Evidence map›Paper›PMID 32487030›Full record

ArticleBMC infectious diseases2020

Genotypic and phenotypic characterization of Mycobacterium tuberculosis resistance against fluoroquinolones in the northeast of Iran.

Mahdieh Sayadi, Hosna Zare, Saeed Amel Jamedar, Seyed Isaac Hashemy, Zahra Meshkat, Saman Soleimanpour, Sven Hoffner, Kiarash Ghazvini

Open access · goldAbstract read
In one paragraph

Article in BMC infectious diseases, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.2field-weighted citation impact, top 33% 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

10 citing papers in PubMed, 17 citations in OpenAlex.

  1. Gemifloxacin resistance inMicrobiology spectrum · 2026
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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

8 authors at 2 institutions in 2 countries.

Mahdieh SayadiAntimicrobial Resistance Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Hosna ZareAntimicrobial Resistance Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Saeed Amel JamedarAntimicrobial Resistance Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Seyed Isaac HashemyDepartment of Clinical Biochemistry, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Zahra MeshkatAntimicrobial Resistance Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Saman SoleimanpourAntimicrobial Resistance Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Sven HoffnerDepartment of Global Public Health, Karolinska Institute, Stockholm, Sweden.
Kiarash GhazviniAntimicrobial Resistance Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. Ghazvinik@mums.ac.ir.ORCID http://orcid.org/0000-0002-8538-1425
Mashhad University of Medical Sciences · IRKarolinska Institutet · SE

Funding

Mashhad University of Medical Sciences 950691
6 · The paper itself

Abstract

backgroundFluoroquinolones are broad-spectrum antibiotics that are recommended, and increasingly important, for the treatment of multidrug-resistant tuberculosis (MDR-TB). Resistance to fluoroquinolones is caused by mutations in the Quinolone Resistance Determining Region (QRDR) of gyrA and gyrB genes of Mycobacterium tuberculosis. In this study, we characterized the phenotypic and genotypic resistance to fluoroquinolones for the first time in northeast Iran.

methodsA total of 123 Mycobacterium tuberculosis isolates, including 111 clinical and 12 collected multidrug-resistant isolates were studied. Also, 19 WHO quality control strains were included in the study. The phenotypic susceptibility was determined by the proportion method on Löwenstein-Jensen medium. The molecular cause of resistance to the fluoroquinolone drugs ofloxacin and levofloxacin was investigated by sequencing of the QRDR region of the gyrA and gyrB genes.

resultsAmong 123 isolates, six (4.8%) were fluoroquinolone-resistant according to phenotypic methods, and genotypically three of them had a mutation at codon 94 of the gyrA gene (Asp→ Gly) which was earlier reported to cause resistance. All three remaining phenotypically resistant isolates had a nucleotide change in codon 95. No mutations were found in the gyrB gene. Five of the 19 WHO quality control strains, were phenotypically fluoroquinolone-resistant, four of them were genotypically resistant with mutations at codon 90, 91 of the gyrA gene and one resistant strain had no detected mutation.

conclusionsMutation at codon 94 of the gyrA gene, was the main cause of fluoroquinolone resistance among M. tuberculosis isolates in our region. In 3/6 fluoroquinolone-resistant isolates, no mutations were found in either gyrA or gyrB. Therefore, it can be concluded that various other factors may lead to fluoroquinolone resistance, such as active efflux pumps, decreased cell wall permeability, and drug inactivation.

Indexed as

Antitubercular AgentsCodonDrug Resistance, BacterialDrug Resistance, Multiple, BacterialFemaleFluoroquinolonesGenotypeHumansIranLevofloxacinMaleMicrobial Sensitivity TestsMutationMycobacterium tuberculosisOfloxacinTuberculosis, Multidrug-ResistantAntitubercular AgentsCodonFluoroquinolonesLevofloxacinOfloxacinFluoroquinoloneMDR-TBMycobacterium tuberculosisResistanceXDR-TB

Identifiers

PMID32487030
PMCPMC7268510
OpenAlexW3032490556

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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.