2. Cholera is an acute diarrheal illness caused by infection
of the intestine with the bacteria Vibrio cholerae.
CHOLERA
2
3. ď A life-threatening secretory diarrhea induced by enterotoxin
secreted by V. cholerae
ď Water-borne illness caused by ingesting water/food
contaminated by copepods infected by V. cholerae
ď An enterotoxic enteropathy (a non-invasive diarrheal disease)
ď A major epidemic disease
CHOLERA
4. 4
1. 1816-1826 - First cholera pandemic: the pandemic began in
Bengal, and then spread across India by 1820. 10,000 British
troops and countless Indians died during this pandemic.
2. 1829-1851 - Second cholera pandemic reached Russia , Hungary
and Germany in 1831, London and Paris in 1832.
3. 1852-1860 - Third cholera pandemic mainly affected Russia, with
over a million deaths. In 1853-4, London's epidemic claimed
10,738 lives.
ďś 1854 - Outbreak of cholera in Chicago took the lives
of 5.5% of the population. The Soho outbreak in
London ended after removal of the handle of the
Broad Street pump by a committee instigated to action
by John Snow.
ďś Deaths in India between 1817 and 1860 are estimated
to have exceeded 15 million persons. Another 23
million died between 1865 and 1917.
HISTORY
5. 5
ď 1863-1875 - Fourth cholera pandemic spread mostly in Europe and
Africa. At least 30,000 of the 90,000 Mecca pilgrims fell victim to the
disease.
ď Cholera claimed 90,000 lives in Russia in 1866.
ď The epidemic of cholera that spread with the Austro-Prussian
War (1866) is estimated to have claimed 165,000 lives in the
Austrian Empire.
ď Hungary and Belgium both lost 30,000 people. In 1867, Italy lost
113,000 lives.
ď 1866 - Outbreak in North America. It killed some 50,000
Americans.
ď 1881-1896 - Fifth cholera pandemic; According to Dr A. J. Wall, the
1883-1887 epidemic cost 250,000 lives in Europe and at least 50,000 in
Americas.
ď Cholera claimed 267,890 lives in Russia (1892); 120,000 in Spain;
90,000 in Japan and 60,000 in Persia. In Egypt cholera claimed
more that 58,000 lives.
6. 6
ď 1899-1923 - Sixth cholera pandemic had little effect in Europe
because of advances in public health, but major Russian cities
were particularly hard hit by cholera deaths.
ď The 1902-1904 cholera epidemic claimed 200,222 lives in
the Philippines.
ď The sixth pandemic killed more than 800,000 in India.
ď1961-1970s - Seventh cholera pandemic began in Indonesia, called
El Tor after the strain, and reached Bangladesh in 1963, India in
1964, and the USSR in 1966.
ďJanuary 1991 to September 1994 - Outbreak in South America,
apparently initiated when a ship discharged ballast water. Beginning
in Peru there were 1.04 million identified cases and almost 10,000
deaths.
7. Recent Cholera Pandemics
ď 1-6th pandemic:
ďˇ 1817- west bengal = home of cholera
ďˇ V. cholerae O1 biotype classical
ďˇ 1817-1923, Asia, Africa, Europe, America and Australia
ď 7th pandemic:
ďˇ V. cholerae O1 biotype El Tor
ďˇ Began in Indonesia in 1961, reached India in 1964
ďˇ Spread to other continents in 1970s and 1980s
ďˇ Spread to Peru in 1991 and then to most of South & Central
America and to U.S. & Canada
ďˇ By 1995 in the Americas, >106 cases; 104 dead
ď 1993: Cholera in Bengal caused by O139
may be cause of 8th pandemic
8. CHOLERA EPIDEMICS IN ENGLAND
1831-1832 - 22,000 deaths
1848-1849 - 52,000 deaths
1853-1854 - John Snowâs work
It was against this background of confusion that
John Snow carried out his work.
9. John Snow mapped cases of
cholera to help give him clues
about the cause.
10. BROAD STREET PUMP
Mapping of cases led John snow to
suspect water from the Broad street
pump as a cause of cholera.
He found that those who were affected
had drunk water from the pump.
11. BROAD STREET PUMP
He identified that a child at number 40
Broad street had been ill with cholera and
that sewage had probably contaminated
the well.
12. REMOVAL OF THE PUMP HANDLE.
John Snow recommended
the pump should not be used
and that itâs handle should be
removed.
14. THE GRAND EXPERIMENT
Two water companies supplied
one area. In 1949 both got water
direct from the Thames in
London. In 1954 the Lambeth
Company moved itâs source
upstream to cleaner water.
15. Comparison of risks of dying from
cholera
Southwark and Vauxhall water company
70 per 10,000 (London Source)
Lambeth water company 5 per 10,000 -
(Source from upstream of London)
16. 1831-1832 - 22,000 deaths
1848-1849 - 52,000 deaths
1853-1854 - John Snowâs work
Massive public concern and sanitary
reform followed.
Final epidemic was in 1866 there
were only around 2,200 deaths.
17. VIBRIO CHOLERA
The organism that causes cholera
was discovered 25 years after John
Snowâs death by Robert Koch
18. ďCholera was prevalent in the 1800s, but due to
proper treatment of sewage and drinking water,
has become rare in developed countries.
ďCholera is a fecal disease, meaning that it
spreads when the feces of an infected person
come into contact with food or water.
ďIncidence: 1 in 100,000 worldwide.
EPIDEMIOLOGY
18
21. ⢠Gram negative.
⢠Oxidase-positive,
⢠Facultative anaerobic,
⢠curved or comma-shaped rods
⢠Highly motile; polar flagellum
⢠Sensitive to low pH and die rapidly in
solutions below pH 6
⢠Proliferate in summers
⢠Pathogenic and nonpathogenic strains
⢠206 serogroups
VIBRIO CHOLERAE
21
22. ď Grows in salt and fresh water
ď Endemic in areas of poor sanitation (India and
Bangladesh ), transmitted by fecal-oral route
ď Can survive and multiply in brackish water by infecting
copepods
ď Only O1 and O139 are toxigenic and cause Cholera
disease
V. CHOLERAE
23. ď Broad temperature & pH range for growth on media
ďˇ 18-37ď°C
ďˇ pH 7.0 - 9.0 (useful for enrichment)
ď Grow on variety of simple media including:
ďˇ MacConkeyâs agar
ďˇ TCBS (Thiosulfate Citrate Bile salts Sucrose) agar
ď V. cholerae grow without salt
ďˇ Most other vibrios are halophilic
Physiology of Vibrio
24. 24
ďąIncubation period: few hours â few days
ďąInfective material: stool and vomitus of cases and carrier
ďąPeriod of infectivity:
ďąCase: 8-10 days
ďąConvalescent carrier: 15-20 days
ďąChronic carrier: months to years
26. SPECIFIC FEATURES OF ELTORE
26
1. Agglutinate chicken & sheep erythrocytes
2. Resistant to polymyxin B & phage IV
3. Survives in adverse condition
4. Produce more number of milder cases
5. Produces more number of carrier state
27. ď Similarities to Enterobacteriaceae
ďˇ G-, Facultative anaerobes
ďˇ Fermentative bacilli
ď Differences from Enterobacteriaceae
ďˇ Polar flagella
ďˇ Oxidase positive
ď Formerly classified together as Vibrionaceae
ďˇ Primarily found in water sources
ďˇ Cause gastrointestinal disease
ďˇ Shown not closely related by molecular methods
Profile of vibrio cholerae
28. V. cholerae
accumulates in
stomach
Produces toxins
Toxins will bind
to G-protein
coupled receptor
Inactivation of
GTPase
G- protein stuck
in "on" position
increase cAMP
activation of ion
channels
NaCl influx into
intestinal lumen
to drag water
into lumen
lead to watery
diarrhea
PATHOPHYSIOLOGY OF CHOLERA
28
29.
30. ďąIncubation period 2hrs-5 days
ďąmost people do not become ill or show any symptoms
ďąOnly about 10-20% of infected people show moderate or
severe symptoms.
ďąModerate symptoms difficult to differentiate from other types
of acute diarrhoea
ďąGroup O blood group highest risk
30
31. Most people remain asymptomatic. The symptoms of
cholera include :
SIGNS & SYMPTOMS
profuse, watery
diarrhea
stomach
pains
leg cramps Mild fever
Vomiting Sunken eyes
and cheeks
Dry mucous
membranes
Decreased
urinary output
31
33. SYMPTOMS
ď Occur 2-3 days after consumption of contaminated
food/water
ď Usually mild, or no symptoms at all
â˘75% asymptomatic
â˘20% mild disease
â˘2-5% severe
ď Vomiting
ď Cramps
ď Watery diarrhea (1L/h)
ď Without treatment, death in 18 h-several days
34. More severe symptoms
Rapid loss of body fluids
6 liters/hour
107 vibrios/mL
Rapidly lose more than 10% of
bodyweight
Dehydration and shock
Death within 12 hours or less
Death can occur within 2-3 hours
35. 35
âcholera cotsâ.
One patient can have as much as 10-20 liters of diarrhea per day. This
type of fluid loss can cause fatal dehydration.
36. ⢠Rare in developed countries
⢠Common in Asia, Africa, & Latin America
Poor sanitary
conditions
⢠Contaminated water, seafood, even in
developed countries.
⢠Especially shellfish.
Raw or
undercooked food
⢠People with low levels of stomach acid
⢠Such as children, older adults, and some
medications.
Hypochlorhydria
⢠Reasons aren't entirely clear
⢠Twice more likelyType O blood
RISK FACTORS
36
37. 37
A very different type of life than what we are used to. Most
notably for todayâs purposes, there is no sewage system.
38. 38
raw sewage literally flowing in the streets. Imagine you are a doctor in a
clinic here. One day a sick young woman enters your clinicâŚ
40. A. The following beliefs about causes of cholera
may reduce effectiveness of key messages:
ďąChildrenâs stools are not dangerous
ďąSoap is believed to wash away luck
B. The following practices increase risks:
ďą defecation often not followed by hand-washing
ďą Handshaking transfers bacteria directly from one person to
the next
40
42. ďąAfter heavy period of rainfall
ďąWhen water temperatures rise
ďąWhen normal diarrhoeal incidence increases
ďąEndemic cholera with good sanitation needs permanent
source of vibrio, but with poor sanitation higher secondary
transmission can maintain endemic status
WHEN DOES CHOLERA BECOME
EPIDEMIC?
42
43. DIAGNOSIS
Clinical diagnosis
Cholera should be considered
in all cases with severe watery
diarrhea and vomiting.
Traveling to affected areas and
eating shellfish
No distinguishing clinical
manifestations for cholera.
Differential diagnosis
Enterotoxigenic e. Coli
Bacterial food poisoning
Viral gastroenteritis
43
44. LABORATORY DIAGNOSIS
⢠Visualization by dark field or phase microscopy
⢠Look like âshooting starsâ
⢠Gram Stain
⢠Red, curved rods of bacteria
⢠Isolate V. cholerae from patientâs stool
⢠Plate on sucrose agar
⢠Yellow colonies form
45.
46. Additional methods of detection include
PCR and monoclonal antibody-based
stool tests.
46
47. Oral rehydration salts
⢠Up to 80% of cases can be treated through this.
Intravenous fluids (Ringer lactate)
⢠For severe cases.
Antimicrobial Therapy
⢠can diminish duration of diarrhea, reduce volume
of rehydration fluids needed, and shorten duration
of V. cholerae excretion.
TREATMENT
47
61. ⢠Basic health education and hygiene
⢠Mass chemoprophylaxis
⢠Provision of safe water and sanitation
⢠Comprehensive Multidisciplinary Approach: water,
sanitation, education, and communication
PREVENTION
61
62. ďąBlocking routes of transmission â water disinfection
(source and /or household), hand washing, sanitation,
good food hygiene and well-cooked
ďąCholera vibrio doesnât like acid environment (block
with acidic water eg. With citrus juice, healthy stomach
acid levels, acid food)
62
63. Parenteral Vaccine : killed
⢠2 doses administered 4 weeks apart
⢠Efficacy of approximately 50% and hardly exceeds 6 months
⢠Not recommended
Oral: Killed WC/rBS Vaccine :
⢠Killed whole-cell V.cholerae in combination with a recombinant B-subunit of cholera toxin
⢠2 doses 15 days apart
⢠Safe in pregnancy and breastfeeding
⢠Efficacy of approximately 50% after 3 years
⢠Only mild side-effects
Oral: Live, attenuated CVD 103-HgR Vaccine :
⢠Protection as early as 1 week after vaccination, with >90%
⢠Unknown efficacy for children under 2
⢠No adverse side-effects
VACCINES
63
64. The prognosis of cholera can range depending on the
severity of the dehydration and how quickly the
patient is given and responds to treatments.
Death (mortality) rates in untreated cholera can be as
high as 50%-60% during large outbreaks but can be
reduced to about 1% if treatment protocols are rapidly
put into action.
PROGNOSIS
64
65. Treatment
centers Set up treatment centers for prompt
treatment.
Sanitary
measures. food safety and animal health measures
Comprehensive
surveillance
data
(adapt to each situation) for a
comprehensive multidisciplinary approach.
CONTROLLING CHOLERA
65