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dc.contributor.advisorPanigraphy, Brundaban
dc.creatorGyimah, Joseph Edmund
dc.descriptionTypescript (photocopy).en
dc.description.abstractSpecific attachment of E. coli (01:K1, 02:K1, 078:K80) to chicken tracheal epithelium was investigated using adherence inhibition studies. The role of pili as an adhesin was examined by blocking pili with antipilus antibodies. The nature of the host cell receptor was determined by blocking bacterial adhesion with specific carbohydrates or lectins and destroying the receptor with sodium metaperiodate. Antipilus antibodies to all 3 serotypes significantly (P [less than or equal to] 0.05) inhibited their adherence, an indication that pili serve as bacterial adhesins. Sodium metaperiodate significantly inhibited the adhesion of all 3 serotypes, suggesting a role for monosaccharides in the host cell receptor. D-mannose and its derivative methyl-α-D-mannopyranoside, inhibited the adhesion of serotypes 01 and 078, implying a role for these sugars in the host cell receptor. This was confirmed by the inhibition of both serotypes following treatment of tracheal epithelial cells with concanavalin A. None of the sugars or lectins used inhibited adhesion of serotype 02. Abrogation of pilus-mediated adhesion by antibodies directed against the pilus was investigated in chickens vaccinated with an oil-emulsified E. coli pilus vaccine against homologous challenge. Compared with positive control chickens, vaccinated chickens were protected against challenge because they suffered low or no mortality, had mild gross lesions, and eliminated challenge E. coli from tissues more efficiently. Protection was still evident when pili from all 3 serotypes were combined as a multivalent vaccine. Immunogenicity of E. coli (01:K1) whole cell bacterin was also evaluated in chickens. Against homologous challenge, vaccinated chickens were protected against active respiratory infection and also eliminated E. coli (01:K1) from tissues more efficiently than positive controls. However E. coli (01:K1) whole cell bacterin did not provide cross-protection against other pathogenic serotypes (02, 078). The results of these studies showed that: (A) adhesin-receptor interaction occurs in the adhesion of pathogenic E. coli to tracheal epithelial cells; (B) this interaction is mediated by pili on the bacterium and mannose-containing receptors on the host cell membrane in the adhesion of serotypes 01, and 078: (C) pili adhesin is a potent an immunogen that provides protection against homologous challenge; (D) whole cell bacterin protects against homologous but not heterologous challenge; (E) the protection afforded by either whole cell or pili was comparable.en
dc.format.extentxiii, 96 leavesen
dc.rightsThis thesis was part of a retrospective digitization project authorized by the Texas A&M University Libraries. Copyright remains vested with the author(s). It is the user's responsibility to secure permission from the copyright holder(s) for re-use of the work beyond the provision of Fair Use.en
dc.subjectMajor veterinary microbiologyen
dc.subject.classification1986 Dissertation G996
dc.subject.lcshEscherichia coli infectionsen
dc.titlePathogenesis and biological control of colibacillosis in chickensen
dc.typeThesisen A&M Universityen of Philosophyen Den
dc.contributor.committeeMemberFanguy, R. C.
dc.contributor.committeeMemberGrumbles, L. C.
dc.contributor.committeeMemberHall, C. F.
dc.format.digitalOriginreformatted digitalen
dc.publisher.digitalTexas A&M University. Libraries

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