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Cholera (Vibrio cholera)

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CHOLERA (VIBRIO CHOLERA) Introduction Cholera, sometimes known as Asiatic cholera or epidemic cholera, is an infectious gastroenteritis caused by the bacterium Vibrio ... – PowerPoint PPT presentation

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Title: Cholera (Vibrio cholera)


1
Cholera (Vibrio cholera)
2
Introduction
  • Cholera, sometimes known as Asiatic cholera or
    epidemic cholera, is an infectious
    gastroenteritis caused by the bacterium Vibrio
    cholerae.12
  • 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.

3
  • 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

4
  • 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.

5
Symptoms
  • 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.

6
Treatment
  • 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.

7
  • 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.

8
Holding or transport media
  • 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

9
Enrichment media
  • Alkaline peptone water at pH 8.6
  • Monsur's taurocholate tellurite peptone water at
    pH 9.2

10
Vaccine for cholera
  • 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,
    Swedentelephone 46-8-7351000,e-mail
    info_at_sblvaccines.sewebsite www.sblvaccines.se

11
  • Pathogenesis and Epidemiology of cholera
  • Virulence factor
  • Colonization 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
  • toxR, ToxS, ToxT System

12
Plating media
  • 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.

13
Biochemistry of the V. cholerae bacterium
  • 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.

14
  • 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 hostif proper sanitation measures
    are not in place

15
  • 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 hostif proper sanitation measures
    are not in place

16
  • 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.

17
  • 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

18
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