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Date of Award
Restricted Thesis: Campus only access
Bachelor of Science
Dr. Laura Runyen-Janecky
Dr. Eugene Wu
The evolution of the Shigella flexneri genome has resulted in Shigella’s pathogenicity. The potential Shigella virulence genes qseC, yegV and ppk, along with the proposed antivirulence fimbrial genes fimD, fimI, fimC and fimA, were investigated for their role in pathogenicity. Mutants lacking virulence genes were created and examined for their ability to invade and kill Henle cells. Strains lacking qseC formed wild type-sized plaques. Strains without yegV formed plaques that were visually, but not statistically, smaller than those formed by wild type Shigella. A strain devoid of ppk was not able to form plaques, suggesting its potential role in virulence. A fimbriated strain of Shigella was created by the addition of an Escherichia coli fim locus and was used to infect human colon cells to investigate the effect of fimbriae on Shigella pathogenicity. The presence of fimbriae on Shigella altered colon cell plaque formation and increased the toxicity of Shigella to those cells. Additionally, analysis of the Shigella fimbrial locus from over 25 strains showed that more than 80% have mutations in at least one fimbrial gene.
Bartlett, Dana Katharine, "Role of potential virulence and antivirulence genes in Shigella flexeneri pathogenicity" (2011). Honors Theses. 123.