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Chapter 23 : Vibrio cholerae: the Genetics of Pathogenesis and Environmental Persistence
Category: Environmental Microbiology
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Cholera is acquired through the consumption of contaminated water or food. After passing through the acid barrier of the stomach, the bacteria penetrate the mucous lining of the small intestine and adhere to intestinal epithelial cells to establish an infection. During colonization of the small intestine, the bacteria begin to express several key virulence factors, including cholera toxin (CT). The action of CT on intestinal epithelial cells is responsible for the massive diarrhea associated with cholera. Key to the ability of Vibrio cholerae to cause disease is the virulence factors that it produces. Extensive research efforts involving innovative techniques have been directed at understanding the mechanisms involved in V. cholerae’s establishing a successful infection. The two most important virulence factors required for the ability of the organism to cause cholera are the CT and the toxin-coregulated pilus (TCP). The evolution of the pathogenic potential of V. cholerae has clearly occurred through the acquisition of several mobile genetic elements. A number of different genetic techniques have been utilized to identify V. cholerae genes important for virulence. Several in vivo transcriptome studies have also shed light on aspects of V. cholerae pathogenesis. Transcriptome profiling of V. cholerae isolated from human stools using microarray analysis has provided the closest understanding of gene expression relevant to the natural host. Considering the severe global impact of cholera, much effort has been directed at vaccine development.
LPS structure of O1 and O139 serogroups of V. cholerae. Reprinted from Reidl and Klose (2002) with permission of Elsevier Science B.V.
The regulatory cascade that controls virulence factor expression in V. cholerae. Reprinted from Reidl and Klose (2002) with permission of Elsevier Science B. V.