Kristi Frank, Ph.D.
Kristi L. Frank, Ph.D.
Name: Kristi L. Frank, Ph.D.
Bacterial pathogenesis and genetics
Treatment and prevention of biofilm infections
2007 Ph.D., Biomedical Sciences-Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, MN
Dr. Frank's lab studies relationships between bacterial pathogens and their hosts in biofilm-associated infections. 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's current efforts focus on Enterococcus faecalis, a Gram-positive bacterium that is both a human commensal and an opportunistic pathogen. 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 Frank Lab pairs animal models of biofilm formation with genetic, molecular, and biochemical approaches to (1) define sensing pathways and regulatory circuits that are involved in triggering transcriptional and stress responses in the host environment, (2) identify biofilm-associated virulence factors in E. faecalis and determine how they affect interactions between the bacterium and its host, (3) test new methods to remove biofilms and prevent their formation, and (4) pursue 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.
Representative publications, projects, and/or deployments
- Frank, K. L., A. M. Barnes, S. M. Grindle, D. A. Manias, P. M. Schlievert, and G. M. Dunny. 2012. Use of recombinase-based in vivo expression technology to characterize Enterococcus faecalis gene expression during infection identifies in vivo-expressed antisense RNAs and implicates the protease Eep in pathogenesis. Infection and Immunity. 80:539-549.
- Frank, K. L., P. S. Guiton, A. M. T. Barnes, D. A. Manias, O. N. Chuang-Smith, P. L. Kohler, A. R. Spaulding, S. J. Hultgren, P. M. Schlievert, and G. M. Dunny. 2013. AhrC and Eep are biofilm infection-associated virulence factors in Enterococcus faecalis. Infection and Immunity. 81:1696-1708.
- Frank, K. L., C. Colomer-Winter, S. M. Grindle, J. A. Lemos, P. M. Schlievert, and G. M. Dunny. 2014. Transcriptome analysis of Enterococcus faecalis during mammalian infection shows cells undergo adaptation and exist in a stringent response state. Plos One. 9:e115839.
- Frank, K. L., P. Vergidis, C. L. Brinkman, K. E. Greenwood-Quaintance, A. M. T. Barnes, J. N. Mandrekar, P. M. Schlievert, G. M. Dunny, and R. Patel. 2015. Evaluation of the Enterococcus faecalis biofilm-associated virulence factors AhrC and Eep in rat foreign body osteomyelitis and in vitro biofilm-associated antimicrobial resistance. Plos One. 10:e0130187.