CHOLERA/BACILLARY

DYSENTRY
Prof. G. N. Lule FRCP(E)

CHOLERA
Infection in the small intestine caused by
Vibrio cholerae.
Gram negative, comma shaped bacillus.
Several strains do exist, commonest being
Vibrio cholerae O1 and O139(serogroups)
Serotype O1 2 biotypes (classical and El Tor)
Each biotype classified as( Inaba or Ogawa)
El Tor now more common mild illness, more
carriers
Others types e.g. V.parahemolyticus

TRANSMISSION

Faecal oral spread

Epidemiology
Affects 3-5 million people world
wide ; 100 to 150,000 deaths per
year.
Remains an epidemic and endemic
in many areas of the world
(Developing)

History
Probably originated from Indian sub
continent(Ganges ),
Reported in Ganges delta since ancient
times.
Russia -1817, Europe, and then Africa
with the arrival of Europeans and other
traders in 10 th century.
Seven pandemics, seventh1961reached
Africa 1971, Americas 1991

Risk Factors
More than 100 million bacteria to cause
cholera in normal adults.
Increased incidence ;
in low gastric acid states.
Children especially below 5 years.
Blood group type O.(AB relative
protection).
People with low immunity eg HIV or
malnourished children

Selective advantage

Cystic fibrosis gene (heterozygous

carriers)

Transmission
Contaminated food or water
Lack of proper sanitation - in the
developing world Africa, Asia, S.America
etc
Overcrowding eg refugee camps, pilgrims ,
slums but can occur in any environment.
Eating sea food (shell fish and plankton)
in the West
Others

Incubation period

Hours to 5 days after ingestion of the

bacteria
For every infected person, 3-100
people do not develop disease.

Symptoms
Sudden onset of profuse painless
diarrhea and vomiting (10-20 litres of
water per day)
Rice water stools with fishy odour

Signs
Severe dehydration
Kidney failure
Other organ failure

Pathogenesis
Ingestion of bacteria - mostly killed
by stomach acid
Surviving bacteria stop activity
while passing through stomach
In small intestine, they penetrate
mucus to the intestinal wall
Vibrio cholerae produce toxins which
give infected person watery diarrhea

Cholera toxin
Made up of 6 sub units
1 type A sub unit ( A1 &A2)
5 type B sub units
B

B
B
s

A1 s
A2
B

MECHANISM
Cholera toxin has 5B subunits
surrounding A subunit
A subunit cleaved into A1 A2
segments.
B subunits binds ganglioside receptors
on intestinal epithelial cells.
This leads to internalisation of the A
subunit

In the Cell
The A1 A2 subunits separate
A1 stimulates ADP breakdown increasing
production cAMP
Increased cAMP change Na/Cl flux across
the cell membrane
Chloride flux followed by massive
outflow of water and electrolytes from
the cell
Leading to profuse (secretory) diarrhea.

Diagnosis
History
Clinical picture
Specimens: fresh stools and swab
samples
Rapid dip stick test determines
presence of V. cholera
Culture and sensitivity (antibiotic)

Enrichment media
Alkaline peptone water at PH 8.6
Monsurs taurocholate tellurite
peptone water at PH 9.2

Plating media
Alkaline bile salt agar (BSA)
Monsurs gelatin tauro cholate trypticase
tellurite agar (GTTA) medium:
TCBS medium: This is the mostly widely used
medium; it contains thiosulphate, citrate, bile
salts and sucrose. Cholera vibrios produce
flat, 2-3 mm diameter, yellow-nucleated
colonies
Serotyping by agglutination with specific cell
ags

Treatment
Fluids
oral rehydration treatment
(Ringers lactate with added K)
-Hospital made solution in severe
cases Intravenous

Antibiotics

Doxycycline
Cotrimoxazole
Erythromycin
Quinolones
Resistance strains emerging

Prognosis
Early diagnosis and treatment,
mortality less than 1%.
Untreated mortality 60%

Prevention

water purification
Proper disposal of infected feaces
Simple hygienic measures
Adequate water supplies
Health education especially pilgrims
Proper sanitation
Sterilization and treatment of faecal
waste

VACCINE
Vaccine mainly oral 2 in use Dukoral and
Sanchoi
Efficacy variable up to 60%..Short and long
term
Injectable vaccine available less effective
below 5 years..not WHO recommended.
Immunization of high risk groups
Antibiotic prophylaxis now not very
recommended.

BACILLARY DYSENTERY

DEFINITION

Frequent blood stained mucoid

stools (shigellosis)

Types of shigella
Shigella sonnei mild disease
Shigella flexneri mod severe
disease
Shigella boydii
Shigella dysenteriae most serious
(Shiga toxin)

Transmission
Faecal oral
Small number of organisms can cause
disease
Shigella bacteria invade the mucosal
cells only up to lamina- propria
Damage is caused by shigella
intracellular division and toxin
production.

Shiga toxin

Hemorrhagic colitis
Hemolytic uremic syndrome

Clinical picture
Diarrhea
Vomiting
Initially watery stools becoming
mucoid and blood stained
Fever
Severe dehydration
Constitutional symptoms

Rieter syndrome
Rieters syndrome associated with S
flexneri.
Chronic seronegative arthritis
Circulating bacterial antigen is the
cause
Genetically linked to HLA-B27 genotype

Investigations
Fresh stool specimen
Microscopy and culture
Selective media like: McConkeys agar,
Selenite F broth (0.4%) etc

Treatment
Oral fluids
Intravenous fluids
Where necessary, antibiotics
Ciprofloxacin or cotrimoxazole.
Others according to culture

Complications

Dehydration
Acute renal failure
Intestinal perforations
Rectal prolapse
Metabolic eg hypoglycaemia
CNS complications

Complications (Rare)
Mainly in severe disease /low
immunity;
1)Toxic megacolon
2)Haemolytic uraemic syndrome(HUS)

Differential Diagnosis

Other bacteria,protozoa etc

Inflammatory bowel diseaseeg
Ulcerative colitis, Crohns
Others eg Tuberculosis/
schistosomiasis

Prevention

Simple personal hygiene

Proper sanitation
Adequate water supply
Vaccine: - No vaccine available

THANK YOU