dr.khalid hama salih

1. Vibrio choleraVibrio choleraVibrio choleraVibrio cholera
Dr.Khalid Hama
salih,
Pediatrics specialist
M.B.Ch.; D.C.H
F.I.B.M.S.ped

2. BACKGROUNDBACKGROUND
The term cholera has ancient origins and is
derived from Greek words meaning “a flow
of bile,

3. V. CHOLERAEV. CHOLERAE
 The organism is a comma-shaped, gram-The organism is a comma-shaped, gram-
negative, aerobic bacillus whose size variesnegative, aerobic bacillus whose size varies
from 1-3 mm in length by 0.5-0.8 mm infrom 1-3 mm in length by 0.5-0.8 mm in
diameter.diameter.
 The antigenic structureof V. cholerae isThe antigenic structureof V. cholerae is
similar to that of other members of thesimilar to that of other members of the
family, Enterobacteriaceae with a flagellarfamily, Enterobacteriaceae with a flagellar
H antigen and a somatic O antigen. The OH antigen and a somatic O antigen. The O
antigen is used to classify V. choleraeantigen is used to classify V. cholerae
further, into serogroups O1 and non-O1further, into serogroups O1 and non-O1

5.  cholera O1 can be classified into threecholera O1 can be classified into three
serotypes according to the presence ofserotypes according to the presence of
somatic antigens and into two biotypessomatic antigens and into two biotypes
according to specific phenotypicaccording to specific phenotypic
characteristics. Serotype Inaba carries thecharacteristics. Serotype Inaba carries the
O antigens A and C, serotype OgawaO antigens A and C, serotype Ogawa
carries the antigens A and B, andcarries the antigens A and B, and
serotype Hikojima carries the threeserotype Hikojima carries the three
antigens A, B, and C.antigens A, B, and C.

6.  The toxinhas five B subunits and twoThe toxinhas five B subunits and two
A subunits. The B subunits allowA subunits. The B subunits allow
binding of the toxin to a specificbinding of the toxin to a specific
receptor,aganglioside (GM1) locatedreceptor,aganglioside (GM1) located
on the surface of the cells lining theon the surface of the cells lining the
mucosa along the intestine of human.mucosa along the intestine of human.

7. Since 1817, there have been 7 cholera
pandemics. The first 6 occurred from 1817-1923
and were caused by V. cholerae, the classical
biotype. The pandemics originated in Asia with
subsequent spread to other continents.
EPIDEMIOLOGY
The seventh pandemic began in Indonesia in
1961 and affected more countries and
continents than the previous 6 pandemics. It
was caused by V. cholerae El Tor.

8. In October 1992, an epidemic of cholera
emerged from Madras, India as a result of a new
serogroup (0139). Some experts regard this as
an eighth pandemic.
This Bengal strain has now spread throughout
Bangladesh, India, and neighboring countries in
Asia.
EPIDEMIOLOGY/2

9. In 1994, 94 countries reported 385,000 cases of
cholera to WHO, but the number reported in 1998
was 121,000. 89% of these cases were reported
from Africa.
REPORTED CASES
The number of cholera patients worldwide is
uncertain because many cases are unreported.
The number of cases is increased during
epidemics & is affected by environmental
factors.

10. Fifty-three countries officially reportedFifty-three countries officially reported
177,963 cases to the WHO in 2007, with 4031177,963 cases to the WHO in 2007, with 4031
deaths; 94% ofthese cases were reported fromdeaths; 94% ofthese cases were reported from
AfricaAfrica

11. V cholerae cause clinical disease by producing
an enterotoxin that promotes the secretion of
fluid and electrolytes into the lumen of the gut.
The result is watery diarrhea with electrolyte
concentrations isotonic to those of plasma.
The enterotoxin acts locally & does not invade
the intestinal wall. As a result few WBC & no
RBC are found in the stool.
PATHOGENESIS

13. Fluid loss originates in the duodenum and
upper jejunum; the ileum is less affected.
The large volume of fluid produced in the
upper intestine, however, overwhelms the
absorptive capacity of the lower bowel, which
results in severe diarrhea.
The colon is usually in a state of absorption
because it is relatively insensitive to the toxin.
PATHOGENESIS/2

14. TRANSMISSION
Cholera is transmitted by the fecal-oral route
through contaminated water & food.
The infectious dose of bacteria required to
cause clinical disease varies with the source. If
ingested with water the dose is in the order of
103
-106
organisms. When ingested with food,
fewer organisms are required to produce
disease, namely 102
-104
.
Person to person infection is rare.

15. V. cholerae is a saltwater organism.
Cholera has 2 main reservoirs, man & water..
V. cholerae is unable to survive in an acid
medium..
TRANSMISSION/2

17. AT RISK GROUPS
All ages but children & elderly are more
severely affected.
Subjects with blood group “O” are more
susceptible.
Subjects with reduced gastric acid.
Social disruption, poverty, poor sanitary and
hygienic conditions, and poor access to
health care

18. CLINICAL PICTURE
Incubation period is 2-5day.
Symptoms begin with sudden onset of
watery diarrhea, which may be followed by
vomiting. Fever is typically absent.
The diarrhea has fishy odor in the
beginning, but became less smelly & more
watery over time.

19. In severe cases stool volume exceeds 250
ml /kg leading to severe dehydration, shock
& death if untreated.
“rice water” diarrhea, which describes
fluid stool with very little fecal material,
appears within 24h from the start of the
illness.
CLINICAL PICTURE/2

21. NB/in children:
Breast-fed infants are protected.
Symptoms are severe & fever is frequent.
Shock, drowsiness & coma are common.
Hypoglycemia is a recognized complication,
which may lead to convulsions.
Rotavirus infection may give similar picture
& need to be excluded.

22. LAB DIAGNOSIS
Organism can be seen in stool by direct
microscopy after gram stain and dark field
illumination is used to demonstrates motility.
Cholera can be cultured on special alkaline
media like triple sugar agar or TCBS agar.

23. polymerase chain reaction (PCR) assaypolymerase chain reaction (PCR) assay
and real-time nucleic acid sequence-basedand real-time nucleic acid sequence-based
amplification assays for detecting vibriosamplification assays for detecting vibrios
in stool and environmental samples. Ain stool and environmental samples. A
rapid diagnosis of cholera can be made inrapid diagnosis of cholera can be made in
the field using a highly sensitive andthe field using a highly sensitive and
specific immunochromatographicspecific immunochromatographic
dipstick test applied to fresh stoolsdipstick test applied to fresh stools

24. OTHER LAB FINDINGS
Dehydration leads to high blood urea &
serum creatinine. Hematocrit & WBC will also
be high due to hemoconcentration.
Dehydration & bicarbonate loss in stool
leads to metabolic acidosis with wide-anion
gap.
Total body potassium is depleted, but serum
level may be normal due to effect of acidosis.

25. TREATMENT
The primary goal of therapy is to replenish
fluid losses caused by diarrhea & vomiting.
Fluid therapy is accomplished in 2 phases:
rehydration and maintenance.
Rehydration should be completed in 4
hours & maintenance fluids should replace
ongoing losses & provide daily requirement.

26. FLUID THERAPY
Ringer lactate solution is preferred over
normal saline because it corrects the associated
metabolic acidosis.
IV fluids should be restricted to patients who
purge >10 ml/kg/h & for those with severe
dehydration.
The oral route is preferred for maintenance &
the use of ORS at a rate of 500-1000 ml/h is
recommended.

27. DRUG THERAPY
The goals of drug therapy are to eradicate
infection, reduce morbidity and prevent
complications.
.
For children erythromycin, cotrimoxazole
and furazolidone are the drugs of choice.

28. DRUG THERAPY/2
Drug therapy reduces volume of stool &
shortens period of hospitalization. It is only
needed for few days (3-5 days).
Drug resistance has been described in some
areas & the choice of antibiotic should be
guided by the local resistance patterns .
Antibiotic should be started when cholera is
suspected without waiting for lab confirmation.

29. COMPLICATIONS
If dehydration is not corrected adequately &
promptly it can lead to hypovolemic shock,
acute renal failure & death.
Electrolyte imbalance is common.
Hypoglycemia occurs in children.
Complications of therapy like over hydration
& side effects of drug therapy are rare.

30. PREVENTION
Education on hygiene practices.
Provision of safe, uncontaminated, drinking
water to the people.
Antibiotic prophylaxis to house-hold
contacts of index cases.
Vaccination against cholera to travellers to
endemic countries & during public gatherings.

31. On drinking boiled water, acidic beverages,
and carbonated water, as well as using
narrow-necked vessels for storing water,
are protective

32. CHOLERA VACCINES
The old killed injectable vaccine is not use
now because it is not effective.
Two new oral vaccines became available in
1997. A Killed & a live attenuated types.
Both provoke a local immune response in
the gut & a blood immune response.
Cholera vaccination is no more required for
international travellers because risk is small.

35.  . cholerae has 2 major biotypes:. cholerae has 2 major biotypes:
classical and El Tor, which was firstclassical and El Tor, which was first
isolated in Egypt in 1905. Currently, Elisolated in Egypt in 1905. Currently, El
Tor is the predominant choleraTor is the predominant cholera
pathogen worldwidepathogen worldwide

36. The toxinhas five B subunits and two A subunits.
The B subunits allow binding
of the toxin to a specific receptor,aganglioside
(GM1) located on thesurface of the cells lining
the mucosa along the intestine of humansand
certain suckling mammals adenylate cyclase results
in a net increase in cyclic adenosine
monophosphate, which blocks the absorption of
sodium and
chloride by microvilli and promotes the secretion of
chloride and
water by crypt cells.