Evidence map›Paper›PMID 40059193›Full record

ArticleBMC microbiology2025

Prevalence of katG and inhA mutations associated with isoniazid resistance in Mycobacterium tuberculosis clinical isolates in Cameroon.

Vanessa Ninkeh Nono, Edouard Akono Nantia, Awelani Mutshembele, Sorelle Nguimfack Teagho, Yannick Willy Kamdem Simo, Brenda Shile Takong, Yvonne Josiane Djieugoue, Yannick Patrick Assolo, Suzanne Magloire Ongboulal, Stanley Nkemnji Awungafac and 4 more

Abstract read
In one paragraph

Article in BMC microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–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

11 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Host range expansion ofFrontiers in microbiology · 2025
    Article
  11. 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

14 authors.

Vanessa Ninkeh NonoDepartment of Biochemistry, Faculty of Science, University of Bamenda, P.O. Box 39, Bambili, Cameroon.
Edouard Akono NantiaDepartment of Biochemistry, Faculty of Science, University of Bamenda, P.O. Box 39, Bambili, Cameroon.
Awelani MutshembeleOffice of AIDS and TB Research, South African Medical Research Council, Pretoria, South Africa.
Sorelle Nguimfack TeaghoMycobacteriology Unit, National Tuberculosis Reference Laboratory, Centre Pasteur du Cameroun, Yaounde, Cameroon.
Yannick Willy Kamdem SimoMycobacteriology Unit, National Tuberculosis Reference Laboratory, Centre Pasteur du Cameroun, Yaounde, Cameroon.
Brenda Shile TakongMycobacteriology Unit, National Tuberculosis Reference Laboratory, Centre Pasteur du Cameroun, Yaounde, Cameroon.
Yvonne Josiane DjieugoueMycobacteriology Unit, National Tuberculosis Reference Laboratory, Centre Pasteur du Cameroun, Yaounde, Cameroon.
Yannick Patrick AssoloMycobacteriology Unit, National Tuberculosis Reference Laboratory, Centre Pasteur du Cameroun, Yaounde, Cameroon.
Suzanne Magloire OngboulalMycobacteriology Unit, National Tuberculosis Reference Laboratory, Centre Pasteur du Cameroun, Yaounde, Cameroon.
Stanley Nkemnji AwungafacMycobacteriology Unit, National Tuberculosis Reference Laboratory, Centre Pasteur du Cameroun, Yaounde, Cameroon.
Sara EyangohCentre Pasteur du Cameroun, Yaounde, Cameroon.
Eric MensahDepartment of Microbiological Pathology, Tuberculosis Research Unit, Sefako Makgatho Health Sciences University, Molotlegi Street, Ga-Rankuwa, Pretoria, 0204, South Africa.
Ndivhuho Agnes MakhadoDepartment of Microbiological Pathology, Tuberculosis Research Unit, Sefako Makgatho Health Sciences University, Molotlegi Street, Ga-Rankuwa, Pretoria, 0204, South Africa.
Valerie Flore Donkeng DonfackMycobacteriology Unit, National Tuberculosis Reference Laboratory, Centre Pasteur du Cameroun, Yaounde, Cameroon. donkeng@pasteur-yaounde.org.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe acquisition of isoniazid (INH) resistance is alarming, considering its importance as a key drug that forms the core of multidrug treatment regimens for tuberculosis (TB). Genetic mutations in the katG and inhA promoter regions play crucial roles in INH resistance, but their prevalence varies geographically. This study aimed to identify the most common mutations in the katG and inhA genes in INH-resistant (INH-R) Mycobacterium tuberculosis (MTB) clinical isolates in Cameroon. The research also explored the relationships between these mutations and patients' demographics (age, sex, and sample type).

methodsWe conducted a retrospective cross-sectional laboratory-based study on 500 INH-R isolates (with or without resistance to other first-line drugs) at the National Tuberculosis Reference Laboratory (NTRL) in Cameroon between January 2014 and December 2020. GenoType MTBDRplus assay was performed on the retrieved isolates and the frequency of katG and inhA mutations were calculated. Chi-square tests were utilized to assess the associations between these mutations and patients' age, sex and sample type.

resultsA total of 410 (85.8%) culture-positive MTB isolates were analyzed, with a male-to-female ratio of 228 (55.6%) to 182 (44.4%) and an average age of 36.3 ± 13.4 years. Mutations in the katG and inhA genes were detected in 354 (86.3%) of cases, while 56 (13.7%) showed no mutations. Among the INH-R isolates, mutations in katG, inhA, and dual katG and inhA genes were present in 247 (60.2%), 76 (18.5%), and 31 (7.6%) isolates, respectively. Our analysis revealed significant associations between mutation prevalence and patient characteristics.

conclusionThis study reaffirmed the importance of the katG S315T substitution as a key indicator of INH resistance, with the inhA C-15T mutation providing additional support. However, a notable proportion of isoniazid-resistant isolates did not exhibit these mutations, underscoring the need to comprehend resistance mechanisms. Given that these mechanisms are strongly associated with varying levels of INH resistance, it is crucial that TB management strategies incorporate genetic profiling alongside patient demographics to optimize treatment outcomes and enhance control measures.

Indexed as

Antitubercular AgentsBacterial ProteinsCatalaseDrug Resistance, BacterialIsoniazidMycobacterium tuberculosisOxidoreductasesAdolescentAdultAgedCameroonChildChild, PreschoolCross-Sectional StudiesFemaleHumansAntitubercular AgentsBacterial ProteinsCatalaseInhA protein, MycobacteriumIsoniazidkatG protein, Mycobacterium tuberculosisOxidoreductasesCamerooninhAIsoniazid resistancekatGMutationsMycobacterium tuberculosis

Identifiers

PMID40059193
PMCPMC11892131

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.