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 cholerae include:^[6]

• Gram negative
• Comma shaped organism
• Flagellated
• Halophillic
• Aerobic or facultatively anaerobic
• Two antigens, H and O

• O polysaccharide antigen
• H flagellar antigen

• Pathogenic factors

• Enterotoxin (cholera toxin)
• “Zona Occludans Toxin” (attacks the zona occludans or “tight” junctions joining epithelial cells)
• Other proteases such as mucinases and chitinases

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

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

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  Crabs have been a repeated source of cholera in the United States and elsewhere, even though they are rarely eaten raw. From Public Health Image Library (PHIL). ^[10]
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  Typical Vibrio cholera contaminated water supply. From Public Health Image Library (PHIL). ^[10]
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  Scanning electron micrograph (SEM) depicts a number of Vibrio parahaemolyticus bacteria; Mag. 19058x. From Public Health Image Library (PHIL). ^[10]
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  Scanning electron micrograph (SEM) depicts a grouping of Vibrio vulnificus bacteria; Mag. 13184x. From Public Health Image Library (PHIL). ^[10]
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  Scanning electron micrograph (SEM) depicts a flagellated Vibrio vulnificus bacterium; Mag. 26367x. From Public Health Image Library (PHIL). ^[10]
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  Scanning electron micrograph (SEM) depicts a grouping of Vibrio vulnificus bacteria; Mag. 13184x. From Public Health Image Library (PHIL). ^[10]
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  Scanning electron micrograph (SEM) depicts a number of Vibrio cholerae bacteria of the serogroup 01; Magnified 22371x. From Public Health Image Library (PHIL). ^[10]

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