启动子区序列变异对耐甲氧西林金黄色葡萄球菌耐药性的影响

F. Habib, Dipa Roy, Momotaj Nity, A. S. Chaity, A. Haque
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引用次数: 0

摘要

耐多药菌株是卫生保健部门关注的问题之一。其中耐甲氧西林金黄色葡萄球菌(MRSA)是医院获得性多药耐药菌株之一。MRSA通过产生由其mecA基因编码的PBP2a(青霉素结合蛋白2a)显示出对甲氧西林和其他青霉素类抗生素的耐药性。在这个过程中,mecR1和mecI基因作为mecA基因的调节因子。本研究的目的是鉴定位于mecA、mecR1和mecI启动子区的序列变异及其与MRSA菌株致病性的关系。在本研究中,我们收集了90例术后感染患者的伤口感染样本。样本采集自孟加拉国拉杰沙希医学院医院。在抗生素敏感性试验中,MRSA仅对氯霉素和杆菌肽100%敏感。它对阿米卡星、伊培南、强力霉素、庆大霉素和新霉素也显示出部分耐药。在HRM分析中,mecA、mecR1和mecI基因共鉴定出TT、AA、CC、GG、GA和CT 6种基因型。在目前的研究中发现了两种类型的突变(T>C和G>A)。在抗生素耐药性和序列方差方面,HRM分析与抗生素敏感性试验进一步相关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effect of Promoter Region Sequence Variations in Relation to Antibiotic Resistance of Methicillin- Resistant Staphylococcus Aureus
Multidrug resistant bacterial strains are one of the concerns of healthcare sector. Among these, Methicillin- resistant Staphylococcus aureus (MRSA) is one of the major hospitals acquired multidrug resistant strains. MRSA shows it is resistant against methicillin and other penicillin like antibiotics by producing PBP2a (penicillin binding protein 2a) which is encoded by its mecA gene. In this process mecR1 and mecI gene act as regulator of mecA gene. The aim of this study is to identify sequence variance located in mecA, mecR1 and mecI promoter region and the effect of those changes in relation to pathogenicity of these MRSA strains. In this current research, work wound infections samples were collected from 90 patients who were infected during post-surgical mamagement. Samples were collected from Rajshahi Medical college hospital, Bangladesh. In antibiotic sensitivity test, MRSA was found 100% sensitive against only Choramphenicol and Bacitracin. It also shows partial resistance against Amikacin, Impenem, Doxycycline, Gentamycin and Neomycin. In HRM, analysis six types of genotypes (TT, AA, CC, GG, GA and CT) were identified in mecA, mecR1 and mecI genes. Two types of mutation (T>C and G>A) were found in current study. This HRM analysis was further correlate with antibiotic sensitivity test in terms of antibiotic resistance and sequence variance.
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