2. CHOLERA
• Is an acute diarrhoeal disease
caused by Vibrio Cholerae.
• Cases range from
symptomless to severe
infections
3. • Typical cases are chracterized
by the sudden onset of
profuse, effortless, watery
diarrhoea followed by
vomiting, rapid dehydration,
muscular cramps and
suppression of urine.
4. • Unless there is rapid
replacement of fluid and
electrolytes, the case fatality
may be high as 30 to 40 %
6. • Cholera transmission is closely
linked to inadequate
environmental management.
• Typical at risk areas include
peri urban slums with poor
basic infrastructure,
7. • A level of such instance could be
due to consequences of disaster
disruption of water and
sanitation system or due to
displacement of population due
to inadequate and over crowded
camps
8. • Cholera remains a high threat
to public health and a key
indicator of lack of social
development.
9. EPIDEMIOLOGICAL FEATURES
• Cholera is both an epidemic and
endemic disease.
• The epidemicity and endemicity of
the disease depends on
characteristics of the agent and the
prevailing environment.
10. • The characteristics of the agent
influencing its distribution
include its ability to survive, its
virulence, average number of
organism required to cause
infection.
11. • Epidemics of cholera are
characteristically abrupt and can
cause an acute public health
problem.
• The epidemics have potentials to
reach a peak and subside
gradually as the force of
infection declines.
12. • Often times by the time control
measures are instituted the
epidemic has already reached its
peak and is waning.
• Thus a cholera epidemic in a
community is self limiting.
13. • This is attributed to the
acquisition of temporary
immunity as well ass due to
occurrence of a large number of
clinical cases.
• The force of infection is
composed of force of infection
through water and force of
infection through living contacts.
14. • Therefore the elimination of
contaminated water does not
immediately bring an outbreak to
an end as the tail of epidemic is
produced due to continuation of
transmission through contacts.
15. • In areas where cholera is
endemic it does not show a
stable endemicity.
• It undergoes seasonal
fluctuations as well as
epidemic outbreaks.
18. AGENT FACTORS
• The agent that causes cholers is
named as Vibrio cholerae.
• Vibrio cholerae are killed within
30 min by heating at 56 deg C, or
with in a few seconds by boiling.
19. • They remain in ice for 4 – 6
weeks or longer.
• Drying and sunshine will kill
them in a few hours.
20. • They are easily destroyed by
coal-tar disinfectants such as
Cresol.
• Bleaching powder (6 mg/lit)
instantly kills the organism.
21. TOXIN PRODUCTION
• The vibrios multiply in the small
intestinal lumen and produce an
exotoxin (enterotoxin).
• This toxin produces diarrhoea
through its effect on the
adenylate cyclase-cyclic AMP
system of the mucosal cells of
the small intestine
22. • The endotoxin has no effect
on other tissues except the
intestinal epithelial cells
23. RESEVOIR OF INFECTION
• The human being is the only
known reservoir
• The individual may be a case or a
carrier
24. • Cases range from inapparent
infections to severe ones
• Individuals with low immunity
(undernourished children,
people with HIV) are at a greater
risk of death if infected
25. • It is the mild and asymptomatic
cases that play a significant role
in maintaining endemic reservoir
26. • Carriers are usually temporary,
rarely chronic
• They make an important
contribution to the reservoir of
infection
27. • Since carriers excrete fewer
vibrios than clinical cases,
carriers best detected by
bacteriological examination of
the purged stool induced by
administration of 30-60 g of
magnesium sulphate in 100 ml of
water by mouth
28. INFECTIVE MATERIAL
• The immediate source of infection
are the stools and vomit of cases
and carriers
• Large number of vibrios (107-1010
vibrios /ml of fluid) are present in
watery stools of patients
29. • An average patient excretes 10-
20 litres of fluid
• Carriers excrete fewer vibrios
than cases (102-105 vibrios / ml
stool)
30. INFECTIVE DOSE
• Cholera is dose related
• Infection occurs when the
number of vibrios ingested
exceeds the dose that is infective
for the individual
31. • Experiments suggests that in a
normal person a very high dose –
10 11 organism is required to
produce clinical disease
33. • Convalescent carriers are
infectious for 2-3 weeks and
chronic carrier state may last
from a month upto 10 years or
more
34. CARRIERS IN CHOLERA
• A cholera carrier may be defined
as an apparently health person
who is excreting V.cholerae
• Four types of cholera carriers
have been identified
35. • PRECLINICAL or INCUBATORY
CARRIERS:The incubatory
carriers are potential patients
(since the incubation period of
cholera is short ;1-5 days,
incubatory carriage is of short
duration)
36. • CONVALESCENT CARRIERS:
Patients who have recovered
from an attack of cholera may
continue to excrete vibrios
during the convalescence period
for 2-3 weeks
37. • Convalescent state has been
reported among patients who
have not received effective
antibiotic treatment
• The convalescent carriers can
often become chronic or long
term carriers
38. • CONTACT or HEALTH CARRIERS: This
is the result f sub clinical infection
contracted through association with
a source f infection (in case of an
infected environment)
• The duration of contact carrier state
is usually less than 10 days. The gall
bladder is not infected and stool
culture is frequently positive for
vibrios
39. • CHRONIC CARRIERS: A chronic
carrier state occurs infrequently
• The gall bladder is infected in
this state. In such case antibody
titre against V.cholerae 01 raises
and remains positive as long as
the person harbours the
organism
40. • This method may be used to
detect long term carriers along
with bacteriological examination
of the stools
41. HOST FACTORS
• AGE & GENDER: Cholera affects
all age and both gender
• In endemic areas attack rate is
highest in children
42. • GADTRIC ACIDITY : Is an efective
barrier
• The vibrio is destroyed at an
acidity of pH 5 or lower.
Condition that affect gastric
acidity may influence individual
susceptibility
43. • POPULATION MOBILITY:
Movement of population
(pilgrimage, marriages, fairs &
festivals) results in increased risk
of exposure to infection
• In this jet age cases and carriers
can easily transfer infection to
other countries
44. • ECONOMIC STATUS: Incidence of
cholera tends to be highest in
the lower socio economic groups
which could be attributed to
poor hygiene
45. • IMMUNITY: An attack of cholera
is followed by immunity to re
infection, but the duration and
degree of immunity are not
known
• Vaccination gives only partial
immunitybfor3-6 months
46. ENVIRONMENTAL FACTORS
• Vibrio transmission is highly
possible in a community with
poor environmental sanitation
• The environmental factors of
importance include
contaminated water and food
47. • These comprise certain human
habits favouring water and soil
pollution, low standards of
personal hygeine, lack of
education and poor quality of
life
48. MODE OF TRANSMISSION
• Transmission occurs from man to
man via faecally contaminated
water, contaminated food and
drinks and by direct contact
50. • CONTAMINATED FOOD AND
DRINKS: Ingestion of
contaminated food and drinks
have been associated with the
outbreak of cholera
• Bottle feeding could be a
significant risk factor for infants
51. • Fruits and vegetables washed
with contaminated water can
also be a source of infection
• Cooked foods can get
contaminated by contaminated
human handling and by flies
52. • DIRECT CONTACT: In developing
countries considerable number of
cases may result from secondary
transmission
• (person to person transmission
through contaminated fingers while
carelessly handling human excreta
or vomitus of patients & through
contaminated linens and fomites
54. PATHOGENESIS
• Diarrhoea is the main symptom
of cholera
• The pathogen gets through the
mucus which overrides the
intestinal epithelium
55. • This probably secretes mucinase
which helps the organism to
move rapidly through the mucus
• Then the vibrio gets attached or
adhered to the intestinal
epithelial cells
56. • When the vibrio becomes
adherent to the mucosa, it
produces its enterotoxin which
consists of 2 parts (the light or L
toxin and heavy or H toxin)
57. • The L toxin combines with
substances in the epithelial cell
membrane called gangliosides
and this binds the vibrios to the
cell wall
• Binding is irreversible
58. • The mode of H toxin is not fully
clear
• However the H toxin activates
the adenyl cyclase in the
intestinal epithelial cells. The
activated adenyl cyclase causes a
rise in in 3,5 adeosine
monophosphate (cAMP)
59. • The cAMP provides energy which
drives the fluid and ions into the
lumen of intestine
• This fluid is isotonic and is secreted
by all segments of small intestine.
The increase in fluid is the cause of
diarrhoea (and not peristalsis)
60. CLINICAL FEATURES
• The severity of cholera depends on
the rapidity and duration of fluid
loss
• A typical case of cholera shows
three stages:
1.Stage of evacuation
2. Stage of collapse
3. Stage of recovery
61. • STAGE OF EVACUATION: The
onset is abrupt with profuse,
painless, watery diarrhoea
followed by vomiting. The
patient may pass as many as 40
stools in a day. The stools may
have rice watery appearance
64. • The classical signs are sunken
eyes, hollow cheeks, scaphoid
abdomen, sub normal
temperature, washer man’s
hands and feet, absent pulse,
unrecordable blood pressure,
loss of skin elasticity, shallow
and quick respirations.
66. • The output of urine decreases
and may ultimately cease. The
patient becomes restless and
complains of intense thirst and
cramps in legs and abdomen.
• Death may occur at this stage,
due to dehydration and acidosis
resulting from diarrhoea
67. • STAGE OF RECOVERY: If death does
not occur then patients begin to
show signs clinical improvement
• The blood pressure begins to raise,
the temperature returns to normal
and urine secretion is re establishd.
If anuria persists, the patient may
die of renal failure
68. LAB DIAGNOSIS
• Lab methods of diagnosis are
required to confirm the diagnosis
• COLLECTION OF STOOLS: a fresh
specimen of stools should be
collected for laboratory
examination
69. • Sample should be collected
before the person is treated with
antibiotics
• Collection may be made in one
of the following ways
70. • RUBBER CATHETHER COLLECTION:
Soft rubber catheter (No.26-28)
sterilized by boiling should be used
• The catheter is introduced (after
lubrication with liquid paraffin) for
atleast 4-5 cm into the rectum
71. • The specimen voided may be
collected directly into a transport
media (VR medium, alkaline
peptone water)
72. • RECTAL SWAB: Swabs consisting
of 15-20 cm long wooden sticks
with one end wrapped with
absorbant cotton, sterilized by
autoclaving can be also used
73. • Rectal swabs should be dipped with
into the holding medium before
being introduced into the rectum
• If no transport medium is available,
a cotton tipped rectal swab should
be soaked in the liquid stool, placed
in a sterile plastic bag, tightly sealed
and sent to testing laboratory
74. • VOMITUS: This is practically never
used as the chances of isolating
vibrios are much less and there is
no advantage
• WATER: Samples containing 1-3
litres of suspect water should be
collected in sterile bottles (for
filter method)
75. • Or 9 volumes of sample water
added to 1 volume of 10 per cent
peptone water and despatched to
the lab by quickest method of
transport
• FOOD SAMPLE : Samples of food
suspected to be contaminated
with vibrios amounting to 1-3 gms
are collected in a transport media
and sent to lab
76. • TRANSPORTATION: the stool
should be transported in
sterilized McCartney bottles 30
ml capacity containing alkaline
peptone water or VR medium
• The specimen should be
transported in alkaline peptone
water or Cary-Blair medium if it
is collected by rectal swab
77. • One gram or one ml of faeces in
10 ml of the holding medium will
suffice
• Rectal swabs should have their
tops broken off hat caps of the
containers can be replaced
78. • If suitable plating media are available
(bile salt agar) at the bedside the stools
should be streaked on to the media and
forwarded to the lab with the transport
media
• DIRECT EXAMINATION: If a microscope
with dark field illumination is available
it may be possible to diagnose about 80
percent of cases within few min
79. • CULTURE METHODS: On arrival
at the laboratory the specimen is
well shaken abd about 0.5 to 1
ml material is inoculated into
Peptone Water Tellurite medium
for enrichment
80. • After 4-6 hrs incubation at 37
deg C, a loop of the culture from
the surface is sub cultured on
Bile Salt Agar medium
• After overnight incubation the
plates are screened under
oblique light illumination for
vibrio colonies
81. • CHARACTERIZATION: Vibrio
usually appears on blue salt agar
as translucent, moist, raised,
smooth easily emulsifiable
colonies about 1mm in diameter
• The typical colonies are picked
up and tested by gram staining
and serological tests
82. • GRAM TESTING: Gram negative
and curved rods with
characteristic scintillating type of
movement in hanging drop
preparations are characteristic of
Vibrio cholerae
83. • SEROLOGICAL TEST: Slide
agglutination test is done by
picking up suspected colonies
and making a homogenous
suspension in 0.85% sterile
saline and adding one drop of
polyvalent anti cholera
diagnostic serum
84. • If agglutination is positive the
test is repeated with Inaba and
Ogawa antisera to determine
subtype
86. • 1. Verification of the diagnosis
• 2. Notification
• 3. Early case finding
• 4. Establishment of treatment
centres
• 5. Rehydration therapy
88. VERIFICATION & DIAGNOSIS
• It is important to confirm the
outbreak of cholera . All cases of
diarrhoea should be investigated
even on slightest suspicion
89. NOTIFICATION
• Cholera is a notifiable disease
locally and nationally (though
not internationally)
• Health workers at all level should
be trained to identify and notify
cases immediately to the local
health authority
90. EARLY CASE FINDING
• An aggressive search for case
(mild, moderate, severe should
be made in the community to be
able to initiate prompt
treatment
91. • Early detection of cases also
permits the detection of infected
household contacts and helps
the epidemiologist in
investigating the means of
spread for deciding on specific
intervention
92. ESTABLISHMENT OF
TREATMENT CENTRES
• In control of cholera no time
should be lost in for providing
treatment to patients. Hence
treatment centres must be
established to the community as
close as possible
93. REHYDRATION THERAPY
• Mortality rated due to cholera
can be effectively brought down
by effective rehydration therapy.
Rehydration may be oral or
intravenous
94. ADJUNCTS TO THERAPY
• Antibiotics should be given as
soon as vomiting stops. The
commonly used antibiotics are
flouroquinolones, tetracycline,
azithromycin, ampicilline and
trimethioprim slfamethoxazole
96. SANITATION MEASURES
• Sanitation measures focusing on
water sanitation, excreta
disposal, food sanitation,
disinfection should be put into
vigorous interventions
98. • Tetracycline is the drug of choice
for mass chemoprophylaxis. It
has to be given over a 3 day
period, in twice daily dose of 500
mg for adults, 125 mg for
children aged 4-13 yrs and 50 mg
for children aged 0-3 years
99. • If the prevailing strains are
resistant to tetracycline,
doxycycline ( 300 mg for adults,
6 mg/kg for children under 15
yrs) has proved to be effective
100. VACCINATION
• Two types of vaccination are
available :
• 1. Dukoral (WC-rBS)
• 2. Sanchol & mORCVAX.
101.
102.
103. • Dukoral (WC-rBS) is a
monovalent vaccine based on
formalin and heat killed whole
cells of V. Cholerae
• Dukoral is not advised for
children less than 2 years
104. • Sanchol & mORCVAX is a closely
related bivalent oral vaccine
based on sero groups.
105. HEALTH EDUCATION
• Health education is the most
effective prophylactic measure.
The benefit of early reporting
and proper hygiene measures
should be taught to the
community
