Cholera

CHOLERA
CHOLERA
CHOLERA
Cholera is an infection of the small intestine caused by the bacterium Vibrio cholerae
.
The main symptoms are profuse watery diarrhea , vomiting and abdominal pain.
Transmission is primarily through contaminated drinking water or food.
The severity of the diarrhea and vomiting can lead to rapid dehydration and
electrolyte imbalance
cholerae is a comma-shaped, gram-negative aerobic bacillus .
Its antigenic structure consists of a flagellar H antigen and a somatic O antigen.
The differentiation of the latter allows for separation into pathogenic and
nonpathogenic strains.
V . cholerae O1 and V . cholerae O139 are associated with epidemic cholera.
TRANSMISION
Cholera is transmitted through ingestion of water contaminated with the cholera
bacterium ( fecal-oral route ) , usually from feces .
The source of the contamination is typically other cholera patients when their
untreated diarrhea discharge is allowed to get into waterways or into groundwater or
drinking water supplies
CHOLERA TRANSMISION
CHOLERA
Vibrio cholerae is the causal agent of the diarrheal disease cholera.
Cholera is a major epidemic disease that has killed millions of people, and continues
to be a major health problem worldwide.
PATHOPHYSIOLOGY

cholerae O1 and V. cholerae O139 cause clinical disease by producing an

enterotoxin that promotes the secretion of fluid and electrolytes into the lumen of
the small intestine.
The enterotoxin is a protein molecule composed of 5 B subunits and 2 A subunits.
The B subunits are responsible for binding to a ganglioside (monosialosyl
ganglioside, GM1) receptor located on the surface of the cells that line the intestinal
mucosa.
 PATHOPHYSIOLOGY
Vibrio cholerae is transmitted to humans through the ingestion of contaminated food
or water, and produces a cholera toxin, which acts on the intestinal mucosa, and
causes severe diarrhea
The activation of the A1 subunit by adenylate cyclase is responsible for the net
increase in cyclic adenosine monophosphate (cAMP).
cAMP blocks the absorption of sodium and chloride by the microvilli and promotes
the secretion of chloride and water by the crypt cells.
The result is watery diarrhea with electrolyte concentrations isotonic to those of
plasma.
WHEN CHOLERA TOXIN IS RELEASED FROM THE
BACTERIA IN THE INFECTED INTESTINE, IT BINDS
TO THE INTESTINAL CELLS KNOWN AS
ENTEROCYTES.
THROUGH THE INTERACTION OF THE PENTAMERIC
B SUBUNIT OF THE TOXIN WITH THE GM1
GANGLIOSIDE RECEPTOR ON THE INTESTINAL
CELL, TRIGGERING ENDOCYTOSIS OF THE TOXIN
CAMP ACTIVATION
the A/B cholera toxin must undergo cleavage of the A1 domain from the A2 domain
in order for A1 to become an active enzyme.
Once inside the enterocyte, the enzymatic A1 fragment of the toxin A subunit enters
the cytosol, where it activates the G protein Gsa through an ADP-ribosylation
reaction that acts to lock the G protein in its GTP-bound form, thereby continually
stimulating adenylate cyclase to produce cAMP.
The high cAMP levels activate the cystic fibrosis transmembrane conductance
regulator (CFTR), causing a dramatic efflux of ions and water from infected
enterocytes, leading to watery diarrhoea.
PATHOPHYSIOLOGY
Fluid loss originates in the duodenum and upper jejunum;
the ileum is less affected. The colon is usually in a state of absorption because it is
relatively insensitive to the toxin.
However, the large volume of fluid produced in the upper intestine overwhelms the
absorptive capacity of the lower bowel, resulting in severe diarrhea.
MORTALITY/MORBIDITY
If untreated, the disease rapidly results in dehydration and can result in death in more
than 50% of infected individuals.
The mortality rate is increased in pregnant women and children
Incubation period is from some hours till 5 days (in average 48 hours).. Stool
volume during cholera is more than that of any other infectious diarrhea.
The characteristic cholera stool is an opaque white liquid that is not malodorous and
often is described as having a rice water
CLINICAL SIGNS
vomiting is a prominent manifestation of illness.
It occurs early in the course of the disease when the vomiting is caused by decreased
gastric and intestinal motility and later in the course of the disease when acidemia is
more likely
- Excessive thirst ,With 5-8% loss of normal body weight - Postural hypotension,
tachycardia, weakness, fatigue, and dry mucous membranes or dry mouth
Oliguria; glassy or sunken eyes; weak, thready, or absent pulse; wrinkled & quot;
washerwoman & quot; skin; and coma. Due to severe dehydration, cholera
manifests itself in decreased skin turgor
LABORATORY STUDIES
An elevated hematocrit value due to hemoconcentration may be found in nonanemic
patients.
Neutrophil leukocytosis may be found, especially in severe cases.
atients have elevated blood urea nitrogen and creatinine levels consistent with
prerenal azotemia. A reduced bicarbonate level
Diagnosis may be confirmed via identification of V. cholerae in the stool
TREATMENT
The primary goal of therapy is to replenish fluid losses caused by diarrhea and
vomiting.
Reserve the intravenous route of rehydration for patients who purge more than 10-20
mL/kg/h and for patients with severe dehydration.
Rehydration is accomplished in 2 phases, rehydration and maintenance
he goal of the rehydration phase is to restore normal hydration status, which should
take no more than 4 hours. Set the rate of infusion in severely dehydrated patients at
50-100 mL/kg/
TREATMENT
Lactated Ringer solution is preferred over isotonic sodium chloride solution because
saline does not correct metabolic acidosis.
Treatment for patient with cholera is drinking oral rehydration solution (ORS) in
order to counteract the cholera-induced dehydration
PRACTICAL GUIDELINES FOR THE
TREATMENT OF CHOLERA
Evaluate the degree of dehydration upon arrival.
Rehydrate the patient in 2 phases
These include rehydration (for 2-4 h) and maintenance (until diarrhea abates).
Register output and intake volumes on predesigned charts and periodically review
these data.
TREATMENT
only use the intravenous route
(1) during the rehydration phase for severely dehydrated patients for whom an
infusion rate of 50-100 mL/kg/h is advised,
(2) for moderately dehydrated patients who do not tolerate the oral route, and
(3) during the maintenance phase in patients considered high stool purgers (ie, >10
mL/kg/h).
TREATMENT
During the maintenance phase, use ORS at a rate of 800-1000 mL/h. Match ongoing
losses with ORS administration
Discharge patients to the treatment center if oral tolerance is greater than or equal to
1000 mL/h, urine volume is greater than or equal to 40 mL/h, and stool volume is
less than or equal to 400 mL/h.
ANTIBIOTICS
Azithromycin (Zithromax) - adult dose: 1 g PO once .
Tetracycline (Sumycin) –
Doxycycline - adult dose: 300 mg PO once .
Ciprofloxacin (Cipro) –
Erythromycin - adult dose:
Trimethoprim and sulfamethoxazole –
Norfloxacin –
Furazolidone (Furoxone) -
PREVENTION
Transmission of cholera is significantly reduced when uncontaminated water is
provided to the population.
Personal hiegine
Vaccines
______The End______