Dr. Jennifer N. Walker
The University of Texas Health Science Center at Houston
McGovern Medical School
Department of Microbiology and Molecular Genetics
We blend multiple scientific disciplines to define the host-pathogen interactions that determine the onset, course, and outcome of chronic infections. Using medical device infections as a model for chronic infections, we are currently pursuing the following questions:
1.How do medical devices become infected?
Despite their prevalence, it is unclear whether device infections occur due to contamination by bacteria from the hospital setting or through the persons’ own microbiome. Additionally, whether certain bacteria or virulence factors are more likely to cause symptomatic vs asymptomatic infection remains unknown. We collaborate closely with physicians and use a combination of animal models, patient samples, and genomics to understand how bacteria initiate device colonization and translate these discoveries into better surveillance, prevention, and treatment strategies.
2. How do medical devices render people susceptible to infection?
Medical devices render people susceptible to atypical or “less pathogenic” bacteria, yet the mechanisms responsible remain largely unknown. We combine the use of animal models and patient samples to understand the inflammatory response to devices with and without infection. This work involves immunology, microbiology, and biochemistry for the identification of biomarkers that predict infection risk and the development of better device materials that reduce infections.
3. What are the staphylococcal mechanisms that facilitate medical device infections?
Staphylococci are the primary cause of device infections and form recalcitrant biofilms on the device surface. Our group recently discovered that staphylococci use different adhesins to attach to various host proteins coating device surfaces to initiate biofilm formation. This work uses bacterial genetics and molecular microbiology to understand the host-pathogen-device interactions that facilitate infection to develop novel antibiotic-sparing treatment strategies.