Wang G, Jiang Q, Taylor D E
Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, Alberta, Canada.
J Clin Microbiol. 1998 Sep;36(9):2730-1. doi: 10.1128/JCM.36.9.2730-2731.1998.
Clarithromycin-susceptible and clarithromycin-resistant Helicobacter pylori isolates from the same patient were investigated for the mode of development and mechanism of clarithromycin resistance. The clarithromycin-resistant strain UA1182 harbors homozygous A-to-G mutations at position 2143 in both copies of the 23S rRNA gene and has a phenotype of resistance to clarithromycin and clindamycin but no significant resistance to streptogramin B. Pulsed-field gel electrophoresis patterns of NruI- and NotI-digested genomic DNA from the Clas and Clar isolates demonstrated that they are genetically distinct, suggesting that the development of clarithromycin resistance is not from the mutation of the existing Clas strain but from a completely new strain.
对来自同一患者的克拉霉素敏感和克拉霉素耐药的幽门螺杆菌分离株进行了克拉霉素耐药性的产生模式和机制研究。克拉霉素耐药菌株UA1182在23S rRNA基因的两个拷贝中的第2143位均存在纯合的A到G突变,并且具有对克拉霉素和克林霉素耐药的表型,但对链阳菌素B无明显耐药性。来自克拉霉素敏感(Clas)和耐药(Clar)分离株的经NruI和NotI消化的基因组DNA的脉冲场凝胶电泳图谱表明它们在基因上是不同的,这表明克拉霉素耐药性的产生并非来自现有的克拉霉素敏感菌株的突变,而是来自一个全新的菌株。