<i>In vivo</i> development of elevated linezolid resistance mediated by a deletion in ribosomal protein L3 in clinical <i>Enterococcus faecium</i>.

ABSTRACT: Gram-positive bacteria can develop resistance to linezolid through mutations in the 50S large-subunit ribosomal proteins, such as L3. However, this mechanism is rarely reported in clinical enterococcal strains. Here, we describe a pair of Enterococcus faecium strains, 1505efm and 1583efm, isolated from a meningioma patient at different stages of linezolid treatment. Strain 1583efm, which was obtained after 17 days of linezolid treatment, exhibited an eightfold higher linezolid MIC (64 mg/L) than the initially isolated strain 1505efm (8 mg/L). Meanwhile, 1583efm became susceptible to erythromycin, tetracycline, and high-level streptomycin due to the loss of plasmid-borne resistance genes erm(A), erm(B), tet(M), ant(6)-Ia, and aph(3')-III. Whole-geno

SUBMITTER: Sun L 

PROVIDER: S-EPMC12691684 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature