Houston Methodist. Leading Medicine.
Houston Methodist. Leading Medicine

Samuel A. Shelburne, M.D., M.S.


Samuel A. Shelburne, M.D., M.S.

Samuel A. Shelburne, M.D., M.S.

Center for Molecular and Translational Human Infectious Diseases Research
Affiliate Member
The Methodist Hospital Research Institute
Assistant Professor, Department of Infectious Diseases
MD Anderson Cancer Center

E-mail: sshelburne@mdanderson.org
Phone: 713-441-5907

Education

B.A.   Princeton University, Princeton NJ
M.D.   University of Texas Medical Branch, Galveston, TX, High Honors
M.S.   Clinical Scientist Training Program, Baylor College of Medicine, Houston, TX (Clinical Research)

Postdoctoral Training

Internship and Residency, Baylor College of Medicine, Houston, TX
Chief Medical Residency, Baylor College of Medicine, Houston, TX
Fellowship, Section of Infectious Diseases, Department of Medicine, Baylor College of Medicine, Houston, TX

 

Biography

After graduating from University of Texas Medical Branch in Galveston, TX with high honors, Dr. Shelburne began his residency training at Baylor College of Medicine in Houston, TX. During his residency, Dr. Shelburne began his research career, first studying immune responses in patients undergoing HIV therapy, and then in the laboratory of Dr. Jim Musser where he began genetically profiling group A Streptococcus (GAS) during its interaction with human saliva. Dr. Shelburne identified a two component system that is activated during GAS colonization of the nasopharynx that controls the expression of several virulence factors and proteins involved in carbohydrate acquisition and metabolism. He has received several awards including an Outstanding Clinical Research Award and an Outstanding Resident Educator from the Baylor College of Medicine, and was awarded a Mentored Clinical Scientist Development Award from the NIH for his work on GAS.

Description of Research

Research in the Shelburne laboratory focuses on understanding the molecular basis of bacterial infections in humans, especially Gram-positive pathogens. Currently he is investigating the relationship between carbon-source utilization and virulence in group A Streptococcus (the “flesh-eating bacteria”). Dr. Shelburne’s laboratory utilizes such molecular techniques as whole genome sequencing, expression microarray analysis, isogenic mutant strain creation, and purified protein analysis to define the contribution of specific group A Streptococcus genes/proteins to disease.

An example of the research in the Shelburne laboratory is shown in the accompanying figure. Through expression microarray analysis, researchers in the Shelburne laboratory were able to elucidate a unique regulatory pathway linking nutrient utilization with virulence factor production. A long-term goal of the Shelburne laboratory is to elucidate novel aspects of bacterial pathogenesis that may be amenable to pharmaceutical intervention or prevention.

Major Areas of Research

group A Streptococcus, strep throat, carbohydrate metabolism

Current Funding

NIH / NIAID (K08-A1064564)
Title: Analysis of group A Streptococcus Saliva Interactions.

Recent Publications

Olsen RJ, Shelburne SA 3rd, Musser JM. Molecular mechanisms underlying group A streptococcal pathogenesis. Cell Microbiol. 2009 11:1-12.

Livorsi DJ, Daver NG, Atmar RL, Shelburne SA, White AC Jr, Musher DM. Outcomes of treatment for hematogenous Staphylococcus aureus vertebral osteomyelitis in the MRSA ERA. J Infect. 2008 2:128-31.

Shelburne SA 3rd, Keith D, Horstaman N, Sumby P, Davenport M, Graviss EA, Brennan RG, Musser JM. A direct link between carbohydrate utilization and virulence in the major human pathogen group A Streptococcus. Proc Natl Acad Sci USA 2008;105:1698-1703.

Shelburne SA 3rd, Keith D, Davenport M, Graviss EA, Musser JM. The contribution of maltose/maltodextrin utilization to group A Streptococcus host-pathogen interaction in the human oropharynx. Mol Micro 2008;69:436-52.

Shelburne SA 3rd, Davenport M, Keith D, Musser JM. The role of complex carbohydrate metabolism in the pathogenesis of invasive streptococci. Trends in Microbiol 2008;16:318-25.