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dc.contributor.advisorSmith, Arnold L.eng
dc.contributor.authorTsao, David L.eng
dc.date.issued2004eng
dc.date.submitted2004 Falleng
dc.descriptionIncludes bibliographical references.eng
dc.descriptionThesis (M.S.) University of Missouri-Columbia 2004.eng
dc.descriptionThe entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file.eng
dc.description"December, 2004"eng
dc.descriptionDissertations, Academic -- University of Missouri--Columbia -- microbiology (Medicine).eng
dc.description.abstract[ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT AUTHOR'S REQUEST.] Since the introduction of Haemophilus influenzae b polysaccharide-protein conjugate vaccines, the incidence of invasive H. influenzae disease dramatically decreased. Currently, invasive disease is caused by other capsular serotypes or strains lacking genes for capsule synthesis, and therefore nontypeable (NTHi). A common feature of invasive H. influenzae is the ability to replicate in human blood, due to resistance to the bactericidal acitivity of serum. Seeking to understand the mechanism of serum-resistance in an invasive NTHi (strain R2866) we studied the strains recovered from the blood of five-day-old rats. We hypothesized that there would be increased virulence and acentuated resistance to normal human serum (NHS) in passaged isolates. We found that the rat passaged strain caused more deaths in the infant rat model, invaded Chang cells better but became more susceptible to the bactericidal action of NHS. This phenotypic shift was associated with modification of the lipooligosaccharide (LOS): more gal-B(1-4)gln epitope was exposed, while less gal-a-(1-3) gal was reactive with the monoclonal antibody. GeneScan® analysis of tetrameric repeats in the R2866 and the passaged strain indicated that expression of a LOS glycosyltransferase was OFF in the rat isolates. We conclude that animal passage of an invasive NTHi selects for increased animal virulence through expression of alternative LOS structures.eng
dc.identifier.merlinb55150445eng
dc.identifier.urihttp://hdl.handle.net/10355/5808
dc.languageEnglisheng
dc.publisherUniversity of Missouri--Columbiaeng
dc.relation.ispartofcollectionUniversity of Missouri--Columbia. Graduate School. Theses and Dissertationseng
dc.rightsAccess is limited to the campuses of the University of Missouri.eng
dc.subject.meshLipopolysaccharides -- chemistryeng
dc.subject.meshHaemophilus influenzae -- drug effectseng
dc.subject.meshVirulenceeng
dc.subject.meshDrug Resistance, Microbialeng
dc.subject.meshModels, Animaleng
dc.subject.meshHaemophilus Infections -- microbiologyeng
dc.subject.meshHaemophilus Vaccines -- immunologyeng
dc.titleSerum resistance of an invasive nontypeable H. influenzaeeng
dc.typeThesiseng
thesis.degree.disciplineMicrobiology (Medicine) (MU)eng
thesis.degree.grantorUniversity of Missouri--Columbiaeng
thesis.degree.levelMasterseng
thesis.degree.nameM.S.eng


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