Related Experiment Video

Updated: Oct 5, 2026

Quantification of Violacein in Chromobacterium violaceum and Its Inhibition by Bioactive Compounds
07:13

Quantification of Violacein in Chromobacterium violaceum and Its Inhibition by Bioactive Compounds

Published on: August 8, 2025

Sub-inhibitory concentrations of vancomycin prevent quinolone-resistance in a penicillin-resistant isolate of

P Cottagnoud1, J M Entenza, M Cottagnoud

  • 1Department of Internal Medicine, Inselspital, Freiburgstrasse, CH-3010 Berne, Switzerland. pcottagn@insel.ch

BMC Microbiology
|July 17, 2001
PubMed
Abstract

Insights

Vancomycin can prevent the development of resistance to fluoroquinolones like trovafloxacin and ciprofloxacin in penicillin-resistant pneumococci. This finding is important for treating pneumococcal infections and combating antimicrobial resistance.

Area of Science:

  • Microbiology
  • Infectious Diseases
  • Pharmacology

Background:

  • Penicillin-resistant pneumococci pose a significant threat to treating pneumococcal infections.
  • Combined resistance to penicillin and quinolones complicates treatment options.
  • Emergence of quinolone resistance is a critical concern in pneumococcal infections.

Purpose of the Study:

  • To identify a treatment strategy to prevent the development of quinolone resistance in pneumococci.
  • To investigate the effect of vancomycin on quinolone resistance selection.

Main Methods:

  • Penicillin-resistant pneumococci were exposed to increasing concentrations of trovafloxacin or ciprofloxacin.
  • Mutant strains were selected to assess resistance development.
  • The effect of sub-inhibitory vancomycin concentrations on resistance was evaluated.

Main Results:

  • Exposure to increasing fluoroquinolone concentrations selected for resistant pneumococcal mutants.
  • Sub-inhibitory vancomycin concentrations prevented the emergence of trovafloxacin resistance.
  • Vancomycin also inhibited the development of high-level ciprofloxacin resistance.

Conclusions:

  • Vancomycin co-administration may be a viable strategy to prevent fluoroquinolone resistance in pneumococci.
  • This approach could be clinically significant in managing infections caused by resistant strains.
  • Further research is warranted to explore clinical applications.

More Related Videos

Nanomechanics of Drug-target Interactions and Antibacterial Resistance Detection11:56

Nanomechanics of Drug-target Interactions and Antibacterial Resistance Detection

Published on: October 25, 2013

Related Concept Videos

Inhibitors of Gram-positive Cell Wall Synthesis01:23

Inhibitors of Gram-positive Cell Wall Synthesis

Bacterial cell walls are typically rigid structures composed mainly of peptidoglycan, a mesh-like polymer that provides mechanical strength and maintains cell shape. The synthesis of peptidoglycan is a crucial process in bacterial growth and serves as a primary target for many antibiotics.Mechanism of Action of Beta-Lactam AntibioticsBeta-lactam antibiotics, such as penicillin, inhibit peptidoglycan synthesis in actively growing cells. These antibiotics share a characteristic four-membered...
Mechanism of Antibiotic Resistance in MRSA01:25

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...
Gene Regulation in Microbial Communities: Quorum Sensing01:28

Gene Regulation in Microbial Communities: Quorum Sensing

Quorum sensing is a mechanism of bacterial communication that enables coordinated gene expression in response to changes in population density. This facilitates collective behaviors that enhance survival, resource acquisition, and ecological adaptation. This process relies on small signaling molecules called autoinducers that accumulate as bacterial populations grow. When a critical threshold concentration of autoinducers is reached, bacterial cells collectively modify gene expression,...
Clinical Significance of Antibiotic Resistance01:25

Clinical Significance of Antibiotic Resistance

Methicillin-resistant Staphylococcus aureus (MRSA) presents a critical public health threat, arising from its capacity to resist β-lactam antibiotics due to acquisition of the mecA gene within the staphylococcal cassette chromosome mec (SCCmec). This gene encodes penicillin-binding protein 2a (PBP2a), which impairs binding efficacy of methicillin and other β-lactams. MRSA has evolved into distinct clonal lineages impacting humans and animals alike, reinforcing its significance within the One...
Inhibitors of Bacterial DNA Synthesis01:28

Inhibitors of Bacterial DNA Synthesis

Bacterial pathogens depend on precise and efficient DNA replication to sustain infection. Two type II topoisomerases—DNA gyrase and topoisomerase IV—are critical to this process, as they resolve DNA supercoiling and unlink chromosomes during replication. Fluoroquinolones, synthetic derivatives of quinolones, exploit this mechanism by stabilizing the transient DNA–enzyme cleavage complex, preventing strand religation, and causing lethal double-strand breaks. These antibiotics are selectively...
Development of Antibiotic Resistance01:30

Development of Antibiotic Resistance

Antibiotic resistance is a major public health concern that arises when bacteria evolve mechanisms to withstand the effects of antibiotic treatments. This resistance can be intrinsic, acquired through genetic mutations, or transferred between bacteria via horizontal gene transfer. The development of antibiotic resistance poses significant challenges in treating bacterial infections and necessitates ongoing research to develop new therapeutic strategies.Intrinsic resistance occurs when bacterial...