Ethionamide cross-and co-resistance in children with isoniazid-resistant tuberculosis

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dc.contributor.authorSchaaf H.S.
dc.contributor.authorVictor T.C.
dc.contributor.authorVenter A.
dc.contributor.authorBrittle W.
dc.contributor.authorJordaan A.M.
dc.contributor.authorHesseling A.C.
dc.contributor.authorMarais B.J.
dc.contributor.authorVan Helden P.D.
dc.contributor.authorDonald P.R.
dc.date.accessioned2011-05-15T16:16:45Z
dc.date.available2011-05-15T16:16:45Z
dc.date.issued2009
dc.description.abstractBACKGROUND: Ethionamide (ETH) is a structural analogue of isoniazid (INH). Both are pro-drugs requiring activation by separate and common enzyme pathways, which could lead to co-and/or cross-resistance. OBJECTIVE: To characterise paediatric INH-resistant mycobacterial isolates to investigate the presence of ETH resistance and mutations in the katG gene and the inhA promoter region. METHODS: Forty-fi ve INH-resistant and 19 INHs usceptible Mycobacterium tuberculosis control isolates from children from the Western Cape Province, South Africa, were analysed to quantify INH minimal inhibitory concentration, test for ETH resistance and investigate mutations in the katG gene and/or inhA promoter region. RESULTS: Among 45 INH-resistant children, ETH resistance was present in 19 of 39 (49%). An inhA promoter mutation was identifi ed in 15 (33.3%); 12/14 (86%) of these isolates were also ETH-resistant. Of the 21 isolates with a katG mutation, six (29%) were ETH-resistant. No isolate had both katG and inhA promoter mutations. Nine (20%) isolates had neither inhA promoter nor katG mutations. Of 15 isolates with inhA promoter mutation, 14 (93%) displayed low-or intermediate-level INH resistance. Among the 19 INH-susceptible isolates, ETH resistance was present in 1/18 (6%) and none showed inhA or katG gene mutations. CONCLUSION: We found a high level of cross-and coresistance with ETH among INH-resistant M. tuberculosis isolates from children in this geographic area. © 2009 The Union.
dc.description.versionArticle
dc.identifier.citationInternational Journal of Tuberculosis and Lung Disease
dc.identifier.citation13
dc.identifier.citation11
dc.identifier.issn10273719
dc.identifier.urihttp://hdl.handle.net/10019.1/13922
dc.subjectethionamide
dc.subjectisoniazid
dc.subjectbacterial protein
dc.subjectcatalase
dc.subjectInhA protein, Mycobacterium
dc.subjectkatG protein, Mycobacterium tuberculosis
dc.subjectoxidoreductase
dc.subjecttuberculostatic agent
dc.subjectantibiotic resistance
dc.subjectarticle
dc.subjectbacterial gene
dc.subjectbacterium isolate
dc.subjectchild
dc.subjectclinical article
dc.subjectcross resistance
dc.subjectgene mutation
dc.subjecthuman
dc.subjectinfant
dc.subjectinhA gene
dc.subjectkatG gene
dc.subjectminimum inhibitory concentration
dc.subjectMycobacterium
dc.subjectpediatrics
dc.subjectpreschool child
dc.subjectpriority journal
dc.subjectpromoter region
dc.subjectSouth Africa
dc.subjecttuberculosis
dc.subjectcase control study
dc.subjectdrug combination
dc.subjectdrug effect
dc.subjectgenetics
dc.subjectgenotype
dc.subjectmicrobiological examination
dc.subjectmicrobiology
dc.subjectmultidrug resistance
dc.subjectmultidrug resistant tuberculosis
dc.subjectmutation
dc.subjectMycobacterium tuberculosis
dc.subjectpathogenicity
dc.subjectphenotype
dc.subjectprospective study
dc.subjecttreatment failure
dc.subjectAntitubercular Agents
dc.subjectBacterial Proteins
dc.subjectCase-Control Studies
dc.subjectCatalase
dc.subjectChild
dc.subjectChild, Preschool
dc.subjectDrug Resistance, Multiple, Bacterial
dc.subjectDrug Therapy, Combination
dc.subjectEthionamide
dc.subjectGenotype
dc.subjectHumans
dc.subjectInfant
dc.subjectIsoniazid
dc.subjectMicrobial Sensitivity Tests
dc.subjectMutation
dc.subjectMycobacterium tuberculosis
dc.subjectOxidoreductases
dc.subjectPhenotype
dc.subjectPromoter Regions, Genetic
dc.subjectProspective Studies
dc.subjectSouth Africa
dc.subjectTreatment Failure
dc.subjectTuberculosis, Multidrug-Resistant
dc.titleEthionamide cross-and co-resistance in children with isoniazid-resistant tuberculosis
dc.typeArticle
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