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Classification and external resources

Scanning electron microscope image of Vibrio cholerae















Cholera is an infection of the small intestine caused by the bacterium Vibrio cholerae.
The main symptoms are watery diarrhea and vomiting. Transmission occurs primarily by drinking water or eating
food that has been contaminated by the feces (waste product) of an infected person, including one with no apparent
symptoms. Severe cholera, requiring hospitalization, results from the accumulation of about a million bacterial cells
within the body.[medical citation needed]
The severity of the diarrhea and vomiting can lead to rapid dehydration and electrolyte imbalance, and death in some
cases. The primary treatment is oral rehydration therapy, typically with oral rehydration solution, to replace water
and electrolytes. If this is not tolerated or does not provide improvement fast enough, intravenous fluids can also be
used. Antibacterial drugs are beneficial in those with severe disease to shorten its duration and severity.
Worldwide, it affects 35 million people and causes 100,000130,000 deaths a year as of 2010[7]. Cholera was one
of the earliest infections to be studied by epidemiological methods.

Signs and symptoms

The primary symptoms of cholera are profuse diarrhea and vomiting of clear fluid. These symptoms usually start
suddenly, half a day to five days after ingestion of the bacteria. The diarrhea is frequently described as "rice water"
in nature and may have a fishy odor. An untreated person with cholera may produce 10 to 20 litres (3 to 5USgal) of
diarrhea a day. Severe cholera kills about half of affected individuals. Estimates of the ratio of asymptomatic to
symptomatic infections have ranged from 3 to 100. Cholera has been nicknamed the "blue death" because a victim's
skin turns bluish-gray from extreme loss of fluids.[8]


If the severe diarrhea is not treated, it can result in life-threatening

dehydration and electrolyte imbalances.
Fever is rare and should raise suspicion for secondary infection.
Patients can be lethargic, and might have sunken eyes, dry mouth, cold
clammy skin, decreased skin turgor, or wrinkled hands and feet.
Kussmaul breathing, a deep and labored breathing pattern, can occur
because of acidosis from stool bicarbonate losses and lactic acidosis
associated with poor perfusion. Blood pressure drops due to
dehydration, peripheral pulse is rapid and thready, and urine output
decreases with time. Muscle cramping and weakness, altered
consciousness, seizures, or even coma due to electrolyte losses and ion
shifts are common, especially in children.

Typical "rice water" diarrhea

Transmission is primarily by the fecal contamination of food and water
caused by poor sanitation. At one time it was thought that cholera was
caused by exposure to toxic gases or miasmas resulting from the
fermentation of composting feces in open cesspools, as was common in
all large cities before the installation of septic systems.[medical citation

About 100 million bacteria must typically be ingested to cause cholera
Vibrio cholerae, the bacterium that causes
in a normal healthy adult. This dose, however, is less in those with
lowered gastric acidity (for instance those using proton pump
inhibitors). Children are also more susceptible, with two- to
four-year-olds having the highest rates of infection. Individuals' susceptibility to cholera is also affected by their
blood type, with those with type O blood being the most susceptible. Persons with lowered immunity, such as
persons with AIDS or children who are malnourished, are more likely to experience a severe case if they become
infected.[9] Any individual, even a healthy adult in middle age, can experience a severe case, and each person's case
should be measured by the loss of fluids, preferably in consultation with a professional health care provider.[medical
citation needed]

The cystic fibrosis genetic mutation in humans has been said to maintain 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.

Cholera is typically transmitted by either contaminated food or water. In the developed world, seafood is the usual
cause, while in the developing world it is more often water. Most cholera cases in developed countries are a result of
transmission by food. This occurs when people harvest oysters in waters infected with sewage, as Vibrio cholerae
accumulates in zooplankton and the oysters eat the zooplankton. Cholera has been found in two animal populations:
shellfish and plankton.


People infected with cholera often have diarrhea, and if this highly liquid stool, colloquially referred to as
"rice-water", contaminates water used by others, disease transmission may occur. The source of the contamination is
typically other cholera sufferers when their untreated diarrheal discharge is allowed to get into waterways,
groundwater or drinking water supplies. Drinking any infected water and eating any foods washed in the water, as
well as shellfish living in the affected waterway, can cause a person to contract an infection. Cholera is rarely spread
directly from person to person. Both toxic and nontoxic strains exist. Nontoxic strains can acquire toxicity through a
temperate bacteriophage. Coastal cholera outbreaks typically follow zooplankton blooms, thus making cholera a
zoonotic disease.[medical citation needed]

When consumed, most bacteria do not survive the acidic conditions of
the human stomach.[10] The few surviving bacteria 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 walls where they can thrive. V. cholerae bacteria start
up production of the hollow cylindrical protein flagellin to make
flagella, the cork-screw helical fibers they rotate to propel themselves
through the mucus of the small intestine.[medical citation needed]
Once the cholera bacteria reach the intestinal wall they no longer need
the flagella to move. The bacteria stop producing the protein flagellin
to conserve energy and nutrients by changing the mix of proteins
which they express 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.[medical citation needed]

Drawing of Death bringing cholera, in Le Petit

Journal (1912)

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), and five copies of the B subunit (part B), connected by a disulfide bond. 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, while the A2 chain fits into the central pore of the B
subunit ring. Upon binding, the complex is taken into the cell via receptor-mediated endocytosis. Once inside the
cell, the disulfide bond is reduced, and the A1 subunit is freed to bind with a human partner protein called
ADP-ribosylation factor 6 (Arf6). Binding exposes its active site, allowing it to permanently ribosylate the Gs alpha
subunit of the heterotrimeric G protein. This results in constitutive cAMP production, which in turn leads to
secretion of H2O, Na+, K+, Cl, and HCO3 into the lumen of the small intestine and rapid dehydration. The gene
encoding the cholera toxin was introduced into V. cholerae by horizontal gene transfer. Virulent strains of V.
cholerae carry a variant of temperate bacteriophage called CTXf or CTX.
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 litres 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.[medical citation needed]
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 a complex cascade of regulatory proteins controls 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, causing diarrhea in the infected person
and allowing 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."

Genetic structure
Amplified fragment length polymorphism fingerprinting of the pandemic isolates of V. 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.Wikipedia:Identifying reliable sources (medicine)

A rapid dipstick test is available to determine the presence of V. cholerae. In those samples that test positive, further
testing should be done to determine antibiotic resistance. In epidemic situations, a clinical diagnosis may be made by
taking a patient history and doing a brief examination. Treatment is usually started without or before confirmation by
laboratory analysis.
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 V. 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 in the United States.


The World Health Organization recommends focusing on prevention,
preparedness, and response to combat the spread of cholera.[11] They
also stress the importance of an effective surveillance system.
Governments can play a role in all of these areas, and in preventing
cholera or indirectly facilitating its spread.
Although cholera may be life-threatening, prevention of the disease is
normally straightforward if proper sanitation practices are followed. In
developed countries, 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
19101911. 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
halted:[medical citation needed]
Sterilization: Proper disposal and treatment of infected fecal waste
Cholera hospital in Dhaka, showing typical
"cholera beds"
water produced by cholera victims and all contaminated materials
(e.g. clothing, bedding, etc.) are essential. All materials that come in
contact with cholera patients should be sanitized 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 disinfected with
chlorinated water or other effective antimicrobial agents.
Sewage: antibacterial treatment of general sewage by chlorine, ozone, ultraviolet 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, ultraviolet light sterilization (e.g. by solar water disinfection), or
antimicrobial 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 or sari filtration, though very basic, have
significantly reduced the occurrence of cholera when used in poor villages in Bangladesh that rely on untreated
surface water. Better antimicrobial 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.

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 provides guidance for improving cholera control activities
for the most vulnerable. For prevention to be effective, it is important that cases be reported to national health


A number of safe and effective oral vaccines for cholera are available.
Dukoral, an orally administered, inactivated whole cell vaccine, has an
overall efficacy of about 52% during the first year after being given
and 62% in the second year, with minimal side effects. It is available in
over 60 countries. However, it is not currently recommended by the
Centers for Disease Control and Prevention (CDC) for most people
traveling from the United States to endemic countries. One injectable
vaccine was found to be effective for two to three years. The protective
efficacy was 28% lower in children less than 5 years old. However, as
of 2010, it has limited availability. Work is under way to investigate
Preventive inoculation against cholera in 1966
the role of mass vaccination. The World Health Organization (WHO)
recommends immunization of high-risk groups, such as children and
people with HIV, in countries where this disease is endemic. If people are immunized broadly, herd immunity
results, with a decrease in the amount of contamination in the environment.

Sari filtration
An effective and relatively cheap method to prevent the transmission of cholera is the use of a folded sari (a long
cloth garment) to filter drinking water. In Bangladesh this practice was found to decrease rates of cholera by nearly
half. It involves folding a sari four to eight times. Between uses the cloth should be rinsed in clean water and dried in
the sun to kill any bacteria on it. A nylon cloth appears to work as well.

Continued eating speeds the recovery of normal intestinal function.
The World Health Organization recommends this generally for cases of
diarrhea no matter what the underlying cause. A CDC training manual
specifically for cholera states: Continue to breastfeed your baby if the
baby has watery diarrhea, even when traveling to get treatment. Adults
and older children should continue to eat frequently.[12]


Cholera patient being treated by medical staff in

The most common error in caring for patients with cholera is to
underestimate the speed and volume of fluids required.
In most
cases, cholera can be successfully treated with oral rehydration therapy (ORT), which is highly effective, safe, and
simple to administer. Rice-based solutions are preferred to glucose-based ones due to greater efficiency. In severe
cases with significant dehydration, intravenous rehydration may be necessary. Ringer's lactate is the preferred
solution, often with added potassium.[] Large volumes and continued replacement until diarrhea has subsided may be
needed. Ten percent of a person's body weight in fluid may need to be given in the first two to four hours. This
method was first tried on a mass scale during the Bangladesh Liberation War, and was found to have much

If commercially produced oral rehydration solutions are too expensive or difficult to obtain, solutions can be made.
One such recipe calls for 1 liter of boiled water, 1/2 teaspoon of salt, 6 teaspoons of sugar, and added mashed banana
for potassium and to improve taste.


As there frequently is initially acidosis, the potassium level may be normal, even though large losses have occurred.
As the dehydration is corrected, potassium levels may decrease rapidly, and thus need to be replaced. This may be
done by eating foods high in potassium like bananas or green coconut water.

Antibiotic treatments for one to three days shorten the course of the disease and reduce the severity of the symptoms.
Use of antibiotics also reduces fluid requirements. People will recover without them, however, if sufficient hydration
is maintained. The World Health Organization only recommends antibiotics in those with severe dehydration.
Doxycycline is typically used first line, although some strains of V. cholerae have shown resistance. Testing for
resistance during an outbreak can help determine appropriate future choices. Other antibiotics proven to be effective
include cotrimoxazole, erythromycin, tetracycline, chloramphenicol, and furazolidone. Fluoroquinolones, such as
norfloxacin, also may be used, but resistance has been reported.
In many areas of the world, antibiotic resistance is increasing. In Bangladesh, for example, most cases are resistant to
tetracycline, trimethoprim-sulfamethoxazole, and erythromycin. Rapid diagnostic assay methods are available for the
identification of multiple drug-resistant cases. New generation antimicrobials have been discovered which are
effective against in in vitro studies.

Zinc supplementation
In Bangladesh zinc supplementation reduced the duration and severity of diarrhea in children with cholera when
given with antibiotics and rehydration therapy as needed. It reduced the length of disease by eight hours and the
amount of diarrheal stool by 10%. Supplementation appears to be also effective in both treating and preventing
infectious diarrhea due to other causes among children in the developing world.

If people with cholera are treated quickly and properly, the mortality rate is less than 1%; however, with untreated
cholera, the mortality rate rises to 5060%. For certain genetic strains of cholera, such as the one present during the
2010 epidemic in Haiti and the 2004 outbreak in India, death can occur within two hours of becoming ill.

Cholera affects an estimated 35million people worldwide, and causes
58,000130,000deaths a year as of 2010. This occurs mainly in the
developing world. In the early 1980s, death rates are believed to have
been greater than 3 million a year. It is difficult to calculate exact
numbers of cases, as many go unreported due to concerns that an
outbreak may have a negative impact on the tourism of a country.
Cholera remains both epidemic and endemic in many areas of the
Although much is known about the mechanisms behind the spread of
cholera, this has not led to a full understanding of what makes cholera
outbreaks happen some places and not others. Lack of treatment of
human feces and lack of treatment of drinking water greatly facilitate

Hand bill from the New York City Board of

Health, 1832the outdated public health advice
demonstrates the lack of understanding of the
disease and its actual causative factors.

its spread, but bodies of water can serve as a reservoir, and seafood shipped long distances can spread the disease.
Cholera was not known in the Americas for most of the 20th century, but it reappeared towards the end of that


The word cholera is from Greek: kholera from khol "bile". Cholera likely has its origins in the Indian
Subcontinent; it has been prevalent in the Ganges delta since ancient times. Choleras first origins, within the Indian
Subcontinent, are believed to have occurred due to the result of poor living conditions as well as the presence of
pools of still water; both of which are ideal living conditions for cholera to thrive. The disease first spread by trade
routes (land and sea) to Russia in 1817, then, through technological advancements, to the rest of Europe, and from
Europe to North America and the rest of the world. Seven cholera pandemics have occurred in the past 200 years,
with the seventh originating in Indonesia in 1961.[15]
The first cholera pandemic occurred in the Bengal region of India
starting in 1817 through 1824. The disease dispersed from India to
Southeast Asia, China, Japan, the Middle East, and southern Russia.
The second pandemic lasted from 1827 to 1835 and affected the United
States and Europe particularly due to the result of advancements in
transportation, such as trade, and increased human migration, including
soldiers. The third pandemic erupted in 1839, persisted until 1856,
extended to North Africa, and reached South America, for the first time
specifically infringing upon Brazil. Cholera hit the sub-Saharan
African region during the fourth pandemic from 1863 to 1875. The
fifth and sixth pandemics raged from 18811896 and 1899-1923.
These epidemics were less fatal due to a greater understanding of the
cholera bacteria. Egypt, the Arabian peninsula, Persia, India, and the
Map of the 20082009 cholera outbreak in
Africa showing the statistics as of 12
Philippines were hit hardest during these epidemics, while other areas,
February 2009.
like Germany in 1892 and Naples from 19101911, experienced severe
outbreaks. The final pandemic originated in 1961 in Indonesia and is
marked by the emergence of a new strain, nicknamed El Tor, which still persists today in developing countries.[16]
From a local disease, cholera became one of the most widespread and deadly diseases of the 19th century, killing an
estimated tens of millions of people.[17] In Russia alone, between 1847 and 1851, more than one million people
perished of the disease.[18] It killed 150,000 Americans during the second pandemic. Between 1900 and 1920,
perhaps eight million people died of cholera in India.[19] Cholera became the first reportable disease in the United
States due to the significant effects it had on health. John Snow, in England, was the first to identify the importance
of contaminated water in its cause in 1854. 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.
In the past, vessels flew a yellow quarantine flag if any crew members or passengers were suffering from cholera. No
one aboard a vessel flying a yellow flag would be allowed ashore for an extended period, typically 30 to 40 days. In
modern sets of international maritime signal flags, the quarantine flag is yellow and black.


Historically many different claimed remedies have existed in folklore.

In the 18541855 outbreak in Naples homeopathic Camphor was used
according to Hahnemann.[20] While T. J. Ritter's "Mother's Remedies"
book lists tomato syrup as a home remedy from northern America.
While elecampagne was recommended in the United Kingdom
according to William Thomas Fernie
Cholera cases are much less frequent in developed countries where
governments have helped to establish water sanitation practices and
effective medical treatments.[21] The United States, for example, used
to have a severe cholera problem similar to those in some developing
countries. There were three large cholera outbreaks in the 1800s, which
can be attributed to Vibrio cholerae's spread through interior
waterways like the Erie Canal and routes along the Eastern Seaboard.
The island of Manhattan in New York City touched the Atlantic
Ocean, where cholera collected just off the coast. At this time, New
York City did not have as effective a sanitation system as it does today,
so cholera was able to spread.[22]

Signal flag "Lima" called the "Yellow Jack"

which when flown in harbor means ship is under
quarantine. A simple yellow flag (also called the
"Yellow Jack") had historically been used to
signal quarantine (it stands for Q among signal
flags), but now indicates the opposite, as a signal
of a ship free of disease that requests boarding
and inspection.

The bacterium was isolated in 1855 by Italian anatomist Filippo Pacini, but its exact nature and his results were not
widely known.
Spanish physician Jaume Ferran i Clua developed a cholera vaccine in 1885, the first to immunize humans against a
bacterial disease.[23]
Ukrainian bacteriologist Waldemar Haffkine developed a cholera vaccine in July 1892.[24]
One of the major contributions to fighting cholera was made by the physician and pioneer medical scientist John
Snow (18131858), who in 1854 found a link between cholera and contaminated drinking water. Dr. Snow proposed
a microbial origin for epidemic cholera in 1849. In his major "state of the art" review of 1855, he proposed a
substantially complete and correct model for the etiology of the disease. In two pioneering epidemiological field
studies, he was able to demonstrate human sewage contamination was the most probable disease vector in two major
epidemics in London in 1854.[25] His model was not immediately accepted, but it was seen to be the more plausible,
as medical microbiology developed over the next 30 years or so.
Cities in developed nations made massive investment in clean water
supply and well-separated sewage treatment infrastructures between
the mid-1850s and the 1900s. This eliminated the threat of cholera
epidemics from the major developed cities in the world. In 1883,
Robert Koch identified V. cholerae with a microscope as the bacillus
causing the disease.[26]
Robert Allan Phillips, working at the US Naval Medical Research Unit
Two in Southeast Asia, evaluated the pathophysiology of the disease
using modern laboratory chemistry techniques and developed a
protocol for rehydration. His research led the Lasker Foundation to
award him its prize in 1967.[citation needed]

Robert Koch (third from the right) on a cholera

research expedition in Egypt in 1884, one year
after he identified V. cholerae.

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,Wikipedia:Please clarify the strains of the pathogen that succeeded in India had a greater incentive
in the longevity of the host. They have become less virulent than the strains prevailing in Bangladesh. These draw
upon the resources of the host population and rapidly kill many victims.
More recently, in 2002, Alam, et al., studied stool samples from patients at the International Centre for Diarrhoeal
Disease 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 the bacterium creates a hyperinfected 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.

Society and culture

In many developing countries, cholera still reaches its victims through contaminated water sources, and countries
without proper sanitation techniques have greater incidence of the disease.[27] Governments can play a role in this. In
2008, for example, the Zimbabwean cholera outbreak was due partly to the government's role, according to a report
from the James Baker Institute. The Haitian governments inability to provide safe drinking water after the 2010
earthquake led to an increase in cholera cases as well.[28] Similarly, South Africas cholera outbreak was exacerbated
by the governments policy of privatizing water programs. The wealthy elite of the country were able to afford safe
water while others had to use water from cholera-infected rivers.Wikipedia:Verifiability[29]
According to Rita R. Colwell of the James Baker Institute, if cholera does begin to spread, government preparedness
is crucial. A government's ability to contain the disease before it extends to other areas can prevent a high death toll
and the development of an epidemic or even pandemic. Effective disease surveillance can ensure that cholera
outbreaks are recognized as soon as possible and dealt with appropriately. Oftentimes, this will allow public health
programs to determine and control the cause of the cases, whether it is unsanitary water or seafood that have
accumulated a lot of Vibrio cholerae specimens. Having an effective surveillance program contributes to a
governments ability to prevent cholera from spreading. In the year 2000 in the state of Kerala in India, the Kottayam
district was determined to be "cholera-affected"; this pronouncement led to task forces that concentrated on
educating citizens with 13,670 information sessions about human health.[30] These task forces promoted the boiling
of water to obtain safe water, and provided chlorine and oral rehydration salts. Ultimately, this helped to control the
spread of the disease to other areas and minimize deaths. On the other hand, researchers have shown that most of the
citizens infected during the 1991 cholera outbreak in Bangladesh lived in rural areas, and were not recognized by the
government's surveillance program. This inhibited physicians' abilities to detect cholera cases early.[31]
According to Colwell, the quality and inclusiveness of a country's health care system affects the control of cholera,
as it did in the Zimbabwean cholera outbreak. While sanitation practices are important, when governments respond
quickly and have readily available vaccines, the country will have a lower cholera death toll. Affordability of
vaccines can be a problem; if the governments do not provide vaccinations, only the wealthy may be able to afford
them and there will be a greater toll on the country's poor.[32] The speed with which government leaders respond to
cholera outbreaks is important.
Besides contributing to an effective or declining public health care system and water sanitation treatments,
government can have indirect effects on cholera control and the effectiveness of a response to cholera. A country's
government can impact its ability to prevent disease and control its spread. A speedy government response backed
by a fully functioning health care system and financial resources can prevent cholera's spread. This limits cholera's
ability to cause death, or at the very least a decline in education, as children are kept out of school to minimize the




risk of infection.

Notable cases
Tchaikovsky's death has traditionally been attributed to cholera, most probably contracted through drinking
contaminated water several days earlier.[33] "Since the water was not boiled and cholera was affecting Saint
Petersburg, such a connection is quite plausible ...."[34] Tchaikovsky's mother died of cholera,[35] and his father
became sick with cholera at this time but made a full recovery.[36] Some scholars, however, including English
musicologist and Tchaikovsky authority David Brown and biographer Anthony Holden, have theorized that his
death was a suicide.[37]
After the 2010 earthquake, an outbreak swept over Haiti, traced to a United Nations base. This marks the worst
cholera outbreak in recent history, as well as the best documented cholera outbreak in modern public health.
Other famous people believed to have died of cholera include:

Sadi Carnot, Physicist, a founder of thermodynamics (d. 1832)[38]

Charles X, King of France (d. 1836)[39]
James K. Polk, eleventh president of the United States (d. 1849)
Carl von Clausewitz, Prussian soldier and German military theorist (d. 1831)[40]


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Prevention and control of cholera outbreaks: WHO policy and recommendations (http:/ / www. emro. who. int/ csr/ Media/ PDF/
cholera_whopolicy. pdf), World Health Organization, Regional Office for the Eastern Mediterranean, undated but citing sources from 07, 04,
03, 04, and 05.
[10] (using the turning off and turning on of gene expression to make toxin proteins in cholera bacteria as a "comprehensive example" of what is
known about the mechanisms by which bacteria change the mix of proteins they express to respond to the changing opportunities for surviving
and thriving in different chemical environments).
[11] "Cholera Fact Sheet", World Health Organization. (http:/ / www. who. int/ mediacentre/ factsheets/ fs107/ en/ index. html).
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[12] Community Health Worker Training Materials for Cholera Prevention and Control (http:/ / www. cdc. gov/ haiticholera/ pdf/
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[33] Brown, Man and Music, 43032; Holden, 371; Warrack, Tchaikovsky, 269270.
[34] (summarizing various theories on what killed the composer Tchaikovsky, including his brother Modest's idea that Tchaikovsky drank
cholera-infested water the day before he became ill).
[35] David Brown, Early Years, 46.
[36] Holden, 23.
[37] Brown, Man and Music, 43135; Holden, 373400.
[38] Asimov, Isaac (1982), Asimov's Biographical Encyclopedia of Science and Technology (2nd rev. ed.), Doubleday
[39] Susan Nagel, Marie Thrse: Child of Terror, p. 349-350.
[40] Smith, Rupert, The Utility of Force, Penguin Books, 2006, page 57

Further reading
Colwell RR (December 1996). "Global climate and infectious disease: the cholera paradigm" (http://www. Science 274 (5295): 202531. doi:
10.1126/science.274.5295.2025 ( PMID 8953025 (http:/
Drasar, B. S.; Forrest, Bruce D., eds. (1996). Cholera and the ecology of Vibrio cholerae (
com/?id=NNQtXqqnVSIC&printsec=frontcover). Springer. p. 355. ISBN0-412-61220-8
Echenberg, Myron (2011) Africa in the Time of Cholera. A History of Pandemics from 1817 to the Present,
Cambridge University Press, New York (Paperback) ISBN 978-0-521-18820-3
Furuque, Shah M.; Nair, G. Balakrish, eds. (2008). Vibrio Cholerae: Genomics and Molecular Biology (http:// Horizon Scientific Press. p. 218.
Gilbert, Pamela K. (2008). Cholera and Nation: Doctoring the Social Body in Victorian England (http://books. SUNY Press. p. 231. ISBN0-7914-7343-0
Henze, Charlotte E. (2011) Disease, Health Care and Government in Late Imperial Russia: Life and Death on the
Volga, 1823-1914. Routledge, Oxon, UK 2011. ISBN 9780415547949.
Jermyn, William S.; O'Shea, Yvonne A.; Quirke, Anne Marie; Boyd, E. Fidelma (2006). "Genomics and the
Evolution of Pathogenic Vibrio Cholerae" (
printsec=frontcover). In Chan, Voon L.; Sherman, Philip M.; Bourke, Billy. Bacterial genomes and infectious
diseases. Humana Press. p. 270. ISBN1-58829-496-X
Johnson, Steven (2006). The Ghost Map: The Story of London's Most Terrifying Epidemic--and How It Changed
Science, Cities, and the Modern World. Riverhead Hardcover. ISBN1-59448-925-4.
McGrew, Roderick (1985) Encyclopedia of Medical History, brief history pp.5964.
Mintz ED, Guerrant RL (March 2009). "A lion in our village--the unconscionable tragedy of cholera in Africa"
( N. Engl. J.
Med. 360 (11): 10603. doi: 10.1056/NEJMp0810559 ( PMID


19279337 (
Pardio Sedas, Violeta T. (2008). "Impact of Climate and Environmental Factors on the Epidemiology of Vibrio
choerae in Aquatic Ecosystems" ( In
Hofer, Tobias N. Marine Pollution: New Research. Nova Science publishers. p. 448. pp.221254.
Ryan, Kenneth J.; Ray, C. George, eds. (2003). Sherris medical microbiology: an introduction to infectious
diseases ( (4th ed.). McGraw-Hill
Professional. p.979. ISBN0-8385-8529-9
Wachsmuth, Kaye; Blake, Paul A.; Olsvik, rjan, eds. (1994). Vibrio cholerae and cholera: molecular to global
perspectives ( ASM Press. p. 465.

External links
Cholera ( Health Organization
The Attenuation of the Causal Agent of Fowl Cholera (
works-of-louis-pasteur-english/the-attenuation-of-the-causal-agent-of-fowl-cholera.html), by Louis Pasteur,
What is Cholera? ( for Disease Control and Prevention
Cholera Epidemic in NYC in 1832 ( New York
Times 15 April 2008
The Cholera Timebomb in The DRC (
45971,news-comment,news-politics,in-pictures-the-cholera-time-bomb)slideshow by The First Post


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