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Causes and pathogenesis of cholera
Last reviewed: 23.04.2024
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Causes of Cholera
The causative agents of classical cholera (biovar vibrio cholera) and El Tor cholera (biovar vibrio cholera eltor) do not differ in morphological, cultural and biochemical properties from each other. These are gram-negative, curved or straight polymorphic sticks with a long flagellum providing active mobility. They facultative anaerobes, spores and capsules do not form, grow well on ordinary nutrient media (especially in meat-peptone broth and alkaline agar), forming a film after 3-4 hours on the surface of the liquid medium. Biovar El-Tor differs from the classical hemolytic properties.
From cholera patients, healthy vibrio-carriers and objects of the external environment, cholera-like vibrios (mutants) are distinguished, which differ from cholerae only in somatic O-antigen and are not causative agents of cholera. They were called "choleroid", and later - NAG-vibrios (not agglutinated with cholera sera vibrios).
According to the antigenic structure, cholera vibrios are divided into serological types:
- type Ogawa (contains antigenic fraction B);
- type Inaba (contains the antigenic fraction C);
- type of Psoshima (contains fractions B and C).
In addition, there are 5 more basic phagotypes (IV). Cholera Vibrio produces exotoxin-cholerogen, which is obtained in pure form and is represented by a protein consisting of two immunologically distinct fragments. He plays an essential role in the mechanism of the development of diarrheal 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 entrance gates of the infection serve only the GI tract, where the pathogen gets 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, responsible for diarrheal syndrome. In addition to exotoxin, other toxic substances and enzymes (mucinase, neuraminidase, proteases, etc.) play an important role in the pathogenesis of the development of the disease.
Under the influence of exotoxin (cholerogen) in intestinal enterocytes, activation of adenylate cyclase activates, 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. The pronounced diarrheal syndrome and frequent vomiting quickly lead to the development of toxicosis with II-III degree exicosis with characteristic clinical manifestations (symptoms of hypokalemia, microcirculatory disorders, development of acute renal and adrenal insufficiency, etc.). The severity of the condition and the clinical manifestations of the disease are directly dependent on the degree of dehydration. With a rapid loss of body weight of the patient (more than 10%) as a result of dehydration, the clinical picture of the cholera algid develops.