Abstract

Objectives Analysis of resistance mechanisms and to determine the place of plasmidic mediated mechanism. Methods They are based on literature search and personal experience. During 30 years, the only known mechanisms of resistance to quinolones were chromosome borne. The first plasmid-mediated resistance determinant to quinolones, QnrA, was discovered in 1998, followed in 2004 by two other markers QnrB and QnrS in several enterobacterial species. These markers interact with quinolones, the topoisomerases, and DNA, thus limiting the binding of the quinolones to their target. In 2005, a second plasmid-borne mechanism, which independantly contributes to the quinolones resistance by modification of the antibiotic molecule was described. This protein, AAC (6’)-Ib-cr, was a variant of the 6’ acetyl transferase, which is known to modify the chemical structure of aminoglycosides, and presented an enlarged enzymatic spectrum toward ciprofloxacin and norfloxacin. Epidemiology of plasmidic resistance to quinolones The plasmid-borne mechanisms of resistance to quinolones are disseminated worldwide among enterobacterial isolates. They confer a high level of resistance to first generation quinolones and confer decreased susceptibility to fluoroquinolones. Conclusion There is no phenotypic criteria allowing difference between chromosome and plasmid-borne mechanisms of resistance to quinolones. A molecular-based approach is required to identify these novel mechanisms of resistance in clinical isolates.

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