Revathi Govind, Associate Professor
346 Ackert Hall
Ph.D. 2006, Texas Tech University HSC. Microbiology and Immunology.
Area(s) of Specialization
Pathogenic Microbiology, Bacterial Genetics.
Hospital acquired infections are a major challenge to patient safety and public health. According to the U.S. Centers for Disease Control and Prevention (CDC), approximately 36 million people are admitted to U.S. hospitals every year, and nearly two million patients annually acquire an infection while being treated; over 80,000 patients die from complications resulting from the infection.
Clostridium difficile (C. difficile) is one of the leading pathogens causing hospital-acquired infection in the United States. People in good health don't usually get sick from C. difficile. Our intestine contains millions of bacteria, which forms a barrier that protects us from this pathogenic bacterial infection. But when we take antibiotics, the drug can destroy some of the helpful bacteria in the gut and without enough healthy bacteria, C. difficile can quickly grow out of control and produce toxins that damage the intestinal cells. This results in diarrheal symptoms and sometime life threatening conditions called pseudomembranous colitis.
The C. difficile toxins, A and B encoding genes (tcdA and tcdB) are part of a pathogenicity locus (PaLoc) which also carry three other genes tcdR, tcdC and tcdE. The research in our lab focuses onC. difficile pathogenesis with a special interest on PaLoc genes and their role in virulence.
Mobile genetic elements such as transposons and temperate phages occupy nearly 11% of C. difficile genome. We are also interested in understanding the role of temperate phage in C. difficiletoxin gene regulation.
Girinathan BP, Ou J, Dupuy B, Govind R. 2018. Pleiotropic roles of Clostridium difficile sin locus. PLoS Pathog 2018 Mar 12;14(3):e1006940. doi: 10.1371/journal.ppat.1006940. eCollection 2018 Mar.
Girinathan BP, Monot M, Boyle D, McAllister KN, Sorg JA, Dupuy B, Govind R. 2017. Effect of tcdR Mutation on Sporulation in the Epidemic Clostridium difficile Strain R20291. mSphere 2017 Feb 15;2(1). pii: e00383-16. doi: 10.1128/mSphere.00383-16. PMID:28217744.
Girinathan BP, Braun S, Sirigireddy AR, Espinola-Lopez J, Govind R. 2016. Importance of Glutamate Dehydrogenase (GDH) in Clostridium difficile Colonization In Vivo. PLoS One 2016 Oct 21;11(10):e0165579. doi: 10.1371/journal.pone.0165579.PMID:27768767.
Govind R, Fitzwater L, Nichols R. 2015. Observations on the Role of TcdE Isoforms in Clostridium difficile Toxin Secretion. J Bacteriol. 2015 Aug 1;197(15):2600-9. doi: 10.1128/JB.00224-15. Epub 2015 May 26. PMID: 26013487.
Girinathan PB, Braun S, Govind R. 2014. The Clostridium difficile glutamate dehydrogenase is a secreted enzyme that confers resistance to hydrogen peroxide. Microbiology. 2014 Jan;160(Pt 1):47-55. PMID: 24145018.
Sirigi Reddy AR, Girinathan PB, Zapotocny R, Govind R. 2013. Identification and Characterization of Clostridium sordellii Toxin Gene Regulator. J Bacteriol. 2013 Sep; 195(18): 4246-5. PMID: 23873908.
Collery M, Govind R, Minton P, Kuehne S. 2013. Pathogenicity Mechanisms of Clostridium difficile. Book Chapter. In Advances with Clostridium difficile. Editors. Karl Weiss & Dr Glenn Tillotson.
Govind R, Dupuy B. 2012. Secretion of Clostridium difficile toxins A and B requires the holin-like protein TcdE. PLoS Pathog. Jun;8(6): e1002727. PMID: 22685398.
Glen Carter, Douce G, Govind R, Howarth P, Mackin K, Spencer J, Buckley A, Antunes A, Kotsanas D, Jenkin G, Dupuy B, J Rood, D Lyras. 2011. The Anti-Sigma Factor TcdC Modulates Hypervirulence in an Epidemic BI/NAP1/027 Isolate of Clostridium difficile. PLoS Pathog. Oct;7(10): e1002317. PMID: 22022270.
Revathi G, Fralick JA, Rolfe RD. 2011. In vivo lysogenization of a Clostridium difficilebacteriophage ФCD119. Anaerobe 2011 Jun;17(3):125-9.
View the complete publication list in NCBI