Adherence of an enteropathogenic strain of Escherichia coli to human intestinal mucosa is mediated by a colicinogenic conjugative plasmid.

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The capacity of a human enteropathogenic Escherichia coli (EPEC) strain serotype O26:K60:H11, to adhere to the mucosa of the human fetal small intestine was shown to be plasmid mediated. Adherence was transferred at a high frequency in a long-term conjugal mating experiment to E. coli K-12 and was lost by treatment of the EPEC strain with the curing agent ethidium bromide. Analysis of radioactively labeled DNA from lysates of the EPEC, transconjugant, and cured strains indicated that adherence was correlated with the presence of plasmid DNA species with an approximate average molecular weight of 56 X 10(6). Resistance to the antibiotics spectinomycin, streptomycin, sulfonamides, and tetracycline and production of colicin Ib were all transferred in long-term mating and lost upon curing coordinately with the property of adherence. In conjugal mating experiments of limited duration between E. coli K-12 strains, however, segregation of colicin production and mucosal adherence from multiple drug resistance was observed. Analysis of plasmid DNA of segregant transconjugant strains confirmed the presence in the 56 X 10(6)-dalton plasmid species of two previously unresolved components, pLG101 designating the ColIb plasmid which also carries the determinant for mucosal adherence and pLG102 representing the slightly smaller multiple drug resistance plasmid.

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