Evidence map›Paper›PMID 36102643›Full record

ArticleMicrobiology spectrum2022

L-Form Switching in Escherichia coli as a Common β-Lactam Resistance Mechanism.

Aleksandra Petrovic Fabijan, David Martinez-Martin, Carola Venturini, Katarzyna Mickiewicz, Neftali Flores-Rodriguez, Jeff Errington, Jonathan Iredell

Open access · goldAbstract read
In one paragraph

Article in Microbiology spectrum, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

16 citing papers in PubMed, 17 citations in OpenAlex.

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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

7 authors at 2 institutions in 2 countries.

Aleksandra Petrovic FabijanCentre for Infectious Diseases and Microbiology, Westmead Institute for Medical Research, Sydney, New South Wales, Australia.ORCID 0000-0003-3172-2375
David Martinez-MartinSchool of Biomedical Engineering, The University of Sydneygrid.1013.3, Sydney, New South Wales, Australia.
Carola VenturiniCentre for Infectious Diseases and Microbiology, Westmead Institute for Medical Research, Sydney, New South Wales, Australia.ORCID 0000-0003-2370-8661
Katarzyna MickiewiczCentre for Bacterial Cell Biology, Bioscience Institute, Newcastle Universitygrid.1006.7, Newcastle upon Tyne, United Kingdom.
Neftali Flores-RodriguezAustralian Centre for Microscopy and Microanalysis, University of Sydneygrid.1013.3, Sydney, New South Wales, Australia.
Jeff ErringtonCentre for Bacterial Cell Biology, Bioscience Institute, Newcastle Universitygrid.1006.7, Newcastle upon Tyne, United Kingdom.
Jonathan IredellCentre for Infectious Diseases and Microbiology, Westmead Institute for Medical Research, Sydney, New South Wales, Australia.
The University of Sydney · AUNewcastle University · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cell wall deficient bacterial L-forms are induced by exposure to cell wall-targeting antibiotics and immune effectors such as lysozyme. L-forms of different bacteria (including Escherichia coli) have been reported in human infections, but whether this is a normal adaptive strategy or simply an artifact of antibiotic treatment in certain bacterial species remains unclear. Here we show that members of a representative, diverse set of pathogenic E. coli readily proliferate as L-forms in supratherapeutic concentrations of the broad-spectrum antibiotic meropenem. We report that they are completely resistant to antibiotics targeting any penicillin-binding proteins in this state, including PBP1A/1B, PBP2, PBP3, PBP4, and PBP5/6. Importantly, we observed that reversion to the cell-walled state occurs efficiently, less than 20 h after antibiotic cessation, with few or no changes in DNA sequence. We defined for the first time a logarithmic L-form growth phase with a doubling time of 80 to 190 min, followed by a stationary phase in late cultures. We further demonstrated that L-forms are metabolically active and remain normally susceptible to antibiotics that affect DNA torsion and ribosomal function. Our findings provide insights into the biology of L-forms and help us understand the risk of β-lactam failure in persistent infections in which L-forms may be common.

Indexed as

Escherichia coliEscherichia coli ProteinsAnti-Bacterial Agentsbeta-Lactam Resistancebeta-LactamsMeropenemMuramidasePenicillin-Binding ProteinsAnti-Bacterial Agentsbeta-LactamsEscherichia coli ProteinsMeropenemMuramidasePBP5 protein, E coliPenicillin-Binding Proteinsantibiotic resistanceEscherichia coliL-formsrefractory infectionsβ-lactams

Identifiers

PMID36102643
PMCPMC9603335
OpenAlexW4295678974

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.