3. Introduction
• Cholera is an ancient disease
• Since 1817, seven (7) cholera pandemics have been recorded. The pandemics
originated from the Indian subcontinent,
• The seventh pandemic of cholera began in 1961; by 1991 it has affected 5
continents and it continues till today. Recognised to be caused by the El Tor
biotype of V Cholerae O1.
• It is common in areas with civil unrest, war, natural disaster (flooding),
crowded living conditions and poor sanitation.
• It is an epidemic prone disease for notification on the integrated disease
surveillance And response Platform in Nigeria (IDSR).
4. • Cholera is an intestinal infection caused
by Vibro cholerae.
• Comma shaped gram negative aerobic
or facultative anaerobic bacillus
• 1.3 um in length by 0.5-0.8um in
diameter.
• Antigenic structure: flagella H antigen
and somatic O antigen (determines
pathogenic and non-pathogenic strain).
• Epidemic cholera serogroup: V cholerae
O1 and V cholerae O139
• Current predominant pathogen the El
Tor biotype of V cholerae.
5. • Serotype Inaba: O antigens A
and C
• Serotype Ogawa: O antigens A
and B
• Serotype Hikojima: O antigens
A, B and C
• Disease caused by 0139 and
O1 strains are similar as they
both produce enterotoxin that
promote secretion of fluid and
electrolytes into the lumen of
the small intestine.
6. Epidemiology
• Cholera can be endemic, an epidemic or a pandemic disease.
• Worldwide : 1 – 4 million reported cases annually
• Mortality : 21,000 to 143,000
• US:Between January 1,1995 and 31st December 2000 61 cases were reported, 37
had travel-associated cases, 24 were acquired in the US.
• International travellers: 1 case per 500,000 population, range of 0.05-3.7 cases
per 100,000 population.
• Between 1970 and 2011, Africa reported 3,221,050 representing 46 % of all cases
reported globally.
• Sub-Saharan Africa accounted for 86 % of reported cases and 99 % of deaths
worldwide in 2011.
• CFR: 0 in many countries to 3.2% in Zambia, 5.2% in Angola and 6.8% in Cha
7. • Nigeria: cholera is endemic and seasonal (late weeks of February to October).
• first series of cholera outbreaks reported between 1970 and 1990.
• Major epidemics also occurred in 1992, 1995-1996, and 1997.
• January - October 2010: 37,289 cases mortality 1,434
• In 2011: 22,797 cases 728, case fatality rate of 3.2%
• Outbreaks were also recorded in 2018 with the NCDC reporting 42,466 suspected cases
including 830 deaths with a case fatality rate of 1.95% from 20 out of 36 States from the
beginning of 2018 to October 2018.
8. • The duodenum, and upper jejunum are
most affected, due to the volume of fluid
produced the absorptive capacity of the
large bowel is overwhelmed, with
resultant severe diarrhea,
shock(dehydration), acidosis (loss of
bicarbonate).
• The enterotoxin acts locally, it does not
invade the intestinal wall. Hence few
neutrophils are appreciated in the stool.
• 0139 Bengal strain: produces novel 0139
lipopolysaccharide (LPS) and an
immunologically related O-antigen
capsule. These enhance virulence and
resistance to human serum in vitro and
sometimes development of bacteremia.
9. • Enterotoxin : protein molecule composed
of 5 B subunits and 2 A subunits.
• B subunit binds to the Monosialosyl
ganglioside, GM1.
• A1 subunit activates adenylate cyclase,
increase cAMP.
• cAMP: blocks absorption of sodium and
chloride by the microvilli, whilst
promoting the secretion of Cl and water
by the crypt cells. Fluid, bicarbonate,
and potassium are lost with the osmotic
pull of the NaCl as it travels down the
intestine.
• Resulting in isotonic watery diarrhea.
10. Host Factors/Risk factor
• Poor sanitary conditions and water contamination
• Age: Children and elderly more susceptible
• Sex: Nil pridelection
• Raw /undercooked food :
• Immunocompromised more susceptible
• Hypochlorhydra: Low gastric acid levels
• Blood group: O greater than B greater than A greater than AB
11. Transmission
• Humans only reservoir
• Casual contact in unsanitary conditions
• Contamination of food and water
12. Communicability
• During acute stage
• Few days after recovery
• By end of week 70% non-nfectious
• By end of third week 98% non-infectious
13. Incubation
• Few hours to 5 says
• Average 1-3 days
• Shorter in people with high gastric pH and consumption of large doses of
bacteria
15. Clinical presentation
• Asymptomatic 75%
• mild 20%
• Severe 2-5%
• Painless watery diarrhea
• Vomiting
• Abdominal cramps
• Nil fever
• Death 18hrs to several days without
treatment.
16. • Cholera gravis : 5% of infected patients, severe watery diarrhea, vomiting,
and dehydration.
• Cholera sicca: ileus and abdominal distention from massive outpouring of
fluid and electrolytes into intestinal loops. High mortality from toxemia
before nausea and vomiting.
17. • Diarrhea: main symptom
• >5yrs : severe dehydration, from acute severe diarrhea (usually without
vomiting).
• >2yrs : acute watery diarrhea in an area where a cholera outbreak was
recorded.
• Volume: >240mL/kg body weight in 24hrs.
• Initially contain fecal matter and progress to opaque white liquid “rice
water” often not malodorous.
18. • Diarrhea: main symptom
• >5yrs : severe dehydration, from acute
severe diarrhea (usually without
vomiting).
• >2yrs : acute watery diarrhea in an
area where a cholera outbreak was
recorded.
• Volume: >240mL/kg body weight in
24hrs.
• Initially contain fecal matter and
progress to opaque white liquid “rice
water” often not malodorous.
19. • Dehydration: develop rapidly within
hours. Isotonic dehydration, which
can lead to Acute tubular necrosis,
and renal failure. When it is Severe,
dehydration can lead to vascular
collapse, shock and death.
• Tachypnea and hypercapnia due to
metabolic acidiosis.
20. • Metabolic/ systemic manifestations:
• Hypoglycemia: convulsion and coma
• Acidemia.
• Hypokalemia: K+ loss in stool, mean
serum K+ app 3.0mmol/L. children
can have normal serum K+ despite
severe K+ depletion.
• Hypocalcemia: rehydration with HCo3
containing fluids. Chvostek and
Trousseau sign present, and
spontaneous tetanic contractions.
22. Investigations
• Direct microscopic examination of stool (dark-field examination), gram stain,
culture and serotype and biotype identification.
• Hematologic test: hematocrit, serum specific gravity and serum protein are
elevated, leukocytosis without a left shift.
• Serum Na: 130-135 mmol/L, K+ normal initially and reduced after correction of
acidiosis, hyperglycemia (systemic release of epinephrine, glucagon, and cortisol).
• Raised BUN and Cr.
• Reduced HCO3: <15mmol/L
• Elevated anion gap (increase in serum lactate, protein and phosphate levels)
• Low arterial pH 7.2
• Mg and Ca elevated due to hemoconcentration
• PCR testing for screening food samples.
• Rapid test kits
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26.
27. Criteria for discharge
• Adequate oral intake Post hydration
• Normal urinary flow
• Maximum diarrhea flow of 400mls /hr
28. Prevention
• Multisectorial approach necessary (health, water and sanitation, fishery and
agriculture and education).
• Sanitation of water supply and making water safer (boiling and addition of
Chlorine).
• Appropriate hygiene for food preparation and personal hygiene.
• Sensitive surveillance and prompt reporting.
29. Vaccine
• 3 oral vaccines identified by the WHO
• Used mostly by travellers
• One vaccine consists of a monovalent killed whole-cell V cholerae O1 with
purified recombinant B-subunit of cholera toxoid (WC/rBS).
• Shanchol and ORCVAX are bivalent vaccines that are based on serogroups
O1 and O139
• CVD 103-HgR is a cholera vaccine developed by the Swiss Serum and
Vaccine Institute in Berne, Switzerland