Medical expert of the article
New publications
Causes and pathogenesis of cholera
Last reviewed: 04.07.2025
All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.
We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.
If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.
Causes of cholera
The causative agents of classical cholera (biovar vibrio cholera) and El Tor cholera (biovar vibrio cholera el tor) do not differ from each other in morphological, cultural and biochemical properties. These are gram-negative, curved or straight polymorphic rods with a long flagellum, providing active mobility. They are facultative anaerobes, do not form spores and capsules, grow well on conventional nutrient media (especially well - in meat-peptone broth and alkaline agar), forming a film on the surface of the liquid medium after 3-4 hours. Biovar El Tor differs from the classical one in its hemolytic properties.
Cholera-like vibrios (mutants) are isolated from cholera patients, healthy vibrio carriers and environmental objects. They differ from cholera vibrios only by the somatic O-antigen and are not pathogens of cholera. They were called "cholera-like" and later - NAG-vibrios (vibrios not agglutinated by cholera serums).
According to the antigenic structure, cholera vibrios are divided into serological types:
- Ogawa type (contains antigenic fraction B);
- Inaba type (contains antigenic fraction C);
- Pshoshima type (contains fractions B and C).
In addition, there are 5 more main phage types (IV). The cholera vibrio produces an exotoxin-cholerogen, which is obtained in pure form and is represented by a protein consisting of two immunologically different fragments. It plays a significant role in the mechanism of development of diarrhea syndrome ("watery" diarrhea). In addition, in the human intestine, cholera vibrios produce destructive enzymes - proteases, mucinases, neuraminidase and some other toxic substances.
[ Pathogenesis of cholera
The only entry point for infection is the gastrointestinal tract, where the pathogen enters through the mouth with infected water, food, or from infected hands, household items, etc. The main place of reproduction of the vibrio is the small intestine. The process of reproduction of the vibrio is accompanied by the release of a large amount of exotoxin, which is responsible for the diarrhea syndrome. In addition to the exotoxin, other toxic substances and enzymes (mucinase, neuraminidase, proteases, etc.) also play a significant role in the pathogenesis of the disease.
Under the influence of exotoxin (cholerogen) in intestinal enterocytes, adenylate cyclase is activated, inducing, in turn, the accumulation of cyclic 3-5-adenosine monophosphate (cAMP), which causes hypersecretion of water and electrolytes by enterocytes into the intestinal lumen. Severe diarrhea syndrome and frequent vomiting quickly lead to the development of toxicosis with exicosis of grade II-III with characteristic clinical manifestations (symptoms of hypokalemia, microcirculatory disorders, development of acute renal and adrenal insufficiency, etc.). The severity of the condition and clinical manifestations of the disease are directly dependent on the degree of dehydration. With rapid loss of body weight of the patient (more than 10%) as a result of dehydration, the clinical picture of cholera algid develops.