Evidence map›Paper›PMID 29611381›Full record

ArticleAnnals of laboratory medicine2018

Determining Genotypic Drug Resistance by Ion Semiconductor Sequencing With the Ion AmpliSeq™ TB Panel in Multidrug-Resistant Mycobacterium tuberculosis Isolates.

Joonhong Park, So Youn Shin, Kyungjong Kim, Kuhn Park, Soyoung Shin, Chunhwa Ihm

Abstract read
In one paragraph

Article in Annals of laboratory medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 2 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

14 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
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  6. Review
  7. Article
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  9. Review
  10. High-Throughput Variant Detection Using a Color-Mixing Strategy.The Journal of molecular diagnostics : JMD · 2022
    Article
  11. Article
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  13. Article
  14. Direct Detection of Rifampin-ResistantFrontiers in microbiology · 2018
    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.

Joonhong Park *Department of Laboratory Medicine, College of Medicine, The Catholic University of Korea, Seoul, Korea.
So Youn Shin *Korean Institute of Tuberculosis, Cheongju, Korea.
Kyungjong KimKorean Institute of Tuberculosis, Cheongju, Korea.
Kuhn ParkDepartment of Thoracic and Cardiovascular Surgery, College of Medicine, The Catholic University of Korea, Seoul, Korea.
Soyoung ShinDepartment of Laboratory Medicine, College of Medicine, The Catholic University of Korea, Seoul, Korea.
Chunhwa IhmDepartment of Laboratory Medicine, Eulji University Hospital, Daejeon, Korea. haneul@eulji.ac.kr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWe examined the feasibility of a full-length gene analysis for the drug resistance-related genes inhA, katG, rpoB, pncA, rpsL, embB, eis, and gyrA using ion semiconductor next-generation sequencing (NGS) and compared the results with those obtained from conventional phenotypic drug susceptibility testing (DST) in multidrug-resistant Mycobacterium tuberculosis (MDR-TB) isolates.

methodsWe extracted genomic DNA from 30 pure MDR-TB isolates with antibiotic susceptibility profiles confirmed by phenotypic DST for isoniazid (INH), rifampin (RIF), ethambutol (EMB), pyrazinamide (PZA), amikacin (AMK), kanamycin (KM), streptomycin (SM), and fluoroquinolones (FQs) including ofloxacin, moxifloxacin, and levofloxacin. Enriched ion spheres were loaded onto Ion PI Chip v3, with 30 samples on a chip per sequencing run, and Ion Torrent sequencing was conducted using the Ion AmpliSeq TB panel (Life Technologies, USA).

resultsThe genotypic DST results revealed good agreement with the phenotypic DST results for EMB (Kappa 0.8), PZA (0.734), SM (0.769), and FQ (0.783). Agreements for INH, RIF, and AMK+KM were not estimated because all isolates were phenotypically resistant to INH and RIF, and all isolates were phenotypically and genotypically susceptible to AMK+KM. Moreover, 17 novel variants were identified: six (p.Gly169Ser, p.Ala256Thr, p.Ser383Pro, p.Gln439Arg, p.Tyr597Cys, p.Thr625Ala) in katG, one (p.Tyr113Phe) in inhA, five (p.Val170Phe, p.Thr400Ala, p.Met434Val, p.Glu812Gly, p.Phe971Leu) in rpoB, two (p.Tyr319Asp and p.His1002Arg) in embB, and three (p.Cys14Gly, p.Asp63Ala, p.Gly162Ser) in pncA.

conclusionsIon semiconductor NGS could detect reported and novel amino acid changes in full coding regions of eight drug resistance-related genes. However, genotypic DST should be complemented and validated by phenotypic DSTs.

Indexed as

AmikacinAntitubercular AgentsBacterial ProteinsDNA, BacterialDrug Resistance, Multiple, BacterialGenotypeHumansKanamycinMicrobial Sensitivity TestsMycobacterium tuberculosisPhenotypePolymerase Chain ReactionSemiconductorsSequence Analysis, DNATuberculosis, Multidrug-ResistantAmikacinAntitubercular AgentsBacterial ProteinsDNA, BacterialKanamycinIon AmpliSeq TB panelIon semiconductor sequencingMultidrug-resistantMutationsMycobacterium tuberculosis

Identifiers

PMID29611381
PMCPMC5895860

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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.