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{{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==
Cholera is a severe diarrheal disease caused by the bacterium ''[[Vibrio cholerae]]''.<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>. Persons infected with cholera have massive diarrhea. This highly liquid [[diarrhea]], which is often compared to "rice water," is loaded with bacteria that can spread under unsanitary conditions to infect water used by other people.
''[[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>
 
==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>
 
'''''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.<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>
 


==Causes==
'''SXT/R391 ICE'''
* '''Cholera''' (or ''Asiatic cholera'' or ''epidemic cholera'') is a severe [[diarrhea]]l disease caused by the [[bacterium]] ''[[Vibrio cholerae]]''.<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>
* ''V. cholerae'' is a [[Gram-negative]] bacteria which produces [[cholera toxin]], an [[enterotoxin]], whose action on the [[mucosa]]l [[epithelium]] lining of the small intestine is responsible for the characteristic massive diarrhea of the disease.<ref name=Sherris />
*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>
===Pathogenicity===
*Following the ingestion the cholera pass through stomach (low pH is known to lower the infectious dose in the infected individuals)
*After passage through the [[stomach]], ''[[Vibrio cholera]]'' has the capacity to survive and [[colonize]] in the [[small intestine]] with the help of the toxin coregulated pili (TCP) by following mechanisms:<ref name=Cho-path>Taylor RK, Miller VL, Furlong DB, and Mekalanos JJ: Use of phoA gene fusions to identify a pilus colonization factor coordinately regulated with cholera toxin. Proc Natl Acad Sci U S A 1987; 84: pp. 2833-2837</ref><ref name=Cholera-patho2> Taylor, Ronald K., et al. "Use of phoA gene fusions to identify a pilus colonization factor coordinately regulated with cholera toxin." Proceedings of the National Academy of Sciences 84.9 (1987): 2833-2837.</ref>
**Mediating bacterium–bacterium interactions and enabling microcolony formation
**Protection against toxic factors produced in the intestine
**promote attachment to the intestinal epithelium
*Following colonizing in the small intestine, ''[[Vibrio cholera]]'' secretes cholera toxin (CT), the AB 5 subunit type protein toxin that causes the secretory diarrhea that is characteristic of cholera.
===Serogroups===
*Vibrio cholerae has many different types or serogroups
*Only two of which can cause epidemic cholera if they also produce the cholera toxin. Those two serogroups include:
**Serogroup O1
**Serogroup O139 (found only in Asia) 
*Serogroups which can cause a less severe diarrheal disease and does not have epidemic potential include:
**Non-O1 and non-O139 Vibrio cholerae (third most commonly reported group of Vibrio bacteria)


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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