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This indicates that the low level resistant strain had a more stable sakacin P resistance phenotype than the high level resistant strain.
Different Ciprofloxacin concentrations selected different low level resistant mutants, and high level resistant mutants emerged from low level resistant mutants if stressed further by Ciprofloxacin.
The high level resistant strain L. monocytogenes L502-1 (hereafter L502-1) shows a slight growth reduction on mannose, with down-regulation of the bacteriocin receptor gene (mptA), compared to that of the wild-type L502.
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Passage with a higher drug concentration of compound 2 selected higher level resistant viruses with a double mutant L26I + A30T.
Furthermore, in depth characterization of the quinolone resistance mechanisms as well as the whole process of becoming a high-level resistant mutant were also a matter of concern.
A gentamicin protection assay was performed to determine if there had been any change in the invasion ability of the high-level resistant mutant (50 64) in comparison with the susceptible isolate, 50-wt.
All clinical strains were similarly high-level resistant to fluoroquinolones.
These isolates were also high-level resistant to clindamycin (MIC ≥ 256 mg/L).
Nonsusceptible isolates encompassed those identified as either intermediate- or high-level resistant.
Of these mutants, three high-level resistant mutants (strains SM7, SM8, and SM10) harboured an additional mutation (i.e. Ser84 → Trp or Leu) in gyrA.
However, all but one of these low-level ciprofloxacin-resistant strains had first-step parC mutations that would favor the appearance of high-level resistant strains.
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