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Antibiotic Selection00:57

Antibiotic Selection

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Constructing Mutants in Serotype 1 Streptococcus pneumoniae strain 519/43
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Microscale insights into pneumococcal antibiotic mutant selection windows.

Robin A Sorg1, Jan-Willem Veening1

  • 1Molecular Genetics Group, Groningen Biomolecular Sciences and Biotechnology Institute, Centre for Synthetic Biology, University of Groningen, Nijenborgh 7, Groningen 9747 AG, The Netherlands.

Nature Communications
|October 31, 2015
PubMed
Summary
This summary is machine-generated.

Emerging antibiotic resistance in Streptococcus pneumoniae is a major concern. This study reveals how bacteriostatic antibiotics promote resistance by allowing gene expression and epigenetic inheritance of reduced susceptibility, aiding further genotypic resistance.

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Area of Science:

  • Microbiology
  • Molecular Biology
  • Genetics

Background:

  • Streptococcus pneumoniae is a significant human pathogen with increasing antibiotic resistance.
  • The fundamental mechanisms driving the de novo emergence of resistance in pneumococci remain unclear.
  • Understanding resistance development is crucial for combating infectious diseases.

Purpose of the Study:

  • To systematically analyze the impact of antibiotics on Streptococcus pneumoniae within the mutant selection window.
  • To differentiate between bacteriostatic and bactericidal antibiotic effects on pneumococcal growth and gene expression.
  • To investigate the mechanisms underlying the emergence of antibiotic heteroresistance and its role in promoting genotypic resistance.

Main Methods:

  • Systematic analysis of antibiotic effects on Streptococcus pneumoniae at sub-inhibitory concentrations.
  • Identification of distinct growth-inhibition profiles for bacteriostatic and bactericidal compounds.
  • Real-time mutation assays and time-lapse microscopy to observe cellular responses and resistance development.
  • Epigenetic analysis to understand the inheritance of heteroresistance.

Main Results:

  • Discrete growth-inhibition profiles were identified, enabling prediction of bacteriostatic vs. bactericidal activity.
  • Bacteriostatic agents promoted continued gene expression, linked to genotypic resistance development.
  • Antibiotic-susceptible pneumococci exhibited growth and death bistability.
  • Subpopulations with decreased susceptibility (heteroresisters) to cell wall synthesis inhibitors were observed.
  • Heteroresistance was found to be epigenetically inherited and potentiated genotypic resistance accumulation.

Conclusions:

  • Antibiotic concentration within the mutant selection window is critical for resistance emergence.
  • Bacteriostatic antibiotics facilitate resistance development through sustained gene expression and epigenetic mechanisms.
  • Heteroresistance is an epigenetically inherited trait that primes pneumococci for further genotypic resistance, posing a significant clinical challenge.