Evidence map›Paper›PMID 35073862›Full record

ArticleBMC infectious diseases2022

Estimating tuberculosis drug resistance amplification rates in high-burden settings.

Malancha Karmakar, Romain Ragonnet, David B Ascher, James M Trauer, Justin T Denholm

Open access · goldAbstract read
In one paragraph

Article in BMC infectious diseases, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

5 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. AI-Driven Enhancements in Drug Screening and Optimization.Methods in molecular biology (Clifton, N.J.) · 2024
    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

5 authors at 4 institutions in 1 country.

Malancha KarmakarComputational Biology and Clinical Informatics, Baker Heart and Diabetes Institute, Melbourne, VIC, Australia.
Romain RagonnetSchool of Public Health and Preventive Medicine, Monash University, Melbourne, Australia.
David B AscherComputational Biology and Clinical Informatics, Baker Heart and Diabetes Institute, Melbourne, VIC, Australia.
James M TrauerSchool of Public Health and Preventive Medicine, Monash University, Melbourne, Australia.
Justin T DenholmVictorian Tuberculosis Program and Department of Microbiology and Immunology, Doherty Institute of Infection and Immunity, University of Melbourne, 792 Elizabeth Street, Melbourne, VIC, 3000, Australia. justin.denholm@mh.org.au.
Monash University · AUBaker Heart and Diabetes Institute · AUPeter Doherty Institute · AUUniversity of Melbourne · AU

Funding

National Health and Medical Research Council APP 1142638National Health and Medical Research Council APP1144570
6 · The paper itself

Abstract

backgroundAntimicrobial resistance develops following the accrual of mutations in the bacterial genome, and may variably impact organism fitness and hence, transmission risk. Classical representation of tuberculosis (TB) dynamics using a single or two strain (DS/MDR-TB) model typically does not capture elements of this important aspect of TB epidemiology. To understand and estimate the likelihood of resistance spreading in high drug-resistant TB incidence settings, we used epidemiological data to develop a mathematical model of Mycobacterium tuberculosis (Mtb) transmission.

methodsA four-strain (drug-susceptible (DS), isoniazid mono-resistant (INH-R), rifampicin mono-resistant (RIF-R) and multidrug-resistant (MDR)) compartmental deterministic Mtb transmission model was developed to explore the progression from DS- to MDR-TB in The Philippines and Viet Nam. The models were calibrated using data from national tuberculosis prevalence (NTP) surveys and drug resistance surveys (DRS). An adaptive Metropolis algorithm was used to estimate the risks of drug resistance amplification among unsuccessfully treated individuals.

resultsThe estimated proportion of INH-R amplification among failing treatments was 0.84 (95% CI 0.79-0.89) for The Philippines and 0.77 (95% CI 0.71-0.84) for Viet Nam. The proportion of RIF-R amplification among failing treatments was 0.05 (95% CI 0.04-0.07) for The Philippines and 0.011 (95% CI 0.010-0.012) for Viet Nam.

conclusionThe risk of resistance amplification due to treatment failure for INH was dramatically higher than RIF. We observed RIF-R strains were more likely to be transmitted than acquired through amplification, while both mechanisms of acquisition were important contributors in the case of INH-R. These findings highlight the complexity of drug resistance dynamics in high-incidence settings, and emphasize the importance of prioritizing testing algorithms which allow for early detection of INH-R.

Indexed as

Mycobacterium tuberculosisTuberculosisTuberculosis, Multidrug-ResistantAntitubercular AgentsDrug ResistanceHumansIsoniazidMicrobial Sensitivity TestsRifampinAntitubercular AgentsIsoniazidRifampinDrug resistant tuberculosisEpidemiological modellingFitness costResistance amplificationTuberculosis transmission dynamics

Identifiers

PMID35073862
PMCPMC8785585
OpenAlexW4206996724

What OpenQuestion holds

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LicenceCC BY
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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.