What is Cholera?

Cholera (lat. Cholera) is an acute intestinal anthroponous infection caused by bacteria of the species Vibrio cholerae. It is characterized by the fecal-oral mechanism of infection, damage to the small intestine, watery diarrhea, vomiting, the fastest loss of body fluid and electrolytes with the development of varying degrees of dehydration up to hypovolemic shock and death.

It spreads, as a rule, in the form of epidemics. Endemic foci are located in Africa, Latin America, India (Southeast Asia).

Causes of Cholera

More than 140 serogroups of Vibrio cholerae are known; they are divided into agglutinating type O1 cholera serum (V. cholerae O1) and non-agglutinating type O1 cholera serum (V. cholerae non 01).

“Classical” cholera is caused by the cholera vibrio of serogroup O1 (Vibrio cholerae O1). Two biovars (biotypes) of this serogroup are distinguished: classical (Vibrio cholerae biovar cholerae) and El Tor (Vibrio cholerae biovar eltor).

According to morphological, cultural and serological characteristics, they are similar: short curved movable sticks having a flagellum, gram-negative aerobes, are well stained with aniline dyes, do not form spores and capsules, grow on alkaline media (pH 7.6-9.2) at a temperature of 10- 40 ° C. El Tor cholerae vibrios, unlike classical ones, are able to hemolize sheep erythrocytes (not always).
Each of these biotypes by O-antigen (somatic) is divided into serotypes. The Inaba serotype contains fraction C, the Ogawa serotype contains fraction B and the Hikoshima serotype (more correctly Hikojima) contains fractions B and C. The cholera vibrio H-antigen (flagellum) is common to all serotypes. Vibrio cholerae form a cholera toxin (CTX) – a protein enterotoxin.

Vibrio cholerae non-01 cause varying severity of cholera-like diarrhea, which can also be fatal.

An example is the large epidemic caused by Vibrio cholerae serogroup O139 Bengal. It began in October 1992 at the port of Madras in South India and, rapidly spreading along the coast of Bengal, reached Bangladesh in December 1992, where in the first 3 months of 1993 alone it caused more than 100,000 cases of the disease.

Pathogenesis during Cholera

The digestive tract is the gateway to infection. Vibrio cholerae often die in the stomach due to the presence of hydrochloric (hydrochloric) acid. The disease develops only when they cross the gastric barrier and reach the small intestine, where they begin to multiply intensively and secrete exotoxin. In experiments on volunteers, it was found that only huge doses of cholera vibrio (10 “microbial cells) caused disease in individuals, and after the preliminary neutralization of hydrochloric acid of the stomach, the disease was able to cause after the introduction of 106 vibrios (i.e., 100,000 times lower dose )

The occurrence of cholera syndrome is associated with the presence of two substances in the vibrio:

  1. protein enterotoxin – cholerogen (exotoxin);
  2. neuraminidases.

Cholerogen binds to a specific enterocyte receptor – ganglioside.

Neuraminidase, breaking down the acid residues of acetylneuraminic acid, forms a specific receptor from gangliosides, thereby enhancing the action of cholerogen. The cholerogen-specific receptor complex activates adenylate cyclase, which, with the participation and through the stimulating action of prostaglandins, increases the formation of cyclic adenosine monophosphate (AMP). AMP regulates the secretion of water and electrolytes from the cell into the intestinal lumen by means of an ion pump. As a result of the activation of this mechanism, the mucous membrane of the small intestine begins to secrete a huge amount of isotonic fluid, which the colon does not have time to absorb. Profuse diarrhea begins with isotonic fluid.

Gross morphological changes in epithelial cells in patients with cholera cannot be detected (with a biopsy). It was not possible to detect cholera toxin neither in the lymph, nor in the blood of vessels departing from the small intestine. In this regard, there is no evidence that a toxin in a person affects any organs other than the small intestine. The fluid secreted by the small intestine is characterized by a low protein content (about 1 g per 1 l), contains the following amounts of electrolytes: sodium – 120 ± 9 mmol / l, potassium – 19 ± 9, bicarbonate – 47 ± 10, chlorides – 95 ± 9 mmol / l. The loss of fluid reaches 1 liter in an hour. As a result, a decrease in plasma volume occurs with a decrease in the amount of circulating blood and its thickening. There is a movement of fluid from the interstitial to the intravascular space, which cannot compensate for the continued loss of the liquid protein-free part of the blood. In this regard, hemodynamic disorders, microcirculation disorders that lead to dehydration shock and acute renal failure quickly ensue. Acidosis that develops in shock is exacerbated by a deficiency of alkalis.

The concentration of bicarbonate in feces is two times higher than its content in blood plasma. There is a progressive loss of potassium, the concentration of which in feces is 3-5 times higher compared to that of blood plasma. If you introduce a sufficient amount of fluid intravenously, then all violations quickly disappear. Incorrect treatment or its absence leads to the development of acute renal failure and hypokalemia. The latter, in turn, can cause intestinal atony, hypotension, arrhythmia, changes in the myocardium. Discontinuation of renal excretory function leads to azotemia. Disruption of blood circulation in the cerebral vessels, acidosis and uremia cause a disorder in the functions of the central nervous system and the patient’s consciousness (drowsiness, stupor, coma).

Diagnosis of Cholera

During an epidemic outbreak, the diagnosis of cholera in the presence of characteristic manifestations of the disease presents no difficulties and can be made on the basis of only clinical symptoms. The diagnosis of the first cases of cholera in an area where it had not existed before must be confirmed bacteriologically. In settlements where cases of cholera have already been reported, patients with cholera and acute gastrointestinal diseases should be actively detected at all stages of medical care, as well as through home visits by medical workers and sanitary officers. When a patient with a gastrointestinal disease is identified, urgent measures are taken to hospitalize him.

The main method of laboratory diagnosis of cholera is a bacteriological study in order to isolate the pathogen. Serological methods have an auxiliary value and can be used mainly for retrospective diagnosis. For bacteriological examination, stool and vomit are taken. If it is not possible to deliver the material to the laboratory within the first 3 hours after capture, preservative media (alkaline peptone water, etc.) are used. The material is collected in individual vessels washed from disinfectant solutions, on the bottom of which a smaller vessel, disinfected by boiling, is placed in a vessel or sheets of parchment paper. Discharge (10-20 ml) using metal disinfected spoons is collected in sterile glass jars or tubes, closed with a tight stopper. For active collection of material, rectal cotton swabs, tubes are used.

When examining convalescents and healthy individuals in contact with sources of infection, they first give a saline laxative (20-30 g of magnesium sulfate). When shipping the material is placed in a metal container and transported in a special transport with an accompanying person. Each sample is provided with a label that indicates the name and surname of the patient, the name of the sample, place and time of taking, the alleged diagnosis and the name of the person who took the material. In the laboratory, the material is seeded in liquid and solid nutrient media to isolate and identify a pure culture. A positive response is given after 12-36 hours, a negative answer is given after 12-24 hours. For serological studies, an agglutination reaction and determination of the titer of vibriocidal antibodies are used. It is better to examine paired sera taken at intervals of 6-8 days. Of the accelerated methods for laboratory diagnosis of cholera, methods of immunofluorescence, immobilization, microagglutination in phase contrast, and RNGA are used.

In the clinical diagnosis of cholera, it is necessary to differentiate from gastrointestinal forms of salmonellosis, acute Sonnet dysentery, acute gastroenteritis caused by protea, enteropathogenic Escherichia coli, staphylococcal food poisoning, rotavirus gastroenteritis. Cholera proceeds without the development of gastritis and enteritis and can only conditionally be attributed to the group of infectious gastroenteritis. The main difference is that with cholera there is no increase in body temperature and there is no abdominal pain. It is important to clarify the appearance of vomiting and diarrhea. With all bacterial acute gastroenteritis and toxic gastritis, vomiting first appears, and then after a few hours – diarrhea. With cholera, on the contrary, diarrhea appears first, and then vomiting (without other signs of gastritis). Cholera is characterized by such a loss of fluid with feces and vomit, which in a very short time (hours) reaches a volume that is practically not encountered with diarrhea of ​​another etiology – in severe cases, the volume of fluid lost may exceed the body weight of the patient with cholera.

Prevention of Cholera

A set of preventive measures is carried out in accordance with official documents.

The organization of preventive measures provides for the allocation of premises and their deployment schemes, the creation of a material and technical base for them, and special training for medical workers. A set of sanitary-hygienic measures is being taken to protect water sources, remove and disinfect sewage, and sanitary-hygienic control of food and water supply. When there is a risk of cholera spread, patients with acute gastrointestinal diseases are actively identified with their mandatory hospitalization in the provisional department and a single study for cholera. Persons who arrived from the foci of cholera without a certificate of observation in the outbreak undergo a five-day observation with a single study for cholera. The control over the protection of water sources and water disinfection is being strengthened. The fight against flies is carried out.

The main anti-epidemic measures for the localization and elimination of the focus of cholera:

  • restrictive measures and quarantine;
  • the identification and isolation of persons in contact with patients, vibriocarriers, as well as with infected environmental objects;
  • treatment of patients with cholera and vibriocarriers;
  • preventive treatment;
  • ongoing and final disinfection.

For persons who have undergone cholera or vibrio-carriage, dispensary monitoring is established, the terms of which are determined by orders of the Ministry of Health. Preventive and sanitary-hygienic measures in settlements are carried out during the year after the elimination of cholera.

For specific prophylaxis, cholera vaccine and cholerogen-toxoid are used. Vaccination is carried out according to epidemic indications. A vaccine containing 8-10 vibrios in 1 ml is administered under the skin, the first time is 1 ml, the second time (after 7-10 days) 1.5 ml. Children 2-5 years old are administered 0.3 and 0.5 ml, 5-10 years old – 0.5 and 0.7 ml, 10-15 years old – 0.7-1 ml, respectively. Cholerogenanatoxin is administered once a year. Revaccination is carried out according to epidemiological indications not earlier than 3 months after primary immunization. The drug is administered strictly under the skin below the angle of the scapula. Adults are injected with 0.5 ml of the drug (for revaccination also 0.5 ml). Children from 7 to 10 years old are injected with 0.1 and 0.2 ml, respectively, 11-14 years old – 0.2 and 0.4 ml, 15-17 years old – 0.3 and 0.5 ml. The international certificate of vaccination against cholera is valid for 6 months after vaccination or revaccination.