Evidence map›Paper›PMID 17728470›Full record

ArticleJournal of clinical microbiology2007

Clonal expansion and microevolution of quinolone-resistant Salmonella enterica serotype typhi in Vietnam from 1996 to 2004.

Thi Anh Hong Le, Laëtitia Fabre, Philippe Roumagnac, Patrick A D Grimont, Maurice R Scavizzi, François-Xavier Weill

Open access · greenAbstract read
In one paragraph

Article in Journal of clinical microbiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
9.2field-weighted citation impact, top 2% 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

30 citing papers in PubMed, 58 citations in OpenAlex.

  1. Trial
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  5. Review
  6. A Single Nucleotide Polymorphism inFrontiers in microbiology · 2021
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  8. Emergence of Resistance Mutations inOpen forum infectious diseases · 2017
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  16. Revised Ciprofloxacin Breakpoints for Salmonella: Is it Time to Write an Obituary?Journal of clinical and diagnostic research : JCDR · 2013
    Article
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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

6 authors at 3 institutions in 3 countries.

Thi Anh Hong LeCentre National de Référence des Salmonella, Unité de Biodiversité des Bactéries Pathogènes Emergentes, Institut Pasteur, 28 rue du Docteur Roux, 75724, Paris Cedex 15, France.
Laëtitia Fabre
Philippe Roumagnac
Patrick A D Grimont
Maurice R Scavizzi
François-Xavier Weill
Institut Pasteur · FRMax Planck Institute for Infection Biology · DENational Institute Of Hygiene And Epidemiology · VN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Salmonella enterica serotype Typhi clinical isolates (n = 91) resistant to nalidixic acid (Nal(r)) were collected from sporadic cases and minor outbreaks throughout Vietnam between 1996 and 2004. These isolates were typed and compared by four methods: Vi phage typing, PstI ribotyping, XbaI and SpeI pulsed-field gel electrophoresis (PFGE), and single-nucleotide polymorphism (SNP) analysis. The results indicated that 65% of the isolates were not typeable by Vi phage typing. In contrast, the ribotyping and, with more accuracy, the SNP analysis methods indicated that all Nal(r) isolates belonged to a single clone (ribotype 3a, haplotype H58) that was found previously and that largely consisted of plasmid-encoded multidrug-resistant serotype Typhi isolates. PFGE demonstrated the occurrence of microevolution within this clone. We identified two major combined PFGE profiles: X1-S1 and X3-S6. X3-S6 predominated between 1996 and 2002 but was replaced by X1-S1 after 2002. Nevertheless, PFGE, with a Simpson's index of 0.78, was not considered an optimal discriminatory method for investigating typhoid fever outbreaks in Vietnam. The rate of quinolone resistance increased and the rate of multidrug resistance decreased during the study period. From 2002 to 2004, 80.6% of the isolates from South Vietnam were resistant only to Nal. The mechanism of Nal resistance in most of the isolates (94%) was a mutation in the quinolone resistance-determining chromosomal region of gyrA that led to the amino acid substitution Ser83Phe. No plasmid-located qnrA, qnrB, or qnrS was detected.

Indexed as

Bacteriophage TypingDrug Resistance, Multiple, BacterialElectrophoresis, Gel, Pulsed-FieldEvolution, MolecularMicrobial Sensitivity TestsPolymorphism, Single NucleotideQuinolonesRibotypingSalmonella typhiTime FactorsVietnamQuinolones

Identifiers

PMID17728470
PMCPMC2168509
OpenAlexW2167891320

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.