Knowledge on cholera in the SW region of Cameroon

Cholera

1. CHOLERA
DR MBUNTUM JASON FRANCIS
MD,MPH,MsC,MRCPH,Cert School Health

2. 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.

3. 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.
V CHOLERAE
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.

4. V. CHOLERAE

5. 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.
EPIDEMIOLOGY
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.

6. The outbreak was declared on 29 October
2021.
As of 30 April 2022,there was
6652 suspected cases of cholera including
134 deaths (CFR 2%) -
CHOLERA IN CAMEROON

7. Division Cases Deaths
SWR 4617 77
Littoral 1704 51
South 183 2
Central 125 4
North 15 0
Far North 8 0
CHOLERA IN CAMEROON

8. CHOLERA IN CAMEROON

9. CHOLERA IN CAMEROON

10. 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.

11. 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

12. 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 adhere to the epithelial surface, probably
by certain factor

13. 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

14. 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)

15. PATHOGENESIS/5
This substance inhibits the absorptive sodium
transport & activates the excretory chloride in the
intestinal cell→ accumulation of NaCl in the
intestinal lumen
This high osmolality is balanced by water
secretion, the result is watery diarrhea

16. 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/6

17. 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.

18. VIBRIO-CHOLERA
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

19. 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

20. TRANSMISSION
Cholera is transmitted by the fecal-oral
route through contaminated water & food.
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 10
3
-10
6
organisms.
When ingested with food, fewer organisms
are required to produce disease, namely 10
2
-
10
4
.
Person to person infection is not
so common.

21. 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.
TRANSMISSION/2

22. The same applies to patients with chronic
gastritis secondary to Helicobacter pylori
infection or those who have had a
gastrectomy
The use of antacids, histamine-receptor
blockers(CIMETIDINE), and proton-pump
inhibitors(Omeprazole) increases the risk of
cholera infection and predisposes patients
to more severe disease as a result of
reduced gastric acidity.
HOST SUSCEPTIBILITY

23. 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

24. 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.

25. 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.

26. 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.

27. LAB DIAGNOSIS
Organism can be seen in stool by direct
microscopy after gram stain & on dark
microscope where 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.

28. 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
Total body potassium is depleted, but
serum level may be normal due to effect of
acidosis.

29. 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.

30. 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
-:

31. 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)

32. 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.

33. 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.

34. 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.

35. PREVENTION
Education on hygienic practices.
Provision of safe, uncontaminated water
to the population.
Antibiotic prophylaxis to house-hold
contacts.
Vaccination against cholera.

36. 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.

37. Steps of epidemic control
Verification of the diagnosis
Early case finding & tracing source of
infection.
Establishment of treatment centers
Notification of the case to MOH & WHO.
Isolation & barrier nursing is indicated

38. THANKS FOR
YOUR
ATTENTION
roe