Cholera[1] is a severe bacterial infection caused by the bacteria Vibrio cholerae, which primarily affects the small intestine

. The main symptoms include profuse watery diarrhea and vomiting. Transmission is primarily by the acquisition of the pathogen through contaminated drinking water or infected food. The severity of the diarrhea and associated vomiting can lead to rapid dehydration and electrolyte loss, which can lead to death. Cholera is a major cause of death in the world. The study of cholera has been used as an example of early epidemiology. Study of the V. cholerae bacterium has also shed light on many of the mechanisms used by bacteria to infect and survive in their hosts.

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1 Signs and symptoms 2 Cause 3 Pathophysiology o 3.1 Susceptibility o 3.2 Transmission  3.2.1 Potential human contribution to transmissibility 4 Diagnosis o 4.1 Enrichment media o 4.2 Plating media 5 Prevention 6 Treatment 7 Epidemiology o 7.1 Pandemic genetic diversity 8 History o 8.1 Origin and spread o 8.2 False historical report o 8.3 Cholera morbus o 8.4 Other historical information o 8.5 Research o 8.6 Notable cases 9 Notes 10 See also 11 References 12 Further reading 13 External links

[edit] Signs and symptoms

When the surviving bacteria exit the stomach and reach the small intestine. Once the cholera bacteria reach the intestinal wall. The five B subunits form a five-membered ring that binds to GM1 gangliosides on the surface of the intestinal epithelium cells. The A1 portion of the A subunit is an enzyme that ADP-ribosylates G proteins. the curly whip-like tails that they rotate to propel themselves through the mucus of the small intestine. and are the result of a toxin produced by the vibrio cholerae bacterium that compels profuse amounts of fluid from the blood supply into the small and large intestines. The bacteria stop producing the protein flagellin. cholerae bacteria start up production of the hollow cylindrical protein flagellin to make flagella. V. severe dehydration and abdominal pain. The cholera toxin (CTX or CT) is an oligomeric complex made up of six protein subunits: a single copy of the A subunit (part A). cholerae start producing the toxic proteins that give the infected person a watery diarrhea. On reaching the intestinal wall. These symptoms start suddenly. the complex is taken . V. Upon binding. usually one to five days after infection. thus again conserving energy and nutrients by changing the mix of proteins which they manufacture in response to the changed chemical surroundings. cholerae bacteria out into the drinking water of the next host if proper sanitation measures are not in place. Cholera may also cause vomiting. [2] An untreated cholera patient may produce several gallons of diarrhoeal fluid a day.[3] The few bacteria that do survive conserve their energy and stored nutrients during the passage through the stomach by shutting down much protein production. cholerae bacteria in the contaminated water consumed by the host do not survive the highly acidic conditions of the human stomach. they need to propel themselves through the thick mucus that lines the small intestine to get to the intestinal wall where they can thrive. connected by a disulfide bond. This carries the multiplying new generations of V. [edit] Cause TEM image of Vibrio cholerae Most of the V. while the A2 chain fits into the central pore of the B subunit ring.The primary symptoms of cholera are profuse diarrhea. and five copies of the B subunit (part B). they do not need the flagella propellers to move any longer.

By inserting separate. the V. and HCO3í into the lumen of the small intestine and rapid dehydration. successive sections of V. which in turn leads to secretion of H2O. 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.into the cell via receptor-mediated endocytosis. Once inside the cell. cholerae carry a variant of lysogenic bacteriophage called CTXf or CTX . Cholera Toxin. passing through the stomach. which through osmosis can pull up to six liters of water per day through the intestinal cells.[5] 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. cholerae responds to the changing chemical environments of the stomach. Virulent strains of V. Na+. cholerae by horizontal gene transfer. This results in constitutive cAMP production. Clí. Researchers have discovered that there is a complex cascade of regulatory proteins that control expression of V. and intestinal wall. 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. The gene encoding the cholera toxin is introduced into V. the disulfide bond is reduced and the A1 subunit is freed to bind with a human partner protein called ADPribosylation factor 6 (Arf6). The delivery region (blue) binds membrane carbohydrates to get into cells. The toxic part (red) is activated inside the cell (PDB code: 1xtc). and on to the intestinal wall. cholerae bacteria produce the TcpP/TcpH .[4] Binding exposes its active site. mucous layers. K+. Microbiologists have studied the genetic mechanisms by which the V. creating an ionic pressure which prevents sodium ions from entering the cell. cholerae virulence determinants. cholerae DNA into the DNA of other bacteria such as E. allowing it to permanently ribosylate the Gs alpha subunit of the heterotrimeric G protein. The chloride and sodium ions create a salt-water environment in the small intestines. creating the massive amounts of diarrhea. researchers have investigated the mechanisms by which V. In responding to the chemical environment at the intestinal wall. coli that would not naturally produce the protein toxins. through the mucous layer of the small intestine.

[edit] Transmission . although increased susceptibility may be observed in those with a weakened immune system."[5] [edit] Pathophysiology [edit] Susceptibility Recent epidemiologic research suggests that an individual's susceptibility to cholera (and other diarrheal infections) is affected by their blood type: those with type O blood are the most susceptible.proteins. the genetic deficiency in the cystic fibrosis transmembrane conductance regulator channel proteins interferes with bacteria binding to the gastrointestinal epithelium. or those who are malnourished. adhere to the cells of) the small intestine. 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. Between these two extremes are the A and B blood types. activate the expression of the ToxT regulatory protein. cholerae infections.[5] Current research aims at discovering "the signal that makes the cholera bacteria stop swimming and start to colonize (that is. cholerae bacteria must typically be ingested to cause cholera in normally healthy adults. 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.[6][7] while those with type AB are the most resistant.[8] In this model. thus reducing the effects of an infection.[citation needed] About one million V. individuals with decreased gastric acidity (as from the use of antacids). together with the ToxR/ToxS proteins. with type A being more resistant than type B. which.

and salt water. in Le Petit Journal People infected with cholera suffer acute diarrhea. When these hyperinfectious bacteria underwent transcription profiles. In a 2002 study at Tufts University School of Medicine.Drawing of Death bringing the cholera. colloquially referred to as "rice-water stool. attached primarily to their chitinous exoskeleton. This highly liquid diarrhea. brackish. Non-toxic strains can acquire toxicity through a lysogenic bacteriophage.[12] In their findings. . Thus. usually from feces or other effluent. 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 supplies. it was found that stomach acidity is a principal agent that advances epidemic spread.[10] Both toxic and non-toxic strains exist. Any infected water and any foods washed in the water. can cause an infection. they were found to possess a unique physiological and behavioral state. the researchers found that human colonization creates a hyperinfectious bacterial state that is maintained after dissemination and that may contribute to epidemic spread of the disease.[9] Cholera is transmitted through ingestion of water contaminated with the cholera bacterium.[11] Coastal cholera outbreaks typically follow zooplankton blooms. V. as well as shellfish living in the affected waterway. cholerae harbors naturally in the zooplankton of fresh. Cholera is rarely spread directly from person to person. the spread of cholera can be expedited by host physiology. thus making cholera a zoonotic disease. [edit] Potential human contribution to transmissibility Cholera bacteria grown in vitro encounter difficulty subsequently growing in humans without additional stomach acid buffering." is loaded with bacteria that can infect water used by other people. characterized by high expression levels of genes required for nutrient acquisition and motility. and low expression levels of genes required for bacterial chemotaxis.

[14][15] Travelers should be aware of how the disease is transmitted and what . [edit] Prevention Although cholera may be life-threatening. due to nearly universal advanced water treatment and sanitation practices. yellow nucleated colonies. bile salts and sucrose. Monsur's gelatin Tauro cholate trypticase tellurite agar (GTTA) medium: Cholera vibrios produce small translucent colonies with a greyish black centre.[edit] Diagnosis In epidemic situations. In the first world. Microscopy is preferred only after enrichment. The last major outbreak of cholera in the United States occurred in 1910-1911. However. Treatment is usually started without or before confirmation by laboratory analysis of specimens. Infection with V. prevention of the disease is normally straightforward if proper sanitation practices are followed. They are classified as follows: [edit] Enrichment media 1. it is necessary to send stool specimens to a reference laboratory. Cholera vibrios produce flat 2±3 mm in diameter. a clinical diagnosis is made by taking a history of symptoms from the patient and by a brief examination only. 3. as this process reveals the characteristic motility of Vibrios and its inhibition by appropriate antiserum. are the most useful specimens for laboratory diagnosis. If V. the laboratory should test for V.6 2. This medium contains thiosulphate. Direct microscopy of stool is not recommended as it is unreliable. Alkaline bile salt agar (BSA): The colonies are very similar to those on nutrient agar. 2. Stool and swab samples collected in the acute stage of the disease. If an epidemic of cholera is suspected. cholerae O1. cholerae serogroup O1 is not isolated. Diagnosis can be confirmed as well as serotyping done by agglutination with specific sera. cholera is no longer a major health threat. cholerae O139. Monsur's taurocholate tellurite peptone water at pH 9. the most common causative agent is Vibrio cholerae O1. The associated diarrheal illness should be referred to as cholera and must be reported. before antibiotics have been administered. Alkaline peptone water at pH 8. citrate.[13] A number of special media have been employed for the cultivation for cholera vibrios.2 [edit] Plating media 1. if neither of these organisms is isolated. TCBS medium: This the mostly widely used medium. cholerae O139 should be reported and handled in the same manner as that caused by V.

or anti-microbal filtration in any area where cholera may be present. All materials that come in contact with cholera patients should be sterilized by washing in hot water using chlorine bleach if possible. have significantly reduced the occurrence of cholera when used in poor villages in Bangladesh that rely on untreated surface water. washing. There are several points along the cholera transmission path at which its spread may be (and should be) halted: Cholera hospital in Dhaka. bedding. Sewage: anti-bacterial treatment of general sewage by chlorine. Hands that touch cholera patients or their clothing. etc.) is essential. chlorination etc. should be thoroughly cleaned and disinfected with chlorinated water or other effective antimicrobial agents. etc. Public health education and adherence to appropriate sanitation practices are of primary importance to help prevent and control transmission of cholera and other diseases.g. though very basic. ultra-violet light sterilization. ozone water treatment. chlorination. are usually sufficient to stop an epidemic. Water purification: All water used for drinking. Effective sanitation practices. .) for possible use. if instituted and adhered to in time.. bedding. Cloth filters. ultraviolet light or other effective treatment before it enters the waterways or underground water supplies helps prevent undiagnosed patients from inadvertently spreading the disease.can be done to prevent it. y y y y Sterilization: Proper disposal and treatment of infected fecal waste water produced by cholera victims and all contaminated materials (e. Sources: Warnings about possible cholera contamination should be posted around contaminated water sources with directions on how to decontaminate the water (boiling. Chlorination and boiling are often the least expensive and most effective means of halting transmission. ozone. showing typical cholera beds. or cooking should be sterilized by either boiling. Better anti-microbial filters like those present in advanced individual water treatment hiking kits are most effective. clothing.

Efficient surveillance systems can also improve the risk assessment for potential cholera outbreaks.[17] Sensitive surveillance and prompt reporting allow for containing cholera epidemics rapidly. This will also aid in the developing indicators for appropriate use of oral cholera vaccine. but prophylactic usage is not currently recommended for routine use by the Centers for Disease Control and Prevention (CDC). alternative homemade solutions using various formulas of water. Two oral cholera vaccines. table salt. cholerae O1 strain CVD 103-HgR. cholerae O139 has influenced efforts in order to develop an effective and practical cholera vaccine since none of the currently available vaccines is effective against this strain. therefore leading to coordinated response and assist in preparation of preparedness plans. occurring annually mostly during rainy seasons. as dehydration and electrolyte depletion occur rapidly. and fruit offer less expensive methods of electrolyte repletion. sugar. and simple to administer: prompt replacement of water and electrolytes is the principal treatment for cholera. baking soda. In severe cholera cases with significant dehydration.[16] During recent years. In most cases cholera can be successfully treated with oral rehydration therapy (ORT). . safe. an orally administered inactivated whole cell vaccine. Surveillance systems can provide early alerts to outbreaks. appears to provide somewhat better immunity and have fewer adverse effects than the previously available vaccine.[13] The newer vaccine (brand name: Dukoral). cholerae O1 in combination with purified recombinant B subunit of cholera toxin and a live-attenuated live oral cholera vaccine.[16] This safe and effective vaccine is available for use by individuals and health personnel. Work is under way to investigate the role of mass vaccination. Cholera exists as a seasonal disease in many endemic countries.[18] [edit] Treatment Cholera patient being treated by medical staff in 1992. containing the genetically manipulated V. are commercially available in several countries: a killed whole-cell V. ORT is highly effective. the administration of intravenous rehydration solutions may be necessary.A vaccine for cholera is available in some countries. Understanding the seasonality and location of outbreaks provide guidance for improving cholera control activities for the most vulnerable. substantial progress has been made in developing new oral vaccines against cholera. which have been evaluated with volunteers from industrialized countries and in regions with endemic cholera. The appearance of V. In situations where commercially produced ORT sachets are too expensive or difficult to obtain.

Antibiotics shorten the course of the disease and reduce the severity of the symptoms. doxycycline.A lack of clean drinking water in Iraq has led to an outbreak of cholera.The cholera epidemic started in Orissa. some 140. the mortality rate is less than 1%. the UN has reported 22 deaths and 4.548 and the number of fatalities. the number of cases of infection by cholera in sub-Saharan Africa had reached 128. erythromycin. cholerae in in vitro studies. cholerae have shown resistance.053. y In 2000.[21] New generation antimicrobials have been discovered which are effective against V. Tetracycline is typically used as the primary antibiotic.[25] July . but resistance has been reported. however. although some strains of V.569 laboratory-confirmed cases. the mortality rate rises to 50±60%.000 cholera cases were officially notified to WHO. chloramphenicol. oral rehydration therapy remains the principal treatment. Koraput and Kalahandi districts where more than 2. 4.[20] Rapid diagnostic assay methods are available for the identification of multi-drug resistant V. The outbreak has affected Rayagada. however. cholerae.[19] Fluoroquinolones such as norfloxacin also may be used. India. with untreated cholera.[22] The success of treatment is significantly affected by the speed and method of treatment. If cholera patients are treated quickly and properly.[27] August 2007 . and furazolidone.[28] y y . Other antibiotics that have been proven effective against V.000 people have been admitted to hospitals. cholerae include cotrimoxazole. Africa accounted for 87% of these cases.December 2007 .[23][24] [edit] Epidemiology By 12 February 2009.[26] As of 2 December 2007.

[30] November 2008 .7%. Two clusters have been identified: Cluster I and Cluster II. the "Crude Case Fatality Ratio (CFR)" had dropped from 4. August 2008 . 4.2% to 3. 377 patients tested positive for cholera. list 1748 cases and 64 fatalities.As of 29 October 2008.201 deaths had been reported.[31] The daily updates for the period 29 March 2009 to 7 April 2009. during the week of 22±28 March 2009. had been verified in Iraq.[32] The CFR had remained above 4.[33] January 2009 . Of those hospitalized.October 2008 . For the most part Cluster I consists of strains from the 1960s and 1970s.591 people in the country have been infected with cholera and. a total of 644 laboratoryconfirmed cholera cases.2.5%).[29] March .[35] [edit] History . giving a weekly CFR of 3.66% (see table above). including eight deaths. bringing the total number of cases treated since November 2008 to 2276. while Cluster II largely contains strains from the 1980s and 1990s. Some 45 cases were reportedly treated between November 7 through 9th.[34] y y y y [edit] Pandemic genetic diversity Amplified fragment length polymorphism (AFLP) fingerprinting of the pandemic isolates of Vibrio cholerae has revealed variation in the genetic structure.The Mpumalanga province of South Africa has confirmed over 381 new cases of Cholera.490 people from 20 provinces throughout Vietnam have been hospitalized with acute diarrhea.April 2009: In the 2008 Zimbabwean cholera outbreak.Doctors Without Borders reported an outbreak in a refugee camp in the Democratic Republic of the Congo's eastern provincial capital of Goma. those for the period 8 April to 16 April list 1375 new cases and 62 deaths (and a resulting CFR of 4. based on the change in the clone structure. which is still continuing. an estimated 96.[32] however.7% for most of January and early February 2009.April 2008 . by 16 April 2009.y August . 19 people have died in the province since the outbreak.[31] According to the World Health Organization. This grouping of strains is best seen in the strains from the African Continent.

then to Western Europe. y 1816-1826 . In London.[42] A two-year outbreak began in England and Wales in 1848 and claimed 52.500 in St. claiming 14. England.000 people. Indonesia (where more than 100. it was the worst outbreak in the city's history. Cholera hit Ireland in 1849 and killed many of the Irish Famine survivors already weakened by starvation and fever. President James K.[39] The epidemic reached Quebec. in Paris. but still heavily affects populations in developing countries.[39] An outbreak in North America took the life of former U.000 British troops and countless Indians died during this pandemic.000 succumbed (out of a population of 650.[44] In 1849 cholera claimed 5. Louis[39] and over 3.000 deaths) and Germany in 1831. One influential UK pamphlet explaining how to nurse cholera patients and prevent the disease was Hints on the Cholera morbus (1832) by the home economics writer Esther Copley. 1849 . the pandemic began in Bengal. 1832. Cholera is now no longer considered a pressing health threat in Europe and North America due to filtering and chlorination of water supplies. London (more than 55.000) with about 100.000 to 12. over twice as many as the 1832 outbreak.Second major outbreak in Paris. killing over 15.000 deaths in all of France. [37] 1829-1851 .000 people died in the United Kingdom)[38] and Paris in 1832. and then spread across India by 1820.000 people in Egypt. The disease spread by trade routes (land and sea) to Russia. y y . Ontario and New York in the same year and the Pacific coast of North America by 1834. spread throughout the Mississippi river system killing over 4. Mormon and Oregon Trails as 6. The outdated public health advice demonstrates the lack of understanding of the disease and its actual causative factors.[42] In 1849 cholera was spread along the California. 20.000 in New Orleans[39] as well as thousands in New York. cholera struck Mecca. In London. and from Europe to North America.137 lives. the disease claimed 6. believed spread from ship(s) from England.536 victims and came to be known as "King Cholera".[40] The 1831 cholera epidemic killed 150.000[45] are believed to have died on their way to the California Gold Rush.[39] Mexico was similarly attacked.Hand bill from the New York City Board of Health.[43] Cholera was found in Dundee in 1832. [edit] Origin and spread Cholera likely has its origins in and is endemic to the Indian subcontinent. 10.308 lives in the port city of Liverpool.Second cholera pandemic reached Russia (see Cholera Riots). Hungary (about 100. Polk.[41] In 1846.[36] The cholera outbreak extended as far as China. England. Cholera.834 in Hull.000 lives. and 1. Deaths in India between 1817 and 1860 are estimated to have exceeded 15 million persons.S.000 people succumbed on the island of Java alone) and the Caspian Sea before receding. Another 23 million died between 1865 and 1917.First cholera pandemic: Previously restricted.

In 1859. with over a million deaths. In 1852.000 and 200. Iraq. an outbreak in Bengal once again led to the transmission of the disease to Iran. Arabia and Russia.000 Americans died during the two pandemics between 1832 and 1849.[39] It is believed that over 150. for example. Italy lost 113.738 lives.[52] Hungary and Belgium both lost 30. At least 30.Third cholera pandemic mainly affected Russia. 1863-1875 .000 lives in the Austrian Empire.5% of the population (about 3. is believed to have killed between 100.[50] This proved that contaminated water (although it didn't identify the contaminant) was the main agent spreading cholera. The Philippines were infected in 1858 and Korea in 1859.000 Mecca pilgrims fell victim to the disease. hospital ward . The Ansei outbreak of 1858-60. In 1867.000 perished.000 lives in Russia in 1866. Cholera claimed 90. It would take almost 50 years for this message to be believed and acted upon.[46][47] 1852-1860 .000 people in Tokyo alone.[42] There were at least seven major outbreaks of cholera in Japan between 1858 and 1902.[51] The epidemic of cholera that spread with the Austro-Prussian War (1866) is estimated to have claimed 165. London's epidemic claimed 10.[39][49] In 1853-4.Fourth cholera pandemic spread mostly in Europe and Africa.500 people).000 people and in the Netherlands 20.000 lives. Building and maintaining a safe water system was and is not cheap²but is absolutely essential. cholera spread east to Indonesia and later invaded China and Japan in 1854.Outbreak of cholera in Chicago took the lives of 5.y y Utah and Oregon in the cholera years of 1849-1855. The Soho outbreak in London ended after removal of the handle of the Broad Street pump by a committee instigated to action by John Snow.000 of the 90.[48] 1854 .[53] y 1892 cholera outbreak in Hamburg.

000 in India.000 in Persia.000 in Japan and over 60.1873 . and more than 20. In the same year more than 21.[57] 27 epidemics were recorded during pilgrimages to Mecca from the 19th century to 1930.600 people. a localized epidemic in the East End claimed 5. This was the last serious European cholera outbreak. there were small outbreaks in Japan and in the South Pacific.[39] Also a minor outbreak at Ystalyfera in South Wales.596 lives just as London was completing its major sewage and water treatment systems²the East End was not quite complete. Wall. including a health care worker on Swinburne Island.000 Americans.000 people dying of cholera during the first quarter of the 20th century)[56] and the Ottoman Empire were particularly hard hit by cholera deaths. 119 died.000 pilgrims died of cholera during the 1907±08 hajj.000 lives in Europe and at least 50. Eleven people died.000 in Americas. The 1902-1904 cholera epidemic claimed 200. There were also many reports of a cholera outbreak near Baku in 1972. y y y y . but major Russian cities (more than 500. disinfection team y 1866 .Seventh cholera pandemic began in Indonesia. From North Africa it spread into Italy by 1973.04 million identified cases and almost 10.000 lives. 1899-1923 . William Farr. the 18831887 epidemic cost 250.[46] In London.Outbreak in South America.Outbreaks in North America. was able to relatively quickly identify the East London Water Company as the source of the contaminated water. Cholera claimed 267.Fifth cholera pandemic . called El Tor after the strain.000 deaths.[56] The sixth pandemic killed more than 800. J. The Netherlands. Although generally held responsible for the virulence of the epidemic.000 lives in the Philippines.[55] 90. Beginning in Peru there were 1. 1881-1896 . cholera spread in the US as epidemic from New Orleans along the Mississippi River and related ports of tributaries.1892 cholera outbreak in Hamburg. The last outbreak in the United States was in 19101911 when the steamship Moltke brought infected people to New York City. January 1991 to September 1994 .Sixth cholera pandemic had little effect in Europe because of advances in public health. Quick action prevented further deaths.000 in Spain.[14][15][58] 1961-1970s . According to Dr A. Vigilant health authorities isolated the infected on Swinburne Island. India in 1964. and reached Bangladesh in 1963. it was mainly its workers and their families who suffered. using the work of John Snow et al. The causative agent was an O1.890 lives in Russia (1892). Caused by the local water works using contaminated canal water.000 people died in Amsterdam.[54] 120. but information about it was suppressed in the USSR. It killed some 50. apparently initiated when a ship discharged ballast water. with thousands dying. the city government went largely unchanged. In the late 1970s. The 1892 outbreak in Hamburg killed 8.[54] In Egypt cholera claimed more that 58. In the 1870s. as to contaminated drinking water being the likely source of the disease. and the USSR in 1966.

he proposed a substantially complete and correct model for the aetiology of the disease. with small differences from the seventh pandemic strain.[60] The other diseases are now known collectively as gastroenteritis. [edit] False historical report Main article: Chicago 1885 cholera epidemic myth A persistent myth states that 90.El Tor strain.[59] In 1885. The bacterium had been originally isolated thirty years earlier (1855) by Italian anatomist Filippo Pacini. In 1992 a new strain appeared in Asia. but its exact nature and his results were not widely known around the world. but is found in many older references. In two . [edit] Other historical information In the past. The term is not in current use. nonagglutinable vibrio (NAG) named O139 Bengal. It is considered to be an intermediate between El Tor and the classic strain and occurs in a new serogroup. 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.[61]. In his major "state of the art" review of 1855. In modern international maritime signal flags the quarantine flag is yellow and black. but this story has no factual basis. India and for a while displaced El Tor in southern Asia before decreasing in prevalence from 1995 to around 10% of all cases. there were no cholera-related deaths. Boats with a yellow flag hung would not be allowed to disembark at any harbor for an extended period. However.000 people died in Chicago of cholera and typhoid fever in 1885.[39] Dr Snow proposed a microbial origin for epidemic cholera in 1849. [edit] Research The Russian-born bacteriologist Waldemar Haffkine developed the first cholera vaccine around 1900. a non-O1. sulfamethoxazole and streptomycin. [edit] Cholera morbus The term cholera morbus was used in the 19th and early 20th centuries to describe both non-epidemic cholera and other gastrointestinal diseases (sometimes epidemic) that resembled cholera. who found a link between cholera and contaminated drinking water in 1854. people traveling in ships would hang a yellow quarantine flag if one or more of the crew members suffered from cholera. though the incident caused the city to become more serious about its sewage treatment. because cholera was not present in the city. It was first identified in Tamil Nadu. typically 30 to 40 days. One of the major contributions to fighting cholera was made by the physician and pioneer medical scientist John Snow (1813±1858). There is evidence of the emergence of wide-spectrum resistance to drugs such as trimethoprim.

the researchers found a correlation between the passage of V.. both regions had cholera pathogens with similar characteristics. Furthermore. thus rapidly killing many victims. They have become less virulent than the strains prevailing in Bangladesh."[63] Other famous people believed to have died of cholera include: y Elliott Frost.[12] [edit] Notable cases The pathos in the last movement of Tchaikovsky's (c.[62] His model was not immediately accepted. This eliminated the threat of cholera epidemics from the major developed cities in the world. The province of Bengal in British India was partitioned into West Bengal and East Pakistan in 1947. in 2002. Cities in developed nations made massive investment in clean water supply and wellseparated sewage treatment infractures was made between the mid-1850s and the 1900s. and formation of periplasmic nitrate reductase complexes were induced just before defecation. More recently. while having lunch with Modest (his brother and biographer). cholerae with a microscope as the bacillus causing the disease in 1885. identified V. As a consequence. the researchers found that the bacterium creates a hyper-infected state where genes that control biosynthesis of amino acids. Robert Koch. but it was seen to be the more plausible as medical microbiology developed over the next thirty years or so. Cholera has been a laboratory for the study of evolution of virulence.pioneering epidemiological field-studies. After 1947.. he is said to have poured tap water from a pitcher into his glass and drunk a few swallows. of patients with a cholera infection. he was able to demonstrate that human sewage contamination was the most probable disease vector in two major epidemics in London in 1854. cholerae through the human digestive system and an increased infectivity state. One observer noted that a week after the premiere of his Sixth Symphony.[clarification needed] the strains of the pathogen that succeeded in India had a greater incentive in the longevity of the host. studied stool samples from patients at the International Centre for Diarrhoeal Disease (ICDDR) in Dhaka. Alam et al. 1840-1893) last symphony made people think that Tchaikovsky had a premonition of death. iron uptake systems. India made more progress on public health than East Pakistan (now Bangladesh). Since the water was not boiled and cholera was once again rampaging St.. Prior to partition. son of American poet Robert Frost[64] . Petersburg. The cause of this indisposition and stomach ache was suspected to be his intentionally infecting himself with cholera by drinking contaminated water. Bangladesh. 30 years later. an environment of limited oxygen and iron. These uninhibitedly draw upon the resources of the host population. The day before. These induced characteristics allow the cholera vibrios to survive in the "rice water" stools. such a connection was quite plausible . "Tchaikovsky was dead--6 November 1893. From the various experiments they conducted.

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