GASTROINTESTINAL DISEASES

CHOLERA

UNIVERSITY OF LUSAKA – MEDICAL SCHOOL

CONTENTS

 General Structure of the GIT and Function

 Characteristics of V. Cholerae
 Structure
 Classification
 Transmission
 Pathophysiology
 Signs and symptoms
 Laboratory diagnosis
 Treatment
 Prevention and control measures
The Gastrointestinal Tract (GIT)
FUNCTIONS - GIT

 Ingestion – taking foods and liquids into the mouth (eating and
drinking)
 Secretion – Water, acids, buffers, and enzymes into the lumen of the
tract
 Mixing and propulsion – Alternating contractions and relaxations of
smooth muscle in the walls of the GIT mix food and secretions and
propel them towards the anus
 Digestion – Mechanical and chemical processes break down ingested
food into smaller molecules.
FUNCTIONS - GIT

 Absorption – entrance of ingested and secreted fluids, ions, and the

products of digestion into the epithelial cells lining the lumen of GIT

 Defecation – Wastes, indigestible substances, bacteria, cells

sloughed from the lining of the GIT, and digested materials that were
not absorbed leave the body through the anus. (faeces or stool)
CHOLERA – General characteristics

 Vibrio cholerae is a bacterium that causes cholera (diarrhoeal

disease)

 It belongs to the family Vibrionaceae and the genus vibrio

 It is gram – negative, motile, flagellated curved rod (coma shaped)

 Species of the bacteria are grouped into Vibrio cholerae and non –
Vibrio cholerae

 Not all vibrio species cause the disease cholera

CLASSIFICATIONS OF V. CHOLERAE STRAINS

 Strains are divided according to differences in their cell wall

composition (O antigens)
 Basis of serotyping scheme that classifies V. cholerae into 139
serogroups
 All pandemic strains agglutinate with a single antiserum designated
01
 The 01 type V. cholerae is further separated into three groups: Inaba,
Ogawa, and Hikojima
 Serogroups are important for epidemiologic studies
CLASSIFICATIONS OF V. CHOLERAE STRAINS

 Epidemic strains of serovar 01 may further be divided into the classic

and EI Tor

 EI Tor is an actively haemolytic biotype of V. cholerae

 It is responsible for most current epidemic outbreaks of cholera

 V. cholerae 01, Ogawa serotype was responsible for the 2017 – 2018
cholera outbreak in Lusaka, Zambia
TRANSMISSION

 V. Cholerae is transmitted by the faecal – oral route when water

supplies become faecally contaminated (water bone disease)

 Mean infective dose is 10p8 – 10p10 CFU

 Transmission can also occur by ingesting contaminated food e.g.

uncooked shellfish, sea foods collected from polluted water sources

 Marine shellfish and plankton are important reservoirs of V. cholerae

TRANSMISSION

 Epidemics occur in crowded living conditions where there is poor

sanitation and water supplies

 In such areas, food safety and hygiene are inadequate

 Risk of cholera epidemics is high following natural or man – made

disasters (flooding)

 Causes faecal contamination of the environment and water supplies

and lack of clean drinking water
TRANSMISSION
TRANSMISSION

 V. Cholerae and other members of the genus are strongly associated

with brackish (salty) waters (Estuaries)

 They can also be spread in contaminated fresh water

 The bacteria form biofilms and colonize copepods, algae and aquatic
plants and plankton (aids the survival of bacteria)

 The bacteria is still highly infectious at this stage

PATHOPHYSIOLOGY - CHOLERA

 V. cholerae 01 and 0139 cause non – inflammatory diarrhoeal

disease (no tissue invasion)
 The bacterium produces a powerful enterotoxin which comprises
subunits A and B (disrupts normal exchange of water and electrolytes
- Na, K, bicarbonate)
 The B subunit binds to the receptors on the intestinal cells, enabling
the A subunit to enter the cells
 Inside the cells, the A subunit activates the enzyme adenylate cyclase
 This in turn increases the levels of cyclic adenosine monophosphate
(cAMP)
PATHOPHYSIOLOGY - CHOLERA

 This causes hypersecretion of fluids and electrolytes into the lumen of

the intestines following the disturbance of normal muscular contractions

 Eventually becomes severe and almost continuous watery diarrhoea

associated with cholera (rice water diarrhoea)

 In acute cholera, this rapid loss of fluid and electrolytes in vomit and
stools leads to severe dehydration (15 – 20 litres/day)

 If this is not corrected leads to renal failure and cardiac arrhythmia

PATHOPHYSIOLOGY - CHOLERA

 Death attributable to:

 Hypovolemic shock – due to abnormally low volume of circulating
fluid (plasma) in the body
 Metabolic acidosis – PH shifts toward acid side due to loss of
bicarbonate buffering capacity

 Incubation period is 2 – 5 days (mortality rates usually high)

PATHOPHYSIOLOGY - CHOLERA
LABORATORY DIAGNOSIS - MICROSCOPY

 V. Cholerae is a gram negative, motile, curved rod with a single

flagellum
LAB DIAGNOSIS – CULTURE (alkaline peptone water)

 V. Cholerae grows rapidly, producing growth (turbidity) on and just

below the surface of the medium (4 – 6 hours)

 Alkaline peptone water is an enrichment medium and its alkalinity

suppresses the growth of intestinal commensals

 To confirm vibrio, examine a wet preparation and a Gram – stained

smear
LAB DIAGNOSIS – CULTURE

 V. Cholerae is an aerobe and facultative anaerobe

 Grows over a wide temperature range of 16 – 40 degrees Celsius with
an optimum of 37 degrees Celsius
 Grows best at alkaline PH (PH 8.2)
 On TCBS, produces sucrose fermenting yellow colonies after
overnight incubation at 35 – 37 degrees Celsius
 All vibrio species are strongly oxidase - positive
LAB DIAGNOSIS – CULTURE
LABORATORY DIAGNOSIS – SEROTYPING AND RAPID
DIPSTICK TESTS

• V. Cholerae 01 and 0139 are serotypeable

• Separate antisera are required to identify V. Cholerae 01 (Inaba, Ogawa and

Hikojima) and V. Cholerae 0139 (Bengal)

• Isolates from TCBS cultures require sub culturing to nutrient agar before
carrying out serotyping
LABORATORY DIAGNOSIS – SEROTYPING AND RAPID
DIPSTICK TESTS

 Rapid dipstick tests to detect V. Cholerae 01 and 0139 in stool and

vomitus are available

 Easy to perform and low cost

 Most applicable in endemic countries for rapid diagnosis

 Known to give false positives, therefore, culture is more reliable.

PREVENTION AND CONTROL MEASURES

 Provision of clean drinking water

 Proper sewerage treatment and sanitation
 High standards of public and personal hygiene:
 Eating warm foods
 Always washing hands after using the toilet
 Thorough washing of food that does not need warming

 Vaccination – especially in endemic areas

PREVENTION AND CONTROL MEASURES

 Control of flies (vectors)

 Isolation of patients and safe disposal of stool and vomit

from the patients

 Identification of carriers and stopping them from working in

food industries
CONCLUSION

 V. Cholerae is gram negative, motile, flagellated, curved rod which

causes cholera
 V. Cholerae is transmitted by the faecal – oral route when water
supplies become faecally contaminated
 Serotypes 01 and 0139 cause non – inflammatory disease by producing
a powerful enterotoxin
 Several Laboratory techniques are available for V. Cholerae
 Water and electrolyte replacement are the priority strategy for cholera
treatment
 Cholera can be controlled by practicing high standard personal and
environmental hygiene