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Quinolone antimicrobial agents: mechanism of action and resistance development.

The primary target of fluoroquinolone antimicrobial agents is the A subunit of DNA gyrase. In several cases a close relationship to ID50 (inhibitory dose-50%) and minimum inhibitory concentration (MIC) has been shown for gram-negative bacteria, although this has not been regularly observed for gram-positive bacteria to date. Cellular entry is by means of diffusion and involves, at least in part, the porin pathway in the outer membrane of gram-negative bacteria. An energy dependent efflux occurs which is more active in brain heart infusion broth than nutrient broth and which, to date, has not been shown to contribute to inhibition of growth or bacterial lethality. The extent of uptake by different gram-negative bacteria varies and may contribute in some cases to determination of the MIC. Resistance to fluoroquinolones is by means of mutations affecting the gyrase gene coding for the A subunit and mutations which affect cell permeability particularly involving porin proteins of the outer membrane. Combined target and permeability resistance has been reported but involves two or more mutational steps. Resistance during clinical treatment has been observed, but is most likely to be of low magnitude and to be detected in patients with significantly compromised host defenses.