study of mutations associated with isoniazid resistance in clinical mycobacterium tuberculosis strains from Tehran & Isfahan province tuberculosis centers by PRC & RFLP


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نویسندگان: پرویز مهاجری

عنوان کنگره / همایش: The 3rd congress of european microbiologists , سوئد , گوتنبرگ ,

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کد مقاله 13
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عنوان لاتین مقاله study of mutations associated with isoniazid resistance in clinical mycobacterium tuberculosis strains from Tehran & Isfahan province tuberculosis centers by PRC & RFLP
نوع ارائه پوستر
عنوان کنگره / همایش The 3rd congress of european microbiologists
نوع کنگره / همایش خارجی
کشور محل برگزاری کنگره/ همایش سوئد
شهر محل برگزاری کنگره/ همایش گوتنبرگ
سال انتشار/ ارائه شمسی
سال انتشار/ارائه میلادی
تاریخ شمسی شروع و خاتمه کنگره/همایش 2009/06/28 الی 2009/07/02
آدرس لینک مقاله/ همایش در شبکه اینترنت
آدرس علمی (Affiliation) نویسنده متقاضی

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پرویز مهاجریاول

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کلمات کلیدیStudy of mutations associated with isoniazid resistance in clinical Mycobacterium tuberculosis strains from Tehran and Isfahan province tuberculosis centers by PCR and RFLP Mohajeri P.1, Tavakoli A.2, Moghim S. 2 1 Kermanshah University of Medical Science, Kermanshah, IRAN 2 Isfahan University of Medical Science, Isfahan, IRAN Background: Although isoniazid is most efficient in killing the tuberculosis bacilli, resistance to this drug also develops most readily. Mutations in katG, inhA and ahpC are responsible for isoniazid resistance in a large proportion of tuberculosis cases. However, the frequency of these mutations varies with population samples. Objectives: Detremination of molecular characterization of isoniazid resistance of M. tuberculosis strains in Teharan and Isfahan Materials and Methods: The study was diagnostic-testing and presence of mutations in specific regions of the katG, inhA and ahpC genes was analyzed with 32 M.tuberculosis isoniazid-resistant strains from Isfahan and Tehran. The katG mutations in codon 315 associated with isoniazid resistance among isoniazid resistant isolates was determined by PCR-RFLP. In this way, 355 bp PCR products were digested by MspI and MspA1I. Mutations in inhA and ahpC genes were detected by sequencing. Results: Mutations in the katG 315(Ser→Thr), inhA and ahpC were detected in 71.9, 18.9 and 6.2% of the 32 isoniazid resistant isolates, respectively. Mutations were not found in one of the isolates. Conclusion: The PCR-RFLP with MspI that detect katG Ser315Thr substitution identified more isoniazid-resistant strains with mutations at codon 315 in the katG. Elucidation of the molecular basis of isoniazid resistance in M. tuberculosis has led to the development of different genotypic approaches for the rapid detection of isoniazid resistance in clinical isolates. The results also suggest that detection of the Ser315Thr in the katG gene may be used as a rapid screening method for identifying isoniazid-resistant clinical M.tuberculosis isolates recovered from Isfahan and Tehran tuberculosis centers.
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