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 on C. 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. difficile toxin gene regulation.
Selected Research Publications
Girinathan PB, Braun S, Govind R*. 2014. The Clostridium difficile glutamate dehydrogenase is a secreted enzyme that confers resistance to hydrogen peroxide. Microbiology. 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
Govind R*, Rolfe RD, Fralick JA. 2011. In vivo lysogenization of Clostridium difficile bacteriophage CD119. Anaerobe. Jun; 17(3): 125-9. PMID: 21664468
Govind R*, Vediyappan G, Rolfe RD, Dupuy B, Fralick JA. 2009. Bacteriophage mediated toxin gene regulation in Clostridium difficile. J. Virology. Dec; 83 (23): 12037-45. PMID: 19776116
Dupuy B, Govind R, Antunes, Matamouros S. 2008. Clostridium difficile toxin synthesis is negatively regulated by TcdC. 2008. J. Med. Microbiol. 57, 685-689. PMID: 18480323
Govind R, Fralick JA, Rolfe RD. 2006. Genomic organization and molecular characterization of C. difficile Bacteriophage CD119. J. Bacteriol. 188 (7): 2568-2577. PMID: 16547044
Govind R, Vediyappan G, Rolfe RD, Fralick JA. 2006. Evidence that Clostridium difficile TcdC, is a membrane associated protein. J. Bacteriol. 188 (10): 3716-20. PMID: 16672625
Kandasamy Revathi, G. Vediyappan, W. L. Chaffin. 2000. Evidence for the presence of PIR-like proteins in Candida albicans. FEMS Microbiol. Lett. 186 (2): 239-243.