1. University of Khartoum
Faculty of Medicine
Department of Community Medicine
Cholera
Amal Ar. Osman

2. OUTLINES
• EPIDIMIOLOGY
• HISTORICAL BACKGROUND
• CAUSE
• TRANSMISSION
• DISTRIBUTION
• CLINICAL MANIFESTATION
• LABROTATY INVESTIGATION
• MANGMENT
• PREVENTION AND CONTROL

3. “Death moved continually about the ranks
of the army, not the death they had been
trained to meet unflinchingly…but a silent ,
unnoticed , almost ignominious summons,
scarcely less sudden and far more painful
than the bullet or the sword cut”
SIR WINSTON CHURCHIL 1899

4. Definition
Cholera is an acute intestinal infection
caused by ingestion of food or water
contaminated with the bacterium Vibrio
cholerae.
Every year, there are an estimated 3–5
million cholera cases and 100 000–
120 000 deaths due to cholera.
 The short incubation period of two
hours to five days, enhances the
potentially explosive pattern of
outbreaks.

5. Historical background
• The condition of ‘dehydrating
diarrhoea’ was mentioned around the time
of Hippocrates (460-377 BC)
• V. cholerae has caused seven worldwide
disease outbreaks or pandemics since
1817, killing millions of people and
infecting millions more.
• Cholera is now endemic in many countries

6. • Prior to 1850, it was thought that
cholera was caused by breathing in
bad air - miasma – and that
protection was offered by strong
smelling substances such as herbs
and camphor.

7. • Deaths in India between 1817 and 1860,
in the first three pandemics of the
nineteenth century, are estimated to have
exceeded 15 million people.
• Another 23 million died between 1865 and
1917, during the next three pandemics.
Cholera deaths in the Russian Empire
during a similar time period exceeded
2 million

8. • 1816–1826: The first cholera pandemic, began
in Bengal, and then spread across India into china
and Indonesia
• 1829–1851: A second cholera pandemic
reached Russia ,Hungary and Germany; it killed
150,000 people in Egypt that year. it reached
London and the United Kingdom (where more than
55,000 people died) and Paris 20,000 died (of a
population of 650,000)
• The epidemic reached Quebec, Ontario, Nova
Scotia and New York in the same year, and the
Pacific coast of North America by 1834
• Over 15,000 people died of cholera in Mecca in
1846

9. • 1852–1860: The third cholera pandemic
mainly affected Russia, with over one
million deaths
• It also spread in south east Asia , Chicago
, London ( ended after john snow
discovered the water source) , Venezuela
and brazil

10. • 1863–1875: The fourth cholera
pandemic spread mostly in Europe and
Africa. At least 30,000 of the 90,000
Mecca pilgrims died from the disease.
• 1881–1896: The fifth cholera pandemic,
the epidemic cost 250,000 lives in Europe
and at least 50,000 in the Americas

11. • 899–1923: The sixth cholera pandemic
had little effect in western Europe because
of advances in public health, but major
Russian cities and the Ottoman Empire
were particularly hard hit by cholera
deaths
• 961–1975: The seventh cholera
pandemic began in Indonesia reached
Bangladesh ,India ,soviet union and Japan

14. historyCholera outbreaks in sudan

15. • The first medical service in Sudan was
established by Turku-Egyptians after
1820was rudimentary and geared the military
machines and its knowledge of the most
serious diseases was limited.
• During the last century the classical cholera
was areal menace to the Sudan and the
several epidemics which hit the country were
not uncommonly heralded by severe famines

16. • A series of major cholera outbreak recurred
successively over practically every decade of the
century after the second pandemic
• The epidemic cycles of the cholera which
devastated the land and caused unprecedented
concern ,came either across the red sea from
Arabia or crept up the Nile from Egypt
• The disease presented grave problems in an
environment which lacked doctors and medical
equipment and its periodic onslaughts resulted in
a frightful mortality rate.

17. • The Sudan faced more than 7 epidemics of cholera during the
ninetieth century several of them were associated with
drought and famine
• 1831 was brought by pilgrims returning from Mecca through
Egypt
• 1835-1837 cholera displayed great activity in Egypt , the
Sudan and Ethiopia
• 1849 by Mecca pilgrims and the ship traffic across the red
sea
• 1857 from Egypt
• 1865 the infection was carried across the red sea from
Jeddah to Suakin and Massawa and penetrated from there
into heartland of Sudan and Ethiopia
• 1872 via Mecca across the red sea
• 1889-1890 after Abyssinian war (Mahadist against king john
of Ethiopia) the epidemic extended over the whole of the
Sudan and ran along the banks of the river Nile as far as
Egypt
• 1896 creep up the Nile from Cairo down to Sudan

18. • During the last century classical cholera
was not detected in Sudan ; the vigorous
enforcement of the international sanitary
regulations under the British medical
administration was a major factor in
ending a century of tragic experience with
this much dreaded disease.

19. 2009

21. Causative Organism
• Vibrio consists of Gram-negative
rods, motile by means of a single
polar flagellum. Vibrios are capable
of both respiratory and fermentative
metabolism.
• O2 is a universal electron acceptor

22. • Most vibrios have relatively simple
growth factor requirements and will
grow in synthetic media with
glucose as a sole source of carbon
and energy. However, since vibrios
are typically marine organisms,
most species require 2-3% NaCl or
a sea water base for optimal
growth.

23. Vibrios are one of the most
common organisms in surface
waters of the world.
They occur in both marine and
freshwater habitats and in
associations with aquatic animals.

24. • V. cholerae and V. parahaemolyticus
are pathogens of humans. Both
produce diarrhea, but in ways that are
entirely different.
• V. parahaemolyticus is an invasive
organism affecting primarily the colon;
• V. cholerae is noninvasive, affecting
the small intestine through secretion of
an enterotoxin.
• Vibrio vulnificus is an emerging
pathogen of humans. This organism
causes wound infections,
gastroenteritis, or a syndrome known
as "primary septicemia

25. Vibrio cholerae

27. • V.Cholerae are killed within 30 mins. by
heating at 56deg c or within few seconds
by boiling . They remain in ice for 4-6 days
or longer .
• Drying and sunshine will kill them in few
hours , while coal tar disinfectant can
easily destroy them
• ElTor tends to be more resistant than
classical biotype

28. • There are two serogroups of V.
cholerae – O1 and O139 – cause
outbreaks. V. cholerae O1 causes
the majority of outbreaks, while
O139 is confined to South-East
Asia.
• Non-O1 and non-O139 V. cholerae
can cause mild diarrhea but do not
generate epidemics.

29. • Recently, new variant strains have
been detected in several parts of
Asia and Africa. Observations
suggest that these strains cause
more severe cholera with higher
case fatality rates

30. • In any single epidemic , one
particular serogroup or biotype
tends to be dominant, but serotype
switching is commonly seen in
cholera epidemics worldwide and is
thought to be driven by the
development of population
immunity to the circulating serotype

31. • El Tor vibrios may be distinguished from
the classical vibrios by the following tests :
1. ElTor vibrios agglutinate chicken and
sheep erythrocytes
2. They are resistant to classical phage IV
3. The VP reaction and haemolytic tests do
not give consistent results

32. • Epidemiologically , cholera due to EL Tor
biotype differs from the classical in the
following
1. Higher incidence of mild and
asymptomatic infections
2. Fewer secondary cases
3. Chronic carriers
4. The organism survives more in the extra
intestinal environment

34. Reservoir
• Include both human and
environment
• Human could be 1-case or 2-
carrier
• 75% of patients doesn’t develop
any symptoms and remain infective
for 7-14 days
• Carriers are usually temporal and
rarely chronic

35. • Cholera transmission is closely
linked to inadequate environmental
management.
• Transmission occurs from man to
man via
1. fecally contaminated water
2. Contaminated food and drinks
3. Direct contact “ secondary
transmission)

36. Bottle feeding could be a significant risk
factor for infants
Fruit and vegetables washed with
contaminated water could be a source of
infection
Cooked food may be contaminated by
handling or flies

37. • Cholera remains a global threat to
public health and a key indicator of
lack of social development

38. Incubation period
• From few hours up to 5 days , Commonly
1-2 days

39. Infective dose
• Cholera is a dose related disease .
• Infection occurs when the number of
vibrios ingested exceed that infective for a
particular individual
• Expermintal work suggest that a very high
dose in a normal person 10)11 organism is
required for producing clinical disease

40. pathophysiology

41. • V. cholerae cells enter the body
and make their way through the
digestive system.
• Approximately two-thirds survive the
acidic conditions of the stomach;
survivors conserve energy
until they enter the small intestine
where they begin production of their
flagella

42. • The flagellum propels each Vibrio cell
forward through the mucus layer to the
intestinal wall.
• V. cholerae also produces enzymes that
digest the layers of mucus, which helps
with access to the epithelial cells lining the
intestine, as well as detachment from cells
that are being
lost due to the body’s defense
mechanisms.

43. • Then it start production of hairlike
appendages called frimbriae or pili which
are formed on the bacterial cell surface.
These structures are made of protein and
allow the bacteria to attach to the lining of
the intestine.
• Growth: For symptoms to persist, the
bacteria must continue to multiply in the
intestine.
• in the intestine, the bacteria invade the
host cell. Production of CT is the final
stage in pathogenesis.

47. Host factors
• Attack rate is higher in children
• Gastric acidity
• Immunity
• availability of surface receptors for CT
on the host cell surface
• Blood group O
Environmental factors
• Contaminated water and food

48. immunology
• Protective immunity in those exposed to cholera is
induced almost exclusively by antibodies produced
in the intestine.
• These antibodies prevent bacterial colonisation and
multiplication, and they inactivatethe CT.
Immunoglobulins IgA, IgG and IgM have all been
detected, although IgA is the most important.
• The antibodies prevent the CT from binding with
receptors on the cell surface. Natural immunity is
provided by IgM followed by a switch to IgG.
• There is a 3- year period post infection where
patients
remain immune to cholera as a result of acquired,
natural immunity.

49. Clinical manifestations

50. • The severity of the disease
depends on the rapidity and
duration of fluid loss
• 90% of ElTor cases are mild and
clinically indistinguishable from
other acute diarrheas

51. • Typical case of cholera shows 3 stages :
 stage of evacuation
Stage of collapse
Stage of recovery

52. • An acute bacterial enteric disease
characterized in its severe form by
sudden onset ,profuse, painless ,
effortless watery diarrhea
• Nausea and profuse vomiting occur
early in the course of illness

53. Watery diarrhea
Cholera
stool
Rotavirus
stool
ETEC
stool
Shigella
stool

54. Complications
• Rapid dehydration
• Acidosis
• Circulatory collapse
• Hypoglycemia in children
• Renal failure
• Electrolyte imbalance (Na ,Ca)
• In severely dehydrated cases (cholera
gravis ) death occurs within few hours
and case fatality rate is up to 50%

55. Diagnosis

56. • Collection of stool:
1. By rubber catherter
2. Rectal swab

57. • For clinical purposes a quick
presumptive diagnosis can be
made by dark field or phase
microscopic visualization of vibrios
in stool moving like “shooting stars “
inhibited by preservative free
serotype specific anti serum

58. • The etiology is confirmed by
isolation if v.cholerae serogroups
from a stool specimen
• Ideally the isolated serogroup
should be tested for cholera toxin
production or cholera toxin gene
sequences (ctxA)
• Strains that don’t possess cholera
toxin can lead to acute watery
diarrhea but not causing cholera or
epidemic

59. • One – step dipstick tests for rapid
antigen detection of V.cholerae O1
and O139 are available and has
shown promise in initial field
evaluation : however these tests do
not yield isolates for subtypes or
antimicrobial resistance .

60. • In epidemics , once laboratory
confirmation and antibiotic susceptibility
have been established its is un necessary
to confirm all subsequent cases . A shift
should be made to the primary use of
WHO clinical case definition of cholera
surveillance as follows :

61. 1. Disease unknown in area : severe
dehydration or death from acute watery
diarrhea in a patient aged 5 years or
older
2. Endemic cholera : acute watery
diarrhea with or without vomiting in
patient aged 5 years or older
3. Epidemic cholera : acute watery
diarrhea with or without vomiting in any
patient

62. • Prolonged outbreak should include
periodic lab confirmation and anti microbial
susceptibility testing of small proportion of
cases to monitor for anti microbial
resistance

65. Treatment

66. Treatment
• Cholera is an easily treatable disease. Up
to 80% of people can be treated
successfully through prompt administration
of oral rehydration salts (WHO/UNICEF
ORS standard sachet)

67. • Very severely dehydrated patients require
administration of intravenous fluids. &
appropriate antibiotics to diminish the
duration of diarrhea, reduce the volume of
rehydration fluids needed, and shorten the
duration of V. cholerae excretion

68. • In order to ensure timely access to
treatment, cholera treatment centers
(CTCs) should be set up among the
affected populations.
• With proper treatment, the case fatality rate
should remain below 1%.

71. • Mass administration of antibiotics is not
recommended, as it has no effect on the
spread of cholera and contributes to
increasing antimicrobial resistance.

72. Steps for successful treatment
1. Assessment of dehydration
2. Rehydration
3. Reassessment of fluid imbalance
4. Antibiotic treatment
5. Avoid/managing complications
6. Zinc for under five
7. When to discharge
8. Consider other conditions
Courtesy of Dr. Ahmed Elamin
FMOH-Epidmology department

73. Assessment of dehydration
• At triage station
Courtesy of Dr. Ahmed Elamin
FMOH-Epidmiology department

74. Ask about:
No
dehydration
Some
dehydration
Severe
dehydration
Diarrhea < 4 /day 4 to 10 motion > 10 episode
Vomiting rare Sometimes Frequent
Thirst None Drinks eagerly and/
or is
Thirsty
Unable to drink
Urine Normal amount Small in amount
and yellowish
No urine for > 6 hours
Courtesy of Dr. Ahmed Elamin
FMOH-Epidmiology department

75. Observe the:
No
dehydratio
n
Some
dehydration
Severe
dehydration
General
condition
Well/ alert Restless/ irritable Lethargic/
unconscious
Eyes Normal Sunken Very sunken
breathing normal Faster than normal Very fast and
deep
Anterior fontanel Normal Sunken Very sunken
Courtesy of Dr. Ahmed Elamin
FMOH-Epidmiology department

76. Examine the:
No dehydration Some
dehydration
Severe
dehydration
Skin pinch Goes back
quickly
Goes back slowly
(≥2 seconds)
Goes back very
slowly
(≥3 seconds)
Radial pulse Full volume Low volume Weak/absent
Courtesy of Dr. Ahmed Elamin
FMOH-Epidmiology department

77. Treatment of some dehydration
Age Weight (kg) Amount of ORS in first
FOUR* or SIX* hours (ml)
<4 months <5 200 - 400
4-11 months 5 – 7.9 400 - 600
1-2 years 8 – 10.9 600 - 800
2-4 years 11 – 15.9 800 - 1200
5-14 years 16 – 29.9 1200 - 2200
>14 years ≥ 30 2200 - 4000
60 4200
70 About 5 liters
Courtesy of Dr. Ahmed Elamin
FMOH-Epidmiology department

78. Maintain rehydration with ORS
Age Approximate ORS amount
following each stool; By
milliliters (ml)
Approximate ORS amount
following
each stool; By household
Measures
Children <2
years
50-100ml 10-20 teaspoons
2-10 years 100-200ml 0.5 - 1 glass
>10 years As much as is
Tolerated
Minimum 1 glass

79. Correction of severe dehydration with IV
fluid
Age Amount of time to give first
30ml/kg
Amount of time to give
remaining 70ml/kg
≥ I year 1 hour 5 hours
< I year 0.5 hour 2.5 hours
Courtesy of Dr. Ahmed Elamin
FMOH-Epidmiology department

80. Regular reassessment of patients:
1. General well-being
2. Vital signs
3. Amount of stool and vomit
4. Look for co-morbid conditions
Courtesy of Dr. Ahmed Elamin
FMOH-Epidmiology department

81. Antibiotics for cholera some and severe
Antibiotics Adults Children
Doxycycline (one dose) 300 mg Not drug of
choice
Tetracycline (3 days) 500 mg/12 hours
Erythromycin (for children and
pregnant women)
250 mg/6 hours 12.5mg/kg/6hour
s
Courtesy of Dr. Ahmed Elamin
FMOH-Epidmiology department

82. Antibiotics for cholera some and severe
• ALWAYS check antimicrobial sensitivity
patterns in your area before dispensing
drugs for cholera:
Courtesy of Dr. Ahmed Elamin
FMOH-Epidmiology department

83. Other recommended antibiotics
Antibiotics Adults Children
Azithromycin 1 g single dose 20 mg/ kg single
dose with max of 1 g
Trimethoprim(TMP)-
Sulfamethoxazole (SMX)
TMP 160 mg and SMX
800 mg 2 times a day for
3 days
TMP 5 mg/ kg and SMX
25 mg/ kg 2 times a day
for 3 days
Ciprofloxacin 500 mg 2 times a day for
3 days***
15 mg/ kg 2 times a day
for 3 days
Courtesy of Dr. Ahmed Elamin
FMOH-Epidmiology department

84. Zinc supplement
• All children aged 5 years and younger
should be given zinc treatment in addition
to fluids and antibiotics as needed.
• Zinc treatment has been shown to
decrease the severity and duration of an
acute diarrheal episode and to decrease
the severity and incidence of subsequent
diarrheal episodes for 2-3 months in
children under 5.

85. Zinc supplement
Age Dose of zinc Duration
0 – 6 months 10 mg once a day 10 – 14 days
6 months – 5 years 20 mg once a day 10 – 14 days

86. Outbreak response
• Once an outbreak is detected, the
usual intervention strategy is to
reduce deaths by ensuring prompt
access to treatment, and to control the
spread of the disease by providing
safe water, proper sanitation and
health education for improved hygiene
and safe food handling practices by
the community.
• The provision of safe water and
sanitation is a formidable challenge
but remains the critical factor in
reducing the impact of cholera

87. Prevention & control

88. Prevention & control
• A multidisciplinary approach based on
prevention, preparedness and response,
along with an efficient surveillance system, is
key for mitigating cholera outbreaks,
controlling cholera in endemic areas and
reducing deaths.

90. Vaccination
• There are two types of safe and
effective oral cholera vaccines.
• Both are whole-cell killed vaccines,
one with a recombinant B-sub unit,
the other without.
• Both have sustained protection of
over 50% lasting for two years in
endemic settings.

91. • Both vaccines are administered in
two doses given between seven
days and six weeks apart.
• The vaccine with the B-subunit
(Dukoral) is given in 150 ml of safe
water.

92. • Both vaccines are WHO-prequalified and
licensed in over 60 countries.
• Dukoral this is a whole-cell, killed V. cholerae
O1 vaccine with part of the CT
protein.
• Has been shown to provide short-term
protection of 85–90% against V. cholerae O1
among all age groups at 4–6 months following
immunization, though protection declines after
6 months in young children and remains at
about 60% in older children and adults after 2
years.
• Dukoral also provides short-term protection
against Escherichia coli enterotoxin, which is
of added benefi to travellers.

93. • (Shanchol) provides longer-term
protection against V. cholerae O1
and O139 in children under five
years of age.

94. • CVD 103-HgR (Orochol) – this
vaccine consists of an attenuated,
live, genetically modifid V. cholerae
O1 Inaba strain that has been
engineered to produce part of the CT.
• It confers high protection (95%)
against O1 (Classical and El Tor) in
virgin volunteers.
• Orochol is the only vaccine available
as a single dose, which, due to
administration logistics, is more viable
for pre-emptive and long-term
outbreak control in ongoing fild
conditions according to WHO.
• However, due to a lack of evidence
for its effectiveness, the vaccine was
withdrawn in 2004.

95. • WHO recommends that
immunization with currently
available cholera vaccines be used
in conjunction with the usually
recommended control measures in
areas where cholera is endemic as
well as in areas at risk of outbreaks.
Vaccines provide a short term effect
while longer term activities like
improving water and sanitation are
put in place.

96. • When used, vaccination should
target vulnerable populations living
in high risk areas and should not
disrupt the provision of other
interventions to control or prevent
cholera epidemics.
• The use of the parenteral cholera
vaccine has never been
recommended by WHO due to its
low protective efficacy and the high
occurrence of severe adverse
reactions.

98. Travel & Trade
• no country requires proof of cholera
vaccination as a condition for entry
• Isolated cases of cholera related to
imported food have been
associated with food in the
possession of individual travelers

99. Situation in south Sudan
• As of 27 July 2015, a total of 1,399
cholera cases including 42 deaths (CFR
3%) have been reported in Juba
and Bor Counties in Central Equatoria and
Jonglei States respectively.
• The initial cases in Juba were traced back
to 18 May 2015 in UN House PoC where
the first cholera case was
confirmed on 1 June 2015.

100. • Cholera was eventually confirmed on
1 June 2015 in Juba after Vibrio
cholerae inaba was isolated from the
one of five samples tested in the
National Public Health Laboratory.
• Since 6 June 2015, sustained and
consistently increasing community
transmission was established in Juba
with increasingly more suspect cases
reported outside UN House Po

102. • The probable risk factors fueling transmission
include: residing in a crowded IDP camp with
poor sanitation and hygiene; using untreated
water from the Water tankers; lack of
household chlorination of drinking water;eating
food from unregulated roadside food vendors
or makeshift markets; open defecation/poor
latrine use; and attending/eating food at a
funeral

103. • The most affected age groups in
Juba and Bor counties are children
under five and 5-9 years
olds.Additionally, a significant
number of cases have occurred
among 25-29 year olds in Juba
County

105. References
1. 1- Todar’s online text book of bacteriology, Vibrio cholerae
and Asiatic Cholera (page1)
http://textbookofbacteriology.net/cholera.html
2. Cholera fact sheet,WHO,
http://www.who.int/mediacentre/factsheets/fs107/en/
3. Cholera ,death by diarrhea by Vicki Symington, The
Society for General Microbiology,
http://www.microbiologyonline.org.uk/media/transfer/doc/fact
file_cholera.pdf
4. Cholera , wikepidia the free enyclopedia ,
https://en.wikipedia.org/?title=Cholera
5. control of communicable disease manual 20th edition
6. Park’s text book of preventive &social medicine edition 22
7. Presentaion from Dr .ahmed mohamed Fmoh epidimiology
directorate