What is Cholera?. Cholera. A life-threatening secretory diarrhea induced by enterotoxin secreted by V. cholerae Water-borne illness caused by ingesting water/food contaminated by copepods infected by V. cholerae An enterotoxic enteropathy (a non-invasive diarrheal disease)
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What is Cholera?
Recent Cholera Pandemics
may be cause of 8th pandemic
小川型 稻叶型 彦岛型
In 1993, an entirely new serogroup (O139) cause an epidemic in Bangladesh.
O139 organisms produce a polysaccharide capsule but do not produce O1 LPS or O1 antigen.
Non-O1, Non-O139 Serogroup
Most are CT (cholera toxin) negative and are not associated with epidemic disease.
Profile of vibrio cholerae
Physiology of Vibrio
People with low gastric acid levels (103 -105 CFU )
Children: 10 × more susceptible than adults
O>> B > A > AB
During acute stage
A few days after recovery
By end of week, 70% of patients non-infectious
By end of third week, 98% non-infectious
More severe symptoms
Rapid loss of body fluids
Rapidly lose more than 10% of bodyweight
Dehydration and shock
Death within 12 hours or less
Death can occur within 2-3 hours
Pathogenesis of V. cholerae
- heat stable endotoxin
- enterotoxin (exotoxin [cholera toxin CT])
CT is antigenically and pharmacologically identical in all sero and bio types
H2O, Na+ and other electrolytes follow due to the osmotic and electrical gradients caused by the loss of Cl-.
The lost H2O and electrolytes in mucosal cells are replaced from the blood.
Thus, the toxin-damaged cells become pumps for water and electrolytes causing the diarrhea, loss of electrolytes, and dehydration that are characteristic of cholera.
cholera from other causes of severe diarrhea:
Enterotoxigenic E. coli
Bacterial food poisoning
Pathogenesis of Hp
CagA (Cytotoxin associated)
VacA (vacuolationg associated)
LPS also play great importance
Flagellum and urease is necessary for its adhesion and inhabitation
Duodenal Ulcer (DU)
Gastric Ulcer (GU)
watery and spreading
round and convex
Pathogenesis of Campylobacter