Related Experiment Video

Updated: Aug 6, 2026

A Robust Pneumonia Model in Immunocompetent Rodents to Evaluate Antibacterial Efficacy against S. pneumoniae, H. influenzae, K. pneumoniae, P. aeruginosa or A. baumannii
09:17

A Robust Pneumonia Model in Immunocompetent Rodents to Evaluate Antibacterial Efficacy against S. pneumoniae, H. influenzae, K. pneumoniae, P. aeruginosa or A. baumannii

Published on: January 2, 2017

Call for the international adoption of microbiological breakpoints for fluoroquinolones and Streptococcus pneumoniae

Kristen N Schurek1, Heather J Adam, Daryl J Hoban

  • 1Department of Medical Microbiology, Faculty of Medicine, University of Manitoba, 5th Floor Basic Medical Sciences Building, 730 William Avenue, Winnipeg, Manitoba, Canada R3E 0W3. kris_schurek@yahoo.com

International Journal of Antimicrobial Agents
|August 15, 2006
PubMed

Insights

Current guidelines for levofloxacin resistance in Streptococcus pneumoniae are insufficient for detecting early resistance mutations. New breakpoints and a second marker like ciprofloxacin are needed to better predict and prevent fluoroquinolone resistance.

Area of Science:

  • Microbiology
  • Clinical Pharmacology
  • Antimicrobial Resistance

Background:

  • Current Clinical and Laboratory Standards Institute (CLSI) levofloxacin breakpoints may not adequately detect fluoroquinolone resistance in Streptococcus pneumoniae.
  • This inadequacy can lead to an underestimation of resistance development risk.

Purpose of the Study:

  • To evaluate the effectiveness of current CLSI levofloxacin breakpoints for detecting fluoroquinolone resistance in Streptococcus pneumoniae.
  • To propose improved methods for identifying resistance, including microbiological breakpoints and additional markers.

Main Methods:

  • Analysis of Streptococcus pneumoniae isolates to assess resistance mechanisms.
  • Evaluation of current and proposed breakpoints for levofloxacin and other fluoroquinolones.
  • Investigation of the correlation between parC mutations and fluoroquinolone susceptibility.

Main Results:

  • Current CLSI levofloxacin breakpoints are inadequate for detecting first-step parC mutations in Streptococcus pneumoniae.
  • ParC mutations are rare in isolates susceptible to fluoroquinolones when using microbiological breakpoints.
  • Ciprofloxacin use as a second marker shows promise in predicting isolates with first-step parC mutations.

Conclusions:

  • Adopting microbiological breakpoints for fluoroquinolones and S. pneumoniae can more accurately reflect resistance emergence.
  • The proposed approach may help prevent future fluoroquinolone treatment failures.
  • Using ciprofloxacin as a secondary marker improves the detection of parC mutations, aiding in resistance surveillance.

More Related Videos

Antibiotic Efficacy Testing in an Ex vivo Model of Pseudomonas aeruginosa and Staphylococcus aureus Biofilms in the Cystic Fibrosis Lung09:26

Antibiotic Efficacy Testing in an Ex vivo Model of Pseudomonas aeruginosa and Staphylococcus aureus Biofilms in the Cystic Fibrosis Lung

Published on: January 22, 2021

Related Concept Videos

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...
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...
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...
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,...