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Cholera, sometimes known as Asiatic or epidemic cholera, is an infectious gastroenteritis caused by enterotoxin-producing strains of the bacterium Vibrio cholerae. Transmission to humans occurs through eating food or drinking water contaminated with Vibrio cholerae from other cholera patients. 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 most salient characteristic, exhaustive diarrhea. 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. 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 (or, in more serious cases, intravenous) rehydration therapy is provided.



It is estimated that most cases of cholera are unreported due to poor surveillance systems, particularly in Africa. Fatality rates are 5% of total cases in Africa, and less than 1% elsewhere. For a map of recent international outbreaks, see:[822]

Treatment



Cholera patient being treated by medical staff in 1992


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 homemade solutions using various formulas of water, sugar, table salt, baking soda, and fruit offer less expensive methods of electrolyte repletion. In severe cholera cases with significant dehydration, 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. Fluoroquinolones such as norfloxacin also may be used, but resistance has been reported.

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

The success of treatment is significantly affected by the speed and method of treatment. If cholera patients are treated quickly and properly, the mortality rate is less than 1%; however, with untreated cholera the mortality rate rises to 50–60%.

Epidemiology

Prevention

Although cholera may be life-threatening, prevention of the disease is normally straightforward if proper sanitation practices are followed. In the first world, due to nearly universal advanced water treatment and sanitation practices, cholera is no longer a major health threat. The last major outbreak of cholera in the United States occurred in 1910-1911. Travelers should be aware of how the disease is transmitted and what can be done to prevent it. Effective sanitation practices, if instituted and adhered to in time, are usually sufficient to stop an epidemic. There are several points along the cholera transmission path at which its spread may be (and should be) halted:



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


A vaccine for cholera is available in some countries, but prophylactic usage is not currently recommended for routine use by the Centers for Disease Control and Prevention (CDC).
 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.
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. 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.

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.

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,

 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.


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.
 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.


Transmission



People infected with cholera suffer acute diarrhea. This highly liquid diarrhea, colloquially referred to as "rice-water stool," is loaded with bacteria that can infect water used by other people. Cholera is transmitted 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. Both toxic and non-toxic strains exist. Non-toxic strains can acquire toxicity through a lysogenic bacteriophage. Coastal cholera outbreaks typically follow zooplankton blooms, thus making cholera a zoonotic disease.

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. 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.

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.

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

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 is the most widely-used carrying medium. This is a buffered solution of sodium chloride, sodium thioglycollate, disodium phosphate and calcium chloride at pH 8.4.
  3. Autoclaved sea water


Enrichment media

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


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.

Biochemistry



Most of the V. cholerae bacteria in the contaminated water consumed by the host do not survive the highly acidic conditions of the human stomach. 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.

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)


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. 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. 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.".

History

Origin and spread

Cholera likely has its origins in and is endemic to the Indian subcontinent. The disease spread by trade routes (land and sea) to Russiamarker, 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 Bengalmarker, and then spread across Indiamarker by 1820. 10,000 British troops and countless Indians died during this pandemic. The cholera outbreak extended as far as Chinamarker, Indonesiamarker (where more than 100,000 people succumbed on the island of Javamarker alone) and the Caspian Seamarker 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. Russianmarker deaths during a similar time period exceeded 2 million.
  • 1829-1851 - Second cholera pandemic reached Russia (see Cholera Riots), Hungarymarker (about 100,000 deaths) and Germanymarker in 1831, Londonmarker (more than 55,000 people died in the United Kingdommarker) and Parismarker in 1832. In London, the disease claimed 6,536 victims and came to be known as "King Cholera"; in Parismarker, 20,000 succumbed (out of a population of 650,000) with about 100,000 deaths in all of Francemarker. The epidemic reached Quebecmarker, Ontariomarker and New Yorkmarker in the same year and the Pacific coast of North America by 1834. The 1831 cholera epidemic killed 150,000 people in Egyptmarker. In 1846, cholera struck Meccamarker, killing over 15,000 people. A two-year outbreak began in England and Wales in 1848 and claimed 52,000 lives.


  • 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. Cholera hit Irelandmarker in 1849 and killed many of the Irish Famine survivors already weakened by starvation and fever. In 1849 cholera claimed 5,308 lives in the port city of Liverpoolmarker, Englandmarker, and 1,834 in Hullmarker, England. An outbreak in North America took the life of former U.S. President James K. Polk. Cholera, believed spread from ship(s) from England, spread throughout the Mississippi river system killing over 4,500 in St. Louismarker and over 3,000 in New Orleansmarker as well as thousands in New Yorkmarker. Mexicomarker was similarly attacked. In 1849 cholera was spread along the California, Mormon and Oregon Trails as 6,000 to 12,000 are believed to have died on their way to the California Gold Rush, Utahmarker and Oregonmarker in the cholera years of 1849-1855. It is believed that over 150,000 Americans died during the two pandemics between 1832 and 1849.
  • 1852-1860 - Third cholera pandemic mainly affected Russia, with over a million deaths. In 1852, cholera spread east to Indonesiamarker and later invaded Chinamarker and Japan in 1854. The Philippinesmarker were infected in 1858 and Koreamarker in 1859. In 1859, an outbreak in Bengal once again led to the transmission of the disease to Iranmarker, Iraqmarker, Arabia and Russia.
  • 1854 - Outbreak of cholera in Chicagomarker took the lives of 5.5% of the population (about 3,500 people). In 1853-4, London's epidemic claimed 10,738 lives. The Sohomarker outbreak in London ended after removal of the handle of the Broad Street pump by a committee instigated to action by John Snow. This proved that contaminated water (although it didn't identify the contaminant) was the main agent spreading cholera. It would take almost 50 years for this message to be believed and acted upon. Building and maintaining a safe water system was and is not cheap—but is absolutely essential.






1892 cholera outbreak in Hamburg, disinfection team


  • 1866 - Outbreak in North America. It killed some 50,000 Americans. 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. Also a minor outbreak at Ystalyferamarker 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 Netherlandsmarker.


  • 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 Russiamarker (1892); 120,000 in Spainmarker; 90,000 in Japanmarker and 60,000 in Persiamarker. In Egyptmarker cholera claimed more that 58,000 lives. The 1892 outbreak in Hamburgmarker 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) and the Ottoman Empire were particularly hard hit by cholera deaths. The 1902-1904 cholera epidemic claimed 200,000 lives in the Philippinesmarker. 27 epidemics were recorded during pilgrimages to Meccamarker from the 19th century to 1930, and more than 20,000 pilgrims died of cholera during the 1907–08 hajj. The sixth pandemic killed more than 800,000 in Indiamarker. The last outbreak in the United States was in 1910-1911 when the steamship Moltke brought infected people to New York City. Vigilant health authorities isolated the infected on Swinburne Islandmarker. Eleven people died, including a health care worker on Swinburne Islandmarker.


  • 1961-1970s - Seventh cholera pandemic began in Indonesiamarker, called El Tor after the strain, and reached Bangladeshmarker 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 Bakumarker in 1972, but information about it was suppressed in the USSRmarker.


  • January 1991 to September 1994 - Outbreak in South America, apparently initiated when a ship discharged ballast water. Beginning in Perumarker 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 Nadumarker, 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.


Recent and ongoing outbreaks

  • In 2000, some 140,000 cholera cases were officially notified to WHO. Africa accounted for 87% of these cases.


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


  • August 2007 - The cholera epidemic started in Orissamarker, Indiamarker. The outbreak has affected Rayagada, Koraput and Kalahandi districts where more than 2,000 people have been admitted to hospitals.


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


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




{| cellpadding="3" border="1" class="wikitable"
! bgcolor="#DDDDDD" colspan="6" | 2008 Zimbabwean cholera outbreak WHO daily updates 
29 March 2009 to 16 April 2009
Date New cases Deaths Date New cases Deaths
29 March 2009 242 15 8 April 2009 130 3
30 March 2009 92 2 9 April 2009 137 0
31 March 2009 76 3 10 April 2009 81 2
1 April 2009 259 7 11 April 2009 84 6
2 April 2009 166 10 12 April 2009 73 1
3 April 2009 44 0 13 April 2009 78 1
4 April 2009 132 1 14 April 2009 363 30
5 April 2009 19 6 15 April 2009 115 9
6 April 2009 536 7 16 April 2009 314 10
7 April 2009 182 13
Total 1748 64 (CFR = 3.66%) Total 1375 62 (CFR=4.51%)
  • 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.


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. For the most part Cluster I consists of strains from the 1960s and 1970s, while Cluster II largely contains strains from the 1980s and 1990s, based on the change in the clone structure. This grouping of strains is best seen in the strains from the African Continent.

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. One observer noted that 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. Petersburgmarker, such a connection was quite plausible ...."

Other famous people believed to have died of cholera include:






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. 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. 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-1850s and the 1900s 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 Bengalmarker 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 Bangladeshmarker). 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 Diseasemarker (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.

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. In 1885, there was a torrential rainstorm that flushed the Chicago Rivermarker 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.

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. The other diseases are now known collectively as gastroenteritis.

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.. In modern international maritime signal flags the quarantine flag is yellow and black.

Notes

See also



References



Further reading





External links




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