Sener Burçin, Köseoglu Ozgen
Department of Microbiology and Clinical Microbiology, Medical Faculty, Hacettepe University, 06100 Ankara, Turkey.
Int J Antimicrob Agents. 2004 Jul;24(1):39-42. doi: 10.1016/j.ijantimicag.2003.11.009.
A collection of 326 strains of Streptococcus pneumoniae isolated from blood, cerebrospinal fluid, bronchoalveolar lavage, transtracheal aspirate or sputum from January 1996-June 2002 were included in this study. The activity of clarithromycin, clindamycin, telithromycin, linezolid and quinupristin/dalfopristin against penicillin G and erythromycin A susceptible and resistant pneumococci were determined; the erythromycin A resistance phenotypes and genotypes were identified and susceptibilities of these agents were assessed according to the resistance genotypes. MICs were determined for all strains of pneumococci using an agar dilution method. MLS(B) resistance phenotypes were determined by the double disk (erythromycin A and clindamycin) diffusion method. Genetic determinants for macrolide resistance were identified by PCR using primers specific for erm(B) and mef(A). Erythromycin A resistance was detected in 13.8% of the strains. MLS(B) resistance phenotype was observed in 82% of these (60% being cMLS(B) and 40% being iMLS(B)), and M type resistance in about 18%. All the MLS(B) phenotype strains except four, revealed the presence of erm(B) gene and all except one M phenotype strains revealed the mef(A) gene. Of the erythromycin A resistant pneumococci about 49% were also resistant to clindamycin. No strains were resistant to telithromycin, quinupristin/dalfopristin and linezolid. Telithromycin had the lowest MIC values for both erythromycin A resistant and susceptible strains of all the antiribosomal agents tested. The most prevalent mechanism of macrolide resistance was mediated by the erm(B) gene leading to the expression of MLS(B) phenotype. Telithromycin was the most active antiribosomal agent, regardless of the macrolide resistance genotype of the pneumococci tested.
本研究纳入了1996年1月至2002年6月期间从血液、脑脊液、支气管肺泡灌洗、经气管抽吸物或痰液中分离出的326株肺炎链球菌。测定了克拉霉素、克林霉素、替利霉素、利奈唑胺和奎奴普丁/达福普汀对青霉素G和红霉素A敏感及耐药肺炎球菌的活性；鉴定了红霉素A耐药表型和基因型，并根据耐药基因型评估了这些药物的敏感性。使用琼脂稀释法测定所有肺炎球菌菌株的最低抑菌浓度（MIC）。通过双纸片（红霉素A和克林霉素）扩散法确定MLS（B）耐药表型。使用针对erm（B）和mef（A）的特异性引物通过聚合酶链反应（PCR）鉴定大环内酯类耐药的遗传决定因素。在13.8%的菌株中检测到红霉素A耐药。在这些菌株中，82%观察到MLS（B）耐药表型（60%为cMLS（B），40%为iMLS（B）），约18%为M型耐药。除4株外，所有MLS（B）表型菌株均显示erm（B）基因的存在，除1株外，所有M表型菌株均显示mef（A）基因的存在。在红霉素A耐药的肺炎球菌中，约49%也对克林霉素耐药。没有菌株对替利霉素、奎奴普丁/达福普汀和利奈唑胺耐药。在所有测试的抗核糖体药物中，替利霉素对红霉素A耐药和敏感菌株的MIC值最低。大环内酯类耐药的最常见机制是由erm（B）基因介导，导致MLS（B）表型的表达。无论测试的肺炎球菌的大环内酯类耐药基因型如何，替利霉素都是最具活性的抗核糖体药物。
