Transcript Document
Cholera
Rose Lee and Ricardo Lé
January 14, 2008
Cholera: The Illness
Clinical Features
Acute diarrhoeal infection
Diarrhoea leads to death by
dehydration and kidney failure
(stool output can reach 0.51L/hour) - hypotension,
tachycardia, and vascular collapse
Short incubation period (2 hours to 5
days)
75% of those infected do not develop
symptoms
100-1000 organisms may cause disease,
although a million are needed to
consistently infect
Transmission
Direct fecal-oral contamination or
ingestion of contaminated water and
food
Linked to inadequate environmental
management (lack of safe water and
sufficient sanitation)
Human-Human contact does not spread
the bacterium
Treatment
Up to 80% of cases can be treated
through oral rehydration salts
Severe cases require intravenous fluids
(Ringer lactate)
Antibiotics can diminish duration of
diarrhoea, reduce volume of rehydation
fluids needed, and shorten duration of
V.cholerae excretion
Parenteral Vaccine
2 doses administered 2 weeks apart
Efficacy of approximately 50%
Protection hardly exceeds 6 months
Does not prevent transmission of
infectious agent
Not recommended for general public
health use
Killed WC/rBS Vaccine
Killed whole-cell V.cholerae in
combination with a recombinant Bsubunit of cholera toxin
Safe in pregnancy and breastfeeding
Efficacy of approximately 50% after 3
years
Only significant side-effects are mild
gastrointestinal disturbances, and
toleration is great for HIV-positive
subjects
Live, attenuated
CVD 103-HgR Vaccine
Protection as early as 1 week after
vaccination, with >90% protection
against moderate or severe cases
Protection lasts at least 6 months,
further data is unknown
Unknown efficacy for children
under 2
No adverse side-effects
Major Issues in Vaccines
Preventative (other measures)
Parenteral: low efficacy, short
duration
WC/rBS: 2 doses (logistics)
CVD 103-HgR: Long term results?
Inefficient for O139 or children <2
Need more tests and trials.
Prevention
Basic health education and
hygiene
Mass chemoprophylaxis
Provision of safe water and
sanitation
Comprehensive Multidisciplinary
Approach: water, sanitation,
education, and communication
Control of Spread
Set up treatment centres for
prompt treatment.
Sanitary measures.
Comprehensive surveillance data
(adapt to each situation) for a
comprehensive multidisciplinary
approach.
Vibrio Cholerae
The Organism
Type of Bacterium
Gram negative (LPS cell wall)
Type of Gammaproteobacteria
Distinguishing factors: Oxidase-
positive, motile via polar flagellum,
and both respiratory and
fermentative metabolism.
Simple growth requirements
History of Cholera
First observed in India then S. Asia
Discovered conclusively in 1883 by
Koch
Spread to Europe and Americas from
1817. 6 epidemics by 1990s.
7th epidemic in 1961 of El Tor biotype
Spread across Asia, Middle East, Africa,
and parts of Europe
Some Definitions:
Strain: Subset of a bacteria differing from
same species.
Biotype: Same genotype, but different
phenotype.
Serotype: Closely related microorganisms
distinguished by a characteristic set of
antigens.
Many strains of Vibio cholerae.
O antigens distinguish 139 serotypes:
O1 (3 biotypes—each has “classical” or
El Tor phenotype), O139 Bengal.
O139 is a new serological strain with
unique O-antigen (no residual
immunity from O1)
Differences
El Tor strain is more virulent
(replacing classical):
Lower ratio of cases to carriers
Longer duration of carriage after
Survives longer in extraintestinal env
O139 Bengal (derived from El Tor)
Different antigenic structure on LPS
Distinct polysaccharide capsule
Possess all El Tor virulence
Virulence Factors
Cholera toxin
Tcp pili
Aggregation, adhesion
Flagellum
withstand propulsive gut
Resistant to bile salts in intestines
If escapes low pH of stomach, easy to survive in
intestines
Cholera toxin
Potent exotoxin
multimeric protein complex of five binding
subunits (B) and one enzymatic (A) subunit.
B subunits bind to intestinal epithelia
cell and A1 subunit enter cell and
activates adenylate cyclase enzyme.
A1 catalyzes ADP-Ribose attachment to Gs Gi cannot
hydrolyze GTP to inactivate adenylate cyclase.
cAMP produced at high rate. Triggers Cl- into intestines.
H O, Na+, bicarbonate, and other electrolytes follow
2
Colonization
Adhesins
Tcp pili, hemagglutinin, acf gene
products
Neuraminidase
Motility
Chemotaxis
Toxin production
Regulation
Enterotoxin is a product of ctx
genes regulated by transcription
Environmental signals
-Temperature, pH, osmolarity, amino acids
ToxR regulatory protein activated
-Induces positive control, binds to DNA
Genes for attachment and toxin
production transcribed
Ecology
Can exist in dormant state
Conversion to infectious state:
-increase Temp, pH, nutrients.
-decrease salinity
Can shift to “rugose form”:
exopolysaccharide production for cell
aggregation, resists chlorine
On our mission we came across a village
in rural Bangladesh. It is very small
but very crowded with poor water
sanitation and irrigation systems.
Its position is dangerously close to the
urban slums that have had cholera
outbreaks within the past few months.
Luckily, there has been no reported
cases of cholera so far within the last 6
months… but now we have some
decisions to make.
Discussion Question 1
What is our plan of action in
regards to this village?
- Where should the emphasis be placed on
protecting a population before an
outbreak occurs? Vaccination or
sanitation?
- What are the pros and cons of each?
Discussion Question 2
Unfortunately, while the members
were debating, an outbreak occurred
in this village. What is the plan now?
-What is the best hybrid solution for controlling
a cholera outbreak? You have short time and
limited resources.
Discussion Question 3
The outbreak has been controlled for
the moment. What should be the
long-term plan for this population?
Discussion Question 4
What are your sentiments and
policies regarding cholera around
the world? How do you feel about
the importance each of these as
aspects?
Scientific Lab Research
Field Work
Infrastructure of Sanitation
Education