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__NOTOC__
{{DiseaseDisorder infobox |
{{DiseaseDisorder infobox |
   Name          = Cholera |
   Name          = Cholera |
  ICD10          = {{ICD10|A|00| |a|00}} |
  ICD9          = {{ICD9|001}} |
   Image          = cholera bacteria SEM.jpg |
   Image          = cholera bacteria SEM.jpg |
   Caption        = ''[[Vibrio cholerae]]'': The bacterium that causes cholera ([[Scanning electron microscope|SEM]] image) |
   Caption        = ''[[Vibrio cholerae]]'': The bacterium that causes cholera ([[Scanning electron microscope|SEM]] image) |
  DiseasesDB    = 2546 |
  ICDO          = |
  OMIM          = |
  MedlinePlus    = |
  eMedicineSubj  = |
  eMedicineTopic = |
  eMedicine_mult = |
  MeshName      = Cholera |
  MeshNumber    = C01.252.400.959.347 |
}}
}}
{{Cholera}}{{About1|Vibrio cholerae}}
'''For patient information click [[{{PAGENAME}} (patient information)|here]]'''
'''For patient information click [[{{PAGENAME}} (patient information)|here]]'''
{{Cholera}}
{{CMG}}


==[[Cholera overview|Overview]]==
{{CMG}}; '''Associate Editors-In-Chief:''' {{TarekNafee}}, {{SaraM}}, {{AAA}}, [[Priyamvada Singh|Priyamvada Singh, MBBS]] [mailto:psingh13579@gmail.com]


==[[Cholera history and symptoms|History & Symptoms]]==
{{SK}} ''Vibrio cholerae'' infection
 
== Treatment ==
 
[[Cholera dietary management|Dietary Management]] | [[Cholera medical therapy|Medical Therapy]]
 
==[[Cholera epidemiology and demographics|Epidemiology & Demographics]]==
==[[Cholera primary prevention|Primary Prevention]]==


==[[Cholera overview|Overview]]==
==[[Cholera historical perspective|Historical Perspective]]==
==[[Cholera classification|Classification]]==
==[[Cholera pathophysiology|Pathophysiology]]==
==[[Cholera causes|Causes]]==
==[[Cholera differential diagnosis|Differentiating Cholera from other Diseases]]==
==[[Cholera epidemiology and demographics|Epidemiology and Demographics]]==
==[[Cholera risk factors|Risk Factors]]==
==[[Cholera risk factors|Risk Factors]]==
==[[Cholera screening|Screening]]==
==[[Cholera natural history, complications, and prognosis|Natural History, Complications, and Prognosis]]==


==[[Cholera laboratory tests|Lab Tests]]==
==Diagnosis==
[[Stool]] and swab collected in the acute stage of the disease are useful specimens for laboratory diagnosis. A number of special media have been employed for the cultivation for Cholera vibrios. They are classified as follows:
[[Cholera history and symptoms|History and Symptoms]] | [[Cholera physical examination|Physical Examination]] | [[Cholera laboratory tests|Laboratory Findings]] | [[Cholera x ray|X ray]] | [[Cholera CT|CT]] | [[Cholera MRI|MRI]] | [[Cholera other diagnostic studies|Other Diagnostic Studies]]


==== Holding or transport media ====
== Treatment ==
#''Venkataraman-ramakrishnan (VR) medium''
[[Cholera medical therapy|Medical Therapy]] | [[Cholera medical therapy|Medical Therapy]] | [[Cholera surgery|Surgery]] | [[Cholera primary prevention|Primary Prevention]] | [[Cholera secondary prevention|Secondary Prevention]]
#''Cary-Blair medium'': This the most popularly carrying media. This is a buffered solution of [[sodium chloride]], sodium thioglycollate, disodium phosphate and [[calcium chloride]] at pH 8.4.


==== Enrichment media ====
==Case Studies==
#''Alkaline peptone water'' at pH 8.6
[[Cholera case study one|Case #1]]
#''Monsur's taurocholate tellurite peptone water'' at pH 9.2


==== Plating media ====
== External Links ==
#''Alkaline bile salt agar'': The colonies are very similar to those on Nutrient Agar.
{{commonscat|Cholera}}
#''Monsur's gelatin Tauro cholate trypticase tellurite agar (GTTA) medium'': Cholera vibrios produce small translucent colonies with a greyish black centre.
#''TCBS medium'': This the mostly widely used medium. This medium contains thiosulphate, citrate, [[bile salts]] and [[sucrose]]. Also in oysters and lobster in some cases. Cholera vibrios produce flat 2-3 mm in diameter, yellow nucleated colonies.
 
==[[Cholera pathophysiology|Pathophysiology]]==
Most of the ''V. cholerae'' bacteria in the contaminated water that a potential host drinks do not survive the very acidic conditions of the [[stomach|human stomach]]<ref name=Hartwell>Hartwell LH, Hood L, Goldberg ML, Reynolds AE, Silver LM, and Veres RC (2004). ''Genetics: From Genes to Genomes.'' Mc-Graw Hill, Boston: p. 551-552, 572-574 (using the turning off and turning on of [[gene expression]] to make toxin proteins in cholera bacteria as a "comprehensive example" of what is known about the mechanisms by which bacteria change the mix of proteins they manufacture to respond to the changing opportunities for surviving and thriving in different chemical environments).</ref> But the few bacteria that manage to survive the stomach's acidity conserve their [[nutrient|energy and stored nutrients]] during the perilous passage through the stomach by shutting down much protein production. When the surviving bacteria manage to exit the [[stomach]] and reach the favorable conditions of the [[small intestine]], they need to propel themselves through the thick [[mucous membrane|mucus]] that lines the small intestine to get to the intestinal wall where they can thrive. So they start up production of the hollow cylindrical protein [[flagellin]] to make [[flagella]], the curly whip-like tails that they rotate to propel themselves through the pasty mucus that lines the small intestine.
 
Once the cholera bacteria reach the [[intestinal wall]], they do not need the flagella propellers to move themselves any more, so they stop producing the protein flagellin, thus again conserving energy and nutrients by changing the mix of proteins that they manufacture, responding to the changed chemical surroundings. And on reaching the intestinal wall, they start producing the toxic proteins that give the infected person a watery [[diarrhea]] which carries the multiplying and thriving new generations of ''V. cholerae'' bacteria out into the drinking water of the next host&mdash;if proper sanitation measures are not in place.
 
[[Image:Cholera Toxin.png|thumb|left|Cholera Toxin. The delivery region (blue) binds membrane carbohydrates to get into cells. The toxic part (red) is activated inside the cell (PDB code: 1xtc)]]
 
[[Microbiologist]]s have studied the [[gene expression|genetic mechanisms]] by which the ''V. cholerae'' bacteria turn off the production of some proteins and turn on the production of other proteins as they respond to the series of chemical environments they encounter, passing through the stomach, through the mucous layer of the small intestine, and on to the intestinal wall.<ref name=DiRita_1991>{{cite journal |author=DiRita V, Parsot C, Jander G, Mekalanos J |title=Regulatory cascade controls virulence in Vibrio cholerae |journal=Proc Natl Acad Sci U S A |volume=88 |issue=12 |pages=5403-7 |year=1991 | url=http://www.pnas.org/cgi/reprint/88/12/5403 |id=PMID 2052618}}</ref> Of particular interest have been the genetic mechanisms by which cholera bacteria turn on the protein production of the toxins that interact with host cell mechanisms to pump [[chloride]] ions into the small intestine, creating an ionic pressure which prevents sodium ions from entering the cell. The [[chloride]] and [[sodium]] ions create a salt water environment in the small intestines which through osmosis can pull up to six liters of water per day through the intestinal cells creating the massive amounts of diarrhea.<ref name=Rabbani_1996 /> The host can become rapidly [[dehydrated]] if an appropriate mixture of dilute salt water and sugar is not taken to replace the blood's water and salts lost in the [[diarrhea]].
 
By inserting separately, successive sections of ''V. cholerae'' DNA into the DNA of other bacteria such as ''[[E. coli]]'' that would not naturally produce the protein toxins, researchers have investigated the mechanisms by which ''V. cholerae'' responds to the changing chemical environments of the stomach, mucous layers, and intestinal wall. Researchers have discovered that there is a complex [[cascade]] of regulatory proteins that control expression of ''V. cholerae'' virulence determinants. In responding to the chemical environment at the intestinal wall, the ''V. cholerae'' bacteria produce the TcpP/TcpH proteins which, together with the ToxR/ToxS proteins, activate the expression of the ToxT regulatory protein. ToxT then directly activates expression of virulence genes that produce the toxins that cause diarrhea in the infected person and that permit the bacteria to colonize the intestine.<ref name=DiRita_1991 /> Current research aims at discovering "the signal that makes the cholera bacteria stop swimming and start to colonize (that is, adhere to the cells of) the small intestine."<ref name=Hartwell>p. 574</ref>


==[[Cholera historical perspective|Historical perspective]]==
* [http://www.who.int/topics/cholera/about/en/index.html Chorela] - [[World Health Organization]]
===Origin and spread===
* [http://www.cdc.gov/cholera/index.html What is Cholera?] - [[Centers for Disease Control and Prevention]]
Cholera was originally [[endemic (epidemiology)|endemic]] to the Indian subcontinent, with the Ganges River likely serving as a contamination reservoir. It spread by trade routes (land and sea) to Russia, then to Western Europe, and from Europe to North America. It is now no longer considered an issue in Europe and North America, due to filtering and [[chlorination]] of the water supply.


* 1816-1826 - '''First Cholera pandemic''': Previously restricted, the pandemic began in Bengal, then spread across India by 1820. It extended as far as China and the Caspian Sea before receding.
* 1829-1851 - '''Second Cholera pandemic''' reached Europe, London and Paris in 1832. In London, it claimed 6,536 victims (see: http://www.mernick.co.uk/thhol/1832chol.html); in Paris, 20,000 succumbed (out of a population of 650,000) with about 100,000 deaths in all of France [http://www.amicale-genealogie.org/Histoires_temps-passe/Epidemies/chol01.htm]. It reached Russia (Cholera Riots), Quebec, Canada, Ontario, Canada] and New York in the same year and the Pacific coast of North America by 1834.
* 1849 - Second major outbreak in Paris. In London, it was the worst outbreak in the city's history, claiming 14,137 lives, ten times as many as the 1832 outbreak. In 1849 cholera claimed 5,308 lives in the port city of Liverpool, England, and 1,834 in Hull, England.<ref>IBMS Institute of Biological Science [http://www.ibms.org/index.cfm?method=science.history_zone&subpage=history_choleraAn ]</ref> An outbreak in North America took the life of former U.S. President James K. Polk. Cholera spread throughout the Mississippi river system killing over 4,500 in St. Louis [http://www.stlgs.org/DBpublicationsNewsCholera.htm] and over 3,000 in New Orleans [http://www.rootsweb.com/~txpanola/epidemics.html] as well as thousands in New York.<ref>The Cholera Years: The United States in 1832, 1849, and 1866 by Charles E. Rosenberg</ref> In 1849 cholera was spread along the California and Oregon trail as hundreds died on their way to the California Gold Rush, Utah and Oregon.<ref>Trails of Hope: California, Oregon and Mormon Trails [http://overlandtrails.lib.byu.edu/ctrail.htm]</ref>
* 1852-1860 - '''Third Cholera pandemic''' mainly affected Russia, with over a million deaths. In 1853-4, London's epidemic claimed 10,738 lives.
* 1854 - Outbreak of cholera in Chicago took the lives of 5.5 per cent of the population (about 3,500 people).[http://www.chipublib.org/004chicago/timeline/riverflow.html]. Soho outbreak in London stopped by removing the handle of the Broad Street pump by a committee instigated to action by John Snow .<ref> On the Mode of Communication of Cholera (1855) by John Snow, M.D. (1813-1858) [http://eee.uci.edu/clients/bjbecker/PlaguesandPeople/week8a.html </ref>
* 1863-1875 - '''Fourth Cholera pandemic''' spread mostly in Europe and Africa.
* 1866 - Outbreak in North America. <!-- taken from above paragraph. Not sure if this is separate from the 4th pandemic --> In London, a localized epidemic in the East End claimed 5,596 lives just as London was completing its major sewage and water treatment systems--the East End was not quite complete. William Farr, using the work of John Snow et al. as to contaminated drinking water being the likely source of the disease, was able to relatively quickly identify the East London Water Company as the source of the contaminated water. Quick action prevented further deaths.<ref> "The Ghost Map" by Steven Johnson, pg. 209 </ref> Also a minor outbreak at Ystalyfera in South Wales. Caused by the local water works using contaminated canal water, it was mainly it's workers and their families who suffered. Only 119 died.
* 1881-1896 - '''Fifth Cholera pandemic '''; The 1892 outbreak in Hamburg, Germany was the only major European outbreak; about 8,600 people died in Hamburg, causing a major political upheaval in Germany, as control over the City was removed from a City Council which had not updated Hamburg's water supplies. This was the last serious European cholera outbreak.
* 1899-1923 - '''Sixth Cholera pandemic''' had little effect in Europe because of advances in public health, but Russia was badly affected again.
* 1961-1970s - '''Seventh Cholera pandemic''' began in Indonesia, called [[El Tor]] after the strain, and reached Bangladesh in 1963, India in 1964, and the USSR in 1966. From North Africa it spread into Italy by 1973. In the late 1970s there were small outbreaks in Japan and in the South Pacific. There were also many reports of a cholera outbreak near Baku in 1972, but information about it was suppressed in the USSR.
* January 1991 to September 1994 - Outbreak in South America, apparently initiated when a ship discharged ballast water. Beginning in Peru there were 1.04 million identified cases and almost 10,000 deaths. The causative agent was an O1, El Tor strain, with small differences from the seventh pandemic strain. In 1992 a new strain appeared in Asia, a non-O1, nonagglutinable vibrio (NAG) named O139 Bengal. It was first identified in Tamil Nadu, India and for a while displaced El Tor in southern Asia before decreasing in prevalence from 1995 to around 10% of all cases. It is considered to be an intermediate between El Tor and the classic strain and occurs in a new serogroup. There is evidence of the emergence of wide-spectrum resistance to drugs such as [[trimethoprim]], [[sulfamethoxazole]] and [[streptomycin]].
* 2007 - The U.N. reported recently of a Cholera outbreak in Iraq.<ref>{{cite news |first= |last= |authorlink= |author= |coauthors= |title=U.N. reports cholera outbreak in northern Iraq |url=http://www.cnn.com/2007/WORLD/meast/08/29/iraq.cholera/index.html |format=HTML |work= |publisher=CNN |id= |pages= |page= |date= |accessdate=2007-08-30 |language=English |quote= }}</ref>


==[[Cholera future or investigational therapies|Future or Investigational Therapies]]==
The major contributions to fighting cholera were made by physician and self-trained scientist [[John Snow (physician)|John Snow]] (1813-1858), who found the link between cholera and contaminated drinking water in 1854 and Henry Whitehead, an Anglican minister, who helped John Snow track down and verify the source of the disease, an infected well in London. Their conclusions and writings were widely distributed and firmly established for the first time a definite link between germs and disease. Clean water and good sewage treatment, despite their major engineering and financial cost, slowly became a priority throughout the major developed cities in the world from this time onward. [[Robert Koch]], 30 years later, identified ''V. cholerae'' with a microscope as the bacillus causing the disease in 1885. The bacterium had been originally isolated thirty years earlier (1855) by Italian anatomist [[Filippo Pacini]], but its exact nature and his results were not widely known around the world.
Cholera has been a laboratory for the study of evolution of virulence. The province of Bengal in British India was partitioned into West Bengal (a state in India) and East Pakistan in 1947. Prior to partition, both regions had cholera pathogens with similar characteristics. After 1947, India made more progress on public health than East Pakistan (now Bangladesh). As a consequence, the strains of the pathogen which succeeded in India had a greater incentive in the longevity of the host and are less virulent than the strains prevailing in Bangladesh, which uninhibitedly draw upon the resources of the host population, thus rapidly killing many in it.
==False report of cholera==
A persistent myth states that [[Chicago 1885 cholera epidemic myth|90,000 people died in Chicago]] of cholera and [[typhoid fever]] in 1885. This story has no factual basis. In 1885 there was a torrential rainstorm that flushed the Chicago river and its attendant pollutants into Lake Michigan far enough that the city's water supply was contaminated. Fortunately, cholera was not present in the city and this is not known to have caused any deaths. It did, however, cause the city to become more serious about their sewage treatment.
==Cholera morbus==
The term ''cholera morbus'' was used in the 19th and early 20th century to describe both non-epidemic cholera and gastrointestinal diseases that mimicked cholera. The term is not in current use, but is found in many older references.<ref>[http://www.antiquusmorbus.com/English/EnglishC.htm Archaic Medical Terms.]</ref>
== References ==
{{Reflist|2}}
== External links ==
{{commonscat|Cholera}}
* [http://www.who.int/cholera Cholera] - [[World Health Organization]]
* [http://www.cdc.gov/ncidod/dbmd/diseaseinfo/cholera_g.htm What is Cholera?] - [[Centers for Disease Control and Prevention]]
* [http://www2.ncid.cdc.gov/travel/yb/utils/ybGet.asp?section=dis&obj=cholera.htm Cholera information for travelers] - Centers for Disease Control and Prevention
* Steven Shapin, [http://www.newyorker.com/printables/critics/061106crbo_books "Sick City: Maps and mortality in the time of cholera"], [[The New Yorker]] May 2006. A review of Steven Johnson, “The Ghost Map: The Story of London’s Most Terrifying Epidemic — and How It Changed Science, Cities, and the Modern World”
*[http://www.itas.fzk.de/tatup/043/turn04a.htm short paper contrasting official responses to cholera in Hamburg, Soho and New York.]
* Kelley Lee and Richard Dogson, "Globalization and Cholera: implications for global governance." in Global Governance, 6:2 (Apr-June 2000)
* [http://www.nashvillepost.com/news/2007/6/1/nashville_now_and_then_of_plagues_and_parasites Nashville's cholera outbreak, Summer 1873]
[[Category:Neurotoxins]]
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Latest revision as of 02:35, 18 July 2021

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This page is about clinical aspects of the disease.  For microbiologic aspects of the causative organism(s), see Vibrio cholerae.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editors-In-Chief: Tarek Nafee, M.D. [2], Sara Mehrsefat, M.D. [3], Aysha Aslam, M.B.B.S[4], Priyamvada Singh, MBBS [5]

Synonyms and keywords: Vibrio cholerae infection

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