TY - JOUR AU - Hooper, David T1 - Emerging Mechanisms of Fluoroquinolone Resistance T2 - Emerging Infectious Disease journal PY - 2001 VL - 7 IS - 2 SP - 337 SN - 1080-6059 AB - Broad use of fluoroquinolones has been followed by emergence of resistance, which has been due mainly to chromosomal mutations in genes encoding the subunits of the drugs' target enzymes, DNA gyrase and topoisomerase IV, and in genes that affect the expression of diffusion channels in the outer membrane and multidrug-resistance efflux systems. Resistance emerged first in species in which single mutations were sufficient to cause clinically important levels of resistance (e.g., Staphylococcus aureus and Pseudomonas aeruginosa). Subsequently, however, resistance has emerged in bacteria such as Campylobacter jejuni, Escherichia coli, and Neisseria gonorrhoeae, in which multiple mutations are required to generate clinically important resistance. In these circumstances, the additional epidemiologic factors of drug use in animals and human-to-human spread appear to have contributed. Resistance in Streptococcus pneumoniae, which is currently low, will require close monitoring as fluoroquinolones are used more extensively for treating respiratory tract infections. KW - Fluoroquinolone Resistance KW - Streptococcus pneumonia KW - resistance mechanisms KW - enzymes KW - United States DO - 10.3201/eid0702.700337 UR - https://wwwnc.cdc.gov/eid/article/7/2/70-0337_article ER - End of Reference