A E T I O L O G Y, M E C H A N I S M S O F I N F E C T I O N ,

PAT H O G E N E S I S A N D L A B O R AT O R Y
DIAGNOSIS OF CHOLERA
INTRODUCTION
• Cholera is a highly infectious disease caused by the bacterium Vibrio cholerae.
• It is transmitted through contaminated water or food and can cause severe
dehydration and even death if left untreated.
• While cholera is not as common in developed countries, it remains a serious
public health issue in many parts of the world.
• particularly in areas with poor sanitation and limited access to clean water. In
fact, cholera outbreaks can have devastating consequences for communities,
leading to widespread illness and death.
• Each year about 1.3 to 4.0 million cases of cholera are reported, and
21,000 to 143,000 deaths are recorded worldwide due to cholera.
• In Nigeria, Since 28 February 2023 and as of 2 April 2023, 664 new cases,
including 54 new deaths have been reported. Since 1 January 2023 and as
of 2 April 2023, 1 336 cases, including 79 deaths have been reported. In
comparison, in 2022 and as of 1 May 2022, 1 861 cases, including 54
deaths were reported.
07/27/2023 Sample Footer Text 4
 A E T I O L O G Y ( V. C H O L E R A E )

• The organism is a comma-shaped, Gram-negative, Aerobic or facultatively anaerobic bacillus

• 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.
• O antigen allows for separation into pathogenic and nonpathogenic strains.
• V. cholerae O1 was the cause of most pandemics until a new strain, termed V. cholerae O139 (non-O1 type)
• V. cholerae O1 is classified into 2 major biotypes: Classic and El Tor.
• Currently, El Tor is the predominant cholera pathogen.
• Organisms in both biotypes are subdivided into serotypes according to the structure of the O antigen, as follows:
• Serotype Inaba - O antigens A and C
• Serotype Ogawa - O antigens A and B
• Serotype Hikojima - O antigens A, B, and C
 TRANSMISSION
Cholera is transmitted by the fecal-oral route
through contaminated water & food.

Person to person infection is rare.

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 blood group “O” are more

susceptible; the cause is unknown.

Subjects with reduced gastric acid.

 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 & more
watery over time.
CLINICAL PICTURE/2
The classical textbook “rice water”
diarrhea, which describes fluid stool with
very little fecal material, appears within
24h from the start of the illness.

In severe cases stool volume exceeds 250

ml /kg leading to severe dehydration, shock
& death if untreated.
• The infectious dose of bacteria required to cause clinical
• disease varies with the mode of administration. If ingested
• with water, the infectious dose is 103-106 organisms. When
• ingested with food, fewer organisms are required to
• produce disease: 102-104 organisms. 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
 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/2
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.
 LAB. STUDIES
• Direct microscopic examination: a Gram‐negative curved bacillus that is motile by means
of a single flagellum which is observed by Gram stain or by direct dark field examination
of the stool.
• Culture: routine differential media (triple sugar iron agar) in which the organism is
sucrose‐positive, lactose‐negative, and oxidase‐positive.
• These media used routinely to differentiate the organism from other intestinal bacteria.
• Selective media: Vibrio species has the ability to grow at a high pH or in bile salts (eg,
thiosulfate‐citrate‐bile‐sucrose‐agar [pH 8.6]).
• These media are recommended to facilitate isolation and lab diagnosis.
• Serotyping and biotyping: by immobilization tests in which specific antisera can be used.
• Classic and El Tor biotypes also can be identified using the same method.
• Hematological tests: In dehydrated patients, Hematocrit, serum‐specific gravity, and
serum protein are elevated. They generally have leukocytosis.
• Serum electrolytes: Serum sodium usually is low. Serum potassium levels are either
normal or low. Bicarbonate concentration usually is less than 15 mmol/L in severely
dehydrated patients and often is non-detectable. Calcium and magnesium levels are
usually high.
• Renal profile: Blood urea, nitrogen and serum creatinine are elevated.
• Blood glucose is elevated, and the arterial pH is usually low (metabolic acidosis).
• Other Tests: More recently, polymerase chain reaction (PCR) has been used with high
sensitivity and specificity.