Download Epidemiology of Cholera

Epidemiology of Cholera
Ashry Gad Mohamed
Professor of Epidemiology
College of Medicine & KKUH
• Greek word for the gutter of a roof,
comparing the deluge of water
following a rainstorm to that of the
anus of an infected person
• Acute intestinal infection caused by the
bacterium Vibrio cholerae
characterized by:
• profuse watery diarrhoea with flecks
of mucous material (rice water
stools), vomiting, abdominal pain
• Rapid onset of dehydration causing
severe weakness, poor skin turgor,
sunken eyes and cheeks
• Often muscular cramps, cyanosis,
subnormal temperature, tachy-cardia,
hypotension; renal failure may follow
inadequate treatment
• Without treatment a healthy person
may become hypotensive within one
hour & may die within 2-3 hours.
• More commonly: from 1st liquid stool to
shock 4-12 hours.
Mechanism
• Entrotoxin activates adenylate cyclase
enzyme in intestinal wall that is
converted into pump that extract water
& electrolytes from blood and tissues
to intestinal lumen with shedding of
mucous and epithelial cells giving rice
water severe diarrhea
Infectious agent: Vibrio cholerae
•
epidemic cholera is caused by two
biotypes of Vibrio cholerae :
– the classical biotype serogroup O1,
and
– since 1961 (7th pandemic), the
biotype El Tor
•
Serogroup O1 includes serotypes Inaba,
Ogawa and Hikojima
•
Serogroup O139: in 1992/93, a new Vibrio
cholerae O139 strain appeared
• Vibrios are one of the most common
organisms in surface waters of the
world. They occur in both marine &
fresh water habitats and in association
with aquatic animals.
• Most infections are subclinical cases, but
excrete the organism in faeces for 7-14
days.
• Only 10% of the infected persons develop
typical cholera.
• 90% of episodes are mild or moderate.
• Case fatality without treatment = 25-50%.
• Case fatality with treatment (ORS) = 1%
• During the 19th century, the classical biotype
of V. cholerae serogroup O1 caused
pandemic cholera, spreading from India to
most of the world; currently confined to the
Indian subcontinent
• Since 1961, the biotype El Tor of V. cholerae
serogroup O1 has spread through Asia into
Africa, Europe (small epidemics), and South
America (since 1991): 7th cholera pandemic
• V. cholera serogroup O139 was mainly
isolated in Asia and represents currently 15%
of isolates
• During 2000, 56 countries have
officially reported
137 000 cases and 4 900 deaths;
however, >150 000 deaths/year
are estimated in developing
countries, about one third in
children <5 years
Current epidemic
7th epidemic
• Due to V cholerae 01,
V eltor &
V cholerae 0139
• Started 1961 in Indonesia.
• Bangladesh 1963
• India 1964
• West Africa 1970
• Latin America 1991
• Bangladesh 1992 (V cholerae 0139)
• South East Asia
• South Africa 2000
Selected morbidity indicators
•
•
•
•
•
•
•
•
•
Cholera
Malaria
Poliomyelitis
Measles
Pulmonary tuberculosis
Diphtheria
7
Tetanus
32
Neonatal tetanus
22
AIDS
63
Meningococcal meningitis
12
1059
0
373
2192
18
2005
2005
2005
2005
2005
2005
2005
2005
2005
2005
• Incubation period: 1-5 days.
• Modes of transmission:
1-Contaminated water and food.
2-Rarely direct from person to person.
• Reservior
1-Aquatic environment (Brackish water & sea
food)
2-Human beings
• Communicability (stool-positive stage):
Usually ends few days after recovery,
occasionally several months carrier state,
antibiotics can shorten the period of
communicability
Prevention and control
•
•
•
-
Hygienic disposal of human faeces.
Adequate supply of safe drinking water.
Good food hygiene
Cooking food thoroughly & eating it hot.
prevent contact of cooked food with raw
contaminated food, water or ice.
- Avoid raw vegetables unless peeled
Boil it, cook it, peel it or forget it.
- Mass chemoprophylaxis has no effect
Vaccination:
o The previous parenteral cholera vaccines had
little efficacy and are not recommended for
use in endemic areas, during outbreaks, or in
people traveling to endemic areas.
oOral immunization:
(1) killed bacterial vaccines
(2) live genetically engineered mutants
deleted of toxin genes
(3) avirulent vectors genetically engineered
to express protective cholera antigens.
Oral killed vaccines
an oral vaccine containing killed V
cholerae O1.
• successful immunity for 6 months, which
later waned.
• Unfortunately, in patients who need the
vaccine most (children), the immunity was
poor.
• Need multiple dosages.
• This vaccine is now disrepute
Oral live vaccines
• Appears to be safe and induces protective
immunity as soon as 8 days after immunization,
even after a single dose in adults.
• It is effective in children and healthy
volunteers.
• Confer 80% immunity against El Tor cholera.
However, its efficacy in endemic and
non-endemic areas and across all populations
is yet to be established.
For a vaccine to be useful in endemic areas, it
should do the following:
– Produce long-lasting immunity
– Be compatible with the Expanded Program on
Immunization
– Be able to produce immunity rapidly, ideally
after one dose, to be useful in epidemics
- Protect against El Tor O1 and O139 Bengal
strains
• Because the secondary attack rate of
cholera in the household is high,
selective antimicrobial prophylaxis of
contacts has been attempted. This is
not feasible as a routine public health
measure.
• Food products from cholera infected
regions:
- Vibrio cholerae 01 survives 5 days in
ambient temperature & 10 days at 5-10
degrees.
-It survives freezing & low temperature.
-It is sensitive to acidity & drying.
-It is sensitive to Gamma irradiation &
temperature above 70 degrees.
Epidemiology
of
Typhoid fever
• An acute infection with prolonged fever due
to Salmonella typhi sometimes lead to
severe complications.
• Globally 16 million cases with 600000
deaths annually.
• Salmonella paratyphi A & B lead to milder
disease.
• S.t. / S.p = 10 – 1
• Peak age 4-19 years.
• Disease caused by S. typhi is typhoid fever.
• In past, many deaths were due to typhoid
fever worldwide.
Now mostly
• localized to developing countries.
• People not only become ill and die but can
become colonized by S. typhi resulting in
being carriers and spread typhoid fever.
• Incubation period for S. typhi is a
week to a month post-ingestion.
• Bacteria multiply in liver and
spleen then released systemically
• (blood). Results in high fever,
chills, anorexia.
Poorer Countries are Vulnerable
• Typhoid Fever seems
to matriculate in
places with poor
sanitary conditions.
• Places where water is
not sanitized provides
the perfect
environment for
Typhoid Fever.
Typhoid Fever
Ingest S. typhi
Bacteria invades intestinal cells and translocates to systemic organs
Multiplies to high number in liver and spleen
Spreads to bloodstream
Bacteria move to gallbladder
Shed in Bile
Bacteria persists
in gallbladder
DEATH
Bacteria shed in
feces
TYPHOID
Risky groups
• Children and young adults in endemic
areas.
• Contacts of chronic carriers.
• Microbiology technicians.
• Food handlers.
• Travelers and military personnel
Incubation period:
• 10-14 days.
Modes of transmission:
• Water contaminated with fecal materials.
• Contaminated food.
• Food handlers.
Reservoir:
Only human (cases & carriers)
Typhoid carriers
• About 1–5% of people who are infected with S.
typhi become asymptomatic chronic carriers.
• The carrier state may follow acute or mild illness
or subclinical infection.
• The incidence of chronic carriage is higher
among women and persons with biliary tract
abnormalities.
• Antibiotic use and antibiotic resistance may also
affect the propensity to become a chronic carrier.
• A chronic urinary carrier state occurs in
individuals with schistosome infection.
• Carriers who handle food without observing
proper hygiene can transmit infection to others.
Transmission
• Typhoid is spread by the faecal-oral route.
Occasionally transmission may be direct,
but usually it occurs following the ingestion
of contaminated water or food.
• In developing countries with contaminated
water supplies and primitive sewage
disposal systems, water is the most likely
vehicle of transmission.
Epidemics originating from water
contamination are particularly explosive.
because
• a water source may serve a large
population.
• Water dilutes gastric acid which would
otherwise inactivate pathogenic agents.
• Water and other beverages remain in the
stomach only very briefly
• In more developed countries, with good
sanitation, typhoid transmission is more
likely to be associated with food
contamination by an undetected carrier or
a breakdown in proper practices of
personal and food hygiene.
Communicability
• Typhoid is communicable as long as S.
typhi organisms are excreted, usually from
the first week and throughout
convalescence.
• About 10% of untreated typhoid fever
patients will excrete bacteria for 3 month
after onset of symptoms.
Prevention and control
• Basic sanitary and hygienic measures
Purifying water supplies.
Improving water delivery and sewage control.
Construction and use of latrines.
Boiling water
Supervision of foodhanders.
Vaccines
•
Three vaccines to typhoid fever:
1. Killed whole bacteria with side effects.
2. Capsular material (Vi antigen) that is safer and more
effective.
3. Live oral vaccine, attenuated S. typhi strain (Ty21a).
Oral vaccines are still being developed to distribute in
developing countries. Ty21a is also being used to
carry foreign antigens from Shigella and V.
cholerae.
Number
Time
of doses
between
necessar
doses
y
Total
time
Minimu
needed
m age
to set
for
aside for vaccinati
vaccinati
on
on
Booster
needed
every...
Vaccine
Name
How
given
Ty21a
(Vivotif
Berna,
Swiss
Serum
and
Vaccine
Institute)
------------
1
capsule
by
mouth
4
2 days
2 weeks
6 years
5 years
ViCPS
(Typhim
Vi,
Pasteur
Merieux)
Injection
1
N/A
2 weeks
2 years
2 years
• Indication of vaccination:
Travellers to endemic areas.
People in refugee camps.
Microbiologists.
• Treatment:
Antibiotics : Ciprofloxacin, pefloxacin &
cephalosporins