- 2013 - present: Associate Professor, Department of Microbiology & Immunology, University of Nevada, Reno School of Medicine, Reno, NV, USA
- 2007 - 2013: Assistant Member, Center for Molecular and Translational Human Infectious Diseases Research, The Methodist Hospital Research Institute, Houston, TX, USA
- 2004 - 2007: Postdoctoral Fellow, The Methodist Hospital Research Institute, Houston, TX, USA.
- 2003 - 2004: Postdoctoral Fellow, Laboratory of Human Bacterial Pathogenesis, Rocky Mountain Laboratories, NIAID, NIH, Hamilton, MT, USA.
- 2002 - 2003: Postdoctoral Fellow, Department of Microbiology, Tufts University, Boston, MA, USA.
- MICR350 – Microbial Genomics & Genetics
The group A Streptococcus (GAS, also known as Streptococcus pyogenes) causes ~700 million human infections, leading to ~550,000 deaths, annually. GAS has a remarkable ability to cause a diverse range of human diseases. For example, GAS is the most common cause of bacterial pharyngitis and a leading cause of superficial skin infections. More severe diseases include necrotizing fasciitis (aka the flesh-eating infection). Importantly, no single virulence factor is sufficient for GAS to cause any particular disease, rather disease potential is attributable to the regulated expression of specific combinations of virulence factors. Dr. Sumby has spent >16 years studying how GAS regulates gene expression in a disease-specific manner. Through understanding of how GAS regulates virulence factor expression the Sumby laboratory aims to develop novel therapeutic and/or preventative regimes, via translational research approaches, that are based upon the manipulation of these regulatory pathways. Research projects in Dr. Sumby's laboratory include:
- Discovering the role of the RocA/CovR/CovS proteins in regulating GAS virulence during invasive and non-invasive infections. The CovR/S proteins form a two-component regulatory system that, along with the accessory protein RocA, negatively regulates ~10% of the GAS transcriptome, including multiple virulence factor-encoding mRNAs. Because of this activity, covR, covS, or rocA mutant strains are positively selected for during invasive infections (and hence patients often contain a mixture of parental and mutant GAS strains), with the resultant mutants being hyper-virulent. While covR, covS, or rocA mutant strains are hyper-virulent during invasive infections they are attenuated for growth in models of non-invasive infections, relative to parental strains. Thus, this regulatory system appears to control the ability of GAS to cycle between invasive and non-invasive infections, and research into this is ongoing.
- Contribution of differential gene regulation and horizontal gene transfer in promoting GAS-serotype disease-phenotype associations. Decades of epidemiological studies have indicated that certain GAS serotypes are non-randomly associated with particular disease manifestations. For example, serotype M3 isolates are associated with particularly severe and lethal invasive infections, while serotype M28 isolates are associated with cases of puerperal sepsis (which is a potentially lethal disease that can occur in women during/following childbirth). We have identified that serotype M3 isolates uniquely harbor mutations in multiple regulator-encoding genes, resulting in M3 isolates producing a distinct virulence factor expression profile. The importance of the regulator gene mutations with regard to the association of M3 isolates with severe invasive infections is currently under study. We are also studying whether the presence of a unique 35 kb pathogenicity island in serotype M28 isolates, of apparent group B Streptococcus origin (which is a normal constituent of the vaginal microflora in ~1/3rd of women), is behind the association of M28 isolates with cases of puerperal sepsis.
- Determination of the molecular mechanisms behind small regulatory RNA (sRNA) - mediated regulation of GAS virulence factor expression. We have characterized the molecular basis behind the ability of the 205 nt sRNA FasX to regulate GAS virulence. Through post-transcriptional regulatory mechanisms FasX enhances the expression of the thrombolytic agent streptokinase, and reduces the expression of multiple cell-surface adhesins. These activities enhance GAS virulence in a mouse model of bacteremia infection and reduce the ability to GAS to adhere to human epithelial cells. Studies aimed at finding additional regulatory targets of FasX, and of identifying how the expression of FasX itself is regulated, are ongoing.
Sumby lectures on medical microbiology to School of Medicine medical students.
- Bacterial Classification, Structure, Nutrition, and Growth
- Sterilization, Disinfection, and Containment
- Laboratory Diagnosis of Bacterial Diseases
- Bacterial Genetics and Pathogenesis
- Survey of Medical Bacteriology
- Skin and Soft Tissue Infections
Current Lab Members
- Ira Jain, Ph.D. graduate student
- Roshika Roshika, Ph.D. graduate student
- Josette Medicielo, M.Sc. graduate student
Past Lab Members
- Jess Danger Ph.D.
- 1994 - 1998: B.S. - Genetics - University of Leicester, England, U.K
- 1998 - 2001: Ph.D. - Molecular Microbiology - University of Nottingham, England, U.K