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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editors-In-Chief: Priyamvada Singh, MBBS [2], Aysha Anwar, M.B.B.S[3]


Vibrio cholerae is a gram negative bacterium with a curved-rod shape that causes cholera in humans.[1] V. cholerae and other species of the genus Vibrio belong to the gamma subdivision of the Proteobacteria.  There are two major strains of V. cholerae, classic and El Tor, and numerous other serogroups.[1][2][3][4][5]


V. cholerae occurs naturally in the plankton of fresh water, brackish water, and saltwater, attached primarily to copepods in the zooplankton. Coastal cholera outbreaks typically follow zooplankton blooms. This makes cholera a typical zoonosis.[2][6]


More than 200 serovars of Vibrio cholera have been identified. Two serogroups, O1 and O139, are mainly associated with major outbreaks of cholera.[3]


There are two main biotypes of Vibrio cholerae:

  • Classic
  • E1 Tor

Each biotype is further associated with three serotypes based on difference in structure of O antigen:[6]

  • Serotype Inaba
  • Serotype Ogawa
  • Serotype Hikcojima

Features of Vibrio cholera

Features of Vibrio cholerae include:[6]

  • O polysaccharide antigen
  • H flagellar antigen
  • Pathogenic factors


The genome of V. cholerae consists of two chromosomes. The following genes may be associated with pathogenesis of Vibrio cholerae.[5][7][8][9]

CtxAB genes

CT is encoded by the ctxAB genes on a specific filamentous bacteriophage. Transduction of this phage is dependent upon bacterial expression of the Toxin Coregulated Pilus (TCP), which is encoded by the V. cholerae pathogenicity island (VPI).

V. cholerae pathogenicity island (VPI)

VPI is generally only present in virulent strains and is laterally transferred. VPI was originally thought to encode a filamentous phage responsible for transfer. This theory was discredited by a study of 46 diverse V. cholerae isolates which found no evidence of VPI phage production. The generalized transduction phage CP-T1 has been shown to transduce the entire VPI, which is then integrated at the same chromosomal location. Also, VPI has been shown to excise and circularize to produce pVPI via a specialized mechanism involving VPI-encoded recombinases. It is not known whether pVPI is involved in CP-T1 transduction or if it is perhaps a component of an alternative VPI mobilization mechanism.[5]


SXT/R391 ICE is associated with the acquisition of antibiotic resistance by acquiring foreign DNA.[7]


  1. 1.0 1.1 Ryan KJ; Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed. ed.). McGraw Hill. ISBN 0838585299.
  2. 2.0 2.1 Wilcox, Bruce A., and Rita R. Colwell. "Emerging and reemerging infectious diseases: biocomplexity as an interdisciplinary paradigm." EcoHealth 2.4 (2005): 244-257.
  3. 3.0 3.1 Harris JB, LaRocque RC, Qadri F, Ryan ET, Calderwood SB (2012). "Cholera". Lancet. 379 (9835): 2466–76. doi:10.1016/S0140-6736(12)60436-X. PMC 3761070. PMID 22748592.
  4. Huq A, Sack RB, Nizam A, Longini IM, Nair GB, Ali A; et al. (2005). "Critical factors influencing the occurrence of Vibrio cholerae in the environment of Bangladesh". Appl Environ Microbiol. 71 (8): 4645–54. doi:10.1128/AEM.71.8.4645-4654.2005. PMC 1183289. PMID 16085859.
  5. 5.0 5.1 5.2 Karaolis DK, Johnson JA, Bailey CC, Boedeker EC, Kaper JB, Reeves PR (1998). "A Vibrio cholerae pathogenicity island associated with epidemic and pandemic strains". Proc Natl Acad Sci U S A. 95 (6): 3134–9. PMC 19707. PMID 9501228.
  6. 6.0 6.1 6.2 Faruque SM, Albert MJ, Mekalanos JJ (1998). "Epidemiology, genetics, and ecology of toxigenic Vibrio cholerae". Microbiol Mol Biol Rev. 62 (4): 1301–14. PMC 98947. PMID 9841673.
  7. 7.0 7.1 Waldor MK, Tschäpe H, Mekalanos JJ (1996). "A new type of conjugative transposon encodes resistance to sulfamethoxazole, trimethoprim, and streptomycin in Vibrio cholerae O139". J Bacteriol. 178 (14): 4157–65. PMC 178173. PMID 8763944.
  8. Taylor RK, Miller VL, Furlong DB, Mekalanos JJ (1987). "Use of phoA gene fusions to identify a pilus colonization factor coordinately regulated with cholera toxin". Proc Natl Acad Sci U S A. 84 (9): 2833–7. PMC 304754. PMID 2883655.
  9. Waldor MK, Mekalanos JJ (1996). "Lysogenic conversion by a filamentous phage encoding cholera toxin". Science. 272 (5270): 1910–4. PMID 8658163.
  10. 10.0 10.1 10.2 10.3 10.4 10.5 10.6 "Public Health Image Library (PHIL)".

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