[Mechanisms for the development of quinolone resistance].
New fluoroquinolones have potent and broad antimicrobial activity and spectra, respectively, against gram-positive and -negative bacteria including P. aeruginosa. As a result of their frequent use, bacterial resistance to the quinolones has gradually developed and limited their therapeutic efficacy in infections, especially, with P. aeruginosa, S. pneumoniae, S. aureus (especially MRSA), and N. gonorrhoeae. Bacterial resistance to the quinolones probably results from : 1) mutations with chromosomal genes of DNA gyrase or DNA topoisomerase in E. coli and S. aureus, 2) decreased permeability of the cell envelope through OmpF, porin-forming protein, in gram-negative bacteria, and 3) activation of active efflux-mediated permeability through the cell membrane protein, either NorA in S. aureus or Opr in P. aeruginosa. Proper use of the quinolones is also proposed to prevent emergence of the bacterial resistance.
Kojima
M
M
Department of Pharmacy, Mie University Hospital, School of Medicine.
D000890:Anti-Infective Agents / Q000378:metabolism / Q000494:pharmacology*; D017920:Antiporters / Q000502:physiology; D001419:Bacteria / Q000187:drug effects / Q000201:enzymology / Q000235:genetics*; D001425:Bacterial Outer Membrane Proteins; D002463:Cell Membrane Permeability; D004264:DNA Topoisomerases, Type I / Q000235:genetics; D004250:DNA Topoisomerases, Type II / Q000235:genetics; D004352:Drug Resistance, Microbial; D024841:Fluoroquinolones; D009154:Mutation
D000890:Anti-Infective Agents; D017920:Antiporters; D001425:Bacterial Outer Membrane Proteins; D024841:Fluoroquinolones; D004264:DNA Topoisomerases, Type I; D004250:DNA Topoisomerases, Type II