2. BACKGROUND
V. cholerae has 2 major biotypes: classical
and El Tor. Currently, El Tor is the predominant
cholera pathogen worldwide.
3. The organism is a comma-shaped, gram-
negative, aerobic bacillus whose size varies from
1-3 mm in length by 0.5-0.8 mm in diameter.
V. CHOLERAE
Its antigenic structure consists of a flagellar H
antigen and a somatic O antigen. It is the
differentiation of the latter that allows for
separation into pathogenic and nonpathogenic
strains.
4. 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.
5. 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
6. 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.
7. 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
8. 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
9. 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.
10. V. cholerae is a saltwater organism & it is
primary habitat is the marine ecosystem.
Cholera has 2 main reservoirs, man & water.
Animals do not play a role in transmission of
disease.
V. cholerae is unable to survive in an acid
medium. Therefore, any condition that reduces
gastric acid production increases the risk of
acquisition.
TRANSMISSION/2
11. The same applies to patients with chronic
gastritis secondary to Helicobacter pylori
infection or those who have had a gastrectomy.
The use of antacids, histamine-receptor
blockers, and proton-pump inhibitors increases
the risk of cholera infection and predisposes
patients to more severe disease as a result of
reduced gastric acidity.
HOST SUSCEPTIBILITY
12. AT RISK GROUPS
All ages but children & elderly are more
severely affected.
Subjects with blood group “O” are more
susceptible; the cause is unknown.
Subjects with reduced gastric acid.
13. CLINICAL PICTURE
Incubation period is 24-48 hours.
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.
14. In severe cases stool volume exceeds 250
ml /kg leading to severe dehydration, shock
& death if untreated.
The classical textbook “rice water”
diarrhea, which describes fluid stool with
very little fecal material, appears within
24h from the start of the illness.
CLINICAL PICTURE/2
15. CHOLERA 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.
16. 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.
Serologic tests are available to define
strains, but this is needed only during
epidemics to trace the source of infection.
17. 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.
18. 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.
19. 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.
20. DRUG THERAPY
The goals of drug therapy are to eradicate
infection, reduce morbidity and prevent
complications.
The drugs used for adults include
tetracycline, doxycycline, cotrimoxazole &
ciprofloxacin.
For children erythromycin, cotrimoxazole
and furazolidone are the drugs of choice.
21. 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.
22. 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.
23. PUBLIC HEALTH ASPECTS
Isolation & barrier nursing is indicated
Trace source of infection.
Resume feeding with normal diet when vomiting
has stopped & continue breastfeeding infants &
young children.
Notification of the case to local authorities &
WHO.
24. 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.
25. CHOLERA VACCINES
The old killed injectable vaccine is obsolete
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.
27. Campylobacter enteritis was not recognized
until the mid-1970s when selective isolation
media were developed for culturing
campylobacters from human feces
Most common form of acute infectious
diarrhea in developed countries; Higher
incidence than Salmonella & Shigella combined
In the U.S., >2 million cases annually, an annual
incidence close to the 1.1% observed in the
United Kingdom; Estimated 200-700 deaths
History of Campylobacter
28. Small, thin (0.2 - 0.5 um X 0.5 - 5.0 um), helical
(spiral or curved) cells with typical gram-negative
cell wall; “Gull-winged” appearance
• Tendency to form coccoid & elongated forms
on prolonged culture or when exposed to O2
Distinctive rapid darting motility
• Long sheathed polar flagellum at one (polar)
or both (bipolar) ends of the cell
• Motility slows quickly in wet mount preparation
Microaerophilic & capnophilic 5%O2,10%CO2,85%N2
Thermophilic (42-43C) (except C. fetus)
• Body temperature of natural avian reservoir
May become nonculturable in nature
Morphology & Physiology of Campylobacter
30. Zoonotic infections in many animals particularly
avian (bird) reservoirs
Spontaneous abortions in cattle, sheep, and
swine, but generally asymptomatic carriage in
animal reservoir
Humans acquire via ingestion of contaminated
food (particularly poultry), unpasteurized milk, or
improperly treated water
Infectious dose is reduced by foods that
neutralize gastric acidity, e.g., milk. Fecal-oral
transmission also occurs
Epidemiology of Campylobacteriosis
31. Contaminated poultry accounts for more than
half of the camylobacteriosis cases in developed
countries but different epidemiological picture in
developing countries
In U.S. and developed countries: Peak
incidence in children below one year of age and
young adults (15-24 years old)
In developing countries where campylobacters
are hyperendemic: Symptomatic disease occurs
in young children and persistent, asymptomatic
carriage in adults
Epidemiology of Campylobacteriosis(cont.)
32. Sporadic infections in humans far outnumber
those affected in point-source outbreaks
Sporadic cases peak in the summer in temperate
climates with a secondary peak in the late fall
seen in the U.S.
Globally, C. jejuni subsp. jejuni accounts for
more than 80% of all Campylobacter enteriti
C. coli accounts for only 2-5% of the total cases
in the U.S.; C. coli accounts for a higher
percentage of cases in developing countries
Epidemiology of Campylobacteriosis(cont.)
33.
34. Infectious dose and host immunity determine
whether gastroenteric disease develops
• Some people infected with as few as 500 organisms
while others need >106 CFU
Pathogenesis not fully characterized
• No good animal model
• Damage (ulcerated, edematous and bloody) to the
mucosal surfaces of the jejunum, ileum, colon
• Inflammatory process consistent with invasion of the
organisms into the intestinal tissue; M-cell (Peyer’s
patches) uptake and presentation of antigen to
underlying lymphatic system
Non-motile & adhesin-lacking strains are avirulent
Pathogenesis & Immunity
35. Cellular components:
Endotoxin
Flagellum: Motility
Adhesins: Mediate attachment to mucosa
Invasins
GBS is associated with C. jejuni serogroup O19
S-layer protein “microcapsule” in C. fetus:
Extracellular components:
Enterotoxins
Cytopathic toxins
Putative Virulence Factors
36. Low incidence potential sequela
Reactive, self-limited, autoimmune disease
Campylobacter jejuni most frequent antecedent
pathogen
Immune response to specific O-antigens cross-
reacts with ganglioside surface components of
peripheral nerves (molecular or antigenic
mimicry)
• Acute inflammatory demyelinating neuropathy
(85% of cases) from cross reaction with
Schwann-cells or myelin
• Acute axonal forms of GBS (15% of cases) from
molecular mimicry of axonal membrane
Guillain-Barre Syndrome (GBS)
37. Gastroenteritis:
•Self-limiting; Replace fluids and electrolytes
•Antibiotic treatment can shorten the excretion period;
Erythromycin is drug of choice for severe or complicated
enteritis & bacteremia; Fluroquinolones are highly active
(e.g., ciprofloxacin was becoming drug of choice) but
fluoroquinolone resistance has developed rapidly since
the mid-1980s apparently related to unrestricted use and
the use of enrofloxacin in poultry
•Azithromycin was effective in recent human clinical trials
•Control should be directed at domestic animal reservoirs
and interrupting transmission to humans
Guillain-Barre Syndrome (GBS)
•Favorable prognosis with optimal supportive care
•Intensive-care unit for 33% of cases
Treatment, Prevention & Control
