Mechanisms of drug resistance: quinolone resistance
By David C. Hooper, G. Jacoby. Annals of the New York Academy of Sciences, 2015
639 citations recorded by the source corpus.
Quinolone antimicrobials are synthetic and widely used in clinical medicine. Resistance emerged with clinical use and became common in some bacterial pathogens. Mechanisms of resistance include two categories of mutation and acquisition of resistance‐conferring genes. Resistance mutations in one or both of the two drug target enzymes, DNA gyrase and DNA topoisomerase IV, are commonly in a localized domain of the GyrA and ParE subunits of the respective enzymes and reduce drug binding to the enzyme–DNA complex. Other resistance mutations occur in regulatory genes that control the expression of native efflux pumps localized in the bacterial membrane(s). These pumps have broad substrate profiles that include quinolones as well as other antimicrobials, disinfectants, and dyes. Mutations of both types can accumulate with selection pressure and produce highly resistant strains. Resistance genes acquired on plasmids can confer low‐level resistance that promotes the selection of mutational high‐level resistance. Plasmid‐encoded resistance is due to Qnr proteins that protect the target enzymes from quinolone action, one mutant aminoglycoside‐modifying enzyme that also modifies certain quinolones, and mobile efflux pumps. Plasmids with these mechanisms often encode additional antimicrobial resistances and can transfer multidrug resistance that includes quinolones. Thus, the bacterial quinolone resistance armamentarium is large.
Subfields: Molecular Biology, Molecular Medicine, Pharmacology
View Paper: https://www.semanticscholar.org/paper/6adb01c0b03e8ef5c3ac13269dcfb32a228626bb
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Citations in the corpus
- Antimicrobial resistance in aquaculture: a crisis for concern (2020, background): “The basic mechanism behind the quinolone resistance is the incidence of mutations in DNA gyrase and DNA topoisomerase along with the plasmid mediated resistance and that of fluoroquinolone resistance due to the QRDR (quinolone resistancedetermining region) based mutation (Hooper and Jacoby 2015).”
- Antibiotic resistance and persistence—Implications for human health and treatment perspectives (2020, positive): “Single amino acid changes in close proximity to the active site tyrosine of the bacterial type II topoisomerase enzymes, DNA gyrase GyrA or DNA topoisomerase IV ParC can cause ciprofloxacin resistance in S. aureus (Sreedharan et al , 1990; Hooper & Jacoby, 2015).”