Virulence Determinants of Enterococcus faecium

Abstract

Enterococcus faecium, a member of the human gut microbiota, has emerged as a notable opportunistic pathogen, contributing to a diverse range of hospital-acquired infections. Its capacity to thrive in various anatomical sites and initiate infections is attributed to an elaborate suite of virulence determinants. Prominent among these are cell surface components and pili structures, which facilitate initial adhesion and subsequent biofilm formation. Additionally, temperature-regulated gene expression augments virulence by enhancing adherence and biofilm formation. E. faecium also employs sophisticated mechanisms to modulate host immune responses, including hindering leukocyte killing through membrane structures like lipoteichoic acids and capsular polysaccharides. Bacteriocins confer a competitive edge by inhibiting competing bacteria, while global regulators orchestrate biofilm formation and stress responses. The stringent response further enhances adaptation to stress conditions. Understanding these virulence factors is paramount for unraveling the intricacies of E. faecium infections and devising effective therapeutic strategies.