ABSTRACT: Unnoticed spread of linear VanA-plasmids in vancomycin-variable Enterococcus faecium strains across different regions: a diagnostics challenge
Project description:Characterization of vanA-harboring plasmids improves differentiation of outbreak-related and sporadic vancomycin-resistant Enterococcus faecium isolates
Project description:This study aims to determine the global gene expression in vancomycin resistant Enterococcus faecium (VRE) in response to a novel essential oil-vancomycin combination, and the individual components (vancomycin, carvacrol and cuminaldehyde) to help determine the mechanism of action of this antimicrobial formulation. This formulation increases the susceptibility of VRE to vancomycin and the array provides data on the synergistic mechanism of action. Five conditions (1. Control; 2. Carvacrol, 1.98 mM; 3. Cuminaldehyde, 4.20 mM; 4. Vancomycin, 0.031 mg/l; 5. Combination, 1.98 mM Carvacrol, 4.2 mM Cuminaldehyde, 0.031 mg/l vancomycin) all with 1% DMSO were tested in triplicate with a 60 minute exposure time before extraction.
Project description:Genomic surveillance of vancomycin-resistant Enterococcus faecium reveals local spread of a linear plasmid conferring a nutrient utilization advantage
Project description:Vancomycin variable Enterococcus faecium clone containing a deletion within vanX
| PRJEB25215 | ENA
Project description:Vancomycin-resistant Enterococcus faecium in Irish hospitals 2017-2019: high prevalence of ST80 and spread of very similar vanA regions via IS1216E and plasmid transfer throughout diverse genetic lineages
Project description:Vancomycin-resistant Enterococcus faecium (VREfm) is a leading cause of healthcare-associated infections globally and demands new approaches for treatment. Here we show that genetic and pharmacological inactivation of a highly conserved NlpC/P60 peptidoglycan hydrolase, secreted antigen A (SagA), enhanced vancomycin susceptibility of VREfm ex vivo and in vivo. Notably, genetic deletion of sagA impaired VREfm peptidoglycan remodeling, growth and increased the activity of vancomycin. We then identified first-in-class covalent NlpC/P60 peptidoglycan hydrolase inhibitors and demonstrated that pharmacological inactivation of SagA activity also impaired peptidoglycan remodeling and increased the efficacy of vancomycin in several VREfm clinical isolates. Our study reveals peptidoglycan hydrolases are druggable targets whose inactivation improves the efficacy of vancomycin against VREfm.
2026-04-13 | PXD075040 | Pride
Project description:Genetic analysis of vancomycin-variable Enterococcus faecium clinical isolates in Italy
| PRJNA993974 | ENA
Project description:Sequencing of multiple Enterococcus faecium isolates from 10 patients harbouring Linear plasmids
