Etiology and epidemiological features
The disease is caused by several variants of the microorganism: the classical cholera vibrio, El Tor vibrio, and the O139 strain. In addition, non-agglutinable (NAG) vibrios can be involved in the infectious process. It is important to consider the serotypes of microorganisms and their pathogenicity factors, among which toxin production undeniably plays the leading role.
The epidemiological pattern of the disease consists of several key links:
- Source of infection and factors contributing to the active spread of the disease among the population.
- Mechanism of infection and transmission routes, where the waterborne route is of primary and critical importance.
- Susceptibility of the population, seasonality of outbreaks, and features of post-infection immunity development.
Special attention should be paid to the specific features of the epidemiology of El Tor cholera, as well as historical and modern aspects of the development of epidemics and pandemics.
Pathogenesis and pathological anatomy
The development of the infection begins by overcoming the nonspecific defense factors of the gastrointestinal tract. The main localization and active reproduction of the pathogen occur in the lumen of the small intestine.
The pathogenetic chain includes the following stages:
- Adhesion of the cholera vibrio directly to the surface of enterocytes.
- Toxin release, where cholera enterotoxin poses the main danger.
- Mechanism of action of the enterotoxin, which has a powerful effect on the regulatory enzyme systems of intestinal cells.
Interference with enzyme systems triggers a cascade of severe disorders. The mechanisms of pathology development rapidly lead to profuse dehydration. This is followed by pronounced water-electrolyte and metabolic disorders. Ultimately, this provokes serious cardiovascular disorders that can culminate in life-threatening hypovolemic shock.
Differential diagnosis
The clinical presentation of cholera requires careful exclusion of other diseases with similar symptoms. Cholera must first be differentiated from:
- Foodborne toxicoinfections (FTI);
- Salmonellosis;
- Escherichiosis;
- Viral gastroenteritis.
Physician action algorithm and hospitalization
Upon detecting a suspected patient, a physician must act according to a strict algorithm, as every minute counts.
Emergency medical care: The cornerstone of treatment is the immediate initiation of rehydration of the patient. Replenishment of fluid losses and detoxification must be continuous, including during transport to the hospital.
Condition assessment and laboratory diagnostics:
- Bacteriological examination: prompt collection of the patient's vomit and stool to isolate the cholera vibrio.
- Assessment of the degree of dehydration: requires simultaneous determination of hematocrit (Ht), acid-base balance (ABB), and blood plasma electrolyte levels.
Organization of hospitalization: Hospitalization is emergent and strictly mandatory. Based on clinical and epidemiological indications, the patient is referred exclusively to an intensive care isolation box.
The physician is obliged to immediately notify the on-duty supervisor of the ambulance station about the identification of a suspected patient and all measures already taken. At the same time, staff safety remains an absolute priority—mandatory adoption of personal prevention measures upon contact with the source of infection.
Briefly: answers to topical questions
What biochemical mechanism underlies the action of cholera enterotoxin inside the enterocyte?
The biochemical mechanism of action of cholera enterotoxin consists of the sustained activation of the enzyme adenylate cyclase and the accumulation of cAMP. The toxin consists of a binding pentamer B and an active subunit A. Inside the cell, subunit A dissociates, and its A1 part inactivates the Gs protein, which acts as a regulator of adenylate cyclase.
Stages of pathogenesis:
- Enzyme stimulation — sustained activation of adenylate cyclase in epithelial cells.
- Growth of secondary messengers — a sharp increase in the level of intracellular cyclic adenosine monophosphate (cAMP).
- Transport impairment — the accumulation of cAMP blocks absorption and provokes massive secretion of water and electrolytes into the lumen of the small intestine, causing watery diarrhea.
Which polyionic crystalloid solutions are used for emergency intravenous rehydration in severe cholera?
For emergency intravenous rehydration in grade III–IV dehydration, polyionic crystalloid solutions administered via rapid IV infusion are used.
Solutions used:
- «Trisol» — «5-4-1» solution: NaCl, NaHCO3, KCl.
- «Acesol» — contains NaCl, Na acetate, KCl.
- «Chlosol» — contains NaCl, Na acetate, KCl.
- «Quartasol» — contains NaCl, Na acetate, NaHCO3, KCl.
To remember the basic algorithm for cholera, use the "three R" rule: Recognize (take cultures and differentiate from FTI), Rehydrate (continuously, even in transit), and Route separately (place in an intensive care isolation box with staff protection).
Class and exam questions
What infections is cholera differentiated from?
First and foremost, cholera is differentiated from foodborne toxicoinfections, salmonellosis, escherichiosis, and various viral gastroenteritis.
Where must a patient with suspected cholera be hospitalized?
The patient is subject to mandatory emergency hospitalization strictly to an intensive care isolation box.
Which blood parameters need to be monitored to assess dehydration?
For an accurate assessment of the degree of dehydration, it is necessary to simultaneously determine the hematocrit (Ht) level, acid-base balance (ABB) indicators, and plasma electrolytes.
What is the main pathogenicity factor of the cholera vibrio?
The ability of the pathogen to produce toxins plays a leading role in pathogenesis, in particular, the release of a specific enterotoxin that disrupts the function of enterocyte enzyme systems.
What else to study on this topic
- Characteristics and mechanism of action of released cholera toxins
- Specific features of the epidemiology of El Tor cholera
- The effect of enterotoxin on the regulatory enzyme systems of intestinal cells
- The role of nonspecific GI defense factors in the development of the disease
- Formation of post-infection immunity and seasonality of the disease
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