Jerse A E, Gicquelais K G, Kaper J B
Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland 21201.
Infect Immun. 1991 Nov;59(11):3869-75. doi: 10.1128/iai.59.11.3869-3875.1991.
Attaching and effacing (A/E) intestinal lesions are produced by enteropathogenic Escherichia coli (EPEC), enterohemorrhagic E. coli (EHEC), and RDEC-1, a pathogen of weanling rabbits. We recently identified a chromosomal locus (eae[E. coli A/E]) which is required for A/E activity in a wild-type EPEC strain. Sequences homologous to those of an eae gene probe were detected in EPEC, RDEC-1, and EHEC isolates. We report here that the eae gene is chromosomally encoded in all EPEC and EHEC strains tested and in RDEC-1. In addition, the eae probe was found to be 100% sensitive and 98% specific in detecting E. coli of EPEC serogroups that demonstrate A/E activity. Ten percent of E. coli of EPEC serogroups that hybridized with the eae probe and produced A/E activity did not hybridize with the EAF (EPEC adherence factor) probe, a plasmid-associated diagnostic probe which is currently used to identify EPEC. In addition to A/E factors, plasmid-associated adhesins also contribute to the pathogenesis of EPEC and RDEC-1. To further investigate the role of plasmid-associated adherence, a hybrid RDEC-1-EPEC strain containing the adherence plasmid of an EPEC strain in the A/E background of RDEC-1 was constructed. This hybrid strain, unlike the parent RDEC-1 strain, produced A/E lesions on human tissue culture cells, which suggests that the EPEC adherence plasmid provides tissue specificity to the hybrid strain and that the A/E factors of RDEC-1 are not host restricted.
黏附和毁损（A/E）性肠道病变由肠致病性大肠杆菌（EPEC）、肠出血性大肠杆菌（EHEC）以及断奶仔兔病原体RDEC-1引起。我们最近鉴定出一个染色体位点（大肠杆菌A/E的eae），它是野生型EPEC菌株中A/E活性所必需的。在EPEC、RDEC-1和EHEC分离株中检测到了与eae基因探针序列同源的序列。我们在此报告，eae基因在所有测试的EPEC和EHEC菌株以及RDEC-1中都是由染色体编码的。此外，发现eae探针在检测表现出A/E活性的EPEC血清群大肠杆菌时，敏感性为100%，特异性为98%。与eae探针杂交并产生A/E活性的EPEC血清群大肠杆菌中有10%不与EAF（EPEC黏附因子）探针杂交，EAF探针是一种目前用于鉴定EPEC的质粒相关诊断探针。除了A/E因子外，质粒相关黏附素也对EPEC和RDEC-1的发病机制有作用。为了进一步研究质粒相关黏附的作用，构建了一种杂交RDEC-1-EPEC菌株，该菌株在RDEC-1的A/E背景中含有EPEC菌株的黏附质粒。与亲本RDEC-1菌株不同，这种杂交菌株在人组织培养细胞上产生了A/E病变，这表明EPEC黏附质粒为杂交菌株提供了组织特异性，并且RDEC-1的A/E因子不受宿主限制。
