A topoisomerase was identified as the bacterial target site for quinolone action in the late 1970s. Since that time, further study identified two bacterial topoisomerases, DNA gyrase and topoisomerase IV, as sites of antibacterial activity DNA gyrase appears to be the primary quinolone target for gram-negative bacteria. Topoisomerase IV appears to be the preferential target in gram-positive organisms, but this varies with the drug. Three mechanisms of resistance against quinolones are mutations of topoisomerases, decreased membrane permeability, and active drug efflux. Although these mechanisms occur singly, several resistance factors are often required to produce clinically applicable increases in minimum inhibitory concentrations. Appropriate drug selection and dosage and prudent human and veterinary interventions are important factors in controlling the emergence of resistance.
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Bearden et al. (2001) studied this question.
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