Vibrio cholerae pathogenesis
Vibrio cholerae is the causative agent of the diarrheal disease cholera. A disease affecting 2.8 million people per year and resulting in the deaths of 91,000, cholera is most common in areas with high population density and low sanitation quality.[1] [2] Not all V. cholerae are pathogenic: only two strains of serogroups O1 and O139 cause cholera.[1] Furthermore, it is considered a facultative human pathogen, as it primarily inhabits surface waters, as opposed to the small intestine.[3]
When entering and colonizing the human host, V. cholerae must endure changing environmental factors such as temperature, acidity, osmolarity, intestinal growth inhibitory substances, and immune system factors.[1] After sufficient colonization, an autoregulatory loop controlling ToxT, cholera toxin, and the toxin-coregulated pilus (TCP) results.[4] Understanding pathogenesis of V. cholerae requires the understanding of colonization and this loop.
Colonization of the Human Small Intestine
ToxR and ToxT Regulon
Toxin-Coregulating Pilus
References
[1] Reidl, J. and K.E. Klose, Vibrio cholerae and cholera: out of the water and into the host. Fems Microbiology Reviews, 2002. 26: p. 125-139.
[2] Ali, M., et al., The global burden of cholera. Bulletin of the World Health Organization, 2012. 90: p. 209-218.
[3] Sack, D.A., et al., Cholera. Lancet, 2004. 363: p. 223-233.
[4] Yu, R.R., and V.J. DiRita, Analysis of an autoregulatory loop controlling ToxT, cholera toxin, and toxin-coregulated pilus production in Vibrio cholerae. J. Baceriol, 1999. 181: p. 2584-2592.
Edited by Tina Solvik, a student of Suzanne Kern in BIOL168L (Microbiology) in The Keck Science Department of the Claremont Colleges Spring 2015.
