CAJ | 학술논문

目的：探讨盐城市东台地区幽门螺杆菌分离菌株gyrA基因突变与左氧氟沙星耐药之间的关系。方法收集2013年5月至2013年10月南通大学附属东台医院消化内科进行胃内窥镜检查的消化性溃疡患者45例胃黏膜组织，接种于含有选择性抑制剂的哥伦比亚血琼脂平板，微需氧条件（5%O2，10%CO2，85%N2）下培养3~5 d，分离培养出23株幽门螺杆菌，所有菌株均采用E?test法进行左氧氟沙星药敏试验，筛选出耐药菌株和敏感菌株；提取幽门螺杆菌菌株基因组DNA，PCR扩增gyrA基因部分片段后进行序列分析。结果左氧氟沙星的耐药率为47.8%（11/23）。11株耐药菌株有10株菌株发生gyrA基因突变，突变形式主要为Asn?87、Asp?91、Val?172，突变菌株数依次为6、3及1株。结论本地区幽门螺杆菌对左氧氟沙星的耐药率较高，其耐药与gyrA基因突变有关，其氨基酸突变形式主要为Asn?87、Asp?91。
목적：탐토염성시동태지구유문라간균분리균주gyrA기인돌변여좌양불사성내약지간적관계。방법수집2013년5월지2013년10월남통대학부속동태의원소화내과진행위내규경검사적소화성궤양환자45례위점막조직，접충우함유선택성억제제적가륜비아혈경지평판，미수양조건（5%O2，10%CO2，85%N2）하배양3~5 d，분리배양출23주유문라간균，소유균주균채용E?test법진행좌양불사성약민시험，사선출내약균주화민감균주；제취유문라간균균주기인조DNA，PCR확증gyrA기인부분편단후진행서렬분석。결과좌양불사성적내약솔위47.8%（11/23）。11주내약균주유10주균주발생gyrA기인돌변，돌변형식주요위Asn?87、Asp?91、Val?172，돌변균주수의차위6、3급1주。결론본지구유문라간균대좌양불사성적내약솔교고，기내약여gyrA기인돌변유관，기안기산돌변형식주요위Asn?87、Asp?91。
Objective To investigate the correlation between gyrA gene mutation of isolated helicobacter pylori (HP) strains and Levofloxacin (LVX) resistance in Dongtai area of Yancheng city. Methods Forty?five gastric mucosal tissues from patients with peptic ulcer,who underwent gastroscopy in the Department of Gastroenterology,Dongtai Hospital Affiliated to Nantong University between May 2013 and October 2013,were included in the study. All gastric mucosal tissues were cultured on Columbia agar plate containing selective inhibitor for 3?5 days under microaerobic condition(5%O2,10%CO2,85%N2). Twenty?three Hp strains were isolated and cultured,and tested for their sensitivity to LVX using the E?test method. The LVX?resistant strains and sensitive strains were screened. The DNA of Hp strain genome was extracted,then the sequence analysis was performed after gyrA gene fragment was amplified by PCR. Results The rate of LVX resistantce was 47.8%(11/23). Among 11 LVX?resistant strains,10 had gyrA gene mutations chiefly including Asn?87(n=6),Asp?91(n=3),and Val?172(n=1). Conclusion The rate of LVX resistance in Hp is high in the Dongtai area,which is correlated with gyrA mutations chiefly presenting as Asn?87 and Asp?91 of amino acid mutations.