Girardeau Jean Pierre, Bertin Yolande, Martin Christine
INRA, UR454 Unité de Microbiologie, F-63122 Saint-Genès Champanelle, France.
Microbiology (Reading). 2009 Apr;155(Pt 4):1016-1027. doi: 10.1099/mic.0.026807-0.
Shiga toxin-producing Escherichia coli (STEC) causes a spectrum of human illnesses such as haemorrhagic colitis and haemolytic-uraemic syndrome. Although the locus of enterocyte effacement (LEE) seems to confer enhanced virulence, LEE-negative STEC strains are also associated with severe human disease, suggesting that other unknown factors enhance the virulence potential of STEC strains. A novel hybrid pathogenicity island, termed PAI I(CL3), has been previously characterized in the LEE-negative O113 : H21 STEC strain CL3. Screening for the presence of PAI I(CL3) elements in 469 strains of E. coli, including attaching and effacing (A/E) pathogens [enteropathogenic E. coli (EPEC) and enterohaemorrhagic E. coli (EHEC)], non-A/E pathogens [LEE-negative STEC, extra-intestinal pathogenic E. coli (ExPEC), enterotoxigenic E. coli (ETEC) and enteroaggregative E. coli (EAEC)] and commensal E. coli isolates, showed that PAI I(CL3) is unique to LEE-negative STEC strains linked to disease, providing a new marker for these strains. We also showed that a PAI I(CL3)-equivalent gene cluster is present in the genome of Citrobacter rodentium, on a 53 kb genomic island inserted into the pheV tRNA locus. While the C. rodentium PAI I(CL3) shows high similarities at the nucleotide level and in organization with the E. coli PAI I(CL3), the genetic context of the integration differs completely. In addition, blast searches revealed that other E. coli pathotypes (O157 : H7 EHEC, ExPEC, EPEC and EAEC) possess incomplete PAI I(CL3) elements that contain only the genes located at the extremities of the island. Six of the 16 sequenced E. coli genomes showed deleted PAI I(CL3) gene clusters which are carried on mobile genetic elements inserted into pheV, selC or serW tRNA loci, which is compatible with the idea that the PAI I(CL3) gene cluster entered E. coli and C. rodentium at multiple times through independent events. The phylogenetic distribution of the PAI I(CL3) variants suggests that a B1 genetic background is necessary for the maintenance of the full complement of PAI I(CL3) genes in E. coli.
产志贺毒素大肠杆菌（STEC）可引发一系列人类疾病，如出血性结肠炎和溶血尿毒综合征。尽管肠细胞脱落位点（LEE）似乎赋予了更强的毒力，但LEE阴性的STEC菌株也与严重的人类疾病相关，这表明其他未知因素增强了STEC菌株的毒力潜能。先前在LEE阴性的O113 : H21 STEC菌株CL3中鉴定出一种新型杂交致病岛，称为PAI I(CL3)。对469株大肠杆菌进行PAI I(CL3)元件筛查，这些菌株包括黏附性和脱落性（A/E）病原体[肠致病性大肠杆菌（EPEC）和肠出血性大肠杆菌（EHEC）]、非A/E病原体[LEE阴性STEC、肠外致病性大肠杆菌（ExPEC）、产肠毒素大肠杆菌（ETEC）和肠聚集性大肠杆菌（EAEC）]以及共生大肠杆菌分离株，结果表明PAI I(CL3)是与疾病相关的LEE阴性STEC菌株所特有的，为这些菌株提供了一个新的标志物。我们还表明，在鼠柠檬酸杆菌基因组中，位于插入pheV tRNA位点的一个53 kb基因组岛上存在一个与PAI I(CL3)等效的基因簇。虽然鼠柠檬酸杆菌PAI I(CL3)在核苷酸水平和组织上与大肠杆菌PAI I(CL3)高度相似，但整合的基因背景完全不同。此外，Blast搜索显示，其他大肠杆菌致病型（O157 : H7 EHEC、ExPEC、EPEC和EAEC）拥有不完整的PAI I(CL3)元件，仅包含位于该岛末端的基因。16个已测序的大肠杆菌基因组中有6个显示PAI I(CL3)基因簇缺失，这些基因簇位于插入pheV、selC或serW tRNA位点的移动遗传元件上，这与PAI I(CL3)基因簇通过独立事件多次进入大肠杆菌和鼠柠檬酸杆菌的观点一致。PAI I(CL3)变体的系统发育分布表明，B1遗传背景对于在大肠杆菌中维持PAI I(CL3)基因的完整互补是必要的。
