K-State Division of Biology


Revathi Govind

Assistant Professor

Ph.D. 2006, Texas Tech University HSC - Microbiology and Immunology

Post Doctoral Research - Institute Pasteur, Paris, France

Pathogenic Microbiology, Bacterial Genetics

346 Ackert Hall
(785) 532-2816

Molecular Cellular Developmental Biology Web

Research Focus

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.


Research Publications

  1. Carter GP, Douce GR, Govind R, Howarth PM, Mackin KE, Spencer J, Buckley AM, Antunes A, Kotsanas D, Jenkin GA, Dupuy B, Rood JI, Lyras D.The anti-sigma factor TcdC modulates hypervirulence in an epidemic BI/NAP1/027 clinical isolate of Clostridium difficile. PLoS Pathog. 2011 Oct;7(10):e1002317.

  2. Revathi G*, Fralick JA, Rolfe RD. In vivo lysogenization of a Clostridium difficile bacteriophage ФCD119. Anaerobe. 2011 Jun;17(3):125-9.

  3. Govind R*, G Vediyappan, R. D. Rolfe, B Dupuy, J. A. Fralick. 2009. Bacteriophage mediated toxin gene regulation in Clostridium difficile. J. Virology. 2009 Dec; 83 (23):12037-45. * Corresponding author.

  4. B. Dupuy, R. Govind, A. Antunes and S. Matamouros. 2008. Clostridium difficile toxin synthesis is negatively regulated by TcdC. 2008. J. Med. Microbiol. 57: 685-689.

  5. Govind R, Vediyappan. G, Rolfe. R. D. and Fralick. J. A. 2006. Evidence that Clostridium difficile TcdC, is a membrane associated protein. J. Bacteriol. 188 (10): 3716-20.

  6. Govind R, J. A. Fralick, R. D. Rolfe. 2006. Genomic organization and molecular characterization of C. difficile Bacteriophage CD119. J. Bacteriol. 188 (7): 2568-2577.

  7. Kandasamy (Govind) R, G. Vediyappan, W. L. Chaffin. 2000. Evidence for the presence of PIR-like proteins in Candida albicans. FEMS Microbiol. Lett. 186 (2): 239-243.


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