Emerging mechanisms of fluoroquinolone resistance.

By D. Hooper. Emerging Infectious Diseases, 2001

654 citations recorded by the source corpus.

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.

Subfields: Epidemiology, Molecular Medicine, Pharmacology

View Paper: https://www.semanticscholar.org/paper/8f46e999d5ef56cc46d2394fa285d01fc57e99f9

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Citations in the corpus

Bacterial resistance: origins, epidemiology, and impact. (2003, neutral): “permeability, or both [14-17].”
Pseudomonas aeruginosa - a phenomenon of bacterial resistance. (2009, background): “aeruginosa: structural changes in target enzymes and active efflux (Hooper, 2001).”
Horizontal transfer of antibiotic resistance genes in clinical environments. (2019, background): “In most bacteria, including 375 Enterobacteriaceae, clinical resistance to fluoroquinolones can only be achieved through the 376 additive contributions of multiple genetic loci (Corkill et al. 2005; Hooper 2001; Kary et al. 377 2017; Sekyere and Amoako 2017).”
Antimicrobial Resistance in ESKAPE Pathogens (2020, background): “The level of resistance achieved by single-target mutations is dependent on both the specific agent and the bacterial species (187), while the accumulation of multiple mutations across both target enzymes often leads to the evolution of a high-level fluoroquinolone resistance phenotype (193).”
Co-occurrence of resistance genes to antibiotics, biocides and metals reveals novel insights into their co-selection potential (2015, background): “Furthermore, large-scale studies on mutation-based resistance [66, 67] as well as crossresistance [68] would provide a more complete picture, as these mechanisms are expected to act in parallel to co-selection via co-occurrence of resistance genes.”