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Associate Professor

Kimberly Davis, PhD, MSc, studies how members of a bacterial population change during infection, to identify strategies to more effectively combat infections.

Contact Info

615 N. Wolfe Street, Room E2628

Research Interests

Bacterial pathogenesis; Host-pathogen interactions; Yersinia; Nitric Oxide; Immunology; Phagocytes

Experiences & Accomplishments
University of Pennsylvania
University of Michigan, Ann Arbor
University of Michigan, Ann Arbor

It has been known for decades that bacterial populations are heterogeneous, but it has been difficult to develop therapeutics that take this into account. Individual bacteria within a population vary in their growth rates, which leads to inherent differences in antimicrobial susceptibility. Additionally, many therapeutics have been designed to target specific virulence factors, which are required for bacterial growth in host organisms. However, it remains unclear if these factors are required at specific stages of infection, and if these factors are produced by the entire bacterial population, or only subsets of bacteria. 

Our lab explores heterogeneity within bacterial populations utilizing approaches that include transcriptional fluorescent reporters to visualize bacterial gene expression at the single cell-level, and immunofluorescence microscopy to visualize heterogeneity within host cell populations.  Our overarching goals are to define the expression patterns of potential drug targets and improve understanding of the pathways that promote altered antibiotic susceptibility, to ultimately develop improved therapeutics. Recently, we have developed molecular tools to identify slow-growing subsets of Yersinia with reduced antibiotic susceptibility, and have generated an antibiotic-sensing reporter to detect tetracycline exposure within host tissues. We have shown that bacteria responding to host-derived nitric oxide are slow-growing and have reduced antibiotic susceptibility, and are currently developing single cell transcriptional approaches to further characterize subpopulations of bacteria that survive antibiotic treatment. We are also studying the role of phenotypic heterogeneity in Staphylococcus aureus abscess  formation, in both ex vivo and mouse model systems.


Honors & Awards

NIAID Career Transition Award, 2017

Fisher Center Discovery Program grant, Johns Hopkins School of Medicine, 2018

Faculty Innovation Fund Award, Johns Hopkins Bloomberg School of Public Health, 2018

Willowcroft Foundation grant, 2021

Finalist for Burroughs Wellcome Fund Investigators in the Pathogenesis of Infectious Disease (PATH) program, 2022

Select Publications

Selected Recent Publications:

  • Alvarez-Manzo HS#, Davidson RK#, Van Cauwelaert de Wyels J, Cotten KL, Nguyen BH, Xiao M, Zhu Z, Anthony J, van Opijnen T, Davis KM. Yersinia pseudotuberculosis doxycycline tolerance strategies include modulating expression of genes linked to cell permeability and tRNA modification. 2022. PLoS Pathogens, 18(5):e1010556. PMID: 35576231 (# equal contribution)

  • Liu B, Braza RE, Cotten KL, Davidson RK, Davis KM. NO-stressed Y. pseudotuberculosis have decreased cell division rates in the mouse spleen. 2022. Infect Immun, 90(8):e0016722. PMID: 35862700

  • Patel P, O’Hara BJ, Aunins E, Davis KM. Modifying TIMER to generate a slow-folding DsRed derivative for optimal use in quickly-dividing bacteria. 2021. PLoS Pathog, 17(7):e1009284. PMID: 34214139

  • Raneses JR, Ellison AL, Liu B, Davis KM. Subpopulations of stressed Y. pseudotuberculosis preferentially survive doxycycline treatment within host tissues. 2020. mBio, 11(4):e00901-20. PMID: 32753491

  • Davis KM. For the greater (bacterial) good: heterogeneous expression of energetically costly virulence factors. 2020. Infect Immun, 88(7):e00911-19. PMID: 32041785