M.P.H. (1998) Hospital and Molecular Epidemiology, University of Michigan, Ann Arbor, Mich.
Ph.D. (2001) Molecular Epidemiology, University of Michigan, Ann Arbor, Mich.
Emerging Infectious Disease Fellowship CDC/APHL 2001-2004
University of Michigan, 2001-2002
Michigan State University, 2004-2010
194 Food Safety & Toxicology Building
Michigan State University
East Lansing, MI 48824
Phone: (517) 884-2033
My laboratory studies the molecular epidemiology and evolutionary genetics of infectious diseases, namely those caused by diarrheagenic Escherichia coli and Streptococcus agalactiae. More specifically, we apply molecular biology, population genetic, and evolutionary methods to answer questions about pathogenesis, emergence, virulence, evolution, and transmission of pathogens in human and animal populations. Our studies of both Shiga toxin-producing E. coli (STEC) O157:H7 and S. agalactiae are similar in that the phylogenetic analysis of genome data and the subsequent epidemiological analysis identified specific strain types to be more important for disease. Most of our current and future research projects are associated with these key findings that will ultimately enhance our understanding of how genetic variation contributes to clinical illness.
S. agalactiae pathogenesis
In collaboration with Drs. David Aronoff of Vanderbilt University and Rita Loch-Caruso of the University of Michigan and funding through the NIH and Global Alliance to Prevent Prematurity and Stillbirth (GAPPS) Foundation, these projects aim to explore transcriptional responses of S. agalactiae following exposure to both placental membranes and human-derived macrophages. The data generated through these projects have uncovered differences in the molecular epidemiology of strain types in circulation, phagocytic uptake frequencies, ability to form biofilms, and transcriptional profiles of phylogenetically distinct S. agalactiae strains after exposure to lung and placental epithelial cells.
The intestinal microbiome and characterization of diarrheagenic E. coli
My laboratory also characterizes intestinal microbial communities from individuals with and without enteric infections through the NIH-funded Enteric Research Investigation Network (ERIN) Cooperative Research Center (CRC). The long term goal of this project is to identify potentially beneficial microbes, microbial communities and/or microbial by-products that can be used to prevent or treat disease. Through the surveillance activities associated with the ERIN and my long-standing collaboration with the Michigan Department of Community Health, we have received a large collection of enteric pathogens for characterization. Our analysis of the E. coli O104:H4 2011 outbreak strain, which caused the highest frequency of hemolytic uremic syndrome (HUS) and death ever recorded in a single E. coli outbreak, demonstrated that biofilm formation is correlated with virulence gene expression in vivo. An interview at WKAR on March 21, 2013 highlights the findings associated with this project.
Ecology of STEC shedding in cattle
The primary goals of this multidisciplinary USDA-funded project are to: 1) identify STEC genotypes and factors important for STEC shedding in multiple herds by examining genotype distributions, genetic diversity and changes in shedding status over time; and 2) compare the composition, diversity and function of the intestinal microbial communities of STEC-shedders and non-shedders. The long term study goal is to assess how the interplay between bacterial, epidemiological, immunological, and host factors affects shedding phenotypes that can facilitate the development of enhanced detection methods and control strategies.