The presence of antibiotic resistance in probiotic bacteria has raised concerns about the safety of the strains used in food systems. This study elucidated the molecular mechanisms underlying vancomycin resistance in Enterococcus faecium KU22001 using integrated genomic and physiological analyses. The minimum inhibitory concentration (MIC) for vancomycin was determined using the broth microdilution method and whole-genome sequencing was performed to identify resistance-associated genes. The E. faecium KU22001 had a very high MIC for vancomycin (1,280 mg/L); genome annotation identified vanZ and several multidrug transporter genes, but did not detect canonical van operon genes; and the high-performance liquid chromatography analysis suggested that there was no enzymatic degradation of vancomycin in E. faecium KU22001 under the test conditions. The physiological assays indicated a partial modulation of cell wall permeability, whereas cell membrane permeability remained largely unchanged. In contrast, the inhibition of efflux pumps after adding reserpine reduced the vancomycin MIC by approximately 1,024-fold. These results suggested that efflux pump–driven antibiotic export plays a major role in vancomycin resistance in E. faecium KU22001. Cell wall–associated adaptive responses also contributed to vancomycin resistance.
Kang et al. (Fri,) studied this question.