Evidence map›Paper›PMID 39012901›Full record

ArticlePloS one2024

Impact of mutations in the mtrR, rpdlVD and rrl genes on azithromycin resistance in Neisseria gonorrhoeae.

Florian Mauffrey, Fabrice Poncet, Damien Jacot, Gilbert Greub, Patrice Nordmann, Dominique S Blanc

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PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
–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

3 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. 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

6 authors.

Florian MauffreyInfection Prevention and Control Unit, Infectious Diseases Service, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland.
Fabrice PoncetInfection Prevention and Control Unit, Infectious Diseases Service, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland.
Damien JacotInstitute for Microbiology, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland.
Gilbert GreubInstitute for Microbiology, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland.
Patrice NordmannSwiss National Reference Center for Emerging Antibiotic Resistance, Fribourg, Switzerland.
Dominique S BlancInfection Prevention and Control Unit, Infectious Diseases Service, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland.ORCID 0000-0002-0324-8437

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionBacterial sexually transmitted infections (STIs) pose a major public health problem. The emergence of antibiotic-resistant strains of Neisseria gonorrhoeae represents a serious threat to successful treatment and epidemiological control. The first extensively drug-resistant (XDR) strains (ceftriaxone-resistant and high-level azithromycin-resistant [HLR AZY]) have been reported.

aimsTo identify molecular mechanisms implicated in azithromycin resistance in strains isolated from patients over a three-year period in a university hospital in Switzerland. MATERIAL AND

methodsFrom January 2020 to December 2022, 34 isolates (one per patient) were recovered from samples analyzed at the University Hospital of Lausanne. Eight genes involved in azithromycin resistance were sequenced: mtrR repressor (mtrCDE operon repressor) and his promotor mtrR-pr, rplD gene (L4 ribosomal protein), rplV gene (L22 ribosomal protein) and the four alleles of the rrl gene (23S rRNA).

resultsWith a cutoff value of 1 mg/L, 15 isolates were considered as being resistant to azithromycin, whereas the remaining 19 were susceptible. The C2597T mutation in 3 or 4 of the rrl allele confer a medium-level resistance to azithromycin (MIC = 16 mg/L, N = 2). The following mutations were significantly associated with MIC values ≥1 mg/L: the three mutations V125A, A147G, R157Q in the rplD gene (N = 10) and a substitution A->C in the mtrR promotor (N = 9). Specific mutations in the mtrR repressor and its promotor were observed in both susceptible and resistant isolates.

conclusionsResistance to azithromycin was explained by the presence of mutations in many different copies of 23S RNA ribosomal genes and their regulatory genes. Other mutations, previously reported to be associated with azithromycin resistance, were documented in both susceptible and resistant isolates, suggesting they play little role, if any, in azithromycin resistance.

Indexed as

Anti-Bacterial AgentsAzithromycinBacterial ProteinsDrug Resistance, BacterialMutationNeisseria gonorrhoeaeRepressor ProteinsFemaleGonorrheaHumansMaleMicrobial Sensitivity TestsRibosomal ProteinsAnti-Bacterial AgentsAzithromycinBacterial ProteinsmtrR protein, Neisseria gonorrhoeaeRepressor ProteinsRibosomal Proteins

Identifiers

PMID39012901
PMCPMC11251580

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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.