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BACTERIAL PATHOGENESIS |
Bacteriology Department, Veterinary Laboratories Agency (Weybridge), New Haw, Addlestone, Surrey KT15 3NB
Corresponding author: Professor M. J. Woodward (e-mail: mwoodward.cvl.wood{at}gtnet.gov.uk).
Received 15 June 1999; accepted 7 Sept. 1999.
Abstract
To investigate the role of fimbriae and flagella in the pathogenesis of avian colibacillosis, isogenic insertionally inactivated mutant strains of Escherichia coli O78:K80 strain EC34195 defective in the elaboration of type-1 and curli fimbriae and flagella were constructed by allelic exchange. Single and multiple non-fimbriate and non-flagellate mutant strains were compared to the wild-type in vitro in adherence assays with a HEp-2 cell line, a mucus-secreting cell line HT2916E, a non-mucus-secreting cell line HT2919A, tracheal explant and proximal gut explant. Mutant strains defective in the elaboration of type-1 fimbriae were significantly less adherent in the order of 90% reduction than the wild-type strain in all assays. Mutant strains defective in the elaboration of flagella were generally as adherent as the wild-type strain except when assayed with the mucus-secreting cell line HT2916E, for which a significant reduction of adherence of the order of 90% compared with the wild-type strain was observed. Mutant strains defective for the elaboration of curli fimbriae adhered as well as the wild-type strain in all assays, except when assayed in tests with gut explant tissue for which a significant reduction of adherence of the order of 80% compared with the wild-type strain was observed. Adherence to explants was to epithelial, not serous, surfaces and was 10-fold greater to tracheal than to gut explants. Together, these data support the hypothesis that type-1 fimbriae are significant factors in adherence, aided by flagella for penetration of mucus and curli fimbriae for adherence to the gut.
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