全部 标题 作者
关键词 摘要

OALib Journal期刊
ISSN: 2333-9721
费用:99美元

查看量下载量

相关文章

更多...

利奈唑胺耐药金黄色葡萄球菌与克林霉素交叉耐药规律

, PP. 408-411

Keywords: 金黄色葡萄球菌,利奈唑胺耐药,交叉耐药,23S核糖体RNA基因

Full-Text   Cite this paper   Add to My Lib

Abstract:

目的阐明体外诱导利奈唑胺耐药金黄色葡萄球菌与克林霉素交叉耐药的变化规律。方法收集2株金黄色葡萄球菌质控菌ATCC29213和ATCC25923,1株乳汁来源的金黄色葡萄球菌和1株血流感染的金黄色葡萄球菌(编号分别为S2、S3、S5和S7菌株,均为利奈唑胺敏感株),通过体外浓度倍增法诱导利奈唑胺耐药;挑取单克隆,37℃培养16h,经E-test条测定MIC值,获得各菌株的耐药浓度梯度,同时测定各菌株对克林霉素的MIC值,提取耐药菌株基因组DNA,PCR扩增23SrRNAV区基因,扩增产物经测序后与野生株比较,获得V区的突变位点。结果经体外多步法诱导利奈唑胺耐药的不同MIC值金黄色葡萄球菌共20株。除S7系列诱导菌株外,其他系列诱导利奈唑胺耐药的菌株,均出现了克林霉素的交叉耐药,PCR测序分析4株母株均无变异位点,G2505A、U2500A、G2576U、C2610C等V区位点可能与克林霉素交叉耐药相关。结论体外多步法诱导产生的金黄色葡萄球菌利奈唑胺菌株,其与克林霉素交叉耐药的机制与23SrRNAV区的位点突变相关。

References

[1]  Meka VG, Gold HS. Antimicrobial resistance to linezolid [J]. Clin Infect Dis, 2004, 39(7): 1010-1015.
[2]  Wemer G, Strommenger B, Klare I, et al.Molecular detection of linezolid resistance in Enterococcus faecium and Enterococcus faecalis by use of 5’nuclease real-time PCR compared to a modified classical approach [J]. J Clin Microbiol, 2004, 42(11): 5327-5331.
[3]  Xiong L, Kloss P. Oxazolidinone resistance mutations in 23srrna of escherichia coli reveal the central region of domain V as the primary site of drug action [J]. J bacteriol, 2000, 182(19): 5325-5331.
[4]  Allen GP, Bierman BC. In vitro analysis of resistance selection by linezolid in vancomycin-susceptible and -resistant Enterococcus faecalis and Enterococcus faecium [J]. Int J Antimicrob Agents, 2009,34(1):21-24.
[5]  Depaidieu F, Perichon B, Courvalin P. Detection of the van alphabet and ident ification of enterococci and Streptococcus at the species level by multiplex PCR [J]. Clin Microbiol, 2004, 42(12): 5857-5860.
[6]  Lin A H, Murray RW, Vidmar TJ, et al. The oxazolidinone eperezolid binds to the 50S ribosomal subunit and competes with binding of chloramphenicol and lincomycin [J]. Antimicrob,Agents Che-mother,1997,41:2127-2131.
[7]  Shinabarger DL, Marotti KR, Murray RW, et al. Mechanism of action of oxazolidinones: effects of linezolid and eperezolid on translation reactions [J]. Antimicrob,Agents Chemother,1997,41:2132-2136.
[8]  Swaney SM, Aoki H, Ganoza MC, et al. The oxazolidinone linezolid inhibits initiation of protein synthesis in bacteria [J]. Antimicrob,Agents Chemother,1998, 42:3251-3255.
[9]  Long KS, Munck C, Andersen TM, et al. Mutations in 23S rRNA at the peptidyl transferase center and their relationship to linezolid binding and cross-resistance [J]. Antimicrob Agents Chemother,2010, 54:4705-4713.
[10]  Li BB, Wu CM, Wang Y,et al. Single and dual mutations at positions 2058, 2503 and 2504 of 23S rRNA and their relationship to resistance to antibiotics that target the large ribosomal subunit [J]. J Antimicrob Chemother, 2011, 66(9):1983-1986.
[11]  Jalava J, Vaara M, Huovinen P. Mutation at the position 2058 of the 23S rRNA as a cause of macrolide resistance in Streptococcus pyogenes [J]. Ann Clin Microbiol Antimicrob, 2004, 3:5.
[12]  Canu A, Malbruny B, Coquemont M, et al. Diversity of ribosomal mutations conferring resistance to macrolides, clindamycin, streptogramin, and telithromycin in Streptococcus pneumoniae [J]. Antimicrob Agents Chemother,2002,46(1):125-131.
[13]  Schlünzen F, Zarivach R, Harms J, et al. Structural basis for the interaction of antibiotics with the peptidyl transferase centre in eubacteria[J]. Nature,2001, 413(6858): 814-821.
[14]  Tu D, Blaha G, Moore PB, et al. Structures of MLSBK antibiotics bound to mutated large ribosomal subunits provide a structural explanation for resistance [J]. Cell, 2005, 121(2):257-270.

Full-Text

Contact Us

service@oalib.com

QQ:3279437679

WhatsApp +8615387084133