Cholera

PATHOPHYSIOLOGY
Modifiable Non modifiable
Ingestion of a significant inoculum
Colonization occurs in the small intestine
Secretion of a potent enterotoxin results in a massive outpouring of isotonic fluid from

the mucosal surface of the intestine
Profuse diarrhea
Dehydration
Vomiting, fluid and electrolyte loss occurs
Hypovolemic shock s/sx: falling blood pressure with fever
Metabolic acidosis hypoactive bowel sounds
Death
Pathophysiology
The species V cholerae has been classified according to the carbohydrate determinants of its
somatic O antigens. Approximately 140 serotypes have been defined and are classified broadly
as those that agglutinate in antisera to the O1 group antigen (V cholerae O1) or those that do not
agglutinate in antisera to the O1 group antigen (non-O1V cholerae).
V cholerae has 2 biotypes, classic and El Tor, which are defined on the basis of their biochemical
and other laboratory parameters. Each biotype has been divided further into 2 serotypes, Inaba
and Ogawa. V cholerae O1 was the cause of most pandemics until a new strain, termed V
cholerae O139 (non-O1 type), was recognized as a cause of epidemic in southern India and parts
of Bangladesh in 1992.
Cholera is a toxin-mediated disease. The clinical features and epidemiologic manifestations of

disease caused by cholera O139 are indistinguishable from those caused by O1 strains. Cholera
toxin (CTX) is a potent protein enterotoxin elaborated by the organism in the small intestine. To
reach the small intestine, however, the organism has to negotiate the normal defense
mechanisms of the GI tract. Because the organism is not acid-resistant, it depends on its large
inoculum size to bypass gastric acidity. Using its own properties, such as motility, chemotaxis,
and elaboration of hemagglutinin/protease, the organism transcends the mucous layer of the
small intestine.
Hemagglutinin/protease is both an agglutinin and a zinc-dependent protease, which cleaves the

mucin and fibronectin as well as a subunit of CTX. Hemagglutinin/protease also may serve to
facilitate the spread and excretion of vibrios within the intestine in stools by detaching them from
the intestinal walls. After the vibrios negotiate these 2 barriers, they adhere to the intestinal wall
mediated by toxin-coregulated pilus (TCP). The synchronous working of TCP, CTX, and a few
other virulence factors all are regulated by toxR gene product, which is designated as the "master
switch."
Once established, the organisms produce CTX that consists of subunits A and B. The B subunit
is the binding subunit, and the A subunit is the enzymatic subunit. These 2 working in harmony,
transfer adenosine diphosphate (ADP) and activate it to cyclic adenosine monophosphate
(cAMP), which inhibits the absorptive sodium transport and activates the excretory chloride
transport in the intestinal crypt cells, eventually leading to an accumulation of sodium chloride in
the intestinal lumen.
The high osmolality in the intestinal lumen is balanced by water secretion that eventually
overwhelms the lumen absorptive capacity and leads to diarrhea. Unless the wasted fluid and
electrolytes are replaced adequately, shock (caused by profound dehydration) and acidosis
(caused by loss of bicarbonate) follow.
The O139 Bengal strain of V cholerae has a very similar pathogenic mechanism except that it
produces a novel O139 lipopolysaccharide (LPS) and an immunologically related O-antigen
capsule. These 2 features enhance its virulence and increase its resistance to human serum in
vitro and occasional development of O139 bacteremia.
ANATOMY AND PHYSIOLOGY
Cholera, sometimes known as Asiatic or epidemic cholera, is an infectious gastroenteritis

caused by enterotoxin-producing strains of the bacterium Vibrio cholerae. Transmission
to humans occurs through eating food or drinking water contaminated with Vibrio
cholerae from other cholera patients. The major reservoir for cholera was long assumed
to be humans themselves, but considerable evidence exists that aquatic environments can
serve as reservoirs of the bacteria. Vibrio cholerae is a Gram-negative bacterium that
produces cholera toxin, an enterotoxin, whose action on the mucosal epithelium lining of
the small intestine is responsible for the disease's most salient characteristic, exhaustive
diarrhea
The small intestine is the part of the gastrointestinal tract (gut) following the stomach and
followed by the large intestine, and is where the vast majority of digestion and absorption
of food takes place. the small intestine in an adult human measures about 7 meters in
length and is approximately 2.5-3 cm in diameter. Although the small intestine is much
longer than the large intestine (typically 4-5 times longer), it gets its name from its
comparatively smaller diameter. Although a simple tube the length and diameter of the
small intestine would have a surface area of only about 0.5m, the surface complexity of
the inner lining of the small intestine increase its surface area by a factor of 500 to
approximately 200m, or roughly the size of a tennis court.
The small intestine is divided into three structural parts:
• Duodenum 26 cm (9.8 in) in length

• Jejunum 2.5 m (8.2 ft)
• Ileum 3.5 m (11.5 ft)
treatment
In most cases cholera can be successfully treated with oral rehydration therapy. Prompt
replacement of water and electrolytes is the principal treatment for cholera, as
dehydration and electrolyte depletion occur rapidly. Oral rehydration therapy or ORT is
highly effective, safe, and simple to administer. In situations where commercially
produced ORT sachets are too expensive or difficult to obtain, alternative homemade
solutions using various formulas of water, sugar, table salt, baking soda, and fruit offer
less expensive methods of electrolyte repletion. In severe cholera cases with significant
dehydration, the administration of intravenous rehydration solutions may be necessary.
Antibiotics shorten the course of the disease, and reduce the severity of the symptoms.
However oral rehydration therapy remains the principal treatment. Tetracycline is
typically used as the primary antibiotic, although some strains of V. cholerae exist that
have shown resistance. Other antibiotics that have been proven effective against V.
cholerae include cotrimoxazole, erythromycin, doxycycline, chloramphenicol, and
furazolidone. Fluoroquinolones such as norfloxacin also may be used, but resistance has
been reported.
Rapid diagnostic assay methods are available for the identification of multidrug resistant
V. cholerae. New generation antimicrobials have been discovered which are effective
against V. cholerae in in vitro studies.
Independent nursing intervention

 sterilization: Proper disposal and treatment of infected fecal waste water produced by
cholera victims and all contaminated materials (e.g. clothing, bedding, etc) is essential.
All materials that come in contact with cholera patients should be sterilized by washing in
hot water using chlorine bleach if possible. Hands that touch cholera patients or their
clothing, bedding, etc, should be thoroughly cleaned and sterilized with chlorinated water
or other effective anti-microbial agents.
 Sewage: anti-bacterial treatment of general sewage by chlorine, ozone, ultra-violet

light or other effective treatment before it enters the waterways or underground water
supplies helps prevent undiagnosed patients from inadvertently spreading the disease.
 Sources: Warnings about possible cholera contamination should be posted around

contaminated water sources with directions on how to decontaminate the water (boiling,
chlorination etc.) for possible use.
 Water purification: All water used for drinking, washing, or cooking should be
sterilized by either boiling, chlorination, ozone water treatment, ultra-violet light
sterilization, or anti-microbal filtration in any area where cholera may be present.
Chlorination and boiling are often the least expensive and most effective means of halting
transmission. Cloth filters, though very basic, have significantly reduced the occurrence
of cholera when used in poor villages in 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.
THE ETIOLOGY OF CHOLERA
Infectious Agent
Cholera is cause by a bacterium called Vibrio Cholerae. There are more than 60 cholera
bacteria, however, current outbreaks in Africa are caused by El Tor biotype of Vibrio
cholera serogroup 01. The serotype of El Tor biotype prevalent in Africa is Inaba. Vibrio
cholerae 0139 serovar is the major causative agent of epidemics in Asia.
Clinical Presentation of Cholera
Most cholera infections are asymptomatic or mild, and indistinguishable from other mild
diarrhoea. In its severe form the following signs and symptoms characterise cholera:
• Onset is typically sudden,

• Diarrhoea is profuse, painless and watery, with flecks of mucus in the stool ("rice
water" stools). The presence of blood in stools is not a characteristic of cholera,
• Vomiting may occur, usually early in the illness,
• Majority of patients are afebrile, children are more often febrile than adults,
• Dehydration occurs rapidly (up to 1000ml/hour of diarrhoea may be produced),
• All complications result from effects of loss of fluids and electrolytes in stool; and
• Vomitus; muscle cramps, acidosis, peripheral vasoconstriction, and ultimately
renal and circulatory failure, arrhythmias and death may occur if treatment is not
given timeously.
Reservoir
For practical purposes, cholera is restricted to humans. Faecally contaminated water is the
most important reservoir of infection and vehicle of transmission, either directly or
indirectly through contaminated food.
Mode of Transmission
Vibrio cholerae is spread mainly via the faecal-oral route. Some of the best-known
sources of infection are as follows:
• Drinking water that has been contaminated at its source, during storage or usage,
• Contaminated foods, vegetables that have been fertilised with human excreta
(nightsoil) or "freshened" with contaminated water,
• Soiled hands can also contaminate clean drinking water and food, and
• Fish, particularly shellfish taken from contaminated water and eaten raw or
insufficiently cooked.
Incubation Period
The incubation period ranges form a few hours to 5 days, (usually 2 - 3 days).
Period of Communicability
Cholera is communicable in the duration of stool-positive stage. Asymptomatic carrier

status may persist for several months.
Population at Risk
The people most at risk of contracting cholera are those who do not have access to piped
safe water and adequate and proper sanitation.

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PATHOPHYSIOLOGY

Modifiable Non modifiable

Ingestion of a significant inoculum

Colonization occurs in the small intestine

Secretion of a potent enterotoxin results in a massive outpouring of isotonic fluid from

Cholera is a toxin-mediated disease. The clinical features and epidemiologic manifestations of

Hemagglutinin/protease is both an agglutinin and a zinc-dependent protease, which cleaves the

ANATOMY AND PHYSIOLOGY

Cholera, sometimes known as Asiatic or epidemic cholera, is an infectious gastroenteritis

The small intestine is divided into three structural parts:

• Duodenum 26 cm (9.8 in) in length

Independent nursing intervention

 Sewage: anti-bacterial treatment of general sewage by chlorine, ozone, ultra-violet

 Sources: Warnings about possible cholera contamination should be posted around

THE ETIOLOGY OF CHOLERA

• Onset is typically sudden,

Cholera is communicable in the duration of stool-positive stage. Asymptomatic carrier

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