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CHOLERA
Dr. Vikas
Assistant Professor
Community Medicine Dept.
SIMS
1
Cholera is an acute diarrheal illness caused by infection
of the intestine with the bacteria Vibrio cholerae.
CHOLERA
2
 A life-threatening secretory diarrhea induced by enterotoxin
secreted by V. cholerae
 Water-borne illness caused by ingesting water/food
contaminated by copepods infected by V. cholerae
 An enterotoxic enteropathy (a non-invasive diarrheal disease)
 A major epidemic disease
CHOLERA
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.
 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.
 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
 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.
 Cholera claimed 90,000 lives in Russia in 1866.
 The epidemic of cholera that spread with the Austro-Prussian
War (1866) is estimated to have claimed 165,000 lives in the
Austrian Empire.
 Hungary and Belgium both lost 30,000 people. In 1867, Italy lost
113,000 lives.
 1866 - Outbreak in North America. It killed some 50,000
Americans.
 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.
 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
 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.
 The 1902-1904 cholera epidemic claimed 200,222 lives in
the Philippines.
 The sixth pandemic killed more than 800,000 in India.
1961-1970s - 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.
January 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.
Recent Cholera Pandemics
 1-6th pandemic:
 1817- west bengal = home of cholera
 V. cholerae O1 biotype classical
 1817-1923, Asia, Africa, Europe, America and Australia
 7th pandemic:
 V. cholerae O1 biotype El Tor
 Began in Indonesia in 1961, reached India in 1964
 Spread to other continents in 1970s and 1980s
 Spread to Peru in 1991 and then to most of South & Central
America and to U.S. & Canada
 By 1995 in the Americas, >106 cases; 104 dead
 1993: Cholera in Bengal caused by O139
may be cause of 8th pandemic
CHOLERA EPIDEMICS IN ENGLAND
1831-1832 - 22,000 deaths
1848-1849 - 52,000 deaths
1853-1854 - John Snow’s work
It was against this background of confusion that
John Snow carried out his work.
John Snow mapped cases of
cholera to help give him clues
about the cause.
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.
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.
REMOVAL OF THE PUMP HANDLE.
John Snow recommended
the pump should not be used
and that it’s handle should be
removed.
THE OUTBREAK SUBSIDED.
After the handle was removed the
outbreak subsided.
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 it’s source
upstream to cleaner water.
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)
1831-1832 - 22,000 deaths
1848-1849 - 52,000 deaths
1853-1854 - John Snow’s work
Massive public concern and sanitary
reform followed.
Final epidemic was in 1866 there
were only around 2,200 deaths.
VIBRIO CHOLERA
The organism that causes cholera
was discovered 25 years after John
Snow’s death by Robert Koch
Cholera was prevalent in the 1800s, but due to
proper treatment of sewage and drinking water,
has become rare in developed countries.
Cholera is a fecal disease, meaning that it
spreads when the feces of an infected person
come into contact with food or water.
Incidence: 1 in 100,000 worldwide.
EPIDEMIOLOGY
18
TYPICAL CHOLERA CURVE
19
DISTRIBUTION
20
• 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
 Grows in salt and fresh water
 Endemic in areas of poor sanitation (India and
Bangladesh ), transmitted by fecal-oral route
 Can survive and multiply in brackish water by infecting
copepods
 Only O1 and O139 are toxigenic and cause Cholera
disease
V. CHOLERAE
 Broad temperature & pH range for growth on media
 18-37C
 pH 7.0 - 9.0 (useful for enrichment)
 Grow on variety of simple media including:
 MacConkey’s agar
 TCBS (Thiosulfate Citrate Bile salts Sucrose) agar
 V. cholerae grow without salt
 Most other vibrios are halophilic
Physiology of Vibrio
24
Incubation period: few hours – few days
Infective material: stool and vomitus of cases and carrier
Period of infectivity:
Case: 8-10 days
Convalescent carrier: 15-20 days
Chronic carrier: months to years
CLASSIFICATION: O1 ANTIGEN
小川型 稻叶型 彦岛
型
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
 Similarities to Enterobacteriaceae
 G-, Facultative anaerobes
 Fermentative bacilli
 Differences from Enterobacteriaceae
 Polar flagella
 Oxidase positive
 Formerly classified together as Vibrionaceae
 Primarily found in water sources
 Cause gastrointestinal disease
 Shown not closely related by molecular methods
Profile of vibrio cholerae
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
Incubation period 2hrs-5 days
most people do not become ill or show any symptoms
Only about 10-20% of infected people show moderate or
severe symptoms.
Moderate symptoms difficult to differentiate from other types
of acute diarrhoea
Group O blood group highest risk
30
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
severe dehydration Shock Renal failure
Death
COMPLICATIONS
32
SYMPTOMS
 Occur 2-3 days after consumption of contaminated
food/water
 Usually mild, or no symptoms at all
•75% asymptomatic
•20% mild disease
•2-5% severe
 Vomiting
 Cramps
 Watery diarrhea (1L/h)
 Without treatment, death in 18 h-several days
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
“cholera cots”.
One patient can have as much as 10-20 liters of diarrhea per day. This
type of fluid loss can cause fatal dehydration.
• 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
A very different type of life than what we are used to. Most
notably for today’s purposes, there is no sewage system.
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 clinic…
Drinking
contaminat
ed water.
eating raw
or
undercook
ed shellfish
CAUSES (TRANSMISSION MODE)
39
A. The following beliefs about causes of cholera
may reduce effectiveness of key messages:
Children’s stools are not dangerous
Soap is believed to wash away luck
B. The following practices increase risks:
 defecation often not followed by hand-washing
 Handshaking transfers bacteria directly from one person to
the next
40
HUMAN TO HUMAN TRANSMISSION
E.G. REFUGEE CAMPS
After heavy period of rainfall
When water temperatures rise
When normal diarrhoeal incidence increases
Endemic 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
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
LABORATORY DIAGNOSIS
• Visualization by dark field or phase microscopy
• Look like “shooting stars”
• Gram Stain
• Red, curved rods of bacteria
• Isolate V. cholerae from patient’s stool
• Plate on sucrose agar
• Yellow colonies form
Additional methods of detection include
PCR and monoclonal antibody-based
stool tests.
46
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
48
Concept behind Use of ORS
Skin
Intestine
Body
49
CHOLERA DIARRHEA
50
Salt
Salt
Salt
51
Salt
Salt
Salt
Salt
Salt
52
Salt
Salt
Salt
Salt
Salt
Net Flow of Water Net Flow of Water
53
HOW WOULD YOU TREAT THE
PATIENT USING OSMOSIS?
54
Salt
Sugar
Salt
Sugar
Salt
Sugar
Salt
Sugar
55
Salt
Sugar
Salt
Sugar
Salt
Sugar
Salt
Sugar
Salt
Sugar
Salt
Sugar
Salt
Sugar
Net Flow of Water
Net Flow of Water
56
57
WHAT HAPPENED TO
THE OSMOSIS WITH 80%
SUCROSE? WHY?
58
Sucrose
Solution
Water
Water
Water
Water
Osmosis59
Sucrose
SolutionNet Flow of Water Net Flow of Water
60
• Basic health education and hygiene
• Mass chemoprophylaxis
• Provision of safe water and sanitation
• Comprehensive Multidisciplinary Approach: water,
sanitation, education, and communication
PREVENTION
61
Blocking routes of transmission – water disinfection
(source and /or household), hand washing, sanitation,
good food hygiene and well-cooked
Cholera vibrio doesn’t like acid environment (block
with acidic water eg. With citrus juice, healthy stomach
acid levels, acid food)
62
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
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
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
THANK YOU
66

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Understanding Cholera: Causes, Symptoms, Treatment

  • 2. Cholera is an acute diarrheal illness caused by infection of the intestine with the bacteria Vibrio cholerae. CHOLERA 2
  • 3.  A life-threatening secretory diarrhea induced by enterotoxin secreted by V. cholerae  Water-borne illness caused by ingesting water/food contaminated by copepods infected by V. cholerae  An enterotoxic enteropathy (a non-invasive diarrheal disease)  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.  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.  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  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.  Cholera claimed 90,000 lives in Russia in 1866.  The epidemic of cholera that spread with the Austro-Prussian War (1866) is estimated to have claimed 165,000 lives in the Austrian Empire.  Hungary and Belgium both lost 30,000 people. In 1867, Italy lost 113,000 lives.  1866 - Outbreak in North America. It killed some 50,000 Americans.  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.  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  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.  The 1902-1904 cholera epidemic claimed 200,222 lives in the Philippines.  The sixth pandemic killed more than 800,000 in India. 1961-1970s - 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. January 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  1-6th pandemic:  1817- west bengal = home of cholera  V. cholerae O1 biotype classical  1817-1923, Asia, Africa, Europe, America and Australia  7th pandemic:  V. cholerae O1 biotype El Tor  Began in Indonesia in 1961, reached India in 1964  Spread to other continents in 1970s and 1980s  Spread to Peru in 1991 and then to most of South & Central America and to U.S. & Canada  By 1995 in the Americas, >106 cases; 104 dead  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 Snow’s 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 it’s handle should be removed.
  • 13. THE OUTBREAK SUBSIDED. After the handle was removed the outbreak subsided.
  • 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 it’s 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 Snow’s 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 Snow’s death by Robert Koch
  • 18. Cholera was prevalent in the 1800s, but due to proper treatment of sewage and drinking water, has become rare in developed countries. Cholera is a fecal disease, meaning that it spreads when the feces of an infected person come into contact with food or water. Incidence: 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.  Grows in salt and fresh water  Endemic in areas of poor sanitation (India and Bangladesh ), transmitted by fecal-oral route  Can survive and multiply in brackish water by infecting copepods  Only O1 and O139 are toxigenic and cause Cholera disease V. CHOLERAE
  • 23.  Broad temperature & pH range for growth on media  18-37C  pH 7.0 - 9.0 (useful for enrichment)  Grow on variety of simple media including:  MacConkey’s agar  TCBS (Thiosulfate Citrate Bile salts Sucrose) agar  V. cholerae grow without salt  Most other vibrios are halophilic Physiology of Vibrio
  • 24. 24 Incubation period: few hours – few days Infective material: stool and vomitus of cases and carrier Period of infectivity: Case: 8-10 days Convalescent carrier: 15-20 days Chronic carrier: months to years
  • 25. CLASSIFICATION: O1 ANTIGEN 小川型 稻叶型 彦岛 型
  • 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.  Similarities to Enterobacteriaceae  G-, Facultative anaerobes  Fermentative bacilli  Differences from Enterobacteriaceae  Polar flagella  Oxidase positive  Formerly classified together as Vibrionaceae  Primarily found in water sources  Cause gastrointestinal disease  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. Incubation period 2hrs-5 days most people do not become ill or show any symptoms Only about 10-20% of infected people show moderate or severe symptoms. Moderate symptoms difficult to differentiate from other types of acute diarrhoea Group 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
  • 32. severe dehydration Shock Renal failure Death COMPLICATIONS 32
  • 33. SYMPTOMS  Occur 2-3 days after consumption of contaminated food/water  Usually mild, or no symptoms at all •75% asymptomatic •20% mild disease •2-5% severe  Vomiting  Cramps  Watery diarrhea (1L/h)  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 “cholera cots”. 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 today’s 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 clinic…
  • 39. Drinking contaminat ed water. eating raw or undercook ed shellfish CAUSES (TRANSMISSION MODE) 39
  • 40. A. The following beliefs about causes of cholera may reduce effectiveness of key messages: Children’s stools are not dangerous Soap is believed to wash away luck B. The following practices increase risks:  defecation often not followed by hand-washing  Handshaking transfers bacteria directly from one person to the next 40
  • 41. HUMAN TO HUMAN TRANSMISSION E.G. REFUGEE CAMPS
  • 42. After heavy period of rainfall When water temperatures rise When normal diarrhoeal incidence increases Endemic 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 “shooting stars” • Gram Stain • Red, curved rods of bacteria • Isolate V. cholerae from patient’s 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
  • 53. Salt Salt Salt Salt Salt Net Flow of Water Net Flow of Water 53
  • 54. HOW WOULD YOU TREAT THE PATIENT USING OSMOSIS? 54
  • 57. 57
  • 58. WHAT HAPPENED TO THE OSMOSIS WITH 80% SUCROSE? WHY? 58
  • 60. Sucrose SolutionNet Flow of Water Net Flow of Water 60
  • 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. Blocking routes of transmission – water disinfection (source and /or household), hand washing, sanitation, good food hygiene and well-cooked Cholera vibrio doesn’t 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