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Mechanism of Antibiotic Resistance in MRSA

Antibiotic resistance in bacteria arises when microorganisms evolve the ability to withstand drugs designed to kill them or inhibit their growth, rendering once-effective treatments useless. This phenomenon, driven by genetic change and selection under antibiotic exposure, poses a profound threat to modern medicine. Mechanisms include drug-inactivating enzymes (e.g., β-lactamases), efflux pumps that eject antibiotics, mutations altering antibiotic targets, decreased drug uptake, and acquisition...
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Related Experiment Video

Updated: May 21, 2026

Cefoperazone-treated Mouse Model of Clinically-relevant Clostridium difficile Strain R20291
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Published on: December 10, 2016

Association between vancomycin-resistant Enterococci bacteremia and ceftriaxone usage.

James A McKinnell1, Danielle F Kunz, Eric Chamot

  • 1Infectious Disease Clinical Outcomes Research Unit, Division of Infectious Disease, Los Angeles Biomedical Research Institute, Harbor-UCLA Medical Center, 1124 West Carson Street, Torrance, CA 90502, USA. Dr.McKinnell@yahoo.com

Infection Control and Hospital Epidemiology
|June 7, 2012
PubMed
Summary

Increased ceftriaxone use correlated with higher vancomycin-resistant enterococci bloodstream infections (VRE-BSI). Limiting ceftriaxone may help reduce hospital-acquired VRE-BSI, improving patient outcomes.

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Published on: July 24, 2021

Area of Science:

  • Infectious Diseases
  • Hospital Epidemiology
  • Antimicrobial Stewardship

Background:

  • Vancomycin-resistant enterococci (VRE) pose a significant public health threat, increasing patient mortality and healthcare costs.
  • The link between hospital antibiotic use and VRE incidence is not well understood, despite animal studies suggesting a ceftriaxone-VRE association.

Purpose of the Study:

  • To investigate the association between antimicrobial usage and vancomycin-resistant enterococci bloodstream infection (VRE-BSI) incidence.
  • To test the hypothesis that increased ceftriaxone usage is linked to a higher incidence of VRE-BSI.

Main Methods:

  • Retrospective cohort study conducted at a 900-bed urban tertiary care hospital from 2005 to 2008.
  • Antimicrobial usage quantified as days of therapy (DOTs) per 1,000 patient-days; VRE-BSI incidence calculated as cases per 1,000 patient-days.
  • Negative binomial regression used to analyze associations between antimicrobial usage and VRE-BSI at hospital and care-unit levels.

Main Results:

  • VRE-BSI incidence rose from 0.06 to 0.17 per 1,000 patient-days during the study period.
  • Prior-month ceftriaxone DOTs were significantly associated with increased VRE-BSI incidence (IRR, 1.38 per 10 DOTs; P = .005).
  • Cephalosporin (class) or vancomycin usage was not predictive of VRE-BSI, nor were other specific antibiotics when analyzed individually.

Conclusions:

  • Prior-month ceftriaxone usage, but not cephalosporin or vancomycin use, was associated with VRE-BSI incidence.
  • Findings suggest that antimicrobial stewardship programs targeting ceftriaxone use could potentially decrease nosocomial VRE-BSI.
  • Intensive care unit type was also identified as a factor related to VRE-BSI incidence.