Dr. Walker is an Assistant Professor in the Department of Microbiology and Molecular Genetics at UTHealth Houston’s McGovern Medical School. Dr. Walker joined the department in 2019 after completing her postdoctoral training with Drs. Scott Hultgren and Michael Caparon at Washington University School of Medicine in St. Louis, MO.
Dr. Walker received her Ph.D. from the Department of Microbiology and Immunology at the University of Iowa after completing her doctoral thesis work.
Dr. Walker is a recipient of the Texas Rising STAR award (2019).
The Walker lab is focused on understanding the host-pathogen interactions that dictate the onset, course, and outcome of chronic infections. Our work uses infections of medical devices as a model for chronic disease. By defining the bacterial and host mechanisms the facilitate these recalcitrant infections, we seek to develop novel antibiotic sparing therapies that can effectively treat common and costly diseases. We use a multidisciplinary approach to blend the use of basic science, model systems, and patient samples to pursue the following questions:
1. How do medical devices become infected?
Millions of medical devices are placed every year and their use is expected to increase due to their efficacy at improving the length and quality of life. However, infections of medical devices are a common, dreaded complication. 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 model systems, 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?
It is a well-known phenomenon that medical devices render people susceptible to atypical or “less pathogenic” bacteria, yet the mechanisms responsible remain largely unknown. Our recent studies indicate the device itself induces inflammation, which may prevent the host from mounting an effective response against these “less pathogenic” bacteria, allowing them to cause disease. To define these interactions, we are combining the use of model systems 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 bacterial 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.
Deposition of Host Matrix Proteins on Breast Implant Surfaces Facilitates Staphylococcus Epidermidis Biofilm Formation: In Vitro Analysis. Aesthet Surg J. 2020 Feb 17;40(3):281-295. doi: 10.1093/asj/sjz099. PubMed PMID: 30953053.
Insights into the Microbiome of Breast Implants and Periprosthetic Tissue in Breast Implant-Associated Anaplastic Large Cell Lymphoma. Sci Rep. 2019 Jul 17;9(1):10393. doi: 10.1038/s41598-019-46535-8. PubMed PMID: 31316085; PubMed Central PMCID: PMC6637124.
Establishment and Characterization of Bacterial Infection of Breast Implants in a Murine Model. Aesthet Surg J. 2019 Jul 1;. doi: 10.1093/asj/sjz190. [Epub ahead of print] PubMed PMID: 31259380.
The Detection of Bacteria and Matrix Proteins on Clinically Benign and Pathologic Implants. Plast Reconstr Surg Glob Open. 2019 Feb;7(2):e2037. doi: 10.1097/GOX.0000000000002037. eCollection 2019 Feb. PubMed PMID: 30881821; PubMed Central PMCID: PMC6416121.
Catheterization alters bladder ecology to potentiate Staphylococcus aureus infection of the urinary tract. Proc Natl Acad Sci U S A. 2017 Oct 10;114(41):E8721-E8730. doi: 10.1073/pnas.1707572114. Epub 2017 Sep 25. PubMed PMID: 28973850; PubMed Central PMCID: PMC5642702.
Antibody-Based Therapy for Enterococcal Catheter-Associated Urinary Tract Infections. mBio. 2016 Oct 25;7(5). doi: 10.1128/mBio.01653-16. PubMed PMID: 27795399; PubMed Central PMCID: PMC5080383.
Fibrinogen Release and Deposition on Urinary Catheters Placed during Urological Procedures. J Urol. 2016 Aug;196(2):416-421. doi: 10.1016/j.juro.2016.01.100. Epub 2016 Jan 28. PubMed PMID: 26827873; PubMed Central PMCID: PMC4965327.
Urinary tract infections: epidemiology, mechanisms of infection and treatment options. Nat Rev Microbiol. 2015 May;13(5):269-84. doi: 10.1038/nrmicro3432. Epub 2015 Apr 8. Review. PubMed PMID: 25853778; PubMed Central PMCID: PMC4457377.
The Staphylococcus aureus ArlRS two-component system is a novel regulator of agglutination and pathogenesis. PLoS Pathog. 2013;9(12):e1003819. doi: 10.1371/journal.ppat.1003819. Epub 2013 Dec 19. PubMed PMID: 24367264; PubMed Central PMCID: PMC3868527.
A coverslip-based technique for evaluating Staphylococcus aureus biofilm formation on human plasma. Front Cell Infect Microbiol. 2012;2:39. doi: 10.3389/fcimb.2012.00039. eCollection 2012. PubMed PMID: 22919630; PubMed Central PMCID: PMC3417647.
Synthetic polymer nanoparticles conjugated with FimH(A) from E. coli pili to emulate the bacterial mode of epithelial internalization. J Am Chem Soc. 2012 Mar 7;134(9):3938-41. doi: 10.1021/ja2091917. Epub 2012 Feb 23. PubMed PMID: 22360307; PubMed Central PMCID: PMC3325780.
Positive selection identifies an in vivo role for FimH during urinary tract infection in addition to mannose binding. Proc Natl Acad Sci U S A. 2009 Dec 29;106(52):22439-44. doi: 10.1073/pnas.0902179106. Epub 2009 Dec 16. PubMed PMID: 20018753; PubMed Central PMCID: PMC2794649.
Small-molecule inhibitors target Escherichia coli amyloid biogenesis and biofilm formation. Nat Chem Biol. 2009 Dec;5(12):913-9. doi: 10.1038/nchembio.242. Epub 2009 Oct 25. PubMed PMID: 19915538; PubMed Central PMCID: PMC2838449.
Bone morphogenetic protein 4 signaling regulates epithelial renewal in the urinary tract in response to uropathogenic infection. Cell Host Microbe. 2009 May 8;5(5):463-75. doi: 10.1016/j.chom.2009.04.005. PubMed PMID: 19454350; PubMed Central PMCID: PMC2696285.
Quantitative metabolomics reveals an epigenetic blueprint for iron acquisition in uropathogenic Escherichia coli. PLoS Pathog. 2009 Feb;5(2):e1000305. doi: 10.1371/journal.ppat.1000305. Epub 2009 Feb 20. PubMed PMID: 19229321; PubMed Central PMCID: PMC2637984.
Utilization of an intracellular bacterial community pathway in Klebsiella pneumoniae urinary tract infection and the effects of FimK on type 1 pilus expression. Infect Immun. 2008 Jul;76(7):3337-45. doi: 10.1128/IAI.00090-08. Epub 2008 Apr 14. PubMed PMID: 18411285; PubMed Central PMCID: PMC2446714.
Molecular variations in Klebsiella pneumoniae and Escherichia coli FimH affect function and pathogenesis in the urinary tract. Infect Immun. 2008 Jul;76(7):3346-56. doi: 10.1128/IAI.00340-08. Epub 2008 May 12. PubMed PMID: 18474655; PubMed Central PMCID: PMC2446687.
LeuX tRNA-dependent and -independent mechanisms of Escherichia coli pathogenesis in acute cystitis. Mol Microbiol. 2008 Jan;67(1):116-28. doi: 10.1111/j.1365-2958.2007.06025.x. Epub 2007 Nov 25. PubMed PMID: 18036139; PubMed Central PMCID: PMC3675907.