Acquisition of double mutation in caused high resistance to sitafloxacin in after unsuccessful eradication with sitafloxacin-containing regimens.

BACKGROUND AND AIM

Although sitafloxacin (STFX)-containing regimens are effective rescue treatments for infection, prevalence of fluoroquinolone resistance in has increased rapidly worldwide. The change in resistance levels and mutations, a major cause of fluoroquinolone resistance, after unsuccessful STFX-containing treatment has not been investigated.

METHODS

We conducted a retrospective, non-randomized study to compare the minimum inhibitory concentrations (MICs) of STFX and the location of mutations in before and after unsuccessful eradication with STFX-containing regimens at Keio University Hospital between December 2011 and March 2015.

RESULTS

A total of 266 patients treated with STFX-containing regimens for third-line eradication were evaluated. Double mutations in were acquired by 20.8% of strains that exhibited seven-fold increased STFX MICs, compared to pre-treatment MICs. The STFX MICs did not increase, however, when the location of the mutations did not change after treatment. Double mutations in developed in 60.0% of the strains in which eradication failed, which exhibited a baseline mutation at position D91, and in 11.1% of strains with baseline mutations at position N87.

CONCLUSION

Acquisition of double mutations in evoked high-level resistance to STFX in after unsuccessful eradication with STFX-containing regimens.