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属于ST100的侵袭性万古霉素异质性耐药金黄色葡萄球菌分离株及其衍生的万古霉素异质性耐药金黄色葡萄球菌突变体中IS256转座增加。

Increase in IS256 transposition in invasive vancomycin heteroresistant Staphylococcus aureus isolate belonging to ST100 and its derived VISA mutants.

作者信息

Di Gregorio Sabrina, Fernandez Silvina, Perazzi Beatriz, Bello Natalia, Famiglietti Angela, Mollerach Marta

机构信息

Cátedra de Microbiología, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, CABA, Argentina.

Laboratorio de Bacteriología Clínica, Hospital de Clínicas José de San Martín, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, CABA, Argentina.

出版信息

Infect Genet Evol. 2016 Sep;43:197-202. doi: 10.1016/j.meegid.2016.05.001. Epub 2016 May 3.

Abstract

In Staphylococcus aureus, transposition of IS256 has been described to play an important role in biofilm formation and antibiotic resistance. This study describes the molecular characterization of two clinical heterogeneous vancomycin-intermediate S. aureus (hVISA) isolates recovered from the same patient (before and after antibiotic treatment) and two VISA derivatives obtained by serial passages in the presence of vancomycin. Our results showed that antibiotic treatment (in vivo and in vitro) could enhance IS256 transposition, being responsible for the eventual loss of agr function. As far as we know this is the first study that reports the increase of IS256 transposition in isogenic strains after antibiotic treatment in a clinical setting.

摘要

在金黄色葡萄球菌中,IS256的转座已被描述为在生物膜形成和抗生素耐药性中发挥重要作用。本研究描述了从同一患者(抗生素治疗前后)分离出的两株临床异质性万古霉素中介金黄色葡萄球菌(hVISA)以及在万古霉素存在下通过连续传代获得的两株VISA衍生物的分子特征。我们的结果表明,抗生素治疗(体内和体外)可增强IS256转座,这是导致agr功能最终丧失的原因。据我们所知,这是第一项报道在临床环境中抗生素治疗后同基因菌株中IS256转座增加的研究。

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