Stationary-Phase Fluoroquinolone Persisters Mostly Avoid DNA Double-Stranded Breaks.

When susceptible bacterial cultures are treated with antibiotics, some cells can survive treatment without heritable resistance, giving rise to susceptible daughter cells in a phenomenon termed antibiotic persistence. Current models of fluoroquinolone (FQ) persistence in stationary-phase cultures posit that post-treatment resuscitation is dependent on double-stranded break (DSB) repair through RecA-mediated homology-directed repair. Previously, we found that stationary-phase does not depend on RecA to persist.

Metabolic and transcriptional activities underlie stationary-phase sensitivity to Levofloxacin.

The bacterial pathogen is responsible for a variety of chronic human infections. Even in the absence of identifiable resistance mutations, this pathogen can tolerate lethal antibiotic doses through phenotypic strategies like biofilm formation and metabolic quiescence. In this study, we determined that maintains greater metabolic activity in the stationary phase compared to the model organism, , which has traditionally been used to study fluoroquinolone antibiotic tolerance.