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粘质沙雷氏菌临床分离株中赋予对单环β-内酰胺类和氧亚氨基头孢菌素耐药性的超广谱β-内酰胺酶

Extended-spectrum beta-lactamases conferring resistance to monobactams and oxyimino-cephalosporins in clinical isolates of Serratia marcescens.

作者信息

Luzzaro F, Pagani L, Porta F, Romero E

机构信息

Clinical Pathology Laboratory, Ospedale di Circolo, Varese, Italy.

出版信息

J Chemother. 1995 Jun;7(3):175-8. doi: 10.1179/joc.1995.7.3.175.

DOI:10.1179/joc.1995.7.3.175
PMID:7562009
Abstract

We studied antibiotic resistance patterns and extended-spectrum beta-lactamases (ES beta Ls) production in Serratia marcescens strains isolated in our hospital during 1993. We examined 210 S. marcescens isolates. Of these, 172 were obtained from 49 patients admitted to an intensive care ward; 157 out of 172 were obtained from February to October and presented the same pattern of antibiotic resistance, including monobactams and oxyimino-cephalosporins. The remaining 15 out of 172 isolates (obtained from September to December) were susceptible to all drugs tested, with the exception of first generation cephalosporins. Thirty-eight additional isolates were recovered, during the same period, from 28 patients admitted to wards other than the intensive care unit; also these strains showed the high susceptibility pattern reported above. Epidemic strains of S. marcescens produced three different types of beta-lactamase with pI 5.4, 5.5, and 8.4. In contrast, non-epidemic strains produced only one type of beta-lactamase with pI 8.4. Conjugation experiments showed that the beta-lactamases having a pI of 5.4 and 5.5 (but not the one with pI 8.4) were plasmid-mediated. Since the beta-lactamase with pI 5.5 was capable of hydrolyzing monobactams and oxyimino-cephalosporins it was classified as ES beta L. Electrophoretic analysis showed that plasmids obtained from multiresistant strains were of about 54 kb; these plasmids appeared also to code for aminoglycoside resistance. Our data indicate that the plasmid-mediated production of ES beta Ls may contribute to the epidemic spread of Serratia marcescens in high-risk wards.

摘要

我们研究了1993年在我院分离出的粘质沙雷氏菌菌株的抗生素耐药模式及超广谱β-内酰胺酶(ESβLs)的产生情况。我们检测了210株粘质沙雷氏菌分离株。其中,172株来自入住重症监护病房的49名患者;172株中的157株是在2月至10月期间获得的,呈现出相同的抗生素耐药模式,包括单环β-内酰胺类和氧亚氨基头孢菌素类。172株中的其余15株(9月至12月获得)除对第一代头孢菌素外,对所有检测药物敏感。同期,从重症监护病房以外病房收治的28名患者中又分离出38株;这些菌株也呈现出上述的高敏感性模式。粘质沙雷氏菌的流行菌株产生了三种不同类型的β-内酰胺酶,其等电点分别为5.4、5.5和8.4。相比之下,非流行菌株仅产生一种等电点为8.4的β-内酰胺酶。接合实验表明,等电点为5.4和5.5的β-内酰胺酶(而非等电点为8.4的)是质粒介导的。由于等电点为5.5的β-内酰胺酶能够水解单环β-内酰胺类和氧亚氨基头孢菌素类,因此被归类为ESβL。电泳分析显示,从多重耐药菌株获得的质粒大小约为54 kb;这些质粒似乎也编码氨基糖苷类耐药性。我们的数据表明,质粒介导的ESβLs产生可能有助于粘质沙雷氏菌在高危病房的流行传播。

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