Cholera

Cause

Vibrio cholerae bacteria

Mode of Transmission

Eating of food or drinking of water contaminated with human waste.

Signs and Symptoms

Sudden onset of frequent painless watery stools

Vomitting

Rapid dehydration (e.g. sunken eyeballs, wrinkled and dry skin)

ImmediateTreatment

Replace lost body fluid by giving Oral Rehydration Solution (ORESOL) or a homemade
solution composed of 1 teaspoon of salt, 4 teaspoons of sugar mix to 1liter of water. If
diarrhea persists, consult your health workers or bring the patient to the nearest hospital.

Prevention and Control

Drink only safe and clean water. If unsure, boil drinking water (Upon reaching boiling
point, extend boiling for two or more minutes), or

Do water chlorination.

Keep food away from insects and rats by covering it.

Wash and cook food properly.

Sanitary disposal of human waste.

Use toilet properly and clean toilet everyday.

Wash hands with soap after using toilet and before eating.

Keep surroundings clean to prevent flies and other insects and rodents from breeding.
Cholera
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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[1] is an infection of the small intestines caused by the bacterium Vibrio cholerae.
The main symptoms are profuse watery diarrhea, vomiting and abdominal pain.
Transmission is primarily through contaminated drinking water or food. The severity of
the diarrhea and vomiting can lead to rapid dehydration and electrolyte imbalance.
Primary treatment is with orals or intravenous rehydration solutions. Antibiotics may in
certain cases be used. Cholera is a major cause of death in the world. Cholera was one of
the earliest infection to be studied by epidemiological methods.
Contents
[hide]

• 1 Signs and symptoms

• 2 Cause
• 3 Pathophysiology
o 3.1 Susceptibility
o 3.2 Transmission
 3.2.1 Human contribution to transmissibility
• 4 Diagnosis
o 4.1 Enrichment media
o 4.2 Plating media
• 5 Prevention
• 6 Treatment
• 7 Epidemiology
o 7.1 Pandemic genetic diversity
• 8 History
o 8.1 Origin and spread
o 8.2 False historical report
o 8.3 Cholera morbus
o 8.4 Other historical information
o 8.5 Research
• 9 Society and culture
o 9.1 Notable cases
o 9.2 Literary works
• 10 Notes
• 11 References
• 12 Further reading

• 13 External links

[edit] Signs and symptoms

The primary symptoms of cholera are profuse diarrhea, severe dehydration and
abdominal pain. Cholera may also cause vomiting. These symptoms start suddenly,
usually one to five days after infection, and are the result of a toxin produced by the
vibrio cholerae bacterium that compels profuse amounts of fluid from the blood supply
into the small and large intestines. [2] An untreated cholera person may produce around 10
litres of diarrhoeal fluid a day.

[edit] Cause
Main article: Vibrio cholerae
TEM image of Vibrio cholerae

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.[3] The few bacteria that do
survive conserve their energy and stored nutrients during the passage through the
stomach by shutting down much protein production. 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
of the small intestine.

Once the cholera bacteria reach the intestinal wall, they do not need the flagella
propellers to move any longer. The bacteria stop producing the protein flagellin, thus
again conserving energy and nutrients by changing the mix of proteins which 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
diarrhoea. 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.

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).[4] 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 is introduced into V. cholerae by horizontal gene transfer. Virulent strains of V.
cholerae carry a variant of lysogenic bacteriophage called CTXf or CTXφ.
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.[5]
Of particular interest have been the genetic mechanisms by which cholera bacteria turn
on the protein production of the toxins that interact with host cell mechanisms to pump
chloride ions into the small intestine, 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.[5] 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."[5]
[edit] Pathophysiology
[edit] Susceptibility

Recent epidemiologic research suggests that an individual's susceptibility to cholera (and

other diarrhoeal infections) is affected by their blood type: those with type O blood are
the most susceptible,[6][7] 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.
[8]
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

Drawing of Death bringing the cholera, in Le Petit Journal

People infected with cholera suffer acute diarrhoea. This highly liquid diarrhoea,
colloquially referred to as "rice-water stool," is loaded with bacteria that can infect water
used by other people.[9] 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 diarrhoea 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 harbours naturally in the zooplankton of fresh, brackish, and salt
water, attached primarily to their chitinous exoskeleton.[10] Both toxic and non-toxic
strains exist. Non-toxic strains can acquire toxicity through a lysogenic bacteriophage.[11]
Coastal cholera outbreaks typically follow zooplankton blooms, thus making cholera a
zoonotic disease.

[edit] 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 agent that advances epidemic
spread.[12] 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
behavioural 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.[13]

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

[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] Prevention

Cholera hospital in Dhaka, showing typical cholera beds.

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
1910-1911.[14][15] Travellers 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 faecal 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 disinfected 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-microbial 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 Bangladesh 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 Centres for Disease Control and Prevention
(CDC).[16] 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.[13] 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.[16] This
safe and effective vaccine is available for use by individuals and health personnel. Work
is under way to investigate the role of mass vaccination.[17]

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.[18]

[edit] Treatment

Cholera patient being treated by medical staff in 1992.

In most cases cholera can be successfully treated with oral rehydration therapy (ORT).
ORT is highly effective, safe, and simple to administer: prompt replacement of water and
electrolytes is the principal treatment for cholera, as dehydration and electrolyte depletion
occur rapidly. 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 have shown
resistance. Other antibiotics that have been proven effective against V. cholerae include
cotrimoxazole, erythromycin, doxycycline, chloramphenicol, and furazolidone.[19]
Fluoroquinolones such as norfloxacin also may be used, but resistance has been reported.
[20]

Rapid diagnostic assay methods are available for the identification of multi-drug resistant
V. cholerae.[21] New generation antimicrobials have been discovered which are effective
against V. cholerae in in vitro studies.[22]

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%.[23][24]
[edit] Epidemiology

By 12 February 2009, the number of cases of infection by cholera in sub-Saharan Africa

had reached 128,548 and the number of fatalities, 4,053.

• In 2000, some 140,000 cholera cases were officially notified to WHO. Africa
accounted for 87% of these cases.[25]

• July - December 2007 - A lack of clean drinking water in Iraq has led to an
outbreak of cholera.[26] As of 2 December 2007, the UN has reported 22 deaths
and 4,569 laboratory-confirmed cases.[27]

• 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.[28]

• August - October 2008 - As of 29 October 2008, a total of 644 laboratory-

confirmed cholera cases, including eight deaths, had been verified in Iraq.[29]

• 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.[30]

• 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 7 through 9th.

• August 2008 - April 2009: In the 2008 Zimbabwean cholera outbreak, which is
still continuing, an estimated 96,591 people in the country have been infected
with cholera and, by 16 April 2009, 4,201 deaths had been reported.[31] According
to the World Health Organization, during the week of 22–28 March 2009, the
"Crude Case Fatality Ratio (CFR)" had dropped from 4.2% to 3.7%.[31] The daily
updates for the period 29 March 2009 to 7 April 2009, list 1748 cases and 64
fatalities, giving a weekly CFR of 3.66% (see table above);[32] however, those for
 the period 8 April to 16 April list 1375 new cases and 62 deaths (and a resulting
CFR of 4.5%).[32] The CFR had remained above 4.7% for most of January and
early February 2009.[33]

• 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.
[34]

• August 2010 - Nigeria is reaching epidemic proportions after wide spread

confirmation of the Cholera outbreaks in 12 of its 36 states. 6400 cases have been
reported with 352 reported deaths. The health ministry blamed the outbreak on
heavy seasonal rainfall and poor sanitation.[35]

[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. 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.[36]

[edit] History

Hand bill from the New York City Board of Health, 1832. The outdated public health
advice demonstrates the lack of understanding of the disease and its actual causative
factors.

[edit] 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 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.[37] 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.[38]

• 1829-1851 - Second cholera pandemic reached Russia (see Cholera Riots),

Hungary (about 100,000 deaths) and Germany in 1831, London (more than
55,000 people died in the United Kingdom)[39] and Paris in 1832. In London, the
disease claimed 6,536 victims and came to be known as "King Cholera"; in Paris,
20,000 succumbed (out of a population of 650,000) with about 100,000 deaths in
all of France.[40] The epidemic reached Quebec, Ontario and New York in the
same year and the Pacific coast of North America by 1834.[41] The 1831 cholera
epidemic killed 150,000 people in Egypt.[42] In 1846, cholera struck Mecca, killing
over 15,000 people.[43] A two-year outbreak began in England and Wales in 1848
and claimed 52,000 lives.[44] Cholera was found in Dundee in 1832. One
influential UK pamphlet explaining how to nurse cholera patients and prevent the
disease was Hints on the Cholera morbus (1832) by the home economics writer
Esther Copley.

• 1849 - 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 Ireland in 1849 and killed many of the Irish Famine survivors already
weakened by starvation and fever.[45] In 1849 cholera claimed 5,308 lives in the
port city of Liverpool, England, and 1,834 in Hull, England.[40] 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. Louis[40] and over 3,000 in New Orleans[40] as
well as thousands in New York.[40] Mexico was similarly attacked.[43] In 1849
cholera was spread along the California, Mormon and Oregon Trails as 6,000 to
12,000[46] are believed to have died on their way to the California Gold Rush,
Utah and Oregon in the cholera years of 1849-1855.[40] It is believed that over
150,000 Americans died during the two pandemics between 1832 and 1849.[47][48]
• 1852-1860 - Third cholera pandemic mainly affected Russia, with over a
million deaths. In 1852, cholera spread east to Indonesia and later invaded China
and Japan in 1854. The Philippines were infected in 1858 and Korea in 1859. In
1859, an outbreak in Bengal once again led to the transmission of the disease to
Iran, Iraq, Arabia and Russia.[43] There were at least seven major outbreaks of
cholera in Japan between 1858 and 1902. The Ansei outbreak of 1858-60, for
example, is believed to have killed between 100,000 and 200,000 people in Tokyo
alone.[49]
• 1854 - Outbreak of cholera in Chicago took the lives of 5.5% of the population
(about 3,500 people).[40][50] In 1853-4, London's epidemic claimed 10,738 lives.
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.[51] 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.

• 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.[52] The epidemic of cholera that spread
with the Austro-Prussian War (1866) is estimated to have claimed 165,000 lives
in the Austrian Empire.[53] Hungary and Belgium both lost 30,000 people and in
the Netherlands 20,000 perished. In 1867, Italy lost 113,000 lives.[54]

1892 cholera outbreak in Hamburg, hospital ward

1892 cholera outbreak in Hamburg, disinfection team

• 1866 - 1873 - Outbreaks in North America. It killed some 50,000 Americans.[47] 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.[40] 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. In the 1870s, cholera spread in the US as epidemic from New
 Orleans along the Mississippi River and related ports of tributaries, with
thousands dying.

• 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);[55] 120,000 in Spain;[56] 90,000 in
Japan and over 60,000 in Persia.[55] In Egypt cholera claimed more that 58,000
lives. The 1892 outbreak in Hamburg 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)[57] and the Ottoman
Empire were particularly hard hit by cholera deaths. The 1902-1904 cholera
epidemic claimed 200,000 lives in the Philippines.[58] 27 epidemics were recorded
during pilgrimages to Mecca from the 19th century to 1930, and more than 20,000
pilgrims died of cholera during the 1907–08 hajj.[57] The sixth pandemic killed
more than 800,000 in India. 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 Island. Eleven
people died, including a health care worker on Swinburne Island.[14][15][59]

• 1961-1970s - Seventh cholera pandemic began in Indonesia, called El Tor after

the strain, and reached East Pakistan (now 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] False historical report

Main article: Chicago 1885 cholera epidemic myth
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.[60] 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.

Cholera
Cholera is an acute intestinal infection caused by ingestion of food or water contaminated
with the bacterium Vibrio cholerae. It has a short incubation period and produces an
enterotoxin that causes a copious, painless, watery diarrhoea that can quickly lead to
severe dehydration and death if treatment is not promptly given. Vomiting also occurs in
most patients.

Most persons infected with V. cholerae do not become ill, although the bacterium is
present in their faeces for 7-14 days. When illness does occur, about 80-90% of episodes
are of mild or moderate severity and are difficult to distinguish clinically from other types
of acute diarrhoea. Less than 20% of ill persons develop typical cholera with signs of
moderate or severe dehydration.

Cholera remains a global threat and is one of the key indicators of social development.
While the disease no longer poses a threat to countries with minimum standards of
hygiene, it remains a challenge to countries where access to safe drinking water and
adequate sanitation cannot be guaranteed. Almost every developing country faces cholera
outbreaks or the threat of a cholera epidemic.

Cholera Outbreak in Misamis Oriental, Philippines Affects

Hundreds

There is a cholera outbreak in Misamis Oriental, Philippines and a State of Calamity was
declared in the province. According to news reports, there are already 960 suspected
cases of cholera with two confirmed deaths.

The causative agent of cholera is Vibrio Cholerae. Just like the typhoid fever outbreak in
Real, Quezon, the modes of transmission of cholera are contaminated food and/or
contaminated water. However, for cholera, one only gets sick if he ingests water and/or
food contaminated by stool or feces of persons infected with the disease.

The diagnostic procedures of cholera are rectal swabbing and stool culture. Signs and
symptoms of cholera include: severe diarrhea (profuse and watery as much as 1 Liter in
an hour), vomiting, muscle cramps and dehydration.
Treatment of cholera involve taking in antibiotics plus fluid and electrolyte replacement
through intravenous solutions.

Cholera prevention include the following:

1. Cholera vaccine
2. Drink only boiled water or distilled water
3. Avoid eating uncooked food

Possible complications of cholera may include the following:

1. Kidney tissue damage

2. Circulatory Collapse
3. Severe Dehydration
4. Metabolic Acidosis

When left untreated, the mortality rate of cholera among infected people is 50% . In view
of Nursing research, I think the incidence of cholera in places like Misamis Oriental is
one good nursing topic for an undergraduate thesis because it will expose and immerse
student-researchers in their own communities (which is the rationale of Community
Health Nursing). The scope of the research could be in one municipality or city only.

Cholera Anatomy
To better understand cholera, it helps to understand the anatomy of the gastrointestinal
tract.

The esophagus is a muscular tube that propels food down to the stomach. The stomach is
the most dilated portion of the digestive tube, situated between the esophagus and the
beginning of the small intestine (duodenum). It lies in the upper central portion of the
abdomen (above the umbilicus) and to the left of the midline. The stomach produces
gastric juice (acidic), which serves to breakdown proteins.

The intestine is a long, continuous, tube inside the body. It lets the body absorb nutrients
from food and liquids. The intestine is about 22 feet long. It includes the large intestine
(colon) and the small intestine.

The small intestine has three parts:

• Duodenum:
o Connects to the stomach
• Jejunum:
o Middle portion of the small intestine
• Ileum:
 o Lower portion of the small intestine that connects to the cecum (first part
of the large intestine)

The large intestine is also known as the colon. It is the last portion of the intestine.

The colon has several parts, including:

• Cecum:
o The portion of the colon that connects to the ileum (small intestine). The
appendix is a finger-like pouch that comes off of the cecum.
• Ascending colon:
o The first section after the small intestine, located on the right side
• Transverse colon:
o Sits horizontally across the upper abdomen
• Descending colon:
o Located on the left side of the abdomen
• Sigmoid:
o A short, S-shaped section above the rectum
• Rectum:
o The lowest internal part of the colon

Gastrointestinal anatomy:

• Esophagus and stomach

• Intestines
• Blood vessels of the intestines
• Entire gastrointestinal tract
 Cholera (El Tor)
January 16, 2009 by Admin · 3 Comments · Email
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Definition:

Cholera is an acute bacterial entric diseases of the

GIT characterized by profuse diarrhea, vomiting, massive loss of fluid and electrolytes
that could result to hypovolemic shock, acidosis and death.

Sometimes known as Asiatic or epidemic cholera

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 during the Irish
immigration period. 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.

Source of Infection:

Vomitus and feces of infected persons and feces of convalescent or healthy carriers.
Contacts may be temporary carriers.

Etiologic Agent:

Vibrio Cholerae/Vibrio coma

1. The organisms are slightly curved rods (coma shape), gram negative (-) and
motile with a single polar flagellum.
2. The organisms survive well at ordinary temperature and can grow well in
temperature ranging from 22-40 degrees centigrade.
3. They can survive well in ordinary temperature and can survive longer in
refrigerated foods.
4. An enterotoxin, choleragen, is elaborated by the organism as they grow in the
intestinal tract.

Incubation Period:

The incubation period ranges from a few hours to five days; usually one to three days.

Period of Communicability:
The organisms are communicable during stool positive stage, usually a few days after
recovery, however occasionally the carrier may have the organism for several months.

Mode of Transmission:

1. Fecal transmission passes via oral route form contaminated water, milk, and other
foods.
2. The organisms are transmitted through ingestion of food or water contaminated
with stool or vomitus of patient.
3. Flies, soiled hands and utensils also serve to transmit the infection.

Pathogenesis and Pathology:

1. Fluid loss is attributed to the enterotoxin elaborated by the organism as they lie in
opposition with the lining cells of the intestines.
2. The toxin stimulates adenylate cyclase, which results in the conversion of the
adenosine truphosphate (ATP) to cyclic adesine monophasphate (CAMP).
3. The mucosal cell is stimulated to increase secretion of chloride, associated with
water and bicarbonate loss.
4. The toxin acts upon the intact epithelium on the vasculator of the bowel, thus,
resulting in outpouring of intestinal fluids.
5. Fluid loss of 5 to 10 percent of the body weight resulting in dehydration and
metabolic acidosis.
6. If treatment is delayed or inadequate, acute renal failure and hypokalemia become
secondary problems.

Clinical Manifestations:

1. There is an acute, profuse, watery diarrhea with no tenesmus or intestinal

cramping.
2. Initially, the stool is brown and contains fecal materials, but soon becomes pale
gray, “rice-water” in appearance with an inoffensive, slightly fishy odor.
3. Vomiting often occurs after diarrhea has been established.
4. Diarrhea causes fluid loss amounting to 1 to 30 liters per day owing to subsequent
dehydration and electrolyte loss.
5. Tissue turgur is poor and eyes are sunken into the orbit.
6. The skin is cold, the fingers and toes are wrinkled, assuming the characteristic
“washer-moman’s hand”.
7. Radial pulse become imperceptible and the blood pressure unobtainable.
8. Cyanosis is present.
9. The voice becomes hoarse and then, is lost, so that the patient speaks in whisper
(aphonia).
10. Breathing is rapid and deep.
11. Despite marked diminished peripheral circulation, consciousness is present.
12. Patients develops oliguria and may even develop anuria.
 13. Temperature could be normal at the onset of the disease but becomes subnormal
in later stage especially if the patient is in shock.
14. When the patient is in deep shock, the passage of diarrhea stops.
15. Death may occur as short as four hours after onset, but usually occurs on the first
or second day if not properly treated.

Susceptibility, Resistance Occurrence:

• Susceptibility and resistance general although variable. Frank clinical attacks

confer a temporary immunity which may afford some protection, for several
years.
• Immunity artificially induced by vaccine is of variable and uncertain duration.
• Appears occasionally in epidemic form in the Philippines and in other parts of the
world.

Diagnostic Exams:

• Rectal Swab
• Darkfield or phase microcopy
• Stool Exam

Modalities of Treatment:

Treatment of cholera consist in correcting the basic abnormalities without delay –

restoring the circulating blood volume and blood electrolytes to normal levels.

1. Intravenous treatment is achieved by rapid intravenous infusion of alkaline saline

solution containing sodium, potassium, chloride and bicarbonate ions in
proportions comparable to that in water-stool.
2. Oral therapy rehydration can be completed by oral route (Oresol, Hydrites) unless
contraindicated or, if the patient is not vomiting.
3. Maintenance of the volume of fluids and electrolytes to ensure rehydration. This
is done by careful intake and output measurement.
4. Antibiotics
1. Tetracycline 500mg every 6 hours might be administered to adults, and
125 mg/kg body weight for children every 6 hours to 72 hours.
2. Furazolidone 100 mg for adults and 125mg/kg for children, might be
given every 6 hours for 72 hours.
3. Chlorampenicol may also be given 500 mg for adults and 18 mg/kg for
children every 6 hours for 72 hours.
4. Cotrimoxazole can also be administered 8mg/kg for 72 hours.

Nursing Management:

1. Medical septic protective care must be provided.

2. Enteric isolation must be observed.
 3. Vital signs must be recorded accurately.
4. Intake and output must be be accurately measured.
5. A thorough and careful personal hygiene must be provided.
6. Excreta must be properly disposed of.
7. Concurrent disinfection must be applied.
8. Food must be properly prepared.
9. Environmental sanitation must be observed.

Prevention:

1. Food and water supply must be protected from fecal contamination.

2. Water should be boiled or chlorinated.
3. Milk should be pasteurized.
4. Sanitary disposal of human excreta is a must.
5. Sanitary supervision is important.

-About 46% to 60% of the average adult’s weight is water, the primary body fluid. In
good health this volume remains relatively constant and the person’s weight varies less
than 0.2kg (0.5lb) in 24 hours, regardless of the amount of fluid ingested.

Water is vital to health and normal cellular function, serving as: (1) a medium for
metabolic reactions within cells (2) a transporter for nutrients, waste products and other
substances (3) a lubricant (4) an insulator and shock absorber (5)one means of regulating
and maintaining body temperature.

• Age, sex, and body fat affect total body water

• Infants have the highest proportion of water, accounting for 70 to 80% of their
body weight, but the proportion of body water decreases with aging
• In people older than 60 years old, it decreases to approximately 50%
• Fat tissue is essentially free of water, whereas lean tissue contain a significant
amount of water
• Water makes up a greater percentage of a lean person’s body weight than an
obese person
• Women, who have proportionately more body fat than men, have a lower
percentage of body water

Cholera is an acute, diarrheal illness caused by infection of the intestine with the
bacterium Vibrio cholerae. The infection is often mild or without symptoms, but
sometimes it can be severe. Approximately one in 20 infected persons has severe
disease characterized by profuse watery diarrhea, vomiting, and leg cramps. In these
persons, rapid loss of body fluids leads to dehydration and shock. Without treatment,
death can occur within hours.