Evidence map›Paper›PMID 22294518›Full record

ArticleGenome research2012

Microevolution of extensively drug-resistant tuberculosis in Russia.

Nicola Casali, Vladyslav Nikolayevskyy, Yanina Balabanova, Olga Ignatyeva, Irina Kontsevaya, Simon R Harris, Stephen D Bentley, Julian Parkhill, Sergey Nejentsev, Sven E Hoffner and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Genome research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
106citing 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

106 citing papers in PubMed, 1 synthesis or guideline pooled it, 184 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Infection & chemotherapy · 2023
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  8. Distribution and origins ofMicrobial genomics · 2023
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  9. Novel and reported compensatory mutations inFrontiers in microbiology · 2023
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  10. Article
  11. Article
  12. The Structural Basis ofMolecules (Basel, Switzerland) · 2022
    Article
  13. Article
  14. Article
  15. Compensatory effects ofEmerging microbes & infections · 2021
    Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

46 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

13 authors at 6 institutions in 4 countries.

Nicola CasaliNational Mycobacterium Reference Laboratory, Blizard Institute, Queen Mary, University of London, London E1 2AT, United Kingdom.
Vladyslav Nikolayevskyy
Yanina Balabanova
Olga Ignatyeva
Irina Kontsevaya
Simon R Harris
Stephen D Bentley
Julian Parkhill
Sergey Nejentsev
Sven E Hoffner
Rolf D Horstmann
Timothy Brown
Francis Drobniewski
Queen Mary University of London · GBWellcome Sanger Institute · GBSamara Medical Institute Reaviz · RUBernhard Nocht Institute for Tropical Medicine · DESwedish Institute · SEUniversity of Cambridge · GB

Funding

Wellcome Trust 095198
6 · The paper itself

Abstract

Extensively drug-resistant (XDR) tuberculosis (TB), which is resistant to both first- and second-line antibiotics, is an escalating problem, particularly in the Russian Federation. Molecular fingerprinting of 2348 Mycobacterium tuberculosis isolates collected in Samara Oblast, Russia, revealed that 72% belonged to the Beijing lineage, a genotype associated with enhanced acquisition of drug resistance and increased virulence. Whole-genome sequencing of 34 Samaran isolates, plus 25 isolates representing global M. tuberculosis complex diversity, revealed that Beijing isolates originating in Eastern Europe formed a monophyletic group. Homoplasic polymorphisms within this clade were almost invariably associated with antibiotic resistance, indicating that the evolution of this population is primarily driven by drug therapy. Resistance genotypes showed a strong correlation with drug susceptibility phenotypes. A novel homoplasic mutation in rpoC, found only in isolates carrying a common rpoB rifampicin-resistance mutation, may play a role in fitness compensation. Most multidrug-resistant (MDR) isolates also had mutations in the promoter of a virulence gene, eis, which increase its expression and confer kanamycin resistance. Kanamycin therapy may thus select for mutants with increased virulence, helping preserve bacterial fitness and promoting transmission of drug-resistant TB strains. The East European clade was dominated by two MDR clusters, each disseminated across Samara. Polymorphisms conferring fluoroquinolone resistance were independently acquired multiple times within each cluster, indicating that XDR TB is currently not widely transmitted.

Indexed as

Evolution, MolecularBacterial ProteinsDNA, BacterialDNA FingerprintingDrug Resistance, MultipleExtensively Drug-Resistant TuberculosisGenome, BacterialGenotypeGeographyHumansMicrobial Sensitivity TestsModels, GeneticMutationMycobacterium tuberculosisPhylogenyPolymorphism, Single NucleotideBacterial ProteinsDNA, Bacterial

Identifiers

PMID22294518
PMCPMC3317155
OpenAlexW2122402674

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.