Cholera
Cholera
Cholera
Cholera is an acute bacterial entric diseases of the GIT characterized by profuse diarrhea,
vomiting, massive loss of fluid and electrolytes that could result to hypovolemic shock,
acidosis and death.
Cholera was originally endemic to the Indian subcontinent, with the Ganges River likely
serving as a contamination reservoir. The disease spread by trade routes (land and sea) to
Russia, then to Western Europe, and from Europe to North America during the Irish
immigration period. Cholera is now no longer considered a pressing health threat in
Europe and North America due to filtering and chlorination of water supplies, but still
heavily affects populations in developing countries.
Source of Infection:
Vomitus and feces of infected persons and feces of convalescent or healthy carriers.
Contacts may be temporary carriers.
Etiologic Agent:
1. The organisms are slightly curved rods (coma shape), gram negative (-) and
motile with a single polar flagellum.
2. The organisms survive well at ordinary temperature and can grow well in
temperature ranging from 22-40 degrees centigrade.
3. They can survive well in ordinary temperature and can survive longer in
refrigerated foods.
4. An enterotoxin, choleragen, is elaborated by the organism as they grow in the
intestinal tract.
Incubation Period:
The incubation period ranges from a few hours to five days; usually one to three days.
Period of Communicability:
The organisms are communicable during stool positive stage, usually a few days after
recovery, however occasionally the carrier may have the organism for several months.
Mode of Transmission:
1. Fecal transmission passes via oral route form contaminated water, milk, and other
foods.
2. The organisms are transmitted through ingestion of food or water contaminated
with stool or vomitus of patient.
3. Flies, soiled hands and utensils also serve to transmit the infection.
1. Fluid loss is attributed to the enterotoxin elaborated by the organism as they lie in
opposition with the lining cells of the intestines.
2. The toxin stimulates adenylate cyclase, which results in the conversion of the
adenosine truphosphate (ATP) to cyclic adesine monophasphate (CAMP).
3. The mucosal cell is stimulated to increase secretion of chloride, associated with
water and bicarbonate loss.
4. The toxin acts upon the intact epithelium on the vasculator of the bowel, thus,
resulting in outpouring of intestinal fluids.
5. Fluid loss of 5 to 10 percent of the body weight resulting in dehydration and
metabolic acidosis.
6. If treatment is delayed or inadequate, acute renal failure and hypokalemia become
secondary problems.
Clinical Manifestations:
Diagnostic Exams:
• Rectal Swab
• Darkfield or phase microcopy
• Stool Exam
Modalities of Treatment:
Nursing Management: