Vibrio cholerae (Cholera)

Last updated: June 19, 2025

Vibrio cholerae (Cholera)

Block 1.5 Digestion & Defence I

Block 1.5 Digestion & Defence I

Anatomy clinical correlates: Viscera of the neck
Anatomy of the salivary glands
Anatomy of the oral cavity
Anatomy of the pharynx and esophagus
Chewing and swallowing
Esophageal motility
Esophagus histology
Gastrointestinal system: Structure and function
Hunger and satiety
Anatomy of the abdominal viscera: Esophagus and stomach
Enteric nervous system
Gastric motility
Gastroesophageal reflux disease (GERD)
Gastrointestinal hormones
Gastrointestinal system anatomy and physiology
Stomach histology
Anatomy of the abdominal viscera: Liver, biliary ducts and gallbladder
Bile secretion and enterohepatic circulation
Biliary colic
Gallbladder histology
Liver anatomy and physiology
Liver histology
Chronic pancreatitis
Pancreas histology
Pancreatic secretion
Colon histology
Lactose intolerance
Vitamins and minerals
Carbohydrates and sugars
Fats and lipids
Proteins
Blood components
Inflammation
Introduction to the immune system
Wound healing
Complement system
Cytokines
Innate immune system
Cell-mediated immunity of CD4 cells
Cell-mediated immunity of natural killer and CD8 cells
MHC class I and MHC class II molecules
T-cell activation
Vaccinations
Antibody classes
B- and T-cell memory
B-cell activation, differentiation, and contraction
Giardia lamblia
Contracting the immune response and peripheral tolerance
Bacterial structure and functions
Cell wall synthesis inhibitors: Penicillins
Mechanisms of antibiotic resistance
Prebiotics and probiotics
Epstein-Barr virus (Infectious mononucleosis)
Viral hepatitis
Hepatitis B and Hepatitis D virus
Hepatitis A and Hepatitis E virus
Hepatitis C virus
Jaundice
Viral structure and functions
Bacillus cereus (Food poisoning)
Campylobacter jejuni
Diarrhea: Clinical
Escherichia coli
Vibrio cholerae (Cholera)
Appendicitis
Glycolysis
Citric acid cycle
Electron transport chain and oxidative phosphorylation
Pentose phosphate pathway
Gluconeogenesis
Fatty acid oxidation
Fatty acid synthesis
Protein structure and synthesis
Amino acid metabolism
Nitrogen and urea cycle
Nucleotide metabolism
Physiological changes during exercise
Ketone body metabolism
Glycogen metabolism
Metabolic acidosis
Approach to diarrhea (pediatrics): Clinical sciences
Rotavirus
Norovirus
Salmonella (non-typhoidal)
VDJ rearrangement

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Cholera is a contagious infection caused by the bacteria Vibrio cholerae, which can in turn cause severe gastroenteritis and excessive watery diarrhea for several days.

Rapid dehydration and electrolyte imbalances can be fatal as suspected in the deaths of James K. Polk, the 11th President of the United States; and Charles the Tenth, King of France.

V. cholerae is a gram-negative, curved bacteria which looks like little red or pink comma-shapes on a gram stain.

It’s positive for oxidase and grows in alkaline media.

It has pili and a single polar flagellum, kind of like a tail, at one end which it uses for movement through the gastrointestinal tract.

It’s a facultative anaerobe so that means it can undergo respiratory and fermentative metabolism.

Transmission of V. cholerae typically occurs through a fecal to oral route.

This includes consuming untreated sewage water, and anything that comes in contact with it, like raw or undercooked fish including shellfish; and improper hygiene, like a lack of hand washing after a bowel movement.

Cholera tends to be more common in developing countries and places lacking advanced sanitation and sewage treatment facilities, with high rates in some locations in Africa and South America.

People who have low gastric acidity or have an O-blood type are particularly at risk for a severe infection.

Now, when V. cholerae enters the stomach it shuts down protein production to conserve energy and nutrients, and to survive the acidic environment.

But once V. cholerae is in the intestines, it uses its flagella to move toward the intestinal walls; propel through the mucous layer on top of the epithelial cells lining the intestines; and attach to the finger-like cellular projections, called villi, on the surface of the epithelial cells.

There, V. cholerae can begin to multiply and produce toxins.

And though V. cholerae does not enter the epithelial cells itself, the toxins do and they can cause a lot of trouble.

Now, the exact toxins produced can depend on the strain of V. cholerae.

Some strains produce toxins that won’t cause any, or maybe just mild clinical symptoms.

But some strains produce cholera enterotoxin, also called choleragen, which is most often the cause significant clinical symptoms.

When cholera enterotoxin enters the epithelial cells, it leads to the ADP-ribosylation of the Gs alpha subunit of G-protein.

So, this causes the G-protein to becomes permanently activated and it keeps activating a membrane-bound protein called adenylate cyclase.
This protein in turn leads to an overproduction of the intracellular secondary messenger protein, cyclic adenosine monophosphate, or simply cAMP.

Increase in cAMP causes chloride channels on the cells to increase the secretion of chloride into the lumen while inhibiting the channels that let sodium and chloride back into the cell.

Key Takeaways

Vibrio cholerae is a bacterium that causes cholera, a severe and contagious diarrheal disease. Cholera is transmitted through contaminated water or food and is most common in areas with poor sanitation and limited access to clean drinking water.

Some strains produce cholera enterotoxin, which acts on the intestinal epithelial cells in the small intestine, causing over-activation of the enzyme adenylate cyclase. This leads to an increase in the intracellular levels of cyclic AMP (cAMP) in the intestinal cells, which in turn leads to the secretion of large amounts of water and electrolytes into the intestinal lumen, resulting in the characteristic watery diarrhea of cholera.

Patients most often present with voluminous, profuse, watery diarrhea, vomiting, and dehydration, all of which lead to fatal dehydration and electrolyte imbalances. Treatment involves rehydration therapy to replace all the fluids and electrolytes that are lost through diarrhea. In severe cases, antibiotics such as tetracyclines, ciprofloxacin, or trimethoprim-sulfamethoxazole may be necessary.