Nallapareddy Sreedhar R, Wenxiang Huang, Weinstock George M, Murray Barbara E
Division of Infectious Diseases, Department of Internal Medicine, University of Texas Medical School at Houston, 6431 Fannin Street, MSB 2.112, Houston, TX 77030, USA.
J Bacteriol. 2005 Aug;187(16):5709-18. doi: 10.1128/JB.187.16.5709-5718.2005.
Enterococcus faecalis, a common cause of endocarditis and known for its capacity to transfer antibiotic resistance to other pathogens, has recently emerged as an important, multidrug-resistant nosocomial pathogen. However, knowledge of its lineages and the potential of particular clones of this species to disseminate and cause disease is limited. Using a nine-gene multilocus sequence typing (MLST) scheme, we identified an evolving and widespread clonal complex of E. faecalis that has caused outbreaks and life-threatening infections. Moreover, this unusual clonal complex was found to contain isolates of unexpected relatedness, including the first known U.S. vancomycin-resistant enterococcus (E. faecalis strain V583), the first known penicillinase-producing (Bla(+)) E. faecalis isolate, and the previously described widespread clone of penicillinase producers, a trait found in <0.1% of E. faecalis isolates. All members of this clonal cluster (designated as BVE for Bla(+) Van(r) endocarditis) were found to contain a previously described putative pathogenicity island (PAI). Further analysis of this PAI demonstrated its dissemination worldwide, albeit with considerable variability, confirmed its association with clinical isolates, and found a common insertion site in different clonal lineages. PAI deletions, MLST, and the uncommon resistances were used to predict the evolution of the BVE clonal cluster. The finding of a virulent and highly successful clonal complex of E. faecalis with different members resistant to the primary therapies of choice, ampicillin and vancomycin, has important implications for the evolution of virulence and successful lineages and for public health monitoring and control.
粪肠球菌是心内膜炎的常见病因,以其向其他病原体传递抗生素耐药性的能力而闻名,最近已成为一种重要的多重耐药医院病原体。然而,关于其谱系以及该物种特定克隆传播和致病潜力的了解有限。我们使用一种九基因多位点序列分型(MLST)方案,鉴定出一种不断演变且广泛存在的粪肠球菌克隆复合体,它已引发疫情和危及生命的感染。此外,发现这个不寻常的克隆复合体包含一些亲缘关系出人意料的分离株,包括首例已知的美国万古霉素耐药肠球菌(粪肠球菌菌株V583)、首例已知的产青霉素酶(Bla(+))粪肠球菌分离株,以及先前描述的广泛存在的产青霉素酶克隆株,这一特征在不到0.1%的粪肠球菌分离株中出现。发现这个克隆簇(命名为BVE,即Bla(+) Van(r)心内膜炎)的所有成员都含有一个先前描述的假定致病岛(PAI)。对该PAI的进一步分析表明,它在全球范围内传播,尽管存在相当大的变异性,证实了它与临床分离株的关联,并在不同克隆谱系中发现了一个共同的插入位点。PAI缺失、MLST和罕见耐药性被用于预测BVE克隆簇的进化。发现一种具有毒力且非常成功的粪肠球菌克隆复合体,其不同成员对首选的主要治疗药物氨苄西林和万古霉素耐药,这对毒力和成功谱系的进化以及公共卫生监测与控制具有重要意义。