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Enhanced antibiotic resistance development from fluoroquinolone persisters after a single exposure to antibiotic

Theresa C Barrett1,2, Wendy W K Mok3,4, Allison M Murawski1,2

  • 1Department of Molecular Biology, Princeton University, Princeton, NJ, 08544, USA.

Nature Communications
|March 14, 2019
PubMed

Insights

Bacterial persisters, tolerant to antibiotics, surprisingly accelerate antibiotic resistance development. Fluoroquinolone treatment damages persister DNA, triggering a response that increases resistant mutant offspring.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Genetics

Background:

  • Bacterial persisters tolerate antibiotics via low metabolic activity.
  • Persister offspring were thought to develop resistance at normal rates.
  • Antibiotic tolerance mechanisms remain incompletely understood.

Purpose of the Study:

  • Investigate the impact of fluoroquinolone treatment on bacterial persisters.
  • Determine if persister populations exhibit altered rates of antibiotic resistance development.
  • Elucidate the molecular mechanisms underlying enhanced resistance in persister offspring.

Main Methods:

  • Time-lapse microscopy of Escherichia coli populations after ofloxacin exposure.
  • Quantification of antibiotic-resistant mutants in populations derived from persisters.
  • Genetic analyses involving RecA, SOS induction, and DNA polymerase V (UmuDC).

Main Results:

  • Persisters exhibited filamentation and induced significant SOS responses upon fluoroquinolone treatment.
  • Populations derived from fluoroquinolone persisters showed significantly higher frequencies of antibiotic resistance.
  • Enhanced resistance development required RecA, SOS induction, recovery time, and UmuDC.

Conclusions:

  • Fluoroquinolones induce DNA damage in bacterial persisters.
  • The SOS response in persisters accelerates the emergence of antibiotic resistance.
  • Persister cells are a significant source of antibiotic resistance evolution.

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