Abstract

Necrotising enterocolitis (NEC) predominantly affects enterally fed premature infants and remains a major cause of morbidity and mortality. It is likely that NEC is a disease with multi-factorial aetiology, but the precise contribution of various potentially adverse events to mucosal injury remains ill-defined. Immaturity of the gastrointestinal mucosal barrier and immune response are thought to make premature infants more susceptible to development of NEC. There is evidence that accumulation of platelet-activating factor and the resulting inflammatory cascade plays a key role in the development of bowel necrosis. Bacterial colonisation of the gastrointestinal tract appears to be a prerequisite for NEC. Although various infectious agents have been implicated, no single organism has consistently been associated with the disease. Compared with full-term newborns, premature infants have delayed gastrointestinal colonisation with a less complex flora comprising predominantly aerobic Gram-negative organisms and few anaerobes. This aberrant colonisation may play a significant role in triggering an inflammatory response. Endotoxin has been shown to stimulate excessive pro-inflammatory cytokine production by immature enterocytes and overgrowth of Enterobacteriaceae may promote bacterial translocation. Several measures, aimed at improving intestinal barrier function, bolstering intestinal immunity and promoting development of a normal gut flora, have been associated with a reduced incidence of NEC.