Abstract：
:Enteropathogenic Escherichia coli (EPEC) produce attaching and effacing lesions. The genes responsible for this lesion are clustered on the chromosome forming a 35.5 kilobase pathogenesis island called LEE. The LEE was identified, characterized and completely sequenced from the human EPEC strain E2348/69. The LEE carries genes coding for: a type III secretion system (genes esc and sep), the translocated intimin receptor (gene tir), the outer membrane protein intimin (gene eae) and the E. coli secreted proteins EspA, EspB, and EspD (genes esp). In addition to man and farm animals, EPEC are also isolated from dogs and cats. We studied structurally and functionally the LEE of dog and cat EPEC. First, we used four probes scattered along the LEE to identify the presence of a LEE in canine and feline EPEC isolates. Second, by PCR, we checked the presence of genes homologous to eae, sep, esp, and tir genes in these strains. Third, since the four types of eae and tir genes were described, we developed a multiplex PCR in order to determine the type of eae and tir genes present in each strain. Fourth, we determined by PCR the site of the LEE insertion on the chromosome. Fifth, we tested several of the canine EPEC in their capacity to induce attaching and effacing lesions in the rabbit intestinal loop assay. We can conclude from this study: first, that the a LEE-like structure is present in all tested strains and that it contains genes homologous to esp, sep, tir, and eae genes; second, that there is some preferential associations between the type of eae gene and the type of tir gene present in a strain; third, that the majority of the tested strains contained a LEE located elsewhere on the chromosome in comparison to the human EPEC strain E2348/69; and fourth that dog EPEC were able to induce attaching and effacing lesions in rabbit ileal loop assay.
journal_name
Adv Exp Med Bioljournal_title
Advances in experimental medicine and biologyauthors
Goffaux F,China B,Janssen L,Pirson V,Mainil Jdoi
10.1007/978-1-4615-4143-1_11subject
Has Abstractpub_date
1999-01-01 00:00:00pages
129-36eissn
0065-2598issn
2214-8019journal_volume
473pub_type
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