Cited by 320Antimicrobial Resistance in StaphylococcusAntibiotic Resistance in BacteriaAntibiotic Use and Resistance

Fluoroquinolone resistance among Gram-positive cocci

Hooper, David C·2002·The Lancet Infectious Diseases

Abstract

Resistance to fluoroquinolones among Gram-positive cocci has emerged as these antimicrobial agents have become extensively used in clinical medicine. Resistance is effected by changes in the bacterial target enzymes DNA gyrase and topoisomerase IV, which reduce drug binding, and by action of native bacterial membrane pumps that remove drug from the cell. In both cases, quinolone exposure selects for spontaneous mutants that are present in large bacterial populations, and which contain chromosomal mutations that alter the target protein or increase the level of pump expression. Resistance among clinical isolates has been greatest in Staphylococcus aureus and particularly among meticillin-resistant strains, in which both selection by quinolone exposure and transmission of clonal strains in health-care settings have contributed to high prevalence. Resistance in Streptococcus pneumoniae has also emerged in the community. Fluoroquinolone resistance has arisen in multidrug-resistant clones and its prevalence has been especially high in Hong Kong and Spain. Further spread and selection of such resistance could compromise the utility of a valuable class of antimicrobial agents, a point that emphasises the importance of the careful use of these agents in appropriate patients and doses, as well as careful infection-control practices.

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Crossref · 10.1016/s1473-3099(02)00369-9

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  • Clinically relevant fluoroquinolone resistance frequently requires accumulation of genetic changes over time, with the first mutation producing minor increases in MIC.

    “Thus, in contrast to the case of RIF, clinically relevant FQ resistance frequently requires an accumulation of genetic changes over time, with the first mutation producing minor increases in the MIC (59).”

    From Mechanisms of Antibiotic Resistance (2016) · cites this paper as [59]

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Authors
Hooper, D. C.
Affiliations
Harvard University (US)
Corresponding author
Hooper, David C
Venue
The Lancet Infectious Diseases
Publisher
Elsevier BV
Published
2002-09
Volume
2
Issue
9
Pages
530-538
ISSN
1473-3099 (ISSN-L)
OpenAlex
W2112722072
Cited by
320
References
121
Citations by year
2026: 4 · 2025: 9 · 2024: 6 · 2023: 7 · 2022: 9 · 2021: 8 · 2020: 13 · 2019: 10 · 2018: 12 · 2017: 15 · 2016: 16 · 2015: 13 · 2014: 16 · 2013: 14 · 2012: 21
FWCI
3.00
Type
journal article
Language
en
Open access
closed
Locations
  • The Lancet Infectious Diseases (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institute of Allergy and Infectious Diseases (R01AI023988)
Topics
  • Health Sciences › Medicine › Infectious Diseases › Antimicrobial Resistance in Staphylococcus
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Medicine › Antibiotic Resistance in Bacteria
  • Life Sciences › Immunology and Microbiology › Applied Microbiology and Biotechnology › Antibiotic Use and Resistance
Keywords
fluoroquinolone resistance, Gram-positive cocci, Staphylococcus aureus, methicillin-resistant Staphylococcus aureus, Streptococcus pneumoniae, DNA gyrase, topoisomerase IV, efflux pumps, multidrug resistance, clonal transmission, antimicrobial resistance, infection control, rational antibiotic use
MeSH terms
Anti-Infective Agents, Gram-Positive Bacteria, Humans, Microbial Sensitivity Tests, Fluoroquinolones, Drug Resistance, Multiple, Bacterial, DNA Gyrase

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