ArticleJAC-antimicrobial resistance2026
Pharmacokinetics determine persister formation in
Article in JAC-antimicrobial resistance, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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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.
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Who cites it
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Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Persisters are bacterial subpopulations of slow- or non-growing cells that are refractory to antimicrobials and can provide a starting point for antimicrobial resistance evolution. Several mechanisms of persister formation have been studied, and it has been shown that a short exposure to sublethal concentrations of antimicrobials can induce persistence. Objectives: We hypothesized that the pharmacokinetics-the temporal changes of drug concentrations under treatment-impact persister formation. We predicted that the slower the rate of drug concentration increase, the longer bacteria spend under sublethal drug concentrations, and the more persisters would form. Methods: Results: We found that faster pharmacokinetics resulted in lower persister numbers compared with slower pharmacokinetics. This finding provides proof of principle that pharmacokinetics, which can be influenced by treatment procedures, has consequences for persister formation. Conclusions: Our results suggest that faster pharmacokinetics could minimize persister numbers and hence lower the risks of bacterial infection relapse and resistance evolution.
Identifiers
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Registered trials
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