Molecular evolution of typical enteropathogenic Escherichia coli:: Clonal analysis by multilocus sequence typing and virulence gene allelic profiling
Molecular evolution of typical enteropathogenic Escherichia coli:: Clonal analysis by multilocus sequence typing and virulence gene allelic profiling
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DOI：
10.1128/jb.01472-06
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发表时间：
2007-01-01
影响因子：
3.2
通讯作者：
Whittam, Thomas S.
中科院分区：
文献类型：
--
作者：
Lacher, David W.;Steinsland, Hans;Whittam, Thomas S.
肠致病性大肠杆菌（EPEC）感染是发展中国家婴儿腹泻的主要原因。典型的EPEC分离株与其他类型的致病性E.大肠杆菌的粘附表现为两种不同的表型，即附着消失和局部粘附。在肠上皮细胞消失（LEE）位点和EPEC粘附因子（EAF）质粒上发现了指定这些表型的基因。为了描述典型的EPEC如何演变，我们通过多位点序列分型（MLST）表征了不同菌株的集合，并对三个毒力基因（eae，bfpA和perA）进行了限制性片段长度多态性（RFLP）分析，以评估等位基因变异。在代表20个O-血清群的129株菌株中，使用MLST鉴定出21个克隆基因型。RFLP分析解决了9个eae，9个bfpA和4个perA等位基因。每个bfpA等位基因仅与一个perA等位基因类相关，这表明重组在单独的EAF质粒之间的bfpA和perA位点的改组中没有发挥很大的作用。EPEC典型菌株中eae等位基因的分布比EAF质粒类型的分布更符合克隆关系。这些结果进一步支持了EPEC致病型在大肠杆菌中多次进化的假设。通过分别获得LEE岛和EAF质粒，在大肠杆菌中表达。
Enteropathogenic Escherichia coli (EPEC) infections are a leading cause of infantile diarrhea in developing nations. Typical EPEC isolates are differentiated from other types of pathogenic E. coli by two distinctive phenotypes, attaching effacement and localized adherence. The genes specifying these phenotypes are found on the locus of enterocyte effacement (LEE) and the EPEC adherence factor (EAF) plasmid. To describe how typical EPEC has evolved, we characterized a diverse collection of strains by multilocus sequence typing (MLST) and performed restriction fragment length polymorphism (RFLP) analysis of three virulence genes (eae, bfpA, and perA) to assess allelic variation. Among 129 strains representing 20 O-serogroups, 21 clonal genotypes were identified using MLST. RFLP analysis resolved nine eae, nine bfpA, and four perA alleles. Each bfpA allele was associated with only one perA allele class, suggesting that recombination has not played a large role in shuffling the bfpA and perA loci between separate EAF plasmids. The distribution of eae alleles among typical EPEC strains is more concordant with the clonal relationships than the distribution of the EAF plasmid types. These results provide further support for the hypothesis that the EPEC pathotype has evolved multiple times within E. coli through separate acquisitions of the LEE island and EAF plasmid.