CHOLERA

Professor Abdelaziz Elamin

College of Medicine
Arabian Gulf University
Bahrain
 BACKGROUND
Cholera, is a Greek word, which means the
gutter of the roof. It is caused by bacteria vibrio
cholerae, which was discovered in 1883 by
Robert Koch during diarrhea outbreak in Egypt.

V cholerae has 2 major biotypes: classical

and El Tor, which was first isolated in Egypt in
1905. Currently, El Tor is the predominant
cholera pathogen.
 V CHOLERAE

The organism is a comma-shaped, gram-

negative, aerobic bacillus whose size varies from
1-3 mm in length by 0.5-0.8 mm in diameter.

Its antigenic structure consists of a flagellar H

antigen and a somatic O antigen. It is the
differentiation of the latter that allows for
separation into pathogenic and nonpathogenic
strains.
V. CHOLERAE
 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.
 EPIDEMIOLOGY/2
In October 1992, an epidemic of cholera
emerged from Madras, India as a result of a new
serogroup (0139).

This Bengal strain has now spread throughout

Bangladesh, India, and neighboring countries in
Asia.

Some experts regard this as an eighth

pandemic.
 REPORTED CASES
The number of cholera patients worldwide is
uncertain because most cases go unreported.
The number of cases is increased during
epidemics & is affected by environmental
factors.

In 1994, 94 countries reported 385000 cases of

cholera to WHO, but the number reported in 1998
was 121000; 89% of these cases were reported in
Africa.
Mortality/ Morbidity

During the six pandemic, the case fatality

rates were very high (50-70%)

After the 1960, dramatic reduction

occurred due to replacement of the
classical type with Eltor serotype and the
advancement in the understanding &
treatment of the disease.
 PATHOGENESIS
MECANISM :-
• Cholera is a toxin- mediated disease
•These toxins acts on the small intestine
• To reach the small intestine, the organisms has
to overcome the defense mechanisms of the
GIT (acidic media in the stomach)
PATHOGENESIS/2

They secrete certain mucinase which

help it to move rapidly through the
mucus
 They also depend on the large
inoculums size (so they bypass the
gastric acidity)
 Then got adherent to the epithelial
surface, probably by certain factor
PATHOGENESIS/3

Then they produce their enterotoxin

which consist of 2 types ,light one( L
toxin) , & heavy ( H toxin)

The L toxin combines with a substance

known as gangliosides , the products make
the organism bind to the cell wall, this
binding is irreversible
PATHOGENESIS/4
The H toxin acts by activating
adenylecyclase, this activation leads to
rise in the level of the so called 3, 5-
adenosine monophosphate (cAMP)
 n
t
e
s
PATHOGENESIS/5 t
i
n
a
This substance inhibits the absorptive
l

sodium transport &l activates the

u
excretory chloridem in the intestinal cell→
e
accumulation of NaCl
n in the intestinal
lumen T
h
This high osmolality
e
is balanced by
water secretion, athe
l
result is watery
diarrhea g
r

e
 PATHOGENESIS/6
Fluid loss originates in the duodenum and
upper jejunum; the ileum is less affected.

The colon usually is in a state of absorption

because it is relatively insensitive to the toxin.
PATHOGENESIS/5

The large volume of fluid produced in the

upper intestine, however, overwhelms the
absorptive capacity of the lower bowel,
which results in severe diarrhea

The enterotoxin acts locally & does not

invade the intestinal wall. As a result few
WBC & no RBC are found in the stool.
AGENT FACTORS
 Resistance:- v. cholerae are killed within
30 minutes at 56 deg.C, or few sec. by
boiling
 Remain in ice for 3-4 weeks or longer
 Drying & sunshine will kill them in few
hours
 Disinfectant kill them also
RESERVOIR OF INFECTION

 Human is the only known reservoir of

cholera infection

 The ratio of severe cases to mild ones is

shown to be 1:5 for classical type & 1:25
for EL Tor
 TRANSMISSION
Cholera is transmitted by the fecal-oral route
through contaminated water & food.

Person to person infection is not

so common.
The infectious dose of bacteria required to
cause clinical disease varies with the source. If
ingested with water the dose is in the order of
103-106 organisms. When ingested with food,
fewer organisms are required to produce
disease, namely 102-104.
 TRANSMISSION/2
V cholerae is a saltwater organism & it is
primary habitat is the marine ecosystem.

Cholera has 2 main reservoirs, man & water.

Animals do not play a role in transmission of
disease.
V cholerae is unable to survive in an acid
medium. Therefore, any condition that reduces
gastric acid production increases the risk of
acquisition.
 HOST SUSCEPTIBILITY

The use of antacids, histamine-receptor

blockers, and proton-pump inhibitors increases
the risk of cholera infection and predisposes
patients to more severe disease as a result of
reduced gastric acidity.

The same applies to patients with chronic

gastritis secondary to Helicobacter pylori
infection or those who have had a gastrectomy
 AT RISK GROUPS
All ages, but children & elderly are more
severely affected.

Subjects with O blood group. Cause is

unknown.

Subjects with reduced gastric acid.

Social class & economic status

 CLINICAL PICTURE
Incubation period is 24-48 hours.
Symptoms begin with sudden onset of watery
diarrhea, which may be followed by vomiting.
Fever is typically absent.
The diarrhea has fishy odor in the beginning,
but became less smelly & like “rice water” in
few hours.
In severe cases stool volume exceeds 250
ml /kg leading to severe dehydration, shock &
death if untreated.
 CHOLERA IN CHILDREN

Breast-fed infants are protected.

Symptoms are severe & fever is frequent.

Shock, drowsiness & coma are common.

Hypoglycemia is a recognized complication,

which may lead to convulsions.
Rotavirus infection may give similar picture.
 COMPLICATIONS
If dehydration is not corrected adequately &
promptly it can lead to hypovolemic shock,
acute renal failure & death.

Electrolyte imbalance.

Hypoglycemia in children.

Complications of therapy like overhydration

& side effects of drug therapy.
 LAB DIAGNOSIS
Organism can be seen in stool by direct
microscopy after gram stain & dark field exam is
used to demonstrates motility.

Cholera can be cultured on special alkaline

media like triple sugar agar or TCBS agar.

Serologic tests are available to define

strains, but this is needed only during
epidemics to trace the source of infection.
 OTHER LAB FINDINGS
Dehydration leads to high blood urea &
serum creatinine. Hematocrit & WBC will also
be high due to hemoconcentration.

Dehydration & bicarbonate loss in stool

leads to metabolic acidosis with wide-anion
gap.

Total body potassium is depleted, but serum

level may be normal due to effect of acidosis.
 TREATMENT
The primary goal of therapy is to replenish
fluid losses caused by diarrhea & vomiting.

Fluid therapy is accomplished in 2 phases:

rehydration and maintenance.

Rehydration should be completed in 4

hours & maintenance fluids will replace
ongoing losses & provide daily requirement.
WHO Guidelines
 Step (1) : Assess degree of dehydration
 Step (2) : Rehydrate the patient &
monitor signs frequently -:
 Step (3): Maintain hydration
 Step (4): Administer oral antibiotics to
patient with severe dehydration
 Step (5): Feed the patient
SEVERE DEHYRATION
 Administer IV fluids immediately
 Monitor the patient very frequently,
(radial pulse & BP)
 Re-assess the patient after 3 hours (if
still having signs, repeat the IV fluid)
 FLUID THERAPY
Ringer lactate solution is preferred over
normal saline because it corrects the associated
metabolic acidosis.

IV fluids should be restricted to patients who

purge >10 ml/kg/h & for severe dehydration.

The oral route is preferred for maintenance &

the use of ORS at a rate of 500-1000 ml/h is
recommended.
 DRUG THERAPY

The goals of drug therapy are to eradicate

infection, reduce morbidity and prevent
complications.

The drugs used for adults include

tetracycline, doxycycline, cotrimoxazole &
ciprofloxacin.
For children erythromycin, cotrimoxazole
and furazolidone are the drugs of choice.
 DRUG THERAPY/2
Drug therapy reduces volume of stool &
shortens period of hospitalization. It is only
needed for few days (3-5 days).

Drug resistance has been described in some

areas & the choice of antibiotic should be
guided by these resistance patterns.

Antibiotic should be started when cholera is

suspected without waiting for lab confirmation.
 PREVENTION

Education on hygienic practices.

Provision of safe, uncontaminated water to

the population.

Antibiotic prophylaxis to house-hold

contacts.
Vaccination against cholera.
 CHOLERA VACCINES
The old killed injectable vaccine is obsolete
now because it is not effective.
Two new oral vaccines became available in
1997. A Killed & a live attenuated types.
Both provoke a local immune response in
the gut & a blood immune response.

Cholera vaccination is no more required

for international travelers coz risk is small.
 Steps of epidemic control

Verification of the diagnosis

Notification of the case to MOH & WHO.

Early case finding & tracing source of

infection.

Establishment of treatment centers

Isolation & barrier nursing is indicated

THANKS
FOR YOUR roe

ATTENTION