A woman with a history of recurrent urinary infections shows increased resistance to levofloxacin. Which bacterial mechanism likely contributed to this outcome?

Increased resistance to levofloxacin in bacterial pathogens can often be attributed to the overexpression of cellular efflux pumps. These pumps are transport proteins that can actively expel antibiotics, including fluoroquinolones like levofloxacin, from the bacterial cell. When bacteria overexpress these pumps, they can effectively lower the intracellular concentration of the antibiotic, reducing its efficacy and allowing the bacteria to survive despite the presence of the drug.

This mechanism is particularly relevant for fluoroquinolones as they rely on sufficient intracellular concentrations to inhibit bacterial DNA replication through interference with topoisomerases. Consequently, if an organism can pump out the antibiotic before it can exert its antimicrobial effect, it can develop resistance.

The other mechanisms involve different processes that do not directly relate to the specific action of levofloxacin. For example, mutations in ribosomal subunits or increased production of dihydrofolate reductase relate to resistance to other classes of antibiotics (like macrolides or trimethoprim/sulfamethoxazole, respectively) but do not effectively explain the resistance to levofloxacin, which targets DNA processes rather than protein synthesis or folate metabolism. Enhanced repair of DNA damage does not directly confer resistance against fluoro