Vibrio Cholerae

Introduction
Vibrios are short Gram negative rods
Curved and actively motile by a single polar
flagellum
The organism is oxidase positive and gives
positive indole reaction
The genus can be divided into:
Halophilic Vibrios (V. parahaemolyticus + V.
vulnificus)
Non- Halophilic Vibrios (V. cholerae)
Most grow at 30C
Vibrios have a low tolerance to acid and prefer
alkaline conditions (Growth range pH 6.8-10.2,
optimum pH 7.4-9.6)

Important Features
More than 130 different O serogroups have been
described
The classical cause of epidemic cholera possesses the O1
antigen, thus known as V. cholerae O1
Strains of other serogroups are known as non O1 V.
cholerae
Some of these strains can cause diarrhoea in man
All strains of V. cholerae share the same flagellar (H)
antigen
Strains of V. cholerae O1 may be further subdivided into
Inaba, Ogawa and Hikojima
There are two biotypes of V. Cholerae O1 i.e Classical and
El Tor biotypes.
V. cholerae O139 has emerged as a new epidemic strain.

Transmission
V. cholerae is transmitted by feco- oral route,
primarily from human sources
Human carriers are deemed as asymptomatic
Main animal reservoirs are marine shellfish, such
as shrimp and oysters
Ingestion of these without adequate cooking can
transmit the disease

Pathogenesis
Pathogenesis of cholera is dependent on colonization of
small intestine by the organism and secretion of
enterotoxin
For colonization to occur, large numbers of bacteria
must be ingested
Adherence to the cells of the gut is related to the
secretion of bac. Enzyme mucinase, which dissolves the
protective glycoprotien coating over the intestinal cells
After adhering, the organism multiplies and secrets an
enterotoxin called choleragen (cholera toxin)
Has the ability to reproduce symptoms of cholera even
in absence of the organism itself.

Choleragen (Cholera toxin)

Consists of A (active) subunit and B (binding) subunit
The B subunit (composed of 5 identical proteins) binds
to the ganglioside receptor on the surface of enterocyte
A subunit is inserted into the cytosol, where it catalyzes
addition of ADP ribose to Gs protein
Locking the Gs protein in on position which causes
persistent stimulation of adenylate cyclase
Resulting overproduction of cyclic AMP activates AMP
dependent protein kinase (phophorylates ion
transporters in cell membrane)
Resulting in loss of water and ions from the cell
Watery efflux enters the lumen of the gut resulting in
watery diarrhea

Clinical Findings
Watery diarrhae
Dry mucous membranes including mouth, throat,
nose and eyelids
Vomiting
No abdominal pain
Dehydration
Low blood pressure
Muscle cramps
Thirst
Acidosis and Hypokalemia also occur as a result
of loss of bicarbonate and potassium

Laboratory Diagnosis
A culture of the diarrhea stool containing V. cholerae will
show colorless colonies on MacConkeys agar
On TSI agar, an alkali slant and an acid butt without gas
or H2S are seen because the organism ferments sucrose
Presumptive diagnosis can be made by the
Immobilization test which is done by observing the wet
smear for distinctive rapid to and fro movement of V.
cholerae
The movement can be stopped by adding one drop of V.
cholera antiserum
Indole Test (positive)
Motility (Positive)

Treatment
Consists of prompt, adequate replacement of
water and electrolytes (orally or intravenously)
Glucose if added to the solution to enhance the
uptake of water and electrolytes
Abx such as tetracycline are not necessary but
they do shorten the duration of symptoms

Prevention
Mainly achieved by public health measures to
ensure clean water and food supply
Killed Vaccine, but has limited usefulness (Only
50% effective for 3 to 6 months)
Live vaccine is available in certain countries but
not in the US
Use of tetracycline for prevention is effective
somehow but cannot help during spread of major
epidemic
Detection of carriers is important in limiting
outbreaks