2004-2021 yılları arasında Düzce Üniversitesi'nde izole edilen mycobacterium tuberculosis suşlarında rifampisin ve ikinci jenerasyon antibiyotik direnç genleri araştırılması
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Tarih
2022
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Düzce Üniversitesi
Erişim Hakkı
info:eu-repo/semantics/openAccess
Özet
Amaç: Çalışmamızın amacı, laboratuvarımızda izole edilen M. tuberculosis komplex suşlarında gelişen antibiyotik direncine neden olan gen paternlerinin moleküler yöntemlerle belirlenmesidir. Gereç ve Yöntem: Çalışmamıza, 2004-2021 yılları arasında identifiye edilmiş ve antibiyotik duyarlılığı belirlenmiş olan rifampisin dirençli 21 M. tuberculosis komplex suşu dahil edildi. Bu suşların Genotype MTBC kiti ile türüne ve Genotype MTBDR plus kiti ile rifampisin direncine neden olan gen paternine bakıldı. Bunların içinden rifampisin ve izoniazid direnci birlikte olan çoklu ilaca dirençli 12 suşa Genotype MTBDR sl kiti ile ikinci nesil ilaç direncine neden olan gen paternine bakıldı. Bulgular ve sonuç: Rifampisin dirençli 21 izolat GenoType MTBC yöntemi değerlendirildiğinde 19'u (%90,4) M. tuberculosis/canetti olarak sonuçlandı, ikisi bu test ile değerlendirilemedi. Bunların yedisi (%36,8) Genotype MTBDR plus ile rifampisine dirençli iken 12'si (%63,2) duyarlı bulundu. Dirençli olanların ise birinde (%14,3) WT8 ve WT6 bantlarında, birinde (%14,3) WT8 bandında silinme gözlenirken, birinde (%14,3) WT7 bandında silinme ile rpoBMUT2A mutasyonu ve dördünde (%57,1) WT8 bandında silinme ile rpoBMUT3 mutasyonu birlikte görüldü. Suşların 7'si (%36,8) Genotype MTBDR plus ile INH için dirençli iken 12'si (%63,2) duyarlı olduğu görüldü. Dirençli olanların ise beşinde (%71,4) katGWT bandında silinme ile katGMUT1 mutasyonu ve ikisinde (%28,6) yalnızca ınhAMUT3B mutasyonu görüldü. Çoklu ilaca dirençli 10 M. tuberculosis izolatının GenoType MTBDR sl ver 2.0 yöntemi ile dokuzunda genotipik olarak ikinci nesil ilaçların hiçbirine karşı direnç paterni gözlenmedi. Bir suş bu test ile değerlendirilemedi. Sonuç olarak fenotipik direnç gözlenen suşlarda her zaman geotipik ilaç direnci gözlenmeyebilir. Laboratuvarımızda rifampisin için en sık rastlan genotipik patern WT8 bandında silinmeyle birlikte rpoBMUT3 olarak belirlendi. Anahtar Kelimeler: M. tuberculosis komplex, Rifampisin direnci, İzoniazid direnci, Çoklu ilaca direnç
ABSTRACT Background: The aim of our study is to determine the gene patterns that cause antibiotic resistance in M. tuberculosis complex strains isolated in our laboratory by molecular methods. Material and Method: In our study, 21 rifampicin-resistant M. tuberculosis complex strains identified between 2004-2021 and antibiotic susceptibility were determined were examined with the Genotype MTBC kit and the gene pattern causing rifampicin resistance with the Genotype MTBDR plus kit. Among them, the gene pattern causing second-generation drug resistance was examined with the Genotype MTBDR sl kit on 12 multi-drug resistant strains with rifampicin and isoniazid resistance together. Results: When the GenoType MTBC method of 21 rifampicin-resistant isolates was evaluated, 19 (90.4%) resulted as M. tuberculosis/canetti, two of which could not be evaluated with this test. Seven of them (36.8%) were resistant to rifampicin with Genotype MTBDR plus, while 12 (63.2%) were susceptible. In the resistant ones, deletion was observed in the WT8/WT6 region in one (14.3%) and in the WT8 region in one (14.3%), while one (14.3%) was deleted in the WT7 region with the rpoBMUT2A mutation and in four (57.1%) the WT8 region. deletion and rpoBMUT3 mutation was observed. While 7 (36.8%) of the strains were resistant to INH with Genotype MTBDR plus, 12 (63.2%) were found to be susceptible. Deletion and katGMUT1 mutation in the katGWT region was observed in five (71.4%) and inhAMUT3B mutation in two (28.6%) of the resistant ones. Genotypically, no resistance pattern was observed against any of the second-generation drugs in nine of the 10 multidrug-resistant M. tuberculosis isolates with the GenoType MTBDR sl ver 2.0 method. One strain could not be evaluated with this test. As a result, geotypic drug resistance may not always be observed in strains with phenotypic resistance. In our laboratory, the most common genotypic pattern for rifampicin was determined as rpoBMUT3 with deletion in the WT8 band. Keywords: M. tuberculosis complex, Rifampicin resistance, Isoniazid resistance, Multidrug resistance
ABSTRACT Background: The aim of our study is to determine the gene patterns that cause antibiotic resistance in M. tuberculosis complex strains isolated in our laboratory by molecular methods. Material and Method: In our study, 21 rifampicin-resistant M. tuberculosis complex strains identified between 2004-2021 and antibiotic susceptibility were determined were examined with the Genotype MTBC kit and the gene pattern causing rifampicin resistance with the Genotype MTBDR plus kit. Among them, the gene pattern causing second-generation drug resistance was examined with the Genotype MTBDR sl kit on 12 multi-drug resistant strains with rifampicin and isoniazid resistance together. Results: When the GenoType MTBC method of 21 rifampicin-resistant isolates was evaluated, 19 (90.4%) resulted as M. tuberculosis/canetti, two of which could not be evaluated with this test. Seven of them (36.8%) were resistant to rifampicin with Genotype MTBDR plus, while 12 (63.2%) were susceptible. In the resistant ones, deletion was observed in the WT8/WT6 region in one (14.3%) and in the WT8 region in one (14.3%), while one (14.3%) was deleted in the WT7 region with the rpoBMUT2A mutation and in four (57.1%) the WT8 region. deletion and rpoBMUT3 mutation was observed. While 7 (36.8%) of the strains were resistant to INH with Genotype MTBDR plus, 12 (63.2%) were found to be susceptible. Deletion and katGMUT1 mutation in the katGWT region was observed in five (71.4%) and inhAMUT3B mutation in two (28.6%) of the resistant ones. Genotypically, no resistance pattern was observed against any of the second-generation drugs in nine of the 10 multidrug-resistant M. tuberculosis isolates with the GenoType MTBDR sl ver 2.0 method. One strain could not be evaluated with this test. As a result, geotypic drug resistance may not always be observed in strains with phenotypic resistance. In our laboratory, the most common genotypic pattern for rifampicin was determined as rpoBMUT3 with deletion in the WT8 band. Keywords: M. tuberculosis complex, Rifampicin resistance, Isoniazid resistance, Multidrug resistance
Açıklama
Anahtar Kelimeler
M. tuberculosis komplex, Rifampisin direnci, İzoniazid direnci, Çoklu ilaca direnç, M. tuberculosis complex, Rifampicin resistance, Isoniazid resistance, Multidrug resistance, Mikrobiyoloji, Microbiology
