Clinical and molecular characterization of vancomycin-resistant enterococci from immunocompromised host and impact on human cell viability in an in vitro colon model

The prevalence of systemic infections caused by vancomycin-resistant Enterococci (VRE) has risen significantly in Europe, posing a critical health risk, especially among immunocompromised patients. This study aimed to comprehensively characterize VRE bloodstream infections in immunocompromised patients and investigate their interaction mechanisms with human cells using an in vitro colorectal cell model.This study involved the isolation and genomic analysis of four VRE strains from patients identified through hospital antimicrobial resistance surveillance programs between June and October 2023. The strains underwent antimicrobial susceptibility testing, molecular characterization, and whole genome sequencing to identify resistance genes and virulence factors. Bacterial adherence and the impact of the bacterial culture supernatants on human colorectal adenocarcinoma cells was assessed using viability assay.Four sequence types (ST117, ST80, ST28, ST179) were identified. All strains were resistant to fluoroquinolones and glycopeptides but susceptible to quinupristin/dalfopristin and linezolid. Genomic analysis revealed resistance genes, including vanA, vanB, and presence of aminoglycoside-modifying enzymes. Only E. faecium isolates presented adhesin genes, while E. faecalis strains carried virulence genes for cytolysin production, capsule, and biofilm formation. Adhesion assays demonstrated that certain strains exhibited greater adherence to CaCo-2 cells compared to the reference strains. VRE supernatants demonstrated a potential cytostatic effect on CaCo-2 cells, reducing cell growth (9.15% to 47.33%) at both 8 and 24 hours (p-values < 0.05). This study revealed significant genetic diversity and varied adhesive profiles in the resistant clinical isolates. The findings suggest a potential cytostatic impact of VRE culture supernatants on colorectal cancer cells. It enhances our understanding of VRE infection mechanisms in immunocompromised patients, highlighting the importance of bacterial adhesion and secreted agents, and warrants further investigation into their mechanisms and potential clinical implications