Evidence map›Paper›PMID 40971933›Full record

ArticleThe Journal of antimicrobial chemotherapy2025

In vitro evolution provides insights into mechanisms of Mycoplasma genitalium resistance to moxifloxacin.

Teck-Phui Chua, Jose L Huaman, Jennifer Danielewski, Catriona S Bradshaw, Dorothy A Machalek, Michael J McDonald, Suzanne M Garland, Gerald L Murray

Abstract read
In one paragraph

Article in The Journal of antimicrobial chemotherapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

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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

2 citing papers in PubMed.

  1. Absence ofOpen forum infectious diseases · 2026
    Article
  2. Novel features ofMicrobial genomics · 2026
    Article
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

8 authors.

Teck-Phui ChuaDepartment of Obstetrics, Gynaecology and Newborn Health, University of Melbourne, Parkville, Victoria, Australia.
Jose L HuamanDepartment of Obstetrics, Gynaecology and Newborn Health, University of Melbourne, Parkville, Victoria, Australia.
Jennifer DanielewskiCentre for Women's Infectious Diseases, The Royal Women's Hospital, Parkville, Victoria, Australia.
Catriona S BradshawMelbourne Sexual Health Centre, Alfred Health, Carlton, Victoria, Australia.
Dorothy A MachalekThe Kirby Institute, University of New South Wales, Sydney, New South Wales, Australia.
Michael J McDonaldSchool of Biological Sciences, Monash University, Clayton, Australia.
Suzanne M GarlandDepartment of Obstetrics, Gynaecology and Newborn Health, University of Melbourne, Parkville, Victoria, Australia.
Gerald L MurrayDepartment of Obstetrics, Gynaecology and Newborn Health, University of Melbourne, Parkville, Victoria, Australia.ORCID 0000-0003-3330-4433

Funding

Australian Government Research Training Program ScholarshipAustralian Research Council Industrial Transformation Research Hub for Antimicrobial Resistance IH190100021NHMRC Investigator Grant APP1197951
6 · The paper itself

Abstract

backgroundCurrent knowledge of Mycoplasma genitalium fluoroquinolone resistance is based on sequence analyses of clinical samples, an approach with limited scope. Many potential resistance mutations have been described but their impact on moxifloxacin efficacy is unclear.

objectiveTo investigate the impact of individual mutations on fluoroquinolone resistance through selection of moxifloxacin-resistant mutants in vitro.

methodsM. genitalium G37 was passaged sequentially in sub-inhibitory concentrations of moxifloxacin. MIC values were determined for moxifloxacin, sitafloxacin, levofloxacin and ciprofloxacin. Bacterial populations were profiled using amplicon sequencing.

resultsAcross three independent experiments, four moxifloxacin mutants were isolated, with mutations encoding the following protein sequence variations: (i) GyrA D99Y/ParE E468K, (ii) ParC S83I/GyrA D99Y/ParE E468K, (iii) ParC D87V/GyrB P462S and (iv) GyrA M95I/ParE E468dup. Moxifloxacin MICs were elevated 16- to 32-fold for mutants with a single GyrA or ParC variation, and 128-fold for the dual GyrA/ParC mutant. Sitafloxacin MICs were elevated but remained lower than moxifloxacin MICs. Mutations did not have a substantial impact on in vitro growth dynamics. Population analysis showed that multiple mutations attained detectable population-wide frequencies, with evidence of clonal interference dynamics, with a minority becoming fixed in the population.

conclusionMutations in multiple genes conferring fluoroquinolone resistance appeared with regularity in vitro. Findings of an additive effect for ParC/GyrA changes, and greater effectiveness of sitafloxacin against resistant bacteria compared with moxifloxacin, are both consistent with clinical data. Improved understanding of fluoroquinolone resistance will inform the development of diagnostic assays predicting fluoroquinolone susceptibility.

Indexed as

Anti-Bacterial AgentsDrug Resistance, BacterialEvolution, MolecularFluoroquinolonesMycoplasma genitaliumDNA GyraseDNA Topoisomerase IVHumansMicrobial Sensitivity TestsMoxifloxacinMutationSelection, GeneticSerial PassageAnti-Bacterial AgentsDNA GyraseDNA Topoisomerase IVFluoroquinolonesMoxifloxacin

Identifiers

PMID40971933
PMCPMC12596053

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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.