Kristi L. Frank, Ph.D.

Kristi L. Frank, Ph.D.


Department of Primary Appointment: Microbiology & Immunology
Position: USU Staff
Title: Assistant Professor

Affiliated Departments: Molecular & Cell Biology,

Research Interests:
Pathogenesis of biofilm-associated infections

Email: (link sends e-mail)
Office Phone: (301) 295-3415
Room: B4092

Department Website
PubMed Listing



Many infections are caused by the formation of microbial biofilms on surfaces in the human body.  Biofilms are organized communities of microbes attached to a surface, or to each other, and are encased in a self-produced extracellular matrix.  Biofilm growth provides protection from adverse environmental conditions, enables evasion of the host immune defenses, and confers resistance to remarkably high concentrations of antimicrobial agents.  Pathogenic bacteria can form biofilms on surfaces throughout a host and on virtually any implantable medical device.  Biofilm infections pose a significant challenge to human health because of their chronic nature and the difficulty associated with treating them.


The Frank lab studies relationships between bacterial pathogens and their hosts in biofilm-associated infections.  In particular, our efforts focus on Enterococcus faecalis, a Gram-positive bacterium that is both a human commensal and an opportunistic pathogen.  The enterococci are exceptionally robust, recalcitrant to many classes of antimicrobial agents, and highly proficient at acquiring virulence factors via horizontal gene transfer.  These characteristics have enabled E. faecalis and other enterococci to emerge as leading causes of healthcare-associated infections.  In immunosuppressed patients, E. faecalis can cause a myriad of infections with biofilm etiology, including endocarditis, surgical site infections, and catheter-associated urinary tract infections.


The questions we are currently investigating grew from initial experiments evaluating E. faecalis gene expression during infection in animal models of endocarditis and subdermal abscess formation.  By pairing these models of biofilm-associated infection with genetic and transcriptomic techniques, we established that (1) an E. faecalis intramembrane metalloprotease called Eep is a biofilm infection-associated virulence factor, and (2) when E. faecalis is introduced into a mammalian host as a pathogen, there is marked genome-wide upregulation of antisense RNA transcripts that occurs concomitantly with activation of a conserved bacterial stress response known as the stringent response.  We are now following up these observations with a combination of in vitro- and in vivo-based approaches.  High throughput sequencing and genetic techniques will be employed to define the sensing pathways and regulatory circuits involved in triggering the bacterial transcriptional and stress responses observed in the host environment.  We are also interested in identifying additional biofilm-associated virulence factors in E. faecalis and how they affect interactions between the bacterium and its host.  Finally, we are pursuing the mechanisms by which E. faecalis colonizes endovascular tissues as part of a broader interest in understanding how biofilm-forming bacteria may affect human cardiovascular health.