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{{Cholera}}
{{Cholera}}


{{CMG}}; '''Associate Editors-In-Chief:''' [[Priyamvada Singh|Priyamvada Singh, MBBS]] [mailto:psingh13579@gmail.com]
{{CMG}}; '''Associate Editors-In-Chief:''' [[Priyamvada Singh|Priyamvada Singh, MBBS]] [mailto:psingh13579@gmail.com], {{AA}}


==Overview==
==Overview==
'''''Vibrio cholerae''''' is a [[gram negative]] [[bacterium]] with a curved-rod shape that causes [[cholera]] in [[human]]s.<ref name=Sherris>{{cite book | author = Ryan KJ; Ray CG (editors) | title = Sherris Medical Microbiology | edition = 4th ed. | publisher = McGraw Hill | year = 2004 | id = ISBN 0838585299 }}</ref> ''V. cholerae'' and other species of the [[genus]] ''[[Vibrio]]'' belong to the gamma subdivision of the [[Proteobacteria]]. &nbsp;There are two major strains of ''V. cholerae'', classic and [[El Tor]], and numerous other serogroups.<ref name=Sherris>{{cite book | author = Ryan KJ, Ray CG (editors) | title = Sherris Medical Microbiology | edition = 4th ed. | pages = 376&ndash;7 |publisher = McGraw Hill | year = 2004 | isbn = 0838585299 }}</ref>
''[[Vibrio cholerae]]'' is a [[gram negative]] [[bacterium]] with a curved-rod shape that causes [[cholera]] in [[human]]s.<ref name=Sherris>{{cite book | author = Ryan KJ; Ray CG (editors) | title = Sherris Medical Microbiology | edition = 4th ed. | publisher = McGraw Hill | year = 2004 | id = ISBN 0838585299 }}</ref> ''V. cholerae'' and other species of the [[genus]] ''[[Vibrio]]'' belong to the gamma subdivision of the [[Proteobacteria]]. &nbsp;There are two major strains of ''V. cholerae'', classic and [[El Tor]], and numerous other serogroups.<ref name=Sherris>{{cite book | author = Ryan KJ, Ray CG (editors) | title = Sherris Medical Microbiology | edition = 4th ed. | pages = 376&ndash;7 |publisher = McGraw Hill | year = 2004 | isbn = 0838585299 }}</ref><ref name=Wilcox> Wilcox, Bruce A., and Rita R. Colwell. "Emerging and reemerging infectious diseases: biocomplexity as an interdisciplinary paradigm." EcoHealth 2.4 (2005): 244-257.</ref><ref name="pmid22748592">{{cite journal| author=Harris JB, LaRocque RC, Qadri F, Ryan ET, Calderwood SB| title=Cholera. | journal=Lancet | year= 2012 | volume= 379 | issue= 9835 | pages= 2466-76 | pmid=22748592 | doi=10.1016/S0140-6736(12)60436-X | pmc=3761070 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22748592  }} </ref><ref name="pmid16085859">{{cite journal| author=Huq A, Sack RB, Nizam A, Longini IM, Nair GB, Ali A et al.| title=Critical factors influencing the occurrence of Vibrio cholerae in the environment of Bangladesh. | journal=Appl Environ Microbiol | year= 2005 | volume= 71 | issue= 8 | pages= 4645-54 | pmid=16085859 | doi=10.1128/AEM.71.8.4645-4654.2005 | pmc=1183289 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16085859  }} </ref><ref name="pmid9501228">{{cite journal| author=Karaolis DK, Johnson JA, Bailey CC, Boedeker EC, Kaper JB, Reeves PR| title=A Vibrio cholerae pathogenicity island associated with epidemic and pandemic strains. | journal=Proc Natl Acad Sci U S A | year= 1998 | volume= 95 | issue= 6 | pages= 3134-9 | pmid=9501228 | doi= | pmc=19707 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9501228  }} </ref>


''V. cholerae'' was first isolated as the cause of cholera by Italian anatomist [[Filippo Pacini]] in 1854, but his discovery was not widely known until [[Robert Koch]], working independently thirty years later, publicized the knowledge and the means of fighting the disease.
==Habitat==
''V. cholerae'' occurs naturally in the plankton of fresh water, brackish water, and saltwater, attached primarily to [[copepod]]s in the zooplankton. Coastal cholera outbreaks typically follow [[algal bloom|zooplankton blooms]]. This makes cholera a typical [[zoonosis]].<ref name=Wilcox> Wilcox, Bruce A., and Rita R. Colwell. "Emerging and reemerging infectious diseases: biocomplexity as an interdisciplinary paradigm." EcoHealth 2.4 (2005): 244-257.</ref><ref name="pmid9841673">{{cite journal| author=Faruque SM, Albert MJ, Mekalanos JJ| title=Epidemiology, genetics, and ecology of toxigenic Vibrio cholerae. | journal=Microbiol Mol Biol Rev | year= 1998 | volume= 62 | issue= 4 | pages= 1301-14 | pmid=9841673 | doi= | pmc=98947 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9841673  }} </ref>
 
==Serovars==
More than 200 serovars of ''[[Vibrio]]'' cholera have been identified. Two serogroups, O1 and O139, are mainly associated with major outbreaks of cholera.<ref name="pmid22748592">{{cite journal| author=Harris JB, LaRocque RC, Qadri F, Ryan ET, Calderwood SB| title=Cholera. | journal=Lancet | year= 2012 | volume= 379 | issue= 9835 | pages= 2466-76 | pmid=22748592 | doi=10.1016/S0140-6736(12)60436-X | pmc=3761070 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22748592  }} </ref>
 
==Biotypes==
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:<ref name="pmid9841673">{{cite journal| author=Faruque SM, Albert MJ, Mekalanos JJ| title=Epidemiology, genetics, and ecology of toxigenic Vibrio cholerae. | journal=Microbiol Mol Biol Rev | year= 1998 | volume= 62 | issue= 4 | pages= 1301-14 | pmid=9841673 | doi= | pmc=98947 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9841673  }} </ref>
*Serotype Inaba
*Serotype Ogawa 
*Serotype Hikcojima
 
==Features of Vibrio cholera==
Features of ''[[Vibrio cholerae]]'' include:<ref name="pmid9841673">{{cite journal| author=Faruque SM, Albert MJ, Mekalanos JJ| title=Epidemiology, genetics, and ecology of toxigenic Vibrio cholerae. | journal=Microbiol Mol Biol Rev | year= 1998 | volume= 62 | issue= 4 | pages= 1301-14 | pmid=9841673 | doi= | pmc=98947 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9841673  }} </ref>
*[[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 [[chitinase|chitinases]]
 
==Genome==
The genome of ''V. cholerae'' consists of two chromosomes. The following genes may be associated with pathogenesis of ''[[Vibrio cholerae]]''.<ref name="pmid9501228">{{cite journal| author=Karaolis DK, Johnson JA, Bailey CC, Boedeker EC, Kaper JB, Reeves PR| title=A Vibrio cholerae pathogenicity island associated with epidemic and pandemic strains. | journal=Proc Natl Acad Sci U S A | year= 1998 | volume= 95 | issue= 6 | pages= 3134-9 | pmid=9501228 | doi= | pmc=19707 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9501228  }} </ref><ref name="pmid8763944">{{cite journal| author=Waldor MK, Tschäpe H, Mekalanos JJ| title=A new type of conjugative transposon encodes resistance to sulfamethoxazole, trimethoprim, and streptomycin in Vibrio cholerae O139. | journal=J Bacteriol | year= 1996 | volume= 178 | issue= 14 | pages= 4157-65 | pmid=8763944 | doi= | pmc=178173 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8763944  }} </ref><ref name="pmid2883655">{{cite journal| author=Taylor RK, Miller VL, Furlong DB, Mekalanos JJ| title=Use of phoA gene fusions to identify a pilus colonization factor coordinately regulated with cholera toxin. | journal=Proc Natl Acad Sci U S A | year= 1987 | volume= 84 | issue= 9 | pages= 2833-7 | pmid=2883655 | doi= | pmc=304754 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2883655  }} </ref><ref name="pmid8658163">{{cite journal| author=Waldor MK, Mekalanos JJ| title=Lysogenic conversion by a filamentous phage encoding cholera toxin. | journal=Science | year= 1996 | volume= 272 | issue= 5270 | pages= 1910-4 | pmid=8658163 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8658163  }} </ref>


==Habitat==
'''''CtxAB'' genes'''
''V. cholerae'' occurs naturally in the plankton of fresh, brackish, and salt water, attached primarily to [[copepod]]s in the zooplankton. Coastal cholera outbreaks typically follow [[algal bloom|zooplankton blooms]]. This makes cholera a typical [[zoonosis]].


==Pathogenesis==
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'' colonizes the [[gastrointestinal]] tract, where it adheres to [[villi|villous]] absorptive cells via pili, and secretes a binary [[toxin]], called [[cholera toxin]] (CT). The two CT subunits are named A and B, and are synthesised in a 1:5 ratio. B subunits bind and internalize A subunits, which are processed to A1. The A1 form catalyses ADP ribosylation from NAD to the regulatory component of [[adenylate cyclase]], thereby activating it. Increased [[adenylate cyclase]] activity increases [[cyclic AMP]] (cAMP) synthesis causing massive fluid and [[electrolyte]] efflux, resulting in [[diarrhea]].


*The major reservoir for cholera was long assumed to be humans, but some evidence suggests that it is the aquatic environment.
**''[[Vibrio cholera]]'' is not dependent on humans for its propagation.
**''[[Vibrio cholera]]'' can grow inbrackish estuaries, coastal seawaters (in close association with copepods or other zooplankton), and water of lower salinity when it is warm and adequate organic material is available.<ref name=Wilcox> Wilcox, Bruce A., and Rita R. Colwell. "Emerging and reemerging infectious diseases: biocomplexity as an interdisciplinary paradigm." EcoHealth 2.4 (2005): 244-257.</ref>


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). 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 specialised 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.
'''''V. cholerae'' pathogenicity island (VPI)'''


Additionally, it produces two different proteases called chitinase and mucinase. [[Chitinase]] is responsible for the ability of ''Vibrio cholerae'' to enter copapods. Mucinase is a non-specific protease that assists entry into the human [[gastro-intestinal tract]].
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.<ref name="pmid9501228">{{cite journal| author=Karaolis DK, Johnson JA, Bailey CC, Boedeker EC, Kaper JB, Reeves PR| title=A Vibrio cholerae pathogenicity island associated with epidemic and pandemic strains. | journal=Proc Natl Acad Sci U S A | year= 1998 | volume= 95 | issue= 6 | pages= 3134-9 | pmid=9501228 | doi= | pmc=19707 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9501228  }} </ref>


Finally, ''Vibrio cholerae'' produces what is called a ZOT toxin, termed as "Zona Occludans Toxin". This toxin specifically attacks the zona occludans or "tight" junctions joining epithelial cells.


'''SXT/R391 ICE'''


SXT/R391 ICE is associated with the acquisition of [[antibiotic resistance]] by acquiring foreign DNA.<ref name="pmid8763944">{{cite journal| author=Waldor MK, Tschäpe H, Mekalanos JJ| title=A new type of conjugative transposon encodes resistance to sulfamethoxazole, trimethoprim, and streptomycin in Vibrio cholerae O139. | journal=J Bacteriol | year= 1996 | volume= 178 | issue= 14 | pages= 4157-65 | pmid=8763944 | doi= | pmc=178173 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8763944  }} </ref>


<gallery>
<gallery>
Image: Cholera10.jpeg| Crabs have been a repeated source of cholera in the United States and elsewhere, even though they are rarely eaten raw. <SMALL><SMALL>''[http://phil.cdc.gov/phil/home.asp From Public Health Image Library (PHIL).] ''<ref name=PHIL> {{Cite web | title = Public Health Image Library (PHIL) | url = http://phil.cdc.gov/phil/home.asp}}</ref></SMALL></SMALL>
Image: Cholera10.jpeg| Crabs have been a repeated source of cholera in the United States and elsewhere, even though they are rarely eaten raw. <SMALL><SMALL>''[http://phil.cdc.gov/phil/home.asp From Public Health Image Library (PHIL).] ''<ref name=PHIL> {{Cite web | title = Public Health Image Library (PHIL) | url = http://phil.cdc.gov/phil/home.asp}}</ref></SMALL></SMALL>
Image: Cholera16.jpeg| Typical Vibrio cholera contaminated water supply. <SMALL><SMALL>''[http://phil.cdc.gov/phil/home.asp From Public Health Image Library (PHIL).] ''<ref name=PHIL> {{Cite web | title = Public Health Image Library (PHIL) | url = http://phil.cdc.gov/phil/home.asp}}</ref></SMALL></SMALL>
Image: Cholera16.jpeg| Typical Vibrio cholera contaminated water supply. <SMALL><SMALL>''[http://phil.cdc.gov/phil/home.asp From Public Health Image Library (PHIL).] ''<ref name=PHIL> {{Cite web | title = Public Health Image Library (PHIL) | url = http://phil.cdc.gov/phil/home.asp}}</ref></SMALL></SMALL>
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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]

Overview

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]

Habitat

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]

Serovars

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

Biotypes

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

Genome

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]

References

  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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