Department of Biological Sciences

School of Natural Sciences and Mathematics

Areas of Study

Kelli Palmer, PhD

B.Sc., Microbiology, University of Oklahoma
PhD, Molecular Genetics and Microbiology, University of Texas at Austin
Postdoctoral Fellow, Ophthalmology, and Microbiology and Immunobiology, Harvard Medical School

Dr. Palmer uses genomic, transcriptomic, and biochemical approaches to study antibiotic resistance in pathogenic bacteria. Her research focuses on microorganisms contributing to significant mortality and cost burdens in the health care industry.

Research Interests

I study antibiotic resistance in, and the in vivo physiology of, pathogenic bacteria. The goals of my research are to: 1) characterize evolutionary and molecular mechanisms contributing to antibiotic resistance in the enterococci and to 2) use in vivo-relevant growth substrates to characterize the physiology of pathogenic bacteria, with each of these goals executed with an eye towards novel antimicrobial development.

1. Genome defense in the enterococci. The enterococci are Gram-positive bacteria and opportunistic pathogens associated with life-threatening infections in humans. Since the 1980s, enterococci have gained increasing notoriety from their association with hospital-acquired infections and multidrug resistance, especially the species Enterococcus faecalis and E. faecium. Multidrug resistance in the enterococci is due in part to the horizontal transfer of mobile genetic elements such as plasmids and transposons. E. faecalis in particular is distinguished by the intraspecies dissemination of pheromone-responsive plasmids, a unique group of plasmids which sense and respond to small peptide signals excreted by plasmid-free E. faecalis cells. Certain phylogenetic lineages of E. faecalis and E. faecium appear to be especially associated with hospital endemicity and drug resistance - these are called the high-risk, or hospital-adapted, lineages. The striking abundance of plasmids, transposons, and viruses in genomes of high-risk strains led me to hypothesize that self-defense mechanisms became compromised in those strains. My current research focuses on the role of CRISPR-Cas systems, which function as prokaryotic acquired immune systems, in regulating mobile element acquisition and dissemination in the enterococci.

2. The host as a growth medium. During infection, bacteria harvest food and energy from their hosts to support survival and growth. However, the in vivo carbon and energy sources for many pathogenic bacteria are unknown or poorly defined. Nutrient availability can also impact virulence factor production. To understand the nature and progression of infectious disease, it is important to study the physiology of pathogenic bacteria either in vivo using animal infection models or in vitro using appropriate growth media. During my graduate training, I studied Pseudomonas aeruginosa, a Gram-negative bacterium that chronically infects the lungs of cystic fibrosis (CF) patients. I utilized sputa expectorated by CF patients as in vitro growth media for P. aeruginosa, and in subsequent work used analytical techniques to create a defined, synthetic growth medium mimicking CF sputum composition. The use of these in vitro media led to significant insights into P. aeruginosa physiology as it relates to CF pathogenesis. This approach - considering the host as a growth medium - will be employed in my lab to study other bacterial pathogens of concern.

Selected Publications:

1. K Palmer, P Godfrey, A Griggs, V Kos, J Zucker, C Desjardins, G Cerqueira, D Gevers, S Walker, J Wortman, M Feldgarden, B Haas, B Birren, and MS Gilmore. 2012. Comparative genomics of enterococci: Variation in E. faecalis, clade structure in E. faecium, and defining characteristics of E. gallinarum and E. casseliflavus. mBio 3(1):e00318-11.

2. KL Palmer, A Daniel, CA Hardy, JA Silverman, and MS Gilmore. 2011. Genetic basis for daptomycin resistance in enterococci. Antimicrob. Agents Chemother. 55:3345-56.

3. KL Palmer and MS Gilmore. 2010. Multidrug resistant enterococci lack CRISPR-cas. mBio 1(4):e00227-10.

4. KL Palmer (co-first author), VN Kos, and MS Gilmore. 2010. Horizontal gene transfer and the genomics of enterococcal antibiotic resistance. Curr Opin Microbiol. 13:632-639.

5. Brown, SA, KL Palmer (co-first author) and M Whiteley. 2008. Revisiting the host as a growth medium. Nat. Rev. Microbiol. 6:657-66.

6. KL Palmer, LM Aye, and M Whiteley. 2007. Nutritional cues control Pseudomonas aeruginosa multi-cellular behavior in cystic fibrosis sputum. J. Bacteriol. 189:8079-8087.

7. KL Palmer, SA Brown, and M Whiteley. 2007. Membrane-bound nitrate reductase is required for anaerobic growth in cystic fibrosis sputum. J. Bacteriol. 189:4449-55.

8. KL Palmer, LM Mashburn, PK Singh, and M Whiteley. 2005. Cystic fibrosis sputum supports growth and cues key aspects of Pseudomonas aeruginosa physiology. J. Bacteriol. 187:5267-77.

  • Updated: December 6, 2016