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| | __NOTOC__ |
| {{DiseaseDisorder infobox | | | {{DiseaseDisorder infobox | |
| Name = Cholera | | | Name = Cholera | |
| ICD10 = {{ICD10|A|00| |a|00}} |
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| ICD9 = {{ICD9|001}} |
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| 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 |
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| ICDO = |
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| OMIM = |
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| MedlinePlus = 000303 |
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| eMedicineSubj = |
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| eMedicineTopic = |
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| eMedicine_mult = |
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| MeshName = Cholera |
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| MeshNumber = C01.252.400.959.347 |
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| }} | | }} |
| | {{Cholera}}{{About1|Vibrio cholerae}} |
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| '''For patient information click [[{{PAGENAME}} (patient information)|here]]''' | | '''For patient information click [[{{PAGENAME}} (patient information)|here]]''' |
| {{SI}}
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| {{CMG}}
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| ==Overview==
| | {{CMG}}; '''Associate Editors-In-Chief:''' {{TarekNafee}}, {{SaraM}}, {{AAA}}, [[Priyamvada Singh|Priyamvada Singh, MBBS]] [mailto:psingh13579@gmail.com] |
| Choleria is a severe bacterial gastrointestinal, diarrheal disease. In its most severe forms, cholera is one of the most rapidly fatal illnesses known. A healthy person may become [[hypotension|hypotensive]] within an hour of the onset of symptoms and may die within 2-3 hours if no treatment is provided.<ref name=Sherris /> More commonly, the disease progresses from the first liquid stool to shock in 4-12 hours, with death following in 18 hours to several days without [[rehydration]] treatment.<ref name=McLeod_2000>{{cite journal |author=McLeod K |title=Our sense of Snow: John Snow in medical geography |journal=Soc Sci Med |volume=50 |issue=7-8 |pages=923-35 |year=2000 |pmid = 10714917}}</ref><ref> WHO Cholera [http://www.who.int/topics/cholera/control/en/index.html]</ref>
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| ==Background==
| | {{SK}} ''Vibrio cholerae'' infection |
| '''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 = 376–7 |publisher = McGraw Hill | year = 2004 | isbn = 0838585299 }}</ref> Transmission to humans is by ingesting contaminated water or food. The major reservoir for cholera was long assumed to be humans, but some evidence suggests that it is the aquatic environment.
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| ''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 /> In its most severe forms, cholera is one of the most rapidly fatal illnesses known. A healthy person may become [[hypotension|hypotensive]] within an hour of the onset of symptoms and may die within 2-3 hours if no treatment is provided.<ref name=Sherris /> More commonly, the disease progresses from the first liquid stool to shock in 4-12 hours, with death following in 18 hours to several days without [[rehydration]] treatment.<ref name=McLeod_2000>{{cite journal |author=McLeod K |title=Our sense of Snow: John Snow in medical geography |journal=Soc Sci Med |volume=50 |issue=7-8 |pages=923-35 |year=2000 |pmid = 10714917}}</ref><ref> WHO Cholera [http://www.who.int/topics/cholera/control/en/index.html]</ref>
| | ==[[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 screening|Screening]]== |
| | ==[[Cholera natural history, complications, and prognosis|Natural History, Complications, and Prognosis]]== |
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| == Symptoms == | | ==Diagnosis== |
| [[Symptoms]] include those of general GA tract (stomach) upset and [[Diarrhea#Acute diarrhea|massive watery diarrhea]]. Symptoms may also include terrible muscle and stomach cramps, vomiting and fever in early stages. In a later stage the diarrhea becomes "rice water stool" (almost clear with flecks of white). Symptoms are caused by massive body fluid loss induced by the [[enterotoxin]]s that ''V. cholerae'' produces. The main enterotoxin, known as '''[[cholera toxin]]''', interacts with [[G protein]]s and [[cyclic AMP]] in the intestinal lining to open [[ion channels]]. As ions flow into the intestinal [[lumen]] (lining), body fluids (mostly water) flow out of the body due to [[osmosis]] leading to massive diarrhea as the fluid is expelled from the body. The body is "tricked" into releasing massive amounts of fluid into the small intestine which shows up in up to 36 liters of liquid diarrhea in a six day period in adults with accompanying massive dehydration.<ref name=Rabbani_1996>{{cite journal |author=Rabbani GH |title=Mechanism and treatment of diarrhoea due to ''Vibrio cholerae'' and ''Escherichia coli'': roles of drugs and prostaglandins |journal=Danish medical bulletin |volume=43 |issue=2 |pages=173-85 |year=1996 |pmid=8741209}}</ref> Radical dehydration can bring death within a day through collapse of the circulatory system. | | [[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]] |
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| == Treatment == | | == Treatment == |
| [[Image:Cholera rehydration nurses.jpg|left|thumb|250px|Nurses encourage patients to drink large amounts of an oral rehydration solution to counteract the massive dehydration resulting from cholera.]] In general, patients must receive as much fluid as they lose, which can be up to 36 L, due to diarrhea. | | [[Cholera medical therapy|Medical Therapy]] | [[Cholera medical therapy|Medical Therapy]] | [[Cholera surgery|Surgery]] | [[Cholera primary prevention|Primary Prevention]] | [[Cholera secondary prevention|Secondary Prevention]] |
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| Treatment typically consists of aggressive [[rehydration]] (restoring the lost body fluids) and [[oral rehydration salt|replacement of electrolytes]] with commercial or hand-mixed sugar-salt solutions (1 tsp salt + 8 tsp sugar in 1 litre of clean/boiled water) or massive injections of liquid given intravenously via an IV in advanced cases. See: [[Oral rehydration therapy]] for easily made rehydration solutions. Without treatment the death rate is as high as 50%; with treatment the death rate can be well below 1%.<ref name=Sack_2004>{{cite journal |author=Sack D, Sack R, Nair G, Siddique A |title=Cholera |journal=Lancet |volume=363 |issue=9404 |pages=223-33 |year=2004 |id=PMID 14738797}}</ref>
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| [[Tetracycline antibiotics]] may have a role in reducing the duration and severity of cholera, although drug-resistance is occurring.<ref name="ExpertOpinPharmacother2003-Bhattacharya">{{cite journal | author=Bhattacharya SK, National Institute of Cholera and Enteric Diseases | title=An evaluation of current cholera treatment | journal=Expert Opin Pharmacother | year=2003 | pages=141-6 | volume=4 | issue=2 | id=PMID 12562304 }}</ref> Oral tetracycline was recommended for reducing the period of vibrio excretion and need for parenteral fluid. Initially cholera vibrios were universally susceptible to all antibiotics active against gram negative bacilli, but since 1979 multiple drug resistant strain have become increasingly common and their effects on overall mortality are questioned.<ref name="PrimCareUpdateObGyns2001-Parsi">{{cite journal | author=Parsi VK | title=Cholera | journal=Prim. Care Update Ob Gyns | year=2001 | pages=106-109 | volume=8 | issue=3 | id=PMID 11378428 }}</ref> Other antibiotics that have been used include [[ciprofloxacin]] and [[azithromycin]],<ref>{{cite journal | author=Saha D, ''et al.'' | title=Single dose azithromycin for the treatment of cholera in adults | journal=New Engl J Med | volume=354 | issue=23 | pages=2452–62 | year=2006 }}</ref> although again, drug-resistance has now been described.<ref>{{cite journal | author=Krishna BVS, Patil AB, Chandrasekhar MR | title=Fluoroquinolone-resistant ''Vibrio cholerae'' isolated during a cholera outbreak in India | jounal=Trans R Soc Trop Med Hyg | year=2006 | volume=100 | issue=3 | pages=224–26 | doi=10.1016/j.rstmh.2005.07.007 }}</ref> | |
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| == Epidemiology ==
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| === Prevention ===
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| Although cholera can be life-threatening, it is nearly always easily prevented, in principle, if proper sanitation practices are followed. In the United States and Western Europe, because of advanced [[water treatment]] and sanitation systems, cholera is no longer a major threat. The last major outbreak of cholera in the United States was in 1911. However, everyone, especially travelers, should be aware of how the disease is transmitted and what can be done to prevent it. Good sanitation practices, if instituted in time, are usually sufficient to stop an epidemic. There are several points along the transmission path at which the spread may be halted:
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| [[Image:Cholera_hospital_in_Dhaka.jpg|left|thumb|Cholera hospital in Dhaka.]]
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| * Sickbed: Proper disposal and treatment of the germ infected fecal waste (and all clothing and bedding that come in contact with it) produced by cholera victims is of primary importance.
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| * Sewage: Treatment of general sewage before it enters the waterways or underground water supplies prevent possible undetected patients from spreading the disease.
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| * Sources: Warnings about cholera contamination posted around contaminated water sources with directions on how to decontaminate the water.
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| * [[Sterilization]]: Boiling, filtering, and chlorination of water kill the bacteria produced by cholera patients and prevent infections, when they do occur, from spreading. All materials (clothing, bedding, etc.) that come in contact with cholera patients should be sterilized in hot water using (if possible) chlorine bleach. Hands, etc. that touch cholera patients or their clothing etc. should be thoroughly cleaned and sterilized. All water used for drinking, washing or cooking should be sterilized by boiling or chlorination in any area where cholera may be present. Water filtration, chlorination and boiling are by far the most effective means of halting transmission. Cloth filters, though very basic, have greatly reduced the occurrence of cholera when used in poor villages in Bangladesh that rely on untreated surface water. In general, public health education and good sanitation practices are the limiting factors in preventing transmission.
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| ===Susceptibility===
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| Recent [[epidemiology|epidemiologic research]] suggests that an individual's susceptibility to cholera (and other [[diarrhea]]l infections) is affected by their [[blood type]]: Those with [[type O blood]] are the most susceptible,<ref name=Swerdlow_1994>{{cite journal |author=Swerdlow D, Mintz E, Rodriguez M, Tejada E, Ocampo C, Espejo L, Barrett T, Petzelt J, Bean N, Seminario L |title=Severe life-threatening cholera associated with blood group O in Peru: implications for the Latin American epidemic |journal=J Infect Dis |volume=170 |issue=2 |pages=468-72 |year=1994 |id=PMID 8035040}}</ref><ref name=Harris_2005>{{cite journal |author=Harris J, Khan A, LaRocque R, Dorer D, Chowdhury F, Faruque A, Sack D, Ryan E, Qadri F, Calderwood S |title=Blood group, immunity, and risk of infection with ''Vibrio cholerae'' in an area of endemicity |journal=Infect Immun |volume=73 |issue=11 |pages=7422-7 |year=2005 |pmid=16239542}}</ref> while those with [[type AB]] are the most resistant. Between these two extremes are the A and B blood types, with type A being more resistant than type B.{{Fact|date=February 2007}}
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| About one million ''V. cholerae'' bacteria must typically be ingested to cause cholera in normally healthy adults, although increased susceptibility may be observed in those with a weakened [[immune system]], individuals with decreased gastric acidity (as from the use of [[antacid]]s), or those who are [[malnutrition|malnourished]].
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| It has also been hypothesized that the [[cystic fibrosis]] genetic [[mutation]] has been maintained in humans due to a selective advantage: [[heterozygous]] carriers of the mutation (who are thus not affected by cystic fibrosis) are more resistant to ''V. cholerae'' infections.<ref name=Bertranpetit_1996>{{cite journal |author=Bertranpetit J, Calafell F |title=Genetic and geographical variability in cystic fibrosis: evolutionary considerations |journal=Ciba Found Symp |volume=197 |issue= |pages=97-114; discussion 114-8 |year=1996 |pmid=8827370}}</ref> In this model, the genetic deficiency in the [[cystic fibrosis transmembrane conductance regulator]] channel proteins interferes with bacteria binding to the [[gastrointestinal]] epithelium, thus reducing the effects of an infection.
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| === Transmission ===
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| [[Image:CholeraLPJ.jpg|thumb|left|200px|Drawing of Death bringing the cholera, in ''Le Petit Journal''.]]
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| 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. Cholera is transmitted from person to person through ingestion of [[feces]] contaminated water loaded with the cholera bacterium. The source of the contamination is typically other cholera patients when their untreated [[diarrhea]] discharge is allowed to get into waterways or into groundwater or drinking water supply. Any infected water and any foods washed in the water, and shellfish living in the affected waterway can cause an infection. Cholera is rarely spread directly from person to person. ''V. cholerae'' occurs naturally in the plankton of fresh, brackish, and salt water, attached primarily to copepods in the zooplankton. Both toxic and non-toxic strains exist. Non-toxic strains can acquire toxicity through a lysogenic [[bacteriophage]].<ref name=Archivist_1997>{{cite journal | author =''Archivist'' | title = Cholera phage discovery | journal =Arch Dis Child | year =1997 | volume =76 | pages = 274 | url=http://adc.bmj.com/cgi/content/full/76/3/274 }}</ref> Coastal cholera outbreaks typically follow zooplankton blooms. This makes cholera a [[zoonosis]].
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| ===Laboratory diagnosis=== | | ==Case Studies== |
| [[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 case study one|Case #1]] |
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| ==== Holding or transport media ====
| | == External Links == |
| #''Venkataraman-ramakrishnan (VR) medium''
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| #''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.
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| ==== Enrichment media ====
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| #''Alkaline peptone water'' at pH 8.6
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| #''Monsur's taurocholate tellurite peptone water'' at pH 9.2
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| ==== Plating media ====
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| #''Alkaline bile salt agar'': The colonies are very similar to those on Nutrient Agar.
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| #''Monsur's gelatin Tauro cholate trypticase tellurite agar (GTTA) medium'': Cholera vibrios produce small translucent colonies with a greyish black centre.
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| #''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.
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| === Biochemistry of the ''V. cholerae'' bacterium ===
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| 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.
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| 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—if proper sanitation measures are not in place.
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| [[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)]]
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| [[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]].
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| 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>
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| == History ==
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| ===Origin and spread===
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| 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.
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| * 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.
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| * 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.
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| * 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>
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| * 1852-1860 - '''Third Cholera pandemic''' mainly affected Russia, with over a million deaths. In 1853-4, London's epidemic claimed 10,738 lives.
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| * 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>
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| * 1863-1875 - '''Fourth Cholera pandemic''' spread mostly in Europe and Africa.
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| * 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.
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| * 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.
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| * 1899-1923 - '''Sixth Cholera pandemic''' had little effect in Europe because of advances in public health, but Russia was badly affected again.
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| * 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.
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| * 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]].
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| * 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>
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| === Research ===
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| 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.
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| 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.
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| ==False report of cholera==
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| 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.
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| ==Cholera morbus==
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| 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>
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| == References ==
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| {{Reflist|2}}
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| == External links == | |
| {{commonscat|Cholera}} | | {{commonscat|Cholera}} |
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| * [http://www.who.int/cholera Cholera] - [[World Health Organization]] | | * [http://www.who.int/topics/cholera/about/en/index.html Chorela] - [[World Health Organization]] |
| * [http://www.cdc.gov/ncidod/dbmd/diseaseinfo/cholera_g.htm What is Cholera?] - [[Centers for Disease Control and Prevention]] | | * [http://www.cdc.gov/cholera/index.html 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
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| * 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”
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| *[http://www.itas.fzk.de/tatup/043/turn04a.htm short paper contrasting official responses to cholera in Hamburg, Soho and New York.]
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| * Kelley Lee and Richard Dogson, "Globalization and Cholera: implications for global governance." in Global Governance, 6:2 (Apr-June 2000)
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| * [http://www.nashvillepost.com/news/2007/6/1/nashville_now_and_then_of_plagues_and_parasites Nashville's cholera outbreak, Summer 1873]
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