Evidence map›Paper›PMID 34504285›Full record

ArticleCommunications biology2021

Pseudomonas aeruginosa adapts to octenidine via a combination of efflux and membrane remodelling.

Lucy J Bock, Philip M Ferguson, Maria Clarke, Vichayanee Pumpitakkul, Matthew E Wand, Paul-Enguerrand Fady, Leanne Allison, Roland A Fleck, Matthew J Shepherd, A James Mason and 1 more

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.0field-weighted citation impact, top 28% 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

12 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Activity of Antiseptics AgainstAntibiotics (Basel, Switzerland) · 2025
    Article
  6. Article
  7. Highly Effective Biocides againstACS infectious diseases · 2024
    Article
  8. Article
  9. The Art of War withAntibiotics (Basel, Switzerland) · 2023
    Review
  10. Article
  11. Role of Efflux Pumps on Antimicrobial Resistance inInternational journal of molecular sciences · 2022
    Review
  12. 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

11 authors at 2 institutions in 1 country.

Lucy J Bock *Technology Development Group, National Infection Service, PHE Porton, Salisbury, UK. Lucy.Bock@phe.gov.uk.ORCID 0000-0001-8336-1909
Philip M Ferguson *Institute of Pharmaceutical Science, School of Cancer & Pharmaceutical Science, King's College London, London, UK.
Maria ClarkeInstitute of Pharmaceutical Science, School of Cancer & Pharmaceutical Science, King's College London, London, UK.ORCID 0000-0003-4129-4810
Vichayanee PumpitakkulInstitute of Pharmaceutical Science, School of Cancer & Pharmaceutical Science, King's College London, London, UK.
Matthew E WandTechnology Development Group, National Infection Service, PHE Porton, Salisbury, UK.ORCID 0000-0002-9277-8869
Paul-Enguerrand FadyInstitute of Pharmaceutical Science, School of Cancer & Pharmaceutical Science, King's College London, London, UK.ORCID 0000-0002-8442-1966
Leanne AllisonCentre for Ultrastructural Imaging, Guy's Campus, King's College London, London, UK.
Roland A FleckCentre for Ultrastructural Imaging, Guy's Campus, King's College London, London, UK.ORCID 0000-0003-1542-6218
Matthew J ShepherdTechnology Development Group, National Infection Service, PHE Porton, Salisbury, UK.
A James MasonInstitute of Pharmaceutical Science, School of Cancer & Pharmaceutical Science, King's College London, London, UK.ORCID 0000-0003-0411-602X
J Mark SuttonTechnology Development Group, National Infection Service, PHE Porton, Salisbury, UK. Mark.Sutton@phe.gov.uk.ORCID 0000-0002-2288-0446
King's College London · GBPublic Health England · GB

Funding

Cancer Research UK FC001029Medical Research Council FC001029Medical Research Council MC_U117533887Wellcome Trust
6 · The paper itself

Abstract

Pseudomonas aeruginosa is an opportunistic pathogen capable of stably adapting to the antiseptic octenidine by an unknown mechanism. Here we characterise this adaptation, both in the laboratory and a simulated clinical setting, and identify a novel antiseptic resistance mechanism. In both settings, 2 to 4-fold increase in octenidine tolerance was associated with stable mutations and a specific 12 base pair deletion in a putative Tet-repressor family gene (smvR), associated with a constitutive increase in expression of the Major Facilitator Superfamily (MFS) efflux pump SmvA. Adaptation to higher octenidine concentrations led to additional stable mutations, most frequently in phosphatidylserine synthase pssA and occasionally in phosphatidylglycerophosphate synthase pgsA genes, resulting in octenidine tolerance 16- to 256-fold higher than parental strains. Metabolic changes were consistent with mitigation of oxidative stress and altered plasma membrane composition and order. Mutations in SmvAR and phospholipid synthases enable higher level, synergistic tolerance of octenidine.

Indexed as

Anti-Bacterial AgentsBiological TransportGenes, BacterialIminesMicrobial Sensitivity TestsMutationPseudomonas aeruginosaPyridinesAnti-Bacterial AgentsIminesoctenidinePyridines

Identifiers

PMID34504285
PMCPMC8429429
OpenAlexW3197866041

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.