CHOLERA
Dr . Haifa Yagoub Osman
Objective
Background
Epidemiology
Pathogenesis
Transmission
Clinical picture
Treatment
BACKGROUND
Cholera, is a Greek word, which means the gutter
of the roof. It is caused by bacteria vibrio cholerae,
which was discovered in 1883 by Robert Koch
during diarrhea outbreak in Egypt.
V cholerae has 2 major biotypes: classical and El
Tor, which was first isolated in Egypt in 1905.
Currently, El Tor is the predominant cholera
pathogen.
V CHOLERAE
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.
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.
Mortality/ Morbidity
During the six pandemic, the case fatality
rates were very high (50-70%)
After the 1960, dramatic reduction occurred
due to replacement of the classical type with
Eltor serotype and the advancement in the
understanding & treatment of the disease.
PATHOGENESIS
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 enterotoxin acts locally & does not invade
the intestinal wall. As a result few WBC & no
RBC are found in the stool.
AGENT FACTORS
Resistance:- v. cholerae are killed within
30 minutes at 56 deg.C, or few sec. by
boiling
Remain in ice for 3-4 weeks or longer
Drying & sunshine will kill them in few
hours
Disinfectant kill them also
RESERVOIR OF INFECTION
Human is the only known reservoir of
cholera infection
The ratio of severe cases to mild ones is
shown to be 1:5 for classical type & 1:25
for EL Tor
Transmission
TRANSMISSION
Cholera is transmitted by the fecal-oral route
through contaminated water & food.
Person to person infection is not so common.
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.
HOST SUSCEPTIBILITY
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.
The same applies to patients with chronic
gastritis secondary to Helicobacter pylori infection
or those who have had a gastrectomy
AT RISK GROUPS
All ages, but children & elderly are more
severely affected.
Subjects with O blood group. Cause is
unknown.
Subjects with reduced gastric acid.
Social class & economic status
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 & like “rice water” in few
hours.
In severe cases stool volume exceeds 250 ml
/kg leading to severe dehydration, shock & death
if untreated.
COMPLICATIONS
If dehydration is not corrected adequately &
promptly it can lead to hypovolemic shock,
acute renal failure & death.
Electrolyte imbalance.
Hypoglycemia in children.
Complications of therapy like overhydration
& side effects of drug therapy.
LAB DIAGNOSIS
Organism can be seen in stool by direct
microscopy after gram stain & dark field exam 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.
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.
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 will replace
ongoing losses & provide daily requirement.
SEVERE DEHYRATION
Administer IV fluids immediately
Monitor the patient very frequently,
(radial pulse & BP)
Re-assess the patient after 3 hours (if
still having signs, repeat the IV fluid)
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 severe dehydration.
The oral route is preferred for maintenance &
the use of ORS at a rate of 500-1000 ml/h is
recommended.
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.
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 these resistance patterns.
Antibiotic should be started when cholera is
suspected without waiting for lab confirmation.
Thanks
Ramadan Mubarak
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