Cholera

Cholera.
Definition:
An acute infection by vibrio cholerae
involving the entire small bowel,
characterized by profuse watery diarrhea,
vomiting, dehydration, oliguria and
collapse.
ETIOLOGY
A causative organism, vibrio cholerae,
serogroups 01 and 0139, is a short,
curved, motile, aerobic rod.
V. Cholera has more than 150 different
serogroups, only two of which cause
epidemic disease.
There are two biotypes of vibrio
Cholerae 01 : classical and EL Tor.
Vibrio Cholera
• Gram-negative
• Curved rod
• .5-.8 μm width
• 1.4-2.6 μm length
• Facultative anaerobe
• Single polar flagellum
• Optimal growth 20-30
degrees
Vibrio Cholera
o Biotype (biovar)
different strains of the same bacterial species
distinguished by a group of phenotypic or genetic traits
o Serogroup
bacteria of the same species with different antigenic
determinants on the cell surface
Epidemiology.
Cholera is endemic in portions of Asia,
the middle east, Africa, south and
central America, and the gulf coast of
the USA.
Cases transported into Europe, Japan
and Australia have caused localized out
breaks.
Cont. epidemiology.
In endemic areas, outbreaks usually
occur during warm months and
incidence is highest in children.
Susceptibility to the infection varies
and is greater for persons whit blood
group O, because the vibrio is
sensitive to gastric acid,
hypochlorhydria and achlorhydria are
predisposing factors.
Cont. epidemiology.
Human are the only known natural host
of vibrio cholerae.
The infective dose is high, 1011bacteria
being required.
The incubation period ranges from few
hours to 5 days.
V. Cholerae does not form spores, is
killed by heating at 55c for 15 minutes.
1883 KOCH demonstrated the bacterial
cause of cholera.
Epidemiology
Since 1817, there have been 7 cholera
pandemics. The first 6 occurred from 1817-1923
and were caused by V. cholerae, the classical
biotype. The pandemics originated in Asia with
subsequent spread to other continents.
The seventh pandemic began in Indonesia in
1961 and affected more countries and continents
than the previous 6 pandemics. It was caused by V.
cholerae El Tor.
Transmission.
Cholera is transmitted by faecal-oral
route through the water or foods
contaminated by the excrement of
persons with symptomatic or
asymptomatic infections.
Spread may occur from case to case
through direct contact with feces or
vomitus. it occurs mostly in hot humid
season.
Pathogenesis
V cholerae cause clinical disease by producing an
enterotoxin that promotes the secretion of fluid and
electrolytes into the lumen of the gut.
The result is watery diarrhea with electrolyte

concentrations isotonic to those of plasma .
The enterotoxin acts locally & does not invade the

intestinal wall. As a result few WBC & no RBC are
found in the stool.
Pathogenesis
Fluid loss originates in the duodenum and upper
jejunum; the ileum is less affected.
The colon is usually in a state of absorption

because it is relatively insensitive to the toxin.
The large volume of fluid produced in the upper

intestine, however, overwhelms the absorptive
capacity of the lower bowel, which results in
severe diarrhea.
Pathogenesis of V. Cholera
Cholera disease begins with ingestion of contaminated water or

food. The bacteria that survive the acidic conditions of the
stomach colonize in the small intestine.
The cholera toxin (CT) is responsible for the severe diarrhea

characteristic of the disease.
Cholera Toxin
CT is a proteinaceous enterotoxin secreted by
V. Cholera
Cholera Toxin
Structure
• Composed of a AB subunit. The B subunit forms a
pentameric “doughnut” like structure that binds the CT to
the receptor on the eukaryotic cells
Pathway
• The A subunit contains the enzymatically active
portion or the toxin
• Proteolytic cleavage of the A subunit results in A1
and A2 peptide units which remain linked by a
disulfide bond
• Once the A subunit is internalized by the eukaryotic
cell, the disulfide bond is reduced
Cholera Toxin
The A1 subunit contains a ADP-ribosyltransferase which

covalently modifies the G protein, which regulates adenylate
cyclase. Adenylate cyclase mediates the formation of cAMP
The increase in cAMP levels bring about the secretion of chloride

and bicarbonate from the mucosal cells into the intestinal
lumen
The change in ion concentrations leads to the secretion of large

amounts of water into the lumen, known as diarrhea
Pathology.
Vibrio cholera multiply in the lumen
of small bowel and are non-invasive.
They secrete a powerful exotoxin
( enterotoxin) which activates
adenyl cyclase in intestinal epithelial
cells of the small intestine producing
hypersecretion of water and chloride
causing massive diarrhea of up to
15 liters per day. Acidosis may occur
Cont. pathology.
Cholera toxin’s comprises two sub-
units: A activate, B binding.
Additional toxins and other factors
are now known to be involved in
cholera pathogenesis.
Immunity to both cholera toxin and
bacterial surface antigens follows
natural infection.
Symptoms
Occur 2-3 days after consumption of
contaminated food/water
Usually mild, or no symptoms at all
75% asymptomatic
20% mild disease
2-5% severe
Vomiting
Cramps
Watery diarrhea (1L/hour)
Without treatment, death in 18 hours-several
days
Cholera Gravis
More severe symptoms
Rapid loss of body fluids
6 liters/hour
107 vibrios/mL
Rapidly lose more than 10% of
bodyweight
Dehydration and shock
Death within 12 hours or less
Death can occur within 2-3 hours
Clinical features.
Stage of evacuation:
Sudden onset with: frequent loose
motions without pain or colic, initially
yellow soon become colorless watery
typical rice-water stools which consist
of clear fluid with flecks of mucus.
Copious watery vomiting follows the
diarrhea.
Stage of collapse:
The enormous loss of fluid and
electrolytes lead to intense
dehydration with:
Muscular cramps due to electrolyte
depletion.
Cold, clammy and wrinkled skin
Sunken eyes
B.P. falls
Pulse not palpable
Urine output diminished.
Consequences of Severe Dehydration
Intravascular volume
depletion
Severe metabolic acidosis
Hypokalemia
Cardiac and renal failure
Sunken eyes, decreased skin
turgor
Almost no urine production
Mortality Rate
Causes 120,000 deaths/year worldwide

With prompt rehydration: <1%
Without treatment: 50%-60%
Complications.
Acidosis due to bicarbonate loss.
Acute renal failure due to dehydration.
Death may occur within few hours
from circulatory shock unless fluid and
electrolytes are replaced.
Mortality rate ranges from less than 1
to 40%.
Diagnosis.
Diagnosis is usually clinical.
Presence of rapidly motile vibrios in fresh
stool by dark-field illumination is diagnostic
(slide under microscope).
Culture of stool or rectal swab should be
taken.
Management.
Replacement of fluid and electrolytes:
ORS in mild cases.
Ringer lactate in sever cases(2-3
liters in first hour followed by
normal saline 1 liter/hour until the
pulse and blood pressure return)
Cont. management.
Drugs:
Ciprofloxacin infusion I.V twice
daily is now used preferably.
tetracycline I.V 6 hourly for 24
hours then 500mg orally 6hourly
for next two days may be
alternative.
Prevention.
Cholera is transmitted by the faecal-
oral route through the contamination
of water or food, hence public health
measures to improve water and
sanitation are essential for long term
control.
The management of out breaks is
based on interrupting transmission.
Cont. prevention.
Appropriate control and management
of cases and contacts.
Effective surveillance.
Health education programmes.
immunization: vaccination for vibrio
cholerae provides protection for short
period.
Chemoprophylaxis with tetracycline
is effective.

Cholera

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Cholera.

The result is watery diarrhea with electrolyte

The enterotoxin acts locally & does not invade the

The colon is usually in a state of absorption

The large volume of fluid produced in the upper

Cholera disease begins with ingestion of contaminated water or

The cholera toxin (CT) is responsible for the severe diarrhea

The A1 subunit contains a ADP-ribosyltransferase which

The increase in cAMP levels bring about the secretion of chloride

The change in ion concentrations leads to the secretion of large

Causes 120,000 deaths/year worldwide

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