Transcript Cholera (Vibrio cholera)

CHOLERA (VIBRIO CHOLERA)
Introduction
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Cholera, sometimes known as Asiatic cholera or
epidemic cholera, is an infectious gastroenteritis
caused by the bacterium Vibrio cholerae.[1][2]
Transmission to humans occurs through ingesting
contaminated water or food.
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.
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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 characteristic massive
diarrhoea of the disease.[1]
In its most severe forms, cholera is one of the most
rapidly fatal illnesses known, and a healthy person
may become hypotensive within an hour of the onset
of symptoms; infected patients may die within three
hours if treatment is not provided.[1]
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In a common scenario, the disease progresses from
the first liquid stool to shock in 4 to 12 hours, with
death following in 18 hours to several days without
oral rehydration therapy.[
Symptoms
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The diarrhea associated with cholera is acute and so severe that,
unless oral rehydration therapy is started promptly, the diarrhea
may within hours result in severe dehydration (a medical
emergency), or even death.
Author Susan Sontag wrote that cholera was more feared than some
other deadly diseases because it dehumanized the victim. Diarrhea
and dehydration were so severe the victim could literally shrink into
a wizened caricature of his or her former self before death.[5]
Other symptoms include rapid dehydration, rapid pulse, dry skin,
tiredness, abdominal cramps, nausea, and vomiting.
Traditionally, Cholera was widespread throughout third world
countries, however more recently outbreaks have occurred in more
rural parts of England and the United States' mid-west region.
Treatment
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Water and electrolyte replacement are essential
treatments for cholera, as dehydration and electrolyte
depletion occur rapidly.
Prompt use of oral rehydration therapy is highly
effective, safe, uncomplicated, and inexpensive.
The use of intravenous rehydration may be absolutely
necessary in severe cases, under some conditions.
In addition, tetracycline is typically used as the primary
antibiotic, although some strains of V. cholerae exist that
have shown resistance.
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Other antibiotics that have been proven effective
against V. cholerae include cotrimoxazole, erythromycin,
doxycycline, chloramphenicol, and furazolidone.[6]
Fluoroquinolones such as norfloxacin also may be used,
but resistance has been reported.[7]
Recently Hemendra Yadav reported his findings at
A.I.I.M.S., New Delhi that Ampicillin resistance has again
decreased in V.cholerae strains of Delhi.
Rapid diagnostic assay methods are available for the
identification of multidrug resistant V. cholerae.[8] New
generation antimicrobials have been discovered which
are effective against V. cholerae in in vitro studies.
Holding or transport media
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Venkataraman-ramakrishnan (VR) medium: This
medium has 20g Sea Salt Powder and 5g Peptone
dissolved in 1L of distilled water.
Cary-Blair medium: This the most widely-used
carrying media. This is a buffered solution of
sodium chloride, sodium thioglycollate, disodium
phosphate and calcium chloride at pH 8.4.
Autoclaved sea water
Enrichment media
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Alkaline peptone water at pH 8.6
Monsur's taurocholate tellurite peptone water at pH
9.2
Vaccine for cholera
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A recently developed oral vaccine for cholera is licensed and
available in other countries (Dukoral from SBL Vaccines).
The vaccine appears to provide somewhat better immunity and have
fewer adverse effects than the previously available vaccine.
However, CDC does not recommend cholera vaccines for most
travelers, nor is the vaccine available in the United States . Further
information about Dukoral can be obtained from the manufacturers:
Dukoral ®
SBL Vaccin AB,
SE-105 21 Stockholm, Sweden
telephone +46-8-7351000,
e-mail: [email protected]
website: www.sblvaccines.se
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Pathogenesis and Epidemiology of cholera
Virulence factor
 Colonization
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of the small Intestinal Mucosa
 Cholera toxin
 Other toxin produced by V. cholerae
Virulence gene Cassette: ctx, ace and zot
Transcriptional Regulation of Virulence Genes
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toxR, ToxS, ToxT System
Plating media
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Alkaline bile salt agar (BSA): The colonies are very similar to those
on nutrient agar.
Monsur's gelatin Tauro cholate trypticase tellurite agar (GTTA)
medium: Cholera vibrios produce small translucent colonies with a
greyish black centre.
TCBS medium: This the mostly widely used medium. This medium
contains thiosulphate, citrate, bile salts and sucrose. Cholera vibrios
produce flat 2-3 mm in diameter, yellow nucleated colonies.
Direct microscopy of stool is not recommended as it is unreliable.
Microscopy is preferred only after enrichment, as this process
reveals the characteristic motility of Vibrios and its inhibition by
appropriate antiserum. Diagnosis can be confirmed as well as
serotyping done by agglutination with specific sera.
Biochemistry of the V. cholerae
bacterium
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Most of the V. cholerae bacteria in the contaminated water that a
host drinks do not survive the very acidic conditions of the human
stomach.
The few bacteria that do survive conserve their energy and stored
nutrients during the passage through the stomach by shutting down
much protein production.
When the surviving bacteria exit the stomach and reach the small
intestine, they need to propel themselves through the thick mucus that
lines the small intestine to get to the intestinal wall where they can
thrive.
V. cholerae bacteria start up production of the hollow cylindrical
protein flagellin to make flagella, the curly whip-like tails that they
rotate to propel themselves through the mucous that lines the small
intestine.
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Once the cholera bacteria reach the intestinal wall, they do
not need the flagella propellers to move themselves any
longer.
The bacteria stop producing the protein flagellin, thus again
conserving energy and nutrients by changing the mix of
proteins that they manufacture in response to the changed
chemical surroundings.
On reaching the intestinal wall, V. cholerae start producing
the toxic proteins that give the infected person a watery
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
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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
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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.
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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 diarrhoea.
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 diarrhoea