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    Katharine Michelle Ng.
    The human intestine is home to a dense community of commensal microbes that have co-evolved with humans for millions of years. In the absence of disturbance, this community modulates gut homeostasis and mounts a state of colonization resistance against enteric pathogens. This is generally thought to occur through highly efficient resource partitioning as well as the induction and modulation of inflammation and antimicrobial defenses. Profound disturbance of the community, often by way of antibiotic treatment, leads to disruption of colonization resistance. In both humans and animal models, recent antibiotic use is associated with increased susceptibility to several pathogens, including Salmonella typhimurium and Clostridium difficile. This dissertation focuses on understanding the specific mechanisms employed by Salmonella typhimurium during post-antibiotic expansion in the intestine. Chapter 1 provides an introduction to Salmonella as well as to the microbiota and the five phases of microbiota-pathogen interactions. Chapter 2 details a specific strategy utilized by S. typhimurium to expand in the gut, which involves the catabolism of the microbiota-liberated mucosal carbohydrates sialic acid and fucose. The work in Chapter 3 addresses some of the potential applications and questions that have resulted from this finding. Chapter 4 concludes with a discussion of future directions for modulating resistance to pathogens, both with respect to this work as well for the field at large.
    Digital Access   2014