Evidence map›Paper›PMID 26261001›Full record

ArticleAnnals of intensive care2015

Mechanisms of antimicrobial resistance in Gram-negative bacilli.

Étienne Ruppé, Paul-Louis Woerther, François Barbier

Open access · goldAbstract read
In one paragraph

Article in Annals of intensive care, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 218 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
218citing papers in PubMed, 3 pooled it
9.4field-weighted citation impact, top 1% 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

218 citing papers in PubMed, 3 syntheses or guidelines pooled it, 483 citations in OpenAlex.

  1. Pooled it
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  4. Trial
  5. Antimicrobial agents and chemotherapy · 2020
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  10. Dissemination of antimicrobial resistance in surface waters: surveillance of enterococci and coliform bacteria in Slovakia.International microbiology : the official journal of the Spanish Society for Microbiology · 2026
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158 more citing papers are in PubMed but not listed here.

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

3 authors at 3 institutions in 2 countries.

Étienne RuppéDepartment of Infectious Diseases, Genomic Research Laboratory, Geneva University Hospitals, Geneva, Switzerland, etienne.ruppe@gmail.com.
Paul-Louis Woerther
François Barbier
Centre hospitalier régional d'Orléans · FRGeneva College · USInstitut Gustave Roussy · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The burden of multidrug resistance in Gram-negative bacilli (GNB) now represents a daily issue for the management of antimicrobial therapy in intensive care unit (ICU) patients. In Enterobacteriaceae, the dramatic increase in the rates of resistance to third-generation cephalosporins mainly results from the spread of plasmid-borne extended-spectrum beta-lactamase (ESBL), especially those belonging to the CTX-M family. The efficacy of beta-lactam/beta-lactamase inhibitor associations for severe infections due to ESBL-producing Enterobacteriaceae has not been adequately evaluated in critically ill patients, and carbapenems still stands as the first-line choice in this situation. However, carbapenemase-producing strains have emerged worldwide over the past decade. VIM- and NDM-type metallo-beta-lactamases, OXA-48 and KPC appear as the most successful enzymes and may threaten the efficacy of carbapenems in the near future. ESBL- and carbapenemase-encoding plasmids frequently bear resistance determinants for other antimicrobial classes, including aminoglycosides (aminoglycoside-modifying enzymes or 16S rRNA methylases) and fluoroquinolones (Qnr, AAC(6')-Ib-cr or efflux pumps), a key feature that fosters the spread of multidrug resistance in Enterobacteriaceae. In non-fermenting GNB such as Pseudomonas aeruginosa, Acinetobacter baumannii and Stenotrophomonas maltophilia, multidrug resistance may emerge following the sole occurrence of sequential chromosomal mutations, which may lead to the overproduction of intrinsic beta-lactamases, hyper-expression of efflux pumps, target modifications and permeability alterations. P. aeruginosa and A. baumannii also have the ability to acquire mobile genetic elements encoding resistance determinants, including carbapenemases. Available options for the treatment of ICU-acquired infections due to carbapenem-resistant GNB are currently scarce, and recent reports emphasizing the spread of colistin resistance in environments with high volume of polymyxins use elicit major concern.

Identifiers

PMID26261001
PMCPMC4531117
OpenAlexW2095741521

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.