COMMON SOURCES OF CHOLERA INFECTION
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Surface or well water. V. cholerae can lie dormant in water for long periods of
time, and contaminated public wells are frequent sources of large-scale
outbreaks. Epidemics are most likely to occur in communities without adequate
sanitation and in areas hard hit by natural disasters or war. People living in
crowded refugee camps are especially at risk. Water stored at home also can
become contaminated. Bathing or washing dishes in water containing cholera
bacteria can spread the disease. AS IS CASE FOR LONDON
Seafood. Eating raw or undercooked seafood, especially shellfish, that originate
from certain locations can expose you to cholera bacteria. Most cases of cholera
occurring in the United States since the 1970s have been traced to oysters and
crab from the Gulf of Mexico and to seafood transported or smuggled from
countries where cholera is endemic. Shellfish are a particular problem because
they filter large amounts of water, concentrating the levels of bacteria.
Raw fruits and vegetables. Raw, unpeeled fruits and vegetables are a frequent
source of cholera infection in areas where cholera is endemic. In developing
nations, uncomposted manure fertilizers or irrigation water containing raw
sewage can contaminate produce in the field. Fruits and vegetables may also
become tainted during harvesting or processing.
Grains. In regions where cholera is widespread, grains such as rice and millet
that are contaminated after cooking and allowed to remain at room temperature
for several hours are a perfect medium for the growth of V. cholerae.
Risk factors
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Malnutrition. Malnutrition and cholera are interconnected. People who are
malnourished are more likely to develop cholera infection, and cholera is more
likely to flourish in places where malnutrition is common, such as refugee camps,
impoverished countries, and areas devastated by famine, war or natural disasters.
Reduced or nonexistent stomach acid (hydrochlorhydria or achlorhydria).
Cholera bacteria can't survive in an acidic environment, and ordinary stomach
acid often serves as a first-line defense against infection. But people with low
levels of stomach acid lack this protection and so are more likely to develop
cholera and to have severe signs and symptoms of the disease. Children and
older adults, especially, tend to have lower than normal stomach acid levels. So
do people who have had gastric surgery, who have untreated Helicobacter pylori
infection, or who are taking antacids, H2 blockers or proton pump inhibitors for
ulcer disease. Antacids help neutralize stomach acid, and H2 blockers and proton
pump inhibitors reduce the amount of acid your body produces.
Household exposure. You're more likely to develop cholera if you live with
someone who has the disease. Up to half of household contacts of infected
people also become sick.
Compromised immunity. If your immune system is compromised for any reason,
you're more susceptible to cholera infection.
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Type O blood. For reasons that aren't entirely clear, people with type O blood
are twice as likely to develop cholera as are people with other blood types.
Raw or undercooked shellfish. Although large-scale cholera outbreaks no longer
occur in industrialized nations, eating raw shellfish — particularly oysters —
from waters known to harbor the bacteria or shellfish transported by travelers
from countries where cholera is endemic greatly increases your risk.
If you're traveling to cholera-endemic areas, your risk of contracting the disease is
extremely low if you follow these precautions:
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Wash your hands. Frequent hand washing is the best way to control infection.
Wash your hands thoroughly with hot, soapy water, especially before eating or
preparing food, after using the toilet, and when you return from public places.
Carry an alcohol-based hand rub for times when water isn't available.
Avoid untreated water. Contaminated drinking water is the most common
source of cholera infection. For that reason, drink only bottled carbonated water
or water you've boiled or disinfected yourself. Hot beverages such as coffee and
tea as well as bottled or canned soft drinks, and wine and beer are generally safe.
Carefully wipe the outside of all bottles and cans before you open them, and ask
for drinks without ice. Use bottled water to brush your teeth.
Get it while it's hot. Choose food that's been thoroughly cooked and is served
piping hot. Cholera bacteria can survive on room temperature food for up to
five days and aren't destroyed by freezing. It's best to avoid street food, but if
you do buy from local vendors, make sure your meal is cooked in your presence
and served hot.
No sushi for you. Avoid raw fish and seafood of all kinds.
Ignore your mother's advice. These days, many experts recommend eating up to
nine servings of fresh fruits and vegetables a day. It's sound advice, but when
you're traveling, make sure that all fruits and vegetables are cooked or have thick
skins that you peel yourself. Avoid lettuce in particular because it may have been
rinsed in contaminated water.
Be careful with dairy foods. Avoid ice cream, which is often contaminated, and
unpasteurized milk.
Cholera (frequently called Asiatic cholera or epidemic cholera) is a severe diarrheal
disease caused by the bacterium Vibrio cholerae. Transmission to humans is by water or
food. The natural reservoir of the organism is not known. It was long assumed to be
humans V. cholerae produces cholera toxin, the model for enterotoxins, whose action
on the mucosal epithelium is responsible for the characteristic diarrhea of the disease
cholera. In its extreme manifestation, cholera is one of the most rapidly fatal illnesses
known. A healthy person may become hypotensive within an hour of the onset of
symptoms and may die within 2-3 hours if no treatment is provided. More commonly,
the disease progresses from the first liquid stool to shock in 4-12 hours, with death
following in 18 hours to several days.
The clinical description of cholera begins with sudden onset of massive diarrhea. The
patient may lose gallons of protein-free fluid and associated electrolytes, bicarbonates
and ions within a day or two. This results from the activity of the cholera enterotoxin
which activates the adenylate cyclase enzyme in the intestinal cells, converting them into
pumps which extract water and electrolytes from blood and tissues and pump it into the
lumen of the intestine. This loss of fluid leads to dehydration, anuria, acidosis and shock.
The watery diarrhea is speckled with flakes of mucus and epithelial cells ("rice-water
stool") and contains enormous numbers of vibrios. The loss of potassium ions may
result in cardiac complications and circulatory failure. Untreated cholera frequently
results in high (50-60%) mortality rates.
Treatment of cholera involves the rapid intravenous replacement of the lost fluid and
ions. Following this replacement, administration of isotonic maintenance solution should
continue until the diarrhea ceases. If glucose is added to the maintenance solution it may
be administered orally, thereby eliminating the need for sterility and iv. administration.
By this simple treatment regimen, patients on the brink of death seem to be
miraculously cured and the mortality rate of cholera can be reduced more than ten-fold.
Most antibiotics and chemotherapeutic agents have no value in cholera therapy, although
a few (e.g. tetracyclines) may shorten the duration of diarrhea and reduce fluid loss.
, but some evidence suggests that it is the aquatic environment.
Antigenic Variation and LPS Structure in Vibrio cholerae
Antigenic variation plays an important role in the epidemiology and virulence of cholera.
The emergence of the Bengal strain, mentioned above, is an example. The flagellar
antigens of V. cholerae are shared with many water vibrios and therefore are of no use in
distinguishing strains causing epidemic cholera. O antigens, however, do distinguish
strains of V. cholerae into 139 known serotypes. Almost all of these strains of V. cholerae
are nonvirulent. Until the emergence of the Bengal strain (which is "non-O1") a single
serotype, designated O1, has been responsible for epidemic cholera. However, there
are three distinct O1 biotypes, named Ogawa, Inaba and Hikojima, and each biotype
may display the "classical" or El Tor phenotype. The Bengal strain (O139) is a new
serological strain with a unique O-antigen which partly explains the lack of residual
immunity.
the toxin-damaged cells become pumps for water and electrolytes causing the diarrhea,
loss of electrolytes, and dehydration that are characteristic of cholera.
Colonization of the Small Intestine
There are several characteristics of pathogenic V. cholerae that are important
determinants of the colonization process. These include adhesins, neuraminidase,
motility, chemotaxis and toxin production. If the bacteria are able to survive the gastric
secretions and low pH of the stomach, they are well adapted to survival in the small
intestine. V. cholerae is resistant to bile salts and can penetrate the mucus layer of the
small intestine, possibly aided by secretion of neuraminidase and proteases (mucinases).
They withstand propulsive gut motility by their own swimming ability and chemotaxis
directed against the gut mucosa.
In Vibrio cholerae, the production of virulence factors is regulated at several levels.
Regulation of genes at the transcriptional level, especially the genes for toxin production
and fimbrial synthesis, has been studied in the greatest detail.
Immunity to Cholera
Infection with V. cholerae results in a spectrum of responses ranging from life-threatening
secretory diarrhea to mild or unapparent infections of no manifestation except a
serologic response. The reasons for these differences are not known. One idea is that
individuals differ in the availability of intestinal receptors for cholera vibrios or for their
toxin, but this has not been proven. Prior immunologic experience is certainly a major
factor. For example, in heavily endemic regions such as Bangladesh, the attack rate is
relatively low among adults in comparison with children.
After natural infection by V. cholerae, circulating antibodies can be detected against
several cholera antigens including the toxin, somatic (O) antigens, and flagellar (H)
antigens. These antibodies are also raised by parenteral injection of antigens as vaccine
components. Antibodies directed against Vibrio O antigens are considered "vibriocidal"
antibodies because they will lyse V. cholerae cells in the presence of complement and
serum components. Vibriocidal antibodies reach a peak 8-10 days after the onset of
clinical illness, and then decrease, returning to the baseline 2 - 7 months later. Their
presence correlates with resistance to infection, but they may not be the mediators of
this protection, and the role of circulating antibodies in natural infection is unclear.
After natural infection, people also develop toxin-neutralizing antibodies but there is no
correlation between antitoxic antibody levels and the incidence of disease in cholera
zones.
Since cholera is essentially a topical disease of the small intestine, it would seem that
topical defense might be a main determinant of protection against infection by V.
cholerae. Recurrent infections of cholera are in fact, rare, and this is probably due to
local immune defense mediated by antibodies secreted onto the surfaces of the
intestinal mucosa. Moreover, in children who are nursing cholera is less likely to occur,
presumably due to protection afforded by secretory antibody in mother's milk.
Cholera, severe infectious disease endemic in India and some other tropical countries
and occasionally spreading to temperate climates. The symptoms of cholera are diarrhea
and the loss of water and salts in the stool. In severe cholera, the patient develops
violent diarrhea with characteristic “rice-water stools,” vomiting, thirst, muscle cramps,
and sometimes circulatory collapse. Death can occur as quickly as a few hours after the
onset of symptoms. The mortality rate is more than 50 percent in untreated cases, but
falls to less than 1 percent with proper treatment. Worldwide in 1999 more than
254,000 people were diagnosed with cholera and there were over 9,100 cholera-related
deaths reported.
The causative agent of cholera is the bacterium Vibrio cholerae, which was discovered in
1883 by the German physician and bacteriologist Robert Koch. Virtually the only means
by which a person can be infected is from food or water contaminated by bacteria from
the stools of cholera patients. Prevention of the disease is therefore a matter of
sanitation. Cholera epidemics swept through Europe and the United States in the 19th
century but did not recur in those areas after improvement of the water supply.
All recent cholera outbreaks in the United States have been traced to raw or
undercooked shellfish