Mechanisms of quinolone action and microbial response.
Over the years, chromosomal mapping of the bacterial genome of Escherichia coli has demonstrated that many loci are associated with quinolone resistance, which is mainly a result of chromosomal mutation or alteration of the quantity or type of porins in the outer membrane of Gram-negative bacteria. There has been one report of a small and confined episode of plasmid-mediated resistance to fluoroquinolones, which did not appear to persist. With the increasingly widespread use of an expanding range of fluoroquinolone antibiotics, a range and mix in individual bacterial isolates of the different mechanisms of resistance to fluoroquinolones will undoubtedly be encountered amongst clinically significant bacteria. Currently, transferable resistance is extremely rare and most resistant bacteria arise from clonal expansion of mutated strains. However, it is conceivable that in the future, horizontal gene transfer may become a more important means of conferring resistance to fluoroquinolones.
Hawkey
Peter M
PM
Public Health Laboratory, Heartlands Hospital, Bordesley Green East, Birmingham B5 9SS, UK. peter.hawkey@heartsol.wmids.nhs.uk
D000890:Anti-Infective Agents / Q000494:pharmacology*; D001419:Bacteria / Q000187:drug effects* / Q000201:enzymology / Q000235:genetics*; D027081:DNA Gyrase / Q000235:genetics; D027101:DNA Topoisomerase IV / Q000235:genetics; D004268:DNA-Binding Proteins / Q000235:genetics; D024881:Drug Resistance, Bacterial / Q000235:genetics*; D006801:Humans; D009154:Mutation; D018272:Porins / Q000235:genetics; D015363:Quinolones / Q000494:pharmacology*
D000890:Anti-Infective Agents; D004268:DNA-Binding Proteins; D018272:Porins; D015363:Quinolones; D027101:DNA Topoisomerase IV; D027081:DNA Gyrase