# Prevalence, Antimicrobial Resistance, and Molecular Characterization of Vancomycin-Resistant Enterococci in a North Indian Tertiary Care Hospital

## TL;DR

This study found a 7.36% prevalence of vancomycin-resistant enterococci in a North Indian hospital, with most cases caused by Enterococcus faecalis and resistance linked to the vanA gene.

## Contribution

The study provides new insights into the prevalence and molecular mechanisms of vancomycin resistance in a North Indian hospital setting.

## Key findings

- Vancomycin-resistant enterococci were found in 7.36% of isolates, with Enterococcus faecalis being the most common species.
- All VRE isolates were resistant to vancomycin but susceptible to linezolid.
- Molecular analysis confirmed the presence of the vanA gene in all tested VRE isolates, with no vanB detected.

## Abstract

Background

Vancomycin-resistant enterococci (VRE) are important nosocomial pathogens with limited treatment options and increasing prevalence in India. This study aimed to determine the prevalence of VRE among hospitalized adults, evaluate their antimicrobial resistance patterns, and characterize genetic determinants of vancomycin resistance.

Methods

A cross-sectional study was conducted from April 2023 to September 2024. Enterococcus spp. isolated from adult inpatients were identified using standard methods and matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS). Antimicrobial susceptibility testing was performed by Kirby-Bauer disc diffusion and Epsilometer strip minimum inhibitory concentration (E-strip MIC) testing. A subset of isolates underwent multiplex real-time polymerase chain reaction (PCR) for vanA and vanB gene detection.

Results

Of 3,176 Enterococcus isolates, 234 (7.36%) were VRE. Urine samples accounted for 210/2,684 (7.8%) and blood cultures for 12/210 (5.7%) of VRE isolates. Overall, Enterococcus faecalis (E. faecalis) (1,960; 61.7%) predominated, while Enterococcus faecium (E. faecium) (1,216; 38.3%) showed higher resistance. Among VRE, E. faecalis contributed 145/234 (61.9%) and E. faecium 89/234 (38.0%). All VRE were resistant to vancomycin (MIC ≥32 µg/mL). Linezolid was effective against all isolates (234/234; 100%). Molecular analysis of 20 representative isolates confirmed the presence of vanA in all (100%), with no vanB detected.

Conclusion

A 7.36% prevalence of VRE was observed, predominantly in urinary and bloodstream infections. Exclusive detection of vanA indicates clonal dissemination of high-level resistance. Routine species-level identification, antimicrobial stewardship, and molecular surveillance are critical to limiting VRE spread in tertiary care settings.