Abstract
Cholera is an acute secretory diarrhoeal disease caused by the bacterium Vibrio cholerae. The key determinants of cholera pathogenicity, cholera toxin (CT), and toxin co-regulated pilus (TCP) are part of the genome of two horizontally acquired Mobile Genetic Elements (MGEs), CTXΦ, and Vibrio pathogenicity island 1 (VPI-1), respectively. Besides, V. cholerae genome harbors several others MGEs that provide antimicrobial resistance, metabolic functions, and other fitness traits. VPI-1, one of the most well characterized genomic island (GI), deserved a special attention, because (i) it encodes many of the virulence factors that facilitate development of cholera (ii) it is essential for the acquisition of CTXΦ and production of CT, and (iii) it is crucial for colonization of V. cholerae in the host intestine. Nevertheless, VPI-1 is ubiquitously present in all the epidemic V. cholerae strains. Therefore, to understand the role of MGEs in the evolution of cholera pathogen from a natural aquatic habitat, it is important to understand the VPI-1 encoded functions, their acquisition and possible mode of dissemination. In this review, we have therefore discussed our present understanding of the different functions of VPI-1 those are associated with virulence, important for toxin production and essential for the disease development.
Highlights
Cholera is an acute gastrointestinal diarrheal disease that is caused by a bacterium, Vibrio cholerae (Kaper et al, 1995)
Vibrio pathogenicity island-1 (VPI-1) has been shown to get transferred from V. cholerae O1 strain C6709 to VPI-negative V. cholerae isolates (468-83, GP6, V69, and 1528-79) by a generalized transducing phage CP-T1.This study proposed an alternative mode of dissemination of VPI1 between V. cholerae strains (O’Shea and Boyd, 2002)
V. cholerae have acquired a number of Mobile Genetic Elements (MGEs) (CTX, VPI-1, Vibrio pathogenicity island-2 (VPI-2), RS1, VSP-1, & Vibrio seventh pandemic island-2 (VSP-2)) that help the pathogen survival under the changing environmental conditions and contribute in causing the pathogenesis
Summary
Cholera is an acute gastrointestinal diarrheal disease that is caused by a bacterium, Vibrio cholerae (Kaper et al, 1995). The second most crucial virulence factor of cholera pathogen, toxin-coregulated pilus (TCP), encoded by the genes present in the TCP locus of VPI-1, helps the pathogen in colonization in the gastrointestinal tract of the host and act as a cell surface receptor for CTX (Manning, 1997) This altogether suggests that the acquisition of the MGEs is the key for the fitness and evolution of the cholera pathogen for different pandemics. All of the seven cholera pandemics are caused by the O1 serotype of V. cholerae, except the spatial emergences of O139 Bengal in eastern part of India and Bangladesh in 1992 (Johnson et al, 1994) All of these pathogenic strains harbored VPI-1 as well as CTX in their chromosomes (Li et al, 2003). Required for conversion of environmental non-pathogenic strains to pathogenic clones
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