1887

Abstract

Certain isolates of from humans and animals with enteric disease attach to enterocytes and cause ‘attaching and effacing’ (AE) lesions. 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 0157: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 ; 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 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. These results indicate that the CVD419 probe is not specific for genes conferring the ability to adhere to HEp-2 or Intestine 407 cells by these and that the adhesins detected , or plasmid-encoded properties, are not required for strain S22–1 to cause AE lesions in gnotobiotic pigs or to cause the accumulation of actin in cells

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1990-04-01
2021-07-27
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