Evidence map›Paper›PMID 38319508›Full record

ArticleEuropean journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology2024

Reduced susceptibility to aztreonam-avibactam conferred by acquired AmpC-type β-lactamases in PBP3-modified Escherichia coli.

Nicolas Helsens, Mustafa Sadek, Christophe Le Terrier, Laurent Poirel, Patrice Nordmann

Abstract read
PubMed Publisher
In one paragraph

Article in European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Antimicrobial agents and chemotherapy · 2026
    Article
  6. Review
  7. Article
  8. Article
  9. Combined resistance mechanisms leading to high-level of cefiderocol resistance among NDM-like producing E. coli ST167 clinical isolates.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2025
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. 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

5 authors.

Nicolas HelsensClinical Microbiology Unit, Pasteur Institute of Lille, 1 Rue du Professeur Calmette, 59000, Lille, France. nicolas.helsens@pasteur-lille.fr.ORCID http://orcid.org/0000-0001-8902-0486
Mustafa SadekDepartment of Food Hygiene and Control, Faculty of Veterinary Medicine, South Valley University, Qena, Egypt.
Christophe Le TerrierMedical and Molecular Microbiology, Department of Medicine, University of Fribourg, Fribourg, Switzerland.
Laurent PoirelMedical and Molecular Microbiology, Department of Medicine, University of Fribourg, Fribourg, Switzerland.
Patrice NordmannMedical and Molecular Microbiology, Department of Medicine, University of Fribourg, Fribourg, Switzerland.

Funding

I-Site ULNE R-TALENTS-20-004Région Hauts-de-France 21008838
6 · The paper itself

Abstract

purposeCarbapenemase-producing Enterobacterales are a growing threat, and very few therapeutic options remain active against those multidrug resistant bacteria. Aztreonam is the molecule of choice against metallo-beta-lactamases (MBL) producers since it is not hydrolyzed by those enzymes, but the co-production of acquired plasmidic cephalosporinases or extended-spectrum β-lactamases leading to aztreonam resistance may reduce the efficacy of this molecule. Hence, the development of the aztreonam-avibactam (AZA) combination provides an interesting therapeutic alternative since avibactam inhibits the activity of both cephalosporinases and extended-spectrum β-lactamases. However, structural modifications of penicillin binding protein PBP3, the target of aztreonam, may lead to reduced susceptibility to aztreonam-avibactam.

methodsHere the impact of various plasmid-encoded AmpC-type β-lactamases (ACC-1, ACT-7, ACT-17, CMY-2, CMY-42, DHA-1, FOX-1, and FOX-5) on susceptibility to aztreonam-avibactam was evaluated using isogenic E. coli MG1655 strains harboring insertions in PBP3 (YRIN and YRIK). The inhibitory activity of various β-lactamase inhibitors (clavulanic acid, tazobactam, avibactam, relebactam, and vaborbactam) were also compared against these enzymes.

resultsHence, we showed that reduced susceptibility to AZA was due to the combined effect of both AmpC production and amino acid insertions in PBP3. The highest resistance level was achieved in strains possessing the insertions in PBP3 in association with the production of ACT-7, ACC-1, or CMY-42.

conclusionAlthough none of the recombinant strains tested displayed clinical resistance to aztreonam-avibactam, our data emphasize that the occurrence of such profile might be of clinical relevance for MBL-producing strains.

Indexed as

AvibactamAztreonamCephalosporinasesE. coliPBP3β-Lactamase inhibitors

Identifiers

What OpenQuestion holds

Textmetadata
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.