Evidence map›Paper›PMID 17108078›Full record

ArticleJournal of clinical microbiology2007

Detection of multidrug resistance in Mycobacterium tuberculosis.

Jun-ichiro Sekiguchi, Tohru Miyoshi-Akiyama, Ewa Augustynowicz-Kopeć, Zofia Zwolska, Fumiko Kirikae, Emiko Toyota, Intetsu Kobayashi, Koji Morita, Koichiro Kudo, Seiya Kato and 3 more

Open access · greenAbstract readEvaluation Study
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 54 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 5 pooled it
3.9field-weighted citation impact, top 6% 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

54 citing papers in PubMed, 5 syntheses or guidelines pooled it, 166 citations in OpenAlex.

  1. Pooled it
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  4. Pooled it
  5. Pooled it
  6. Predicting isoniazid resistance inJournal of clinical microbiology · 2026
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  10. Multi-drug resistant gene mutation analysis inIranian journal of microbiology · 2024
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  20. Clinical implication of novel drug resistance-conferring mutations in resistant tuberculosis.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2017
    Review
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 2 countries.

Jun-ichiro SekiguchiInternational Medical Center of Japan, 1-21-1 Toyama, Shinjuku, Tokyo 162-8655, Japan.
Tohru Miyoshi-Akiyama
Ewa Augustynowicz-Kopeć
Zofia Zwolska
Fumiko Kirikae
Emiko Toyota
Intetsu Kobayashi
Koji Morita
Koichiro Kudo
Seiya Kato
Tadatoshi Kuratsuji
Toru Mori
Teruo Kirikae
Saitama International Medical Center · JPJapan Anti Tuberculosis Association · JPNational Institute of Public Health · PLKyorin University · JPMitsubishi Group (Japan) · JPNational Center For Child Health and Development · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We developed a DNA sequencing-based method to detect mutations in the genome of drug-resistant Mycobacterium tuberculosis. Drug resistance in M. tuberculosis is caused by mutations in restricted regions of the genome. Eight genome regions associated with drug resistance, including rpoB for rifampin (RIF), katG and the mabA (fabG1)-inhA promoter for isoniazid (INH), embB for ethambutol (EMB), pncA for pyrazinamide (PZA), rpsL and rrs for streptomycin (STR), and gyrA for levofloxacin, were amplified simultaneously by PCR, and the DNA sequences were determined. It took 6.5 h to complete all procedures. Among the 138 clinical isolates tested, 55 were resistant to at least one drug. Thirty-four of 38 INH-resistant isolates (89.5%), 28 of 28 RIF-resistant isolates (100%), 15 of 18 EMB-resistant isolates (83.3%), 18 of 30 STR-resistant isolates (60%), and 17 of 17 PZA-resistant isolates (100%) had mutations related to specific drug resistance. Eighteen of these mutations had not been reported previously. These novel mutations include one in rpoB, eight in katG, one in the mabA-inhA regulatory region, two in embB, five in pncA, and one in rrs. Escherichia coli isolates expressing individually five of the eight katG mutations showed loss of catalase and INH oxidation activities, and isolates carrying any of the five pncA mutations showed no pyrazinamidase activity, indicating that these mutations are associated with INH and PZA resistance, respectively. Our sequencing-based method was also useful for testing sputa from tuberculosis patients and for screening of mutations in Mycobacterium bovis. In conclusion, our new method is useful for rapid detection of multiple-drug-resistant M. tuberculosis and for identifying novel mutations in drug-resistant M. tuberculosis.

Indexed as

Antitubercular AgentsBacterial ProteinsDNA, BacterialDrug Resistance, Multiple, BacterialEscherichia coli ProteinsHumansMicrobial Sensitivity TestsMutationMycobacterium tuberculosisPolymerase Chain ReactionRibosomal Protein S9Sensitivity and SpecificitySequence Analysis, DNATemperatureTuberculosis, Multidrug-ResistantTuberculosis, PulmonaryAntitubercular AgentsBacterial ProteinsDNA, BacterialEscherichia coli ProteinsRibosomal Protein S9RpsI protein, E coli

Identifiers

PMID17108078
PMCPMC1828975
OpenAlexW2150863863

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.