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Cholera Classification and external resources
Scanning Electron Microscope image of Vibrio cholerae
ICD-10	A00.,
ICD-9	001
DiseasesDB	29089
MedlinePlus	000303
eMedicine	med/351
MeSH	D002771

Cholera, sometimes known as Asiatic or epidemic cholera, is an infectious gastroenteritis caused by enterotoxin-producing strains of the bacterium Vibrio cholerae.^[1][2] Transmission to humans occurs through eating food or drinking water contaminated with cholera vibrios. The major reservoir for cholera was long assumed to be humans themselves, but considerable evidence exists that aquatic environments can serve as reservoirs of the bacteria.

Vibrio cholerae is a Gram-negative bacterium that produces cholera toxin, an enterotoxin, whose action on the mucosal epithelium lining of the small intestine is responsible for the disease's infamous characteristic, exhaustive diarrhea.^[1] In its most severe forms, cholera is one of the most rapidly fatal illnesses known, and a healthy person's blood pressure may drop to hypotensive levels within an hour of the onset of symptoms; infected patients may die within three hours if medical treatment is not provided.^[1] In a common scenario, the disease progresses from the first liquid stool to shock in 4 to 12 hours, with death following in 18 hours to several days, unless oral rehydration therapy is provided.^[3][4]

Contents 1 Symptoms 2 Treatment 3 Epidemiology 3.1 Prevention 3.2 Susceptibility 3.3 Transmission 3.3.1 Potential human contribution to transmissibility 3.4 Diagnosis 3.4.1 Holding or transport media 3.4.2 Enrichment media 3.4.3 Plating media 3.5 Biochemistry 4 History 4.1 Origin and spread 4.1.1 Recent and ongoing outbreaks 4.2 Pandemic genetic diversity 4.3 Famous victims 4.4 Research 4.5 False historical report 4.6 Cholera morbus 4.7 Other historical information 5 References 6 See also 7 Further reading 8 External links

[edit] Symptoms

The incubation period is the period from infection until symptoms occur. In cholera this is usually 24-72 hours. The severity of symptoms depends on the dose, i.e. the number of bacteria ingested. Some otherwise healthy individuals may not develop any symptoms at all. Of those who do, only a small proportion develop severe disease.

The principal symptom of infection is diarrhea, which is watery and brown at first, but quickly changes to large volumes of pale fluid stools ('rice-water stools'). In the most severe cases dramatic fluid loss from the continuous diarrhea can lead to hypovolemic shock and collapse within 1 to 4 hours. Depending upon the treatment provided, unconsciousness and death can occur anytime from 12 to 18 hours afterwards, although some individual cases may persist for several days.

Fever is not a prominent feature of cholera.

Other symptoms include nosebleed, rapid pulse, dry skin, tiredness, abdominal cramps, nausea, leg cramps, and vomiting.

[edit] Treatment

In most cases cholera can be successfully treated with oral rehydration therapy. Prompt replacement of water and electrolytes is the principal treatment for cholera, as dehydration and electrolyte depletion occur rapidly. Oral rehydration therapy or ORT is highly effective, safe, and simple to administer. In situations where commercially produced ORT sachets are too expensive or difficult to obtain, alternative home made solutions using various formulas of water, sugar, table salt, baking soda and fruit have proven effective.

In severe cases the administration of intravenous rehydration solutions may be necessary.

Antibiotics shorten the course of the disease, and reduce the severity of the symptoms. However Oral rehydration therapy remains the principal treatment. Tetracycline is typically used as the primary antibiotic, although some strains of V. cholerae exist that have shown resistance. Other antibiotics that have been proven effective against V. cholerae include cotrimoxazole, erythromycin, doxycycline, chloramphenicol, and furazolidone.^[5] Fluoroquinolones such as norfloxacin also may be used, but resistance has been reported.^[6] Recently Hemendra Yadav reported his findings at the All India Institute of Medical Sciences, New Delhi, that Ampicillin resistance has again decreased in the V.cholerae strains of Delhi.

Rapid diagnostic assay methods are available for the identification of multidrug resistant V. cholerae.^[7] New generation antimicrobials have been discovered which are effective against V. cholerae in in vitro studies.^[8]

The success of treatment is greatly impacted by the speed and method of treatment. If treated quickly and properly, the mortality rate is less than 1%, however, untreated the mortality rate rises to 50–60%.^[9][10]

[edit] Epidemiology

[edit] Prevention

Although cholera can be life-threatening, prevention of the disease is straightforward if proper sanitation practices are followed. In the first world, due to advanced water treatment and sanitation systems, cholera is no longer a major health threat. The last major outbreak of cholera in the United States occurred in 1910-1911 .^[11][12] 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:

• Sterilization: Proper disposal and treatment of the germ infected fecal waste produced by cholera victims (and all clothing and bedding that come in contact with it) is of primary importance. All materials (such as clothing and bedding) that come in contact with cholera patients should be sterilized in hot water using chlorine bleach if possible. Hands that touch cholera patients or their clothing and bedding should be thoroughly cleaned and sterilized.
• Sewage: Treatment of general sewage before it enters the waterways or underground water supplies prevents undiagnosed patients from spreading the disease.
• Sources: Warnings about cholera contamination posted around contaminated water sources with directions on how to decontaminate the water.
• Water purification: All water used for drinking, washing, or cooking should be sterilized by boiling or chlorination in any area where cholera may be present. Boiling, filtering, and chlorination of water kill the bacteria produced by cholera patients and prevent infections from spreading. Water filtration, chlorination, and boiling are by far the most effective means of halting transmission. Cloth filters, though very basic, have significantly reduced the occurrence of cholera when used in poor villages in Bangladesh that rely on untreated surface water. Public health education and appropriate sanitation practices are important to help prevent and control transmission.

A vaccine is available in some countries (not the US), but this prophylactic is not currently recommended for routine use by the US Centers for Disease Control and Prevention (CDC)^[13]. During recent years, substantial progress has been made in developing new oral vaccines against cholera. Two oral cholera vaccines, which have been evaluated with volunteers from industrialized countries and in regions with endemic cholera, are commercially available in several countries: a killed whole-cell V. cholerae O1 in combination with purified recombinant B subunit of cholera toxin and a live-attenuated live oral cholera vaccine, containing the genetically manipulated V. cholerae O1 strain CVD 103-HgR. The appearance of V. 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.^[14] The newer vaccine (brand name: Dukoral), an orally administered inactivated whole cell vaccine, appears to provide somewhat better immunity and have fewer adverse effects than the previously available vaccine.^[13] 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.^[15]

Sensitive surveillance and prompt reporting allow for containing cholera epidemics rapidly. Cholera exists as a seasonal disease in many endemic countries, occurring annually mostly during rainy seasons. Surveillance systems can provide early alerts to outbreaks, therefore leading to coordinated response and assist in preparation of preparedness plans. Efficient surveillance systems can also improve the risk assessment for potential cholera outbreaks. Understanding the seasonality and location of outbreaks provide guidance for improving cholera control activities for the most vulnerable. This will also aid in the developing indicators for appropriate use of oral cholera vaccine.^[16]

[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,^[17][18] 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.^{[citation needed]}

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 antacids), or those who are malnourished.

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.^[19] 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.

[edit] Transmission

People infected with cholera suffer acute diarrhea. This highly liquid diarrhea, referred to as rice-water stool, is loaded with bacteria that can infect water used by other people. Cholera is transmitted from person to person through ingestion of water contaminated with the cholera bacterium, usually from faeces 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. Any infected water and any foods washed in the water, as well as shellfish living in the affected waterway, can cause an infection. Cholera is rarely spread directly from person to person. V. cholerae harbors naturally in the zooplankton of fresh, brackish, and salt water, attached primarily to their chitinous exoskeleton.^[20] Both toxic and non-toxic strains exist. Non-toxic strains can acquire toxicity through a lysogenic bacteriophage.^[21] Coastal cholera outbreaks typically follow zooplankton blooms, 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. In a 2002 study at Tufts University School of Medicine, it was found that stomach acidity is a principal factor that contributes to epidemic spread.^[22] In their findings, 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. When these hyperinfectious bacteria underwent transcription profiles, they were found to possess a unique physiological and behavioral state, characterized by high expression levels of genes required for nutrient acquisition and motility, and low expression levels of genes required for bacterial chemotaxis. Thus, the spread of cholera can be expedited by host physiology.

[edit] Diagnosis

In epidemic situations a clinical diagnosis is made by taking a history of symptoms from the patient and by a brief examination only. Treatment is usually started without or before confirmation by laboratory analysis of specimens.

Stool and swab samples collected in the acute stage of the disease, before antibiotics have been administered, are the most useful specimens for laboratory diagnosis. If an epidemic of cholera is suspected, the most common causative agent is Vibrio cholerae O1. If V. cholerae serogroup O1 is not isolated, the laboratory should test for V. cholerae O139. However, if neither of these organisms is isolated, it is necessary to send stool specimens to a reference laboratory. Infection with V. cholerae O139 should be reported and handled in the same manner as that caused by V. cholerae O1. The associated diarrheal illness should be referred to as cholera and must be reported as a case of cholera to the appropriate public health authorities.^[14]

A number of special media have been employed for the cultivation for cholera vibrios. They are classified as follows:

[edit] Holding or transport media

1. Venkataraman-Ramakrishnan (VR) medium: This medium has 20g Sea Salt Powder and 5g Peptone dissolved in 1L of distilled water.
2. Cary-Blair medium: This the most widely-used carrying media. This is a buffered solution of sodium chloride, sodium thioglycollate, disodium phosphate and calcium chloride at pH 8.4.
3. Autoclaved sea water

[edit] Enrichment media

1. Alkaline peptone water at pH 8.6
2. Monsur's taurocholate tellurite peptone water at pH 9.2

[edit] Plating media

1. Alkaline bile salt agar (BSA): The colonies are very similar to those on nutrient agar.
2. Monsur's gelatin Tauro cholate trypticase tellurite agar (GTTA) medium: Cholera vibrios produce small translucent colonies with a greyish black centre.
3. TCBS medium: This the mostly widely used medium. This medium contains thiosulphate, citrate, bile salts and sucrose. Cholera vibrios produce flat 2-3 mm in diameter, yellow nucleated colonies.

Direct microscopy of stool is not recommended as it is unreliable. Microscopy is preferred only after enrichment, as this process reveals the characteristic motility of Vibrios and its inhibition by appropriate antiserum. Diagnosis can be confirmed as well as serotyping done by agglutination with specific sera.

[edit] Biochemistry

Most of the V. cholerae bacteria in the contaminated water that a host drinks do not survive the very acidic conditions of the human stomach.^[23] The few bacteria that do survive conserve their energy and stored nutrients during the passage through the stomach by shutting down much protein production. When the surviving bacteria exit the stomach and reach the small intestine, they need to propel themselves through the thick mucus that lines the small intestine to get to the intestinal wall where they can thrive. V. cholerae bacteria 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 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 longer. The bacteria stop producing the protein flagellin, thus again conserving energy and nutrients by changing the mix of proteins that they manufacture in response to the changed chemical surroundings. On reaching the intestinal wall, V. cholerae start producing the toxic proteins that give the infected person a watery diarrhea. This carries the multiplying new generations of V. cholerae bacteria out into the drinking water of the next host—if proper sanitation measures are not in place.

Microbiologists have studied the 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.^[24] 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. 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 separate, 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.^[24] 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."^[24]

[edit] History

[edit] Origin and spread

Cholera was originally endemic to the Indian subcontinent, with the Ganges River likely serving as a contamination reservoir. The disease spread by trade routes (land and sea) to Russia, then to Western Europe, and from Europe to North America. Cholera is now no longer considered a pressing health threat in Europe and North America due to filtering and chlorination of water supplies, but still heavily affects populations in developing countries.

• 1816-1826 - First cholera pandemic: Previously restricted, the pandemic began in Bengal, and then spread across India by 1820. 10,000 British troops and countless Indians died during this pandemic.^[25] The cholera outbreak extended as far as China, Indonesia (where more than 100,000 people succumbed on the island of Java alone) and the Caspian Sea before receding. Deaths in India between 1817 and 1860 are estimated to have exceeded 15 million persons. Another 23 million died between 1865 and 1917. Russian deaths during a similar time period exceeded 2 million.^[26]
• 1829-1851 - Second cholera pandemic reached Russia (see Cholera Riots), Hungary (about 100,000 deaths) and Germany in 1831, London (more than 55,000 persons died in the United Kingdom)^[27] and Paris in 1832. In London, the disease claimed 6,536 victims; in Paris, 20,000 succumbed (out of a population of 650,000) with about 100,000 deaths in all of France.^[28] The epidemic reached Quebec, Ontario and New York in the same year and the Pacific coast of North America by 1834. ^[29] A two-year outbreak began in England and Wales in 1848 and claimed 52,000 lives.^[30]

• 1849 - Second major outbreak in Paris. In London, it was the worst outbreak in the city's history, claiming 14,137 lives, over twice 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.^[28] 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^[28] and over 3,000 in New Orleans^[28] as well as thousands in New York.^[28] 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.^[28] It is believed that over 150,000 Americans died during the two pandemics between 1832 and 1849.^[31][32]
• 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% of the population (about 3,500 people).^[28] 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.^[33]

• 1863-1875 - Fourth cholera pandemic spread mostly in Europe and Africa. At least 30,000 of the 90,000 Mecca pilgrims fell victim to the disease. Cholera claimed 90,000 lives in Russia in 1866.^[34] The epidemic of cholera that spread with the Austro-Prussian War (1866) is estimated to have claimed 165,000 lives in the Austrian Empire.^[35] Hungary and Belgium both lost 30,000 people and in the Netherlands 20,000 perished. In 1867, Italy lost 113,000 lives.^[36]

• 1866 - Outbreak in North America. It killed some 50,000 Americans.^[31] 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.^[28] Also a minor outbreak at Ystalyfera in South Wales. Caused by the local water works using contaminated canal water, it was mainly its workers and their families who suffered, 119 died. In the same year more than 21,000 people died in Amsterdam, The Netherlands.

• 1881-1896 - Fifth cholera pandemic ; According to Dr A. J. Wall, the 1883-1887 epidemic cost 250,000 lives in Europe and at least 50,000 in Americas. Cholera claimed 267,890 lives in Russia (1892);^[37] 120,000 in Spain^[38]; 90,000 in Japan and 60,000 in Persia. In Egypt cholera claimed more that 58,000 lives. The 1892 outbreak in Hamburg, Germany killed 8,600 people. Although generally held responsible for the virulence of the epidemic, the city government went largely unchanged. 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 major Russian cities (more than 500,000 people dying of cholera during the first quarter of the 20th century)^[39] and the Ottoman Empire were particularly hard hit by cholera deaths. The 1902-1904 cholera epidemic claimed 200,222 lives in the Philippines.^[40] The sixth pandemic killed more than 800,000 in India. The last outbreak in the United States was in 1910-1911 when the SMS Moltke brought infected people to New York City. Vigilant health authorities isolated the infected on Swinburne Island. Eleven people died, including a health care worker on Swinburne Island.^[41][11][12]

• 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.

[edit] Recent and ongoing outbreaks

• July - December 2007 - A lack of clean drinking water in Iraq has led to an outbreak of cholera.^[42] As of 2 December 2007, the UN has reported 22 deaths and 4,569 laboratory-confirmed cases.^[43]

• August 2007 - The cholera epidemic started in Orissa, India. The outbreak has affected Rayagada, Koraput and Kalahandi districts where more than 2,000 people have been admitted to hospitals.^[44]

• August - October 2008 - As of 29 October 2008, a total of 644 laboratory-confirmed cholera cases, including eight deaths, had been verified in Iraq.^[45]

• March - April 2008 - 2,490 people from 20 provinces throughout Vietnam have been hospitalized with acute diarrhea. Of those hospitalized, 377 patients tested positive for cholera.^[46]

• November 2008 - Doctors Without Borders reported an outbreak in a refugee camp in the Democratic Republic of the Congo's eastern provincial capital of Goma. Some 45 cases were reportedly treated between November 7th through 9th.

Wikinews has related news: Wikinews Shorts: November 25, 2008#53 die in Zimbabwe after cholera outbreak Number of Zimbabwe cholera deaths nears 500

• August 2008 - February 2009 - More than an estimated 79,000 people in Zimbabwe are believed to be infected with more than 3,700 recorded deaths observed during a current and ongoing outbreak.^[47] The number of people infected is believed to be significantly higher and the government is accused of underestimating the spread of the epidemic. The outbreak is a result of mismanagement of water purification infrastructure. Subsequent outbreaks are being observed in neighbouring countries as the medical infrastructure in Zimbabwe is severely crippled by hyperinflation leading to several Zimbabwean citizens seeking medical care elsewhere. The continuing closure of several local hospitals and the scarcity of basic medical commodities such as medicines and personnel is believed to be a major contributor to the spread. According to the World Health Organization, Zimbabwe's government has asked for urgent international help to tackle its cholera outbreak.^[48] Médecins Sans Frontières warned that the epidemic could last until March 2009 at the earliest.^[49][50]

• January 2009 - The Mpumalanga province of South Africa has confirmed over 381 new cases of Cholera, bringing the total number of cases treated since November 2008 to 2276. 19 people have died in the province since the outbreak. ^[51]

[edit] Pandemic genetic diversity

Amplified fragment length polymorphism (AFLP) fingerprinting of the pandemic isolates of Vibrio cholerae has revealed variation in the genetic structure. Two clusters have been identified: Cluster I and Cluster II. Cluster I consists mainly of strains from the 1960s and 1970s, while cluster II contains mainly strains from the 1980s and 1990s, based on a the change in the clone structure. This grouping of strains is best seen in the strains from the African Continent.^[52]

[edit] Famous victims

The pathos in the last movement of Tchaikovsky's (c. 1840-1893) last symphony made people think that Tchaikovsky had a premonition of death. "A week after the premiere of his Sixth Symphony, Tchaikovsky was dead--6 November 1893. The cause of this indisposition and stomach ache was suspected to be his intentionally infecting himself with cholera by drinking contaminated water. The day before, while having lunch with Modest (his brother and biographer), he is said to have poured tap water from a pitcher into his glass and drunk a few swallows. Since the water was not boiled and cholera was once again rampaging St. Petersburg, such a connection was quite plausible ...."^[53]

Other famous people who succumbed to the disease include:

[edit] Research

The Russian-born bacteriologist Waldemar Haffkine developed the first cholera vaccine around 1900. 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. One of the major contributions to fighting cholera was made by the physician and pioneer medical scientist John Snow (1813-1858), who found a link between cholera and contaminated drinking water in 1854.^[28] Dr Snow proposed a microbial origin for epidemic cholera in 1849 and in his major state of the art review of 1855 he proposed a substantially complete and correct model for the aetiology of the disease. In two pioneering epidemiological field-studies he was able to demonstrate that human sewage contamination was the most probable disease vector in two major epidemics in London in 1854.^[55]His model was not immediately accepted but was seen to be the more plausible as medical microbiology developed over the next thirty years or so. Massive investment in clean water supply and well separated sewage treatment infractures was made between the mid-1850's and the 1900's which eliminated the threat of cholera epidemics from the major developed cities in the world. Robert Koch, 30 years later, identified V. cholerae with a microscope as the bacillus causing the disease in 1885. Cholera has been a laboratory for the study of evolution of virulence. The province of Bengal in British India was partitioned into West Bengal 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 that 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 victims.

More recently, in 2002, Alam et al. studied stool samples from patients at the International Centre for Diarrhoeal Disease (ICDDR) in Dhaka, Bangladesh. From the various experiments they conducted, the researchers found a correlation between the passage of V. cholerae through the human digestive system and an increased infectivity state. Furthermore, the researchers found that the bacterium creates a hyper-infected state where genes that control biosynthesis of amino acids, iron uptake systems, and formation of periplasmic nitrate reductase complexes were induced just before defecation. These induced characteristics allow the cholera vibrios to survive in the rice water stools, an environment of limited oxygen and iron, of patients with a cholera infection.^[22]

[edit] False historical report

A persistent myth states that 90,000 people died in Chicago of cholera and typhoid fever in 1885, but this story has no factual basis.^[56] 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. However, because cholera was not present in the city, there were no cholera-related deaths, though the incident caused the city to become more serious about its sewage treatment.

[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. The term is not in current use, but is found in many older references.^[57] The other diseases are now known collectively as gastroenteritis.

[edit] Other historical information

In the past, people traveling in ships would hang a yellow quarantine flag if one or more of the crew members suffered from cholera. Boats with a yellow flag hung would not be allowed to disembark at any harbor for an extended period, typically 30 to 40 days.^[58]. In modern international maritime signal flags the quarantine flag is yellow and black.

[edit] References

[edit] See also

• The Ghost Map: The Story of London's Most Terrifying Epidemic - and How it Changed Science, Cities and the Modern World - which tells the story of how John Snow found the cause of a cholera epidemic, which was the start of modern epidemiology.
• The Painted Veil (2006 film), starring Naomi Watts and Edward Norton, in which cholera is a prominent subject, based on the novel of the same name by W. Somerset Maugham.
• The Horseman on the Roof (1995 film), starring Juliette Binoche and Olivier Martinez, in which the 1832 cholera outbreak in southern France is a major influence to the story line.
• The Dress Lodger by Sheri Holman - A historical novel set in Sunderland, England during the cholera epidemic of 1831.
• In the novel Death in Venice by Thomas Mann (also a 1971 film by Lucino Visconti starring Dirk Bogard), the main character dies of cholera in Venice; the epidemic is a recurring sub-plot of the story.

[edit] Further reading

• Crump J, Bopp C, Greene KD, Kubota KA, Middendorf RL, Wells JG, Mintz ED (2003). "Emergence of toxigenic Vibrio cholerae O141 causing cholera-like diarrhea and bloodstream infection in the United States". Journal of Infectious Diseases 187: 866–8. 

• Steinberg EB, Green KD, Bopp CA, Cameron DN, Wells JG, Mintz ED (2001). "Cholera in the United States, 1995-2000: trends at the end of the millennium". J Infect Dis 184: 799–802. 

[edit] External links

Wikimedia Commons has media related to: Cholera

Look up cholera in Wiktionary, the free dictionary.

• Cholera - World Health Organization
• What is Cholera? - Centers for Disease Control and Prevention
• Cholera information for travelers - Centers for Disease Control and Prevention
• Steven Shapin, "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”
• Cholera Epidemic in NYC in 1832 New York Times 15 April 2008

v • d • e Cholera Cholera Symptoms - Treatment - Prevention - Susceptibility - Transmission - Diagnosis - History Cholera Bacteria Vibrio cholerae - Strains: Classic -El Tor Discovery:1854 Broad Street cholera outbreak - John Snow - Reverend Henry Whitehead Treatment Oral rehydration therapy Antibiotics:Tetracycline - cotrimoxazole - erythromycin - doxycycline - chloramphenicol - furazolidone Fluoroquinolones:norfloxacin Outbreaks Cholera Pandemics: First cholera pandemic - Second cholera pandemic - Third cholera pandemic - Fourth cholera pandemic - Fifth cholera pandemic - Sixth cholera pandemic - Seventh cholera pandemic 1854 Broad Street cholera outbreak - 2007 Central Luzon hog cholera outbreak - 2007 Iraq cholera outbreak - 2008 Congo cholera outbreak - 2008–2009 Zimbabwean cholera outbreak

v • d • e Infectious diseases · Bacterial diseases: Proteobacterial G- (primarily A00-A79, 001-041,080-109) α Rickettsiales Rickettsiaceae/ (Rickettsioses) Typhus Rickettsia typhi (Murine typhus) · Rickettsia prowazekii (Epidemic typhus) Spotted fever Tick-borne disease Rickettsia rickettsii (Rocky Mountain spotted fever) · Rickettsia conorii (Boutonneuse fever) Other Rickettsia akari (Rickettsialpox) · Orientia tsutsugamushi (Scrub typhus) Anaplasmataceae Ehrlichia/Anaplasma: Anaplasma phagocytophilum (Human granulocytic ehrlichiosis) · Ehrlichia chaffeensis (Human monocytic ehrlichiosis) Rhizobiales Brucellaceae Brucella abortus (Brucellosis) Bartonellaceae Bartonellosis: Bartonella henselae (Cat scratch fever) · Bartonella quintana (Trench fever) · either henselae or quintana (Bacillary angiomatosis) · Bartonella bacilliformis (Carrion's disease) β Neisseriales M+ Neisseria meningitidis/meningococcus (Meningococcal disease, Waterhouse-Friderichsen syndrome) M- Neisseria gonorrhoeae/gonococcus (Gonorrhea) · Moraxella catarrhalis ungrouped: Eikenella corrodens · Kingella kingae Burkholderiales Burkholderia pseudomallei (Melioidosis) · Burkholderia mallei (Glanders) · Burkholderia cepacia complex · Bordetella pertussis/Bordetella parapertussis (Pertussis) γ Enterobacteriales (OX-) Lac+ Klebsiella pneumoniae (Rhinoscleroma, Klebsiella pneumonia) · Klebsiella granulomatis (Granuloma inguinale) · Klebsiella oxytoca Escherichia coli · Escherichia coli O157:H7 (Hemolytic-uremic syndrome) · Enterotoxigenic Enterobacter aerogenes/Enterobacter cloacae Slow/weak Serratia marcescens (Serratia infection) · Citrobacter Lac- Yersinia pestis (Plague/Bubonic plague) · Yersinia enterocolitica · Yersinia pseudotuberculosis Salmonella enterica (Typhoid fever, Paratyphoid fever, Salmonellosis) · Shigella dysenteriae/sonnei/flexneri (Shigellosis, Bacillary dysentery) · Proteus mirabilis/Proteus vulgaris Pasteurellales Haemophilus: influenzae (Haemophilus meningitis, Brazilian purpuric fever) · ducreyi (Chancroid) Pasteurella multocida (Pasteurellosis) · Actinobacillus (Actinobacillosis) Aggregatibacter actinomycetemcomitans Legionellales Legionella pneumophila/Legionella longbeachae (Legionellosis) · Coxiella burnetii (Q fever) Thiotrichales Francisella tularensis (Tularemia) Vibrionales Vibrio cholerae (Cholera) · Vibrio vulnificus · Vibrio parahaemolyticus · Plesiomonas shigelloides Pseudomonadales Pseudomonas aeruginosa (Pseudomonas infection) Cardiobacteriales Cardiobacterium hominis ε Campylobacterales Campylobacter jejuni (Campylobacteriosis) · Helicobacter pylori (Peptic ulcer, MALT lymphoma)