| Literature DB >> 1975834 |
G A Hall1, C R Dorn, N Chanter, S M Scotland, H R Smith, B Rowe.
Abstract
Certain isolates of Escherichia coli from humans and animals with enteric disease attach to enterocytes and cause 'attaching and effacing' (AE) lesions. E. coli strain S22-1, serotype O103:H2, isolated from a child with diarrhoea, contained two plasmids; one of these (pDEP12) hybridized with the CVD419 DNA probe derived from a plasmid found in E. coli O157:H7 and associated with expression of fimbriae and ability to adhere to Intestine 407 cells. Strain S102-9, serotype O5:H-, isolated from a calf with dysentery, contained six plasmids, one of which also hybridized with the CVD419 probe. Loss of pDEP12 coincided with reduced adhesion to HEp-2 or Intestine 407 cells cultured in vitro; reintroduction of this plasmid restored adhesiveness. Loss of the plasmid in strain S102-9 that hybridized with the CVD419 probe did not cause a decrease in adhesion. Accumulations of actin were seen in vitro in the fluorescence actin staining (FAS) test of strains S22-1, S102-9 and their derivatives, irrespective of the plasmid content of these strains or the prevalence of attached bacteria. Strain S22-1 and its plasmidless derivative caused AE lesions of equal severity in experimentally infected gnotobiotic piglets; piglets inoculated with an isolate from a healthy human or pig did not develop these lesions.(ABSTRACT TRUNCATED AT 250 WORDS)Entities:
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Year: 1990 PMID: 1975834 DOI: 10.1099/00221287-136-4-779
Source DB: PubMed Journal: J Gen Microbiol ISSN: 0022-1287