- 2005 PhD Northwestern University
- 2004 MPH Northwestern University
- 1996 BA Saint Olaf College
- 2011 Instructor, Department of Molecular Microbiology, Washington University School of Medicine, Saint Louis, Missouri, USA.
- 2005-2010 Postdoctoral Fellow, Department of Molecular Microbiology, Washington University School of Medicine, Saint Louis, Missouri, USA. Laboratory of Scott Hultgren.
- 2007-2009 Visiting Postdoctoral Fellow, Karolinska Institute, Stockholm, Sweden. Laboratory of Drs. Birgitta Henriques-Normark and Staffan Normark.
Enterococci are one of the leading causes of hospital-acquired infections and cause a variety of disease states including endocarditis, bacteremia, meningitis, wound infections, and urinary tract infections. The ability to form biofilms in vivo and in the environment is critical for many enterococcus infections. Enterococcal and other Gram positive infections are increasingly problematic due to the rising prevalence of antibiotic resistance. Vancomycin-resistant enterococci (VRE) are of particular concern in hospital settings. Enterococcus faecalis can also share antibiotic resistance genes with methicillin-resistant Staphylococcus aureus (MRSA) resulting in bacterial infections that are exceptionally difficult to treat. Therefore, discovering new strategies to combat infections caused by these organisms is of utmost importance.
E. faecalis must interact with other bacteria to transfer genetic material and with host cells to cause disease, and utilize extracellular proteins and polymers (pili) to mediate these processes. Thus, understanding protein secretion and the pathways that assemble and attach the extracellular proteins to the cell surface promotes our understanding of pathogenesis. We previously demonstrated that several E. faecalis surface proteins are secreted, polymerized, and anchored to the cell wall at distinct focal sites on the bacterial surface. Using a combination of genetics, genomics, biochemistry, and imaging, we are exploring the molecular mechanisms that dictate site selection, organization, and maintenance of localized virulence factor assembly sites in bacteria. We integrate studies of basic cellular processes with in vivo infection models to assess the contribution of localized surface structure biogenesis to disease progression. We have developed several urinary tract infection models to study the pathogenesis of Gram positive organisms. These and other models enable the study of in vivo biofilm formation, infection dynamics, and the host response.
Collectively, we assess the functional consequence of perturbing focal localization of virulence factor assembly at the single cell level, at the bacterial population level, and in models of disease. The overarching goal of these studies is to understand new aspects of fundamental biological processes and to identify novel anti-infective and therapeutic targets.