Evidence map›Paper›PMID 26190223›Full record

ReviewAnnals of the New York Academy of Sciences2015

Mechanisms of drug resistance: quinolone resistance.

David C Hooper, George A Jacoby

Open access · greenAbstract readReview
In one paragraph

Review in Annals of the New York Academy of Sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 344 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
344citing papers in PubMed, 3 pooled it
11.1field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

344 citing papers in PubMed, 3 syntheses or guidelines pooled it, 653 citations in OpenAlex.

  1. Global prevalence of fluoroquinolone resistance inFrontiers in cellular and infection microbiology · 2026
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  20. Genomic Characterization, Antimicrobial Resistance Profiles, andAnimals : an open access journal from MDPI · 2026
    Article

284 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

David C HooperDivision of Infectious Diseases, Massachusetts General Hospital, Boston, Massachusetts.
George A JacobyLahey Hospital and Medical Center, Burlington, Massachusetts.
Harvard University · USLahey Medical Center · US

Funding

Technical Mother Machine CoreP01AI083214 · NIAID · SCHEPENS EYE RESEARCH INSTITUTE · PI Michael S Gilmore · 2009 to 2026
$39.4M
Plasmid-mediated Quinolone ResistanceR01AI057576 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI HOOPER, DAVID C · 2004 to 2018
$5.3M
Quinolone and multidrug resistance in Staphylococcus aureusR37AI023988 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI HOOPER, DAVID C · 2008 to 2017
$4.1M
QUINOLONE RESISTANCE MECHANISMS IN STAPHYLOCOCCUS AUREUSR01AI023988 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI HOOPER, DAVID C · 1986 to 2007
$3.0M
NIAID NIH HHS P01 AI083214NIAID NIH HHS R01 AI023988NIAID NIH HHS R01 AI057576NIAID NIH HHS R37 AI023988
6 · The paper itself

Abstract

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.

Indexed as

MutationAnti-Bacterial AgentsBacteriaBacterial InfectionsBacterial ProteinsDNA GyraseDNA Topoisomerase IVDrug Resistance, BacterialHumansQuinolonesAnti-Bacterial AgentsBacterial ProteinsDNA GyraseDNA Topoisomerase IVQuinolonesDNA gyraseefflux pumpsplasmidsquinolonetopoisomerase

Identifiers

PMID26190223
PMCPMC4626314
OpenAlexW1592445079

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.