[A study on the active efflux mechanism in Staphylococcus aureus resistant to quinolone]

To explore the effect, the characteristic, and potential approaches to the active efflux mechanism in straphylococcus aureus (S. a) resistant to quinolones.

S. a standard strain ATCC25923 and clinical isolates susceptible to quinolone were inoculated onto MH agar containing ofloxacin at a concentration of 4 x MIC (in the presence or absence of 20 micro g of reserpine/ml). Following incubation at 35 degrees C for 48 h, the inhibiting effect of reserpine on the occurrence of induced resistance was observed and the MIC of the induced resistant strain to ethidium bromide (EB), ofloxacin and ciprofloxacin (in the presence or absence of 20 micro g of reserpine/ml) was determined. The influence of reserpine to the MIC of induced resistant strains was also determined. The accumulation and loss of EB was determined based on the fact that EB's fluorescence can be strengthened when combined with DNA. Reserpine inhibition test was used to study the active efflux in clinical S. a resistant to quinolone.

The active efflux mechanism in S. a resistant to second generation quinolones was confirmed by the reserpine's influence on the level of ethidium bromide (EB) in the cytoplasm of S. a. Reserpine reduced the 50 percent resistant rate to quinolone in induced resistant S. a, and decreased the MIC of induced resistant strains. Reserpine inhibited the active efflux of EB from the cytoplasm of S. a.

Active efflux is an important mechanism in S. a resistant to quinolone. Reserpine can inhibit its active efflux mechanism, and has synergistic effect with quinolone, which hold therapeutic potential for S. a resistant to quinolones.