Evidence map›Paper›PMID 35928205›Full record

ReviewFrontiers in cellular and infection microbiology2022

Link Between Antibiotic Persistence and Antibiotic Resistance in Bacterial Pathogens.

Wolfgang Eisenreich, Thomas Rudel, Jürgen Heesemann, Werner Goebel

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Frontiers in cellular and infection microbiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06305455 (Change in the Resistance Profile of Escherichia Coli in Infections of Community Origin), which is not on this map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.4field-weighted citation impact, top 3% 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.

NCT06305455 unknown statusnot on this mapstarted 2024, after this paper: background citation

Change in the Resistance Profile of Escherichia Coli in Infections of Community Origin: The Importance of Antimicrobial Stewardship

TypeobservationalSponsorJosé Raimundo Araujo de AzevedoRan2024 to 2024Enrolled200ConditionsAntimicrobial ResistanceArmsEscherichia coli ESBL
3 · Its place in the literature

Who cites it

41 citing papers in PubMed, 68 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Outer membrane vesicles fromMicrobiology spectrum · 2026
    Article
  7. Article
  8. Transcriptional Reprogramming ofInternational journal of molecular sciences · 2026
    Article
  9. Observational
  10. Review
  11. Review
  12. Article
  13. Molecular Basis of Persister Awakening and Lag-Phase Recovery inInternational journal of molecular sciences · 2026
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Heterogeneous subpopulations inFrontiers in cellular and infection microbiology · 2025
    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

4 authors at 3 institutions in 1 country.

Wolfgang EisenreichBavarian NMR Center - Structural Membrane Biochemistry, Department of Chemistry, Technische Universität München, Garching, Germany.
Thomas RudelChair of Microbiology, Biocenter, University of Würzburg, Würzburg, Germany.
Jürgen HeesemannMax von Pettenkofer-Institute, Ludwig Maximilian University of Munich, München, Germany.
Werner GoebelMax von Pettenkofer-Institute, Ludwig Maximilian University of Munich, München, Germany.
Ludwig-Maximilians-Universität München · DETechnical University of Munich · DEUniversity of Würzburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Both, antibiotic persistence and antibiotic resistance characterize phenotypes of survival in which a bacterial cell becomes insensitive to one (or even) more antibiotic(s). However, the molecular basis for these two antibiotic-tolerant phenotypes is fundamentally different. Whereas antibiotic resistance is genetically determined and hence represents a rather stable phenotype, antibiotic persistence marks a transient physiological state triggered by various stress-inducing conditions that switches back to the original antibiotic sensitive state once the environmental situation improves. The molecular basics of antibiotic resistance are in principle well understood. This is not the case for antibiotic persistence. Under all culture conditions, there is a stochastically formed, subpopulation of persister cells in bacterial populations, the size of which depends on the culture conditions. The proportion of persisters in a bacterial population increases under different stress conditions, including treatment with bactericidal antibiotics (BCAs). Various models have been proposed to explain the formation of persistence in bacteria. We recently hypothesized that all physiological culture conditions leading to persistence converge in the inability of the bacteria to re-initiate a new round of DNA replication caused by an insufficient level of the initiator complex ATP-DnaA and hence by the lack of formation of a functional orisome. Here, we extend this hypothesis by proposing that in this persistence state the bacteria become more susceptible to mutation-based antibiotic resistance provided they are equipped with error-prone DNA repair functions. This is - in our opinion - in particular the case when such bacterial populations are exposed to BCAs.

Indexed as

Anti-Bacterial AgentsBacteriaDrug Resistance, BacterialDrug Resistance, MicrobialAnti-Bacterial AgentsATP-DnaA complexbacterial pathogensDNA replication initiationpersistenceresistance

Identifiers

PMID35928205
PMCPMC9343593
OpenAlexW4285796036

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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 Socratic graph.