Cholera– an acute quarantine infectious disease that occurs with severe diarrhea, vomiting, leading to dehydration. Etiology. The causative agent is a mobile gram-negative bacterium Vibrio cholerae (cholera vibrio, or Koch’s comma). There are 3 types of pathogens – Vibrio cholerae asiaticae (the causative agent of classical cholera), Vibrio cholerae eltor (the causative agent of El Tor cholera) and serovar 0,T (Bengal) (the causative agent of cholera in Southeast Asia). The motility of bacteria is very pronounced, and its determination (using the hanging or crushed drop method) is an important diagnostic feature. Cell division occurs very quickly and on alkaline peptone water, the pathogen gives growth visible to the naked eye after 6 hours. Epidemiology. Cholera is a typical intestinal infection. The only natural reservoir is the sick and bacteria carriers, the main way of dereki is fecal-oral, less often by contact. Transmission factors: food, water, environmental objects. A certain role is played by flies that can transfer the pathogen from feces to food. Despite the fact that the release of the pathogen into the environment occurs within a short time, a large number of latent forms support the circulation of the pathogen. The only historical endemic focus of cholera is the delta of the Ganges and the Brahmaputra. There are 2 types of cholera epidemics: epidemic outbreaks with a single source of infection and distribution routes, characterized by the simultaneous appearance of a large number of cases, and low-level epidemics with a small constant incidence and difficult to detect routes of transmission of the pathogen. In the bulk of cases, an increase in the incidence is observed in the warm season. Pathogenesis. In the human body, most of the vibrios die under the action of the acidic environment of the stomach, and only a small part of them reach the small intestine. In response to the penetration of bacteria, the intestinal epithelium secretes an alkaline secret saturated with bile (bile is an ideal medium for the propagation of the pathogen). Clinical manifestations of cholera determine the ability to form exotoxins

    • Exotoxin (cholerogen) is a thermolabile protein, the toxin molecule includes 2 components: component B interacts with the monosialic ganglioside receptor, which causes component A to enter the cell. Component A consists of subunit A, (active center) and subunit A2, which binds both components. The A{ subunit catalyzes the ribosylation of the guanyl-dependent component of adenylate cyclase, leads to an increase in the intracellular content of cyclic 3,5-adenosine monophosphate and the release of fluid and electrolytes from the cells of the Lieberkühn glands

into the intestinal lumen. The toxin is not able to realize its action on any other cells. Serovar 0139 bacteria also produce an exotoxin with similar properties, but in smaller quantities; toxin formation is encoded by both chromosomal and plasmid genes

    • Hemolysins play a certain role in the lesions caused by the El Tor biotype.

Clinical picture

    • Most infected individuals are asymptomatic or may have mild diarrhoea. The ratio of severe lesions to the number of erased manifestations for classical cholera is 1:5-1:10, for El Tor cholera -1:25-1:100.
    • For clinically expressed cases, the incubation period varies from several hours to 5 days (approximately -2-3 days), characterized by general malaise, abdominal pain, vomiting and the development of severe diarrheal syndrome. The latter is characterized by the release of a significant amount (up to 10 l / day) of watery, colorless stools (rice water). Another characteristic feature is the sweetish, fishy (but not fecal) smell of stools.
    • In severe cases, diuresis sharply decreases in patients with the development of acute renal failure. Characterized by hoarseness or aphonia. The leading pathogenetic factor is hypovolemia and electrolyte deficiency. As a result, arterial hypotension, coronary insufficiency, impaired consciousness and hypothermia develop. A similar condition is defined as cholera algid. They note the characteristic manifestation of fades hippocratica (sunken eyes, pointed facial features with sharply protruding cheekbones). The duration of manifestations depends on the timely started, adequately conducted treatment and varies from several hours to several days. In the absence of treatment, the lethality of patients in the algid stage can reach 60%.
    • Recovery is accompanied by the development of short-term immunity, cases of re-infection are not often noted.

Research methods

    • Isolation and identification of the pathogen; the objectives of the research are to identify patients and bacteria carriers, establish the final diagnosis in the study of the dead, monitor the effectiveness of treating sick people and sanitation of carriers, control over environmental objects and the effectiveness of disinfection measures Materials for research – feces, vomit, bile, sectional material (fragments of the small intestine and gallbladder), bed and underwear, water, sludge, sewage, hydrobionts, washings from environmental objects, food products, flies, etc. The most objective results are obtained by examining samples taken before starting antibiotic therapy.
    • Blood test – signs of dehydration (acidemia, acidosis, hypokalemia, hyponatremia, hypochloremia, hypoglycemia, polycythemia, minor neutrophilic leukocytosis)

Differential diagnosis is made with various severe diarrheas (for example, caused by Shigella species, E. coli or enteropathogenic viruses).


    • Etiotropic therapy
    • Adults and children over 8 years old – doxycycline 300 mg

1 r / day, or 100 mg 2 r / day or tetracycline 50 mg / day

kg/day for 3 days.

    • Children under 8 years old – trimethoprim-sulfamethoxazole (co-tri-moxazole) 4 mg / kg trimethoprim and 20 mg / kg sulfamethoxazole after 12 hours or furazolidone 5-10 mg / kg / day in 4 doses every 6 hours for 3 days.
    • Pregnant women – furazolidone 100 mg 4 r / day for 7-10 days.
    • Compensation for the loss of fluid and electrolytes in accordance with the degree of dehydration of the diseased.
    • In mild and moderate forms – oral rehydration (solution of rehydration salt [NaCl 3.5 g, potassium chloride 1.5 g, glucose 20 g, trisodium citrate 2.9 g in 1 liter of water], glucosolan or citraglucosolan).
    • In severe form – the introduction of saline solutions in / in (tri-salt, chlosol, acesol, etc.).


    • Asiatic cholera
    • epidemic cholera
    • rice water diarrhea


  • AOO Cholera
  • A00.9 Cholera unspecified Literature. 129: 277—281

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