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本文引用的文献

1
Clonal spread of fluoroquinolone non-susceptible Streptococcus pyogenes.对氟喹诺酮不敏感的化脓性链球菌的克隆传播。
J Antimicrob Chemother. 2005 Mar;55(3):320-5. doi: 10.1093/jac/dki011. Epub 2005 Feb 10.
2
Interspecies recombination in type II topoisomerase genes is not a major cause of fluoroquinolone resistance in invasive Streptococcus pneumoniae isolates in the United States.在美国侵袭性肺炎链球菌分离株中,II型拓扑异构酶基因的种间重组并非氟喹诺酮耐药性的主要原因。
Antimicrob Agents Chemother. 2005 Feb;49(2):779-80. doi: 10.1128/AAC.49.2.779-780.2005.
3
Fibronectin-binding protein gene recombination and horizontal transfer between group A and G streptococci.纤连蛋白结合蛋白基因在A组和G组链球菌之间的重组与水平转移。
J Clin Microbiol. 2004 Nov;42(11):5357-61. doi: 10.1128/JCM.42.11.5357-5361.2004.
4
Levofloxacin-resistant invasive Streptococcus pneumoniae in the United States: evidence for clonal spread and the impact of conjugate pneumococcal vaccine.美国耐左氧氟沙星的侵袭性肺炎链球菌:克隆传播的证据及肺炎球菌结合疫苗的影响
Antimicrob Agents Chemother. 2004 Sep;48(9):3491-7. doi: 10.1128/AAC.48.9.3491-3497.2004.
5
Seven years survey of susceptibility to marbofloxacin of bovine pathogenic strains from eight European countries.来自八个欧洲国家的牛致病菌株对马波沙星敏感性的七年调查。
Int J Antimicrob Agents. 2004 Sep;24(3):268-78. doi: 10.1016/j.ijantimicag.2003.12.011.
6
High-level fluoroquinolone resistance in a clinical Streptoccoccus pyogenes isolate in Germany.
Clin Microbiol Infect. 2004 Jul;10(7):659-62. doi: 10.1111/j.1469-0691.2004.00890.x.
7
Reemergence of macrolide resistance in pharyngeal isolates of group a streptococci in southwestern Pennsylvania.宾夕法尼亚州西南部A组链球菌咽部分离株中大环内酯耐药性的再度出现。
Antimicrob Agents Chemother. 2004 Feb;48(2):473-6. doi: 10.1128/AAC.48.2.473-476.2004.
8
First Streptococcus agalactiae isolates highly resistant to quinolones, with point mutations in gyrA and parC.首批无乳链球菌分离株对喹诺酮类药物高度耐药,gyrA和parC基因存在点突变。
Antimicrob Agents Chemother. 2003 Nov;47(11):3605-9. doi: 10.1128/AAC.47.11.3605-3609.2003.
9
Viridans group streptococci are donors in horizontal transfer of topoisomerase IV genes to Streptococcus pneumoniae.草绿色链球菌是拓扑异构酶IV基因向肺炎链球菌进行水平转移的供体。
Antimicrob Agents Chemother. 2003 Jul;47(7):2072-81. doi: 10.1128/AAC.47.7.2072-2081.2003.
10
Fluoroquinolone resistance in Streptococcus pyogenes.
Clin Infect Dis. 2003 Feb 1;36(3):380-3. doi: 10.1086/345904. Epub 2003 Jan 14.

侵袭性化脓性链球菌分离株中由于自发突变和水平基因转移导致的氟喹诺酮耐药性。

Fluoroquinolone resistance in invasive Streptococcus pyogenes isolates due to spontaneous mutation and horizontal gene transfer.

作者信息

Pletz M W R, McGee L, Van Beneden C A, Petit S, Bardsley M, Barlow M, Klugman K P

机构信息

Department of Global Health, Rollins School of Public Health, Emory University, Atlanta, Georgia, USA.

出版信息

Antimicrob Agents Chemother. 2006 Mar;50(3):943-8. doi: 10.1128/AAC.50.3.943-948.2006.

DOI:10.1128/AAC.50.3.943-948.2006
PMID:16495255
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1426425/
Abstract

Fluoroquinolone resistance in Streptococcus pyogenes has been described only anecdotally. In this study we describe two invasive ciprofloxacin-resistant S. pyogenes isolates (ciprofloxacin MICs, 8 mg/liter), one of which shows evidence of interspecies recombination. The quinolone resistance-determining regions of gyrA and parC were sequenced. In both isolates, there was no evidence for an efflux pump and no mutation in gyrA. Both isolates had an S79F mutation in parC that is known to confer fluoroquinolone resistance. In addition, a D91N mutation in parC, which is not related to fluoroquinolone resistance but is a feature of the parC sequence of Streptococcus dysgalactiae, was found in one isolate. The parC nucleotide sequence of that isolate showed greater diversity than that of S. pyogenes. A GenBank search and phylogenetic analysis suggest that this isolate acquired resistance by horizontal gene transfer from S. dysgalactiae. Statistical testing for recombination confirmed interspecies recombination of a 90-bp sequence containing the S79F mutation from S. dysgalactiae. For the other isolate, we could confirm that it acquired resistance by spontaneous mutation by identifying the susceptible ancestor in an outbreak setting.

摘要

化脓性链球菌对氟喹诺酮类药物耐药的情况仅有零星报道。在本研究中,我们描述了两株对环丙沙星耐药的侵袭性化脓性链球菌分离株(环丙沙星 MIC 为 8 mg/L),其中一株显示存在种间重组的证据。对 gyrA 和 parC 的喹诺酮耐药决定区进行了测序。在这两株分离株中,均未发现存在外排泵的证据,且 gyrA 未发生突变。两株分离株的 parC 均有 S79F 突变,已知该突变可导致对氟喹诺酮类药物耐药。此外,在其中一株分离株中发现 parC 存在 D91N 突变,该突变与氟喹诺酮耐药无关,但却是停乳链球菌 parC 序列的一个特征。该分离株的 parC 核苷酸序列显示出比化脓性链球菌更高的多样性。GenBank 搜索和系统发育分析表明,该分离株通过水平基因转移从停乳链球菌获得耐药性。重组的统计检验证实了包含来自停乳链球菌 S79F 突变的 90 bp 序列发生了种间重组。对于另一株分离株,我们通过在一次暴发疫情中鉴定出易感祖先,从而证实它是通过自发突变获得耐药性的。