RESEARCH

The focus of the Escherichia coli research is based on trying to understand the underlying rules governing colonization of the mammalian intestine. Previous work from this lab identified the core set of nutrients necessary to colonize and to compete during colonization of the streptomycin-treated mouse intestine. An intestine-adapted strain was isolated that had characteristics of colonizing the intestine better than its wild-type parent. Genome sequencing revealed a single deletion responsible for making the intestine-adapted strain non-motile and able to grow faster on carbon sources within the intestine. We are focusing on understanding the switch controlling deletion at the flhDC locus. Quorum sensing not only communicates from the microbiome to E. coli, but the absence of at least QseC directly affects lag and nutrient preference.


The focus of the Citrobacter rodentium research is to model pathogenesis of enterohemorrhagic E. coli in the mammalian intestine. Previous work has sequenced the commonly used strain of Citrobacter rodentium strain DBS100. We are developing the continuous streptomycin-treated mouse model of Citrobacter rodentium. Use of streptomycin-treatment during the entire infection causes pathogenesis to cease while promoting colonization. The absence of competition removes the pathogenesis and the presence of competition drives pathogenesis. Not only is colonization divorced from pathogenesis, but adhesins are required for pathogenesis and not for colonization. The microbiome during colonization differs significantly from the microbiome during pathogenesis.