Infectious diseases. Cholera. Etiology. Epidemiology. Pathogenesis (most important)

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Infectious diseases. Cholera. Etiology. Epidemiology. Pathogenesis (most important)

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6. Cholera. Etiology. Epidemiology. Pathogenesis

Cholera is an acute intestinal disease caused by Vibrio cholerae (serotype 01) capable of producing an enterotoxin. Manifestations of cholera range from asymptomatic to extremely severe forms, when the onset of the disease leads to hypovolemic shock, metabolic acidosis and, in untreated cases, death.

Etiology. The causative agent of cholera is a short, slightly curved, mobile Gram-negative bacillus with a single, polarly located flagellum. There are about 70 serotypes of the pathogen, but only serotype 01 causes true cholera. Vibrio grows well on various nutrient media. The causative agent of serotype 01 forms opaque, yellow colonies on them. Two different biotypes of V. cholerae 01 have been identified: classical and El Tor.

Epidemiology. Endemic outbreaks and epidemics of cholera are characterized by a pronounced seasonal pattern. The source of infection in cholera is only a sick person, or vibrio carrier. Individuals with asymptomatic or mild cholera play an important role in spreading the infection. Long-term bacteriocarrier, when the gallbladder of adults who have had cholera caused by El Tor, serves as the reservoir of the pathogen, does not occur in children. The mechanism of infection transmission is carried out through the external environment - the water way of infection is more important.

Pathomorphology and pathophysiology. The entrance gate of infection is the gastrointestinal tract, the main breeding site of vibrios is the lumen of the small intestine, where they attach to the surface of the epithelial cells of the mucous layer and produce enterotoxin, which is fixed on the receptors of the cell membrane. The active subunit of the toxin enters the cell and activates the enzyme adenylate cyclase. This contributes to increased production of cAMP, which leads to a decrease in the active absorption of sodium and chloride and an increase in the active secretion of sodium by crypt cells. The result of these changes is a massive release of water and electrolytes into the intestinal lumen.

A biopsy of the mucous membrane of the small intestine during this period of the disease reveals an intact epithelium with minimal reactive changes in the cells. Histological examination reveals an increase in the size and clarification of goblet cells, which indicates an increase in their secretion of mucus. There is also a slight edema of the lamina propria, an expansion of the blood and lymphatic vessels in the region of the tips of the intestinal villi.

The liquid released into the intestinal lumen is isotonic with plasma, it contains a large amount of sodium and potassium bicarbonate. The feces of children with cholera contain more potassium, and sodium, chloride and bicarbonate - less compared to the feces of adults with cholera. The loss of fluid leads to a deficiency of sodium and water, the development of acidosis and a decrease in potassium levels.

Author: Pavlova N.V.

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