Transcript cholera - muhadharaty.com

CHOLERA
Al- Abbasi A.M, PhD, FRCP, DCN, DTM
&H
Prof. Of infections Diseases &
Clinical Immunology, Coll. Of Med.,
Univ. of Baghdad, Baghdad, Iraq.
Robert Koch (third from the right) on a cholera research
expedition in Egypt in 1884, one year after he identified V. cholerae.
Black and yellow Jack signal flags on ships
IDENTIFICATION
An acute bacterial enteric disease characterized in
its sever form by:
 Sudden onset, profuse painless
 watery stool (rice-water stool),
 nausea and profuse vomiting
early in the course of illness.
 In untreated cases, rapid dehydration,
 acidosis, circulatory collapse,
 hypoglycemia in children, and renal failure can rapidly
lead to death.
Dehydration
Single flagellum
CASE DEFINITION
WHO, CDC
 DISEASE UNKNOWN IN AREA:
Severe dehydration or death from acute watery
diarrhea in a patient aged 5 or more.
 ENDEMIC CHOLERA:
Acute watery diarrhea with or without vomiting in
a patient aged 5 or more.
 EPIDEMIC CHOLERA:
Acute watery diarrhea with or without vomiting in
any patient.
Vibrio cholerae
Gram-negative, comma-shaped bacterium.
V. cholerae is a facultative anaerobic organism and has a flagellum at
one cell pole.
During infection, V. cholerae secretes
cholera toxin, a protein causes profuse, watery
diarrhea.
Two sero groups, O1 and O139, cause outbreaks of cholera.
O1 causes the majority of outbreaks, while O139 – first identified
in Bangladesh in 1992 – is confined to South-East Asia.
In 1996 Matthew K. Waldor and John J. Mekalanos of the U.S. reported a
stunning discovery about the toxin.
The toxin was for the first time shown to be not a part of the
bacterium but actually that of a virus (bacteriophage) that got
integrated into the V. cholerae genome.
Normally this virus remains silent within V. cholerae but during infection it
gets activated.
It then multiplies within the bacterium and escapes to infect other V. cholerae
cells.
Under certain laboratory conditions it is possible to activate and release this
virus or phage from V. cholerae.
It is called CTX phage, CT standing for cholera toxin.
Along with the toxin, a specific pilus called toxin- corregulated pilus (TCP) is
also produced on the surface of V. cholerae.
Scanning electron microscope image of Vibrio cholerae
CHOLERA SYNDROM
ENZYMATIC DIARRHOEA
Vibrionaceae Family: four genera
Cholera: 139 strains
01 of Classical type & ELTOR biological type are the causes.
Now O139 is blamed to cause the 8th pandemic.
Some other cause of a brief enzymatic diarrhea are:NAG, NCV&NVC.
NAG: Short sporadic diarrhea by non O1 vibrios especially
V. parahemolyticus group 6.
NCV: Diarrhea by Aeromonas, Plasiomonas genera.
NVC: Other enzymatic diarrhea by non vibrio
microorganisms e.g. E.coli.
NB: Vibrios of non O1 group might cause septicemia, wound
infection, otitis media..etc.
PATHOGENESIS OF CHOLERA
Ingestion
Small Intestine
Gastric acid
Attachment
Secrtory IgA
Local B cell
T cell dependence
Systemic
B cells
Agglutinating
Vibriocidal
Agglutinating
Copro Ab IgG IgM IgA
Destroyed in gut.
Serum Ab.
Antigen
absorption
Nutrition
Vaccination
Effect of strain
Entrotoxin
Production
Attachment for
Life of cell
AC
cAMP
not opsonizing SECRETION
Cholera
Kinetics water/ Electrolyte Absorption
UPPER G.I. 8 LITERS DAILY
Intake
Saliva
Intestine
Gastric
Biliary
Pancreas
Active transport resorption in small GI:500-1000 mI only
Large intestine
Net secretion of water stool/ day=100mI
ATP
Cholera
Toxin
phosphodiesterase
Irreversible
AC
cAMP
AMP
activation
80% Na+ absorbed actively with glucose/ amino acid, only 20%
with CL-.Glucose absorption not affected by cholera toxin.
Electrolyte composition of diarrheal stools, oral and
intravenous replacement solutions (mEq/L)for cholera.

3
Na+
Cl-
K+
HCO
Adult
135
100
15
45
-
Child
105
90
25
30
-
Oral solution*
90
80
20
30
111
IV solution †
134
99
13
48
optional
Substance
glucose
Stool
*WHO solution, 3.5 gm NaCl, 2.5 gm NaHCO3, 1.5 gm KCl, glucose
20 gm/L (or sucrose 40 gm/L).
† Dacca solution (5/4/1)= 5 gm NaCl, 4 gm NaHCO3, 1 gm KCl /L.
CHOLERA : CLINICAL
Subclinical / A symptomatic / mild: common
Florid causes Loss water & electrolytes > One
liter/hour.
1.p = 1 - 5 days usually 12 – 48 hours.
Abrupt onset of painless, odorless effortless
diarrhea of up to 40 bowel motion / day, followed
by profuse vomiting.
Early signs of collapse
Loss of skin turger , washer – woman hand
Dehydration 12% is fatal
Major cause of death in adults: acute renal failure,
in children : hypokalemia .
Diarrhea "rice water" in nature and may have a
fishy odor.
An untreated person with cholera may produce 10
to 20 liters (3 to 5 US gal) of diarrhea a day with
fatal results.
For every symptomatic person, 3 to 100 people get
the infection but remain asymptomatic.
Cholera has been nicknamed the "blue death"
as victim's skin turns bluish-gray from extreme
loss of fluids.
Cholera/ Food poisoning
Symptoms
Cholera
Food poisoninmg
Nausia,retching & pain in
stomach
Vomiting
Rare
common
Watery follows Diarrhoea
Diarrhoea
Rice water
Contain food
particles,precedes
diarrhoea
Offensive foecal matter
Pain & gripping
Absent
present
Muscle cramps
Common
Rare
Urine
Suppressed
No Suppression
Collapse
Common
Rare
Fever
Rare
> 37.3 C
Headach
Rare
Common
History of common meal
Rare
Common
I V. Fluid
Na+
K+
HCO3-
Cl-
Ca++
Plasma
Sod.chloride
0.9%
Hartmans
Sod.bicarb.
1.4%
Sod.lactate M/6
142
150
4.5
-
26
-
103
150
2.5
-
131
167
5
-
29
167
111
-
2
-
167
-
167
-
-
FACTORS FAVORING ERADICATION
 V. cholerae is fragile microorganism
 Large doses are required for infection 1
billion mo.Vs 1 million for S. typhi & 100 mo for
shigellosis
 No bactremia
 Lack of person-person transmission
 Short incubation period
 Impact of non-specific control measures
 Public motivation
FACTORS IMPEDING ERADICATION
 Persistence of V.cholerae in the aquatic environment
 Increase in the population density
 Non existence of an adequate vaccine
 Limited protection from natural immune system
 Failure of other traditional public- health measures e.g.
Chemoprophylaxis, quarantine, trade embargo
 Rapid development of microbial resistance and lack of
effective treatment
 Flexibility & variety of microbial toxigenic strains
THANK YOU