Vancomycin-resistant Enterococcus faecium (VREfm) is recognised by the World Health Organization (WHO) as a high-priority pathogen due to its capacity to cause severe infections in hospitalised patients and its resistance to nearly all available antibiotics. Of increasing concern is the emergence of resistance to daptomycin, one of the few remaining therapeutic options for treating VREfm infections. Despite its clinical significance, the molecular basis of daptomycin resistance in VREfm remains poorly understood.
This project aims to elucidate the molecular and cellular mechanisms that enable VREfm to survive daptomycin exposure. Through an integrated approach combining bacterial genetics, comparative genomics, multi-omics, and targeted in vitro assays, we will identify and characterise novel resistance pathways and key effector molecules that contribute to reduced daptomycin susceptibility. Particular emphasis will be placed on how these effectors influence membrane physiology, modulate stress responses, and promote antibiotic tolerance.
By deepening our understanding of the fundamental biology underlying daptomycin resistance in VREfm, this project will provide a foundation for the development of new therapeutic strategies to prevent or overcome resistance, improve treatment outcomes, and help preserve the clinical utility of daptomycin.
Public Health
