Evidence map›Paper›PMID 18508939›Full record

ArticleJournal of clinical microbiology2008

Biological and molecular characteristics of Mycobacterium tuberculosis clinical isolates with low-level resistance to isoniazid in Japan.

Chiyoji Abe, Ikuo Kobayashi, Satoshi Mitarai, Masako Wada, Yoshiko Kawabe, Tetsuya Takashima, Katsuhiro Suzuki, Li-Hwei Sng, Suxing Wang, Hla Hla Htay and 1 more

Open access · greenAbstract readComparative Study
In one paragraph

Article in Journal of clinical microbiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

22 citing papers in PubMed, 54 citations in OpenAlex.

  1. Predicting isoniazid resistance inJournal of clinical microbiology · 2026
    Article
  2. Prevalence and resistance spectrum ofMicrobiology spectrum · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. The occurrence and frequency of genomic mutations that mediate Isoniazid and Rifampicin resistance inMalawi medical journal : the journal of Medical Association of Malawi · 2018
    Article
  10. Comparative Genomic Analysis of Two Clonally Related Multidrug ResistantFrontiers in cellular and infection microbiology · 2017
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. 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

11 authors at 7 institutions in 3 countries.

Chiyoji AbeFukushima Laboratory, Nippon Becton Dickinson Diagnostic Systems, Tsuchifune, Fukushima 960-2152, Japan. abe_chiyoji@yahoo.co.jp
Ikuo Kobayashi
Satoshi Mitarai
Masako Wada
Yoshiko Kawabe
Tetsuya Takashima
Katsuhiro Suzuki
Li-Hwei Sng
Suxing Wang
Hla Hla Htay
Hideo Ogata
Singapore General Hospital · SGFukushima University · JPJapan Anti Tuberculosis Association · JPLaboratoire National de Référence · MANational Kinki Chuo Hospital for Chest Disease · JPOsaka Prefectural Medical Center · JPTokyo National Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We reevaluated the BACTEC MGIT 960 antimicrobial susceptibility testing system (MGIT 960 AST) by using 1,112 isolates of Mycobacterium tuberculosis. When the results of MGIT 960 AST were compared with that of the proportion method using Ogawa medium (Ogawa PM), discrepant results were obtained for 30 strains with isoniazid, all resistant by MGIT 960 AST but susceptible by Ogawa PM. For 93% of the strains that produced discrepant results, the MIC was 0.4 or 0.8 microg/ml, showing resistance by the proportion method using Middlebrook agar plates. Furthermore, it was also established by analyses of the katG and inhA genes that strains resistant only by MGIT 960 AST have a low level of isoniazid (INH) resistance, indicating that MGIT 960 AST is a reliable method. Ninety-six strains were resistant to 0.1 microg/ml INH by MGIT 960 AST. When they were divided into three groups, Low-S (susceptible at 0.2 microg/ml), Low-R (resistant at 0.2 microg/ml), and High-R (resistant at 1.0 microg/ml), by Ogawa PM, 43.3% of the Low-S strains had mutations in the promoter region of inhA and no mutations were detected in katG codon 315, while 61.7% of the High-R strains had katG codon 315 mutations or a gross deletion of katG. These results suggest that mutations in inhA are associated with low-level resistance to INH and katG codon 315 mutations are associated with high-level resistance to INH. In addition, the analyses demonstrated some relationship of mutations in the inhA gene with ethionamide resistance for the Low-S strains, but not for the High-R strains.

Indexed as

Antitubercular AgentsBacterial ProteinsCatalaseCodon, NonsenseDNA, BacterialDrug Resistance, BacterialEthionamideGene DeletionHumansIsoniazidJapanMicrobial Sensitivity TestsMutationMutation, MissenseMycobacterium tuberculosisOxidoreductasesAntitubercular AgentsBacterial ProteinsCatalaseCodon, NonsenseDNA, BacterialEthionamideInhA protein, MycobacteriumIsoniazidkatG protein, Mycobacterium tuberculosisOxidoreductases

Identifiers

PMID18508939
PMCPMC2446907
OpenAlexW2164139498

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.