ArticleNature microbiology2026
Quantifying the real-world impact of antibiotic use and genetic determinants of resistance on gonococcal dynamics.
Article in Nature microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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.
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.
Who cites it
3 citing papers in PubMed.
- Heterogeneity of azithromycin resistance markers inNew microbes and new infections · 2026Review
- Genetic Background Modulates Zoliflodacin and Gepotidacin Cross-Resistance and Fitness in Neisseria gonorrhoeae.The Journal of infectious diseases · 2026Article
- Fluoroquinolone resistance-conferringbioRxiv : the preprint server for biology · 2026Article
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10 authors.
Funding
Abstract
The dynamics of antimicrobial resistance in bacterial populations are influenced by the fitness impact of genetic determinants of resistance and antibiotic pressure. However, estimates of real-world fitness impact have been lacking. To address this gap, we developed a hierarchical Bayesian phylodynamic model to quantify contributions of resistance determinants to strain success in a 20-year collection of Neisseria gonorrhoeae isolates. Fitness contributions varied with antibiotic use, which over this period included ciprofloxacin, cefixime, ceftriaxone and azithromycin, and genetic pathways to phenotypically identical resistance conferred distinct fitness effects. These findings were supported by competition experiments both in vitro and in the mouse model of gonococcal infection. Quantifying these fitness contributions to lineage dynamics reveals opportunities for investigation into other genetic and environmental drivers of fitness. This work thus establishes a method for linking pathogen genomics and antibiotic use to define factors shaping ecological trends.
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