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可转移的β-内酰胺酶。粪肠球菌体外青霉素耐药的一种新机制。

Transferable beta-lactamase. A new mechanism for in vitro penicillin resistance in Streptococcus faecalis.

作者信息

Murray B E, Mederski-Samaroj B

出版信息

J Clin Invest. 1983 Sep;72(3):1168-71. doi: 10.1172/JCI111042.

Abstract

Although enterococci are relatively resistant to penicillin, the mechanism of resistance is largely unknown and enzymatic inactivation does not play a role. In this study, an isolate of Streptococcus faecalis was found to have beta lactamase activity resulting in complete inactivation of penicillin. With a high inoculum, this strain was resistant to greater than 1,000 micrograms/ml of penicillin. Penicillin resistance and beta lactamase activity were transferred by conjugation at a high frequency to an enterococcal laboratory recipient strain together with two plasmids of molecular size 34 X 10(6) and 56 X 10(6), thus demonstrating the emergence of plasmid-mediated penicillin resistance in the genus Streptococcus.

摘要

尽管肠球菌对青霉素相对耐药,但其耐药机制很大程度上尚不清楚,且酶失活不起作用。在本研究中,发现一株粪链球菌具有β-内酰胺酶活性,导致青霉素完全失活。在高接种量时,该菌株对大于1000微克/毫升的青霉素耐药。青霉素耐药性和β-内酰胺酶活性通过接合高频转移至一株肠球菌实验室受体菌株,同时伴有两个分子大小分别为34×10⁶和56×10⁶的质粒,从而证明在链球菌属中出现了质粒介导的青霉素耐药性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0fec/1129285/7c26c0443a30/jcinvest00769-0429-a.jpg

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