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β溶血性链球菌和肺炎链球菌中可诱导的克林霉素耐药性。

Inducible clindamycin resistance in β-hemolytic streptococci and Streptococcus pneumoniae.

作者信息

Megged Orli, Assous Marc, Weinberg Gila, Schlesinger Yechiel

机构信息

Pediatric Infectious Diseases Unit, Shaare Zedek Medical Center, affiliated with Hadassah-Hebrew University Medical School, Jerusalem, Israel.

出版信息

Isr Med Assoc J. 2013 Jan;15(1):27-30.

PMID:23484235
Abstract

BACKGROUND

Resistance to macrolides in beta-hemolytic streptococci and Streptococcus pneumoniae arises primarily due to Erm(B) or Mef(A). Erm(B) typically confers high level resistance to macrolides, lincosamides and streptogramin B (MLSB phenotype), whereas Mef(A) confers low level resistance to macrolides only (M phenotype).

OBJECTIVES

To investigate the incidence of macrolide resistance mechanisms in isolates of beta-hemolytic streptococci and pneumococci in Israel, with particular emphasis on inducible MLSB phenotype.

METHODS

We collected 316 clinical isolates of streptococci during May-August 2010. Erythromycin resistance mechanism was determined by the erythromycin-clindamycin double disk diffusion method.

RESULTS

Erythromycin and clindamycin resistance rates were 19.4% and 13.4% for S. pneumoniae, 4.7% and 1.6% for group A Streptococcus (GAS), 17% and 17% for group B Streptococcus (GBS), and 38.8% and 27.8% for group G Streptococcus (GGS) respectively. The most common resistance mechanism for all streptococci was constitutive MLSB (cMLSB). Inducible MLSs (iMLSB) mechanism was found in 3% of all strains and represented 25% of resistance mechanisms.

CONCLUSIONS

The prevalence of macrolide resistance and the distribution of resistance mechanisms differ among beta-hemolytic streptococci and S. pneumoniae, with GBS, GGS and S. pneumoniae showing the highest resistance rate. Macrolide or lincosamide cannot be empirically used for severe streptococcal infections before strains are proved to be susceptible. Continuous surveillance of erythromycin and clindamycin resistance patterns among streptococci is needed.

摘要

背景

β溶血性链球菌和肺炎链球菌对大环内酯类药物的耐药性主要由Erm(B)或Mef(A)引起。Erm(B)通常赋予对大环内酯类、林可酰胺类和链阳菌素B的高水平耐药性(MLSB表型),而Mef(A)仅赋予对大环内酯类的低水平耐药性(M表型)。

目的

调查以色列β溶血性链球菌和肺炎球菌分离株中大环内酯类耐药机制的发生率,特别关注诱导型MLSB表型。

方法

我们在2010年5月至8月期间收集了316株链球菌临床分离株。通过红霉素-克林霉素双碟扩散法确定红霉素耐药机制。

结果

肺炎链球菌对红霉素和克林霉素的耐药率分别为19.4%和13.4%,A组链球菌(GAS)为4.7%和1.6%,B组链球菌(GBS)为17%和17%,G组链球菌(GGS)为38.8%和27.8%。所有链球菌最常见的耐药机制是组成型MLSB(cMLSB)。在所有菌株的3%中发现了诱导型MLS(iMLSB)机制,占耐药机制的25%。

结论

β溶血性链球菌和肺炎链球菌之间大环内酯类耐药性的流行情况和耐药机制的分布有所不同,GBS、GGS和肺炎链球菌显示出最高的耐药率。在菌株被证明敏感之前,大环内酯类或林可酰胺类不能凭经验用于严重的链球菌感染。需要持续监测链球菌中红霉素和克林霉素的耐药模式。

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