Etiology and Epidemiology
The disease is caused by the Gram-negative bacterium Vibrio cholerae (cholera bacillus). In clinical practice, the most significant serogroups are O1 (including the El Tor biotype / El Tor and Inaba serotype / Inaba) and O139 (the Bengal strain / Bengal). Additionally, non-O1/non-O139 (NAG) vibrios exist, which are not agglutinated by cholera O1 antiserum.
The infection is endemic to several countries in Southeast Asia. The transmission mechanism is fecal-oral (via contaminated water, swimming, unwashed hands). Susceptibility to the disease is extremely high.
Clinical presentation
The disease has an acute onset. Unlike many other intestinal infections, cholera does not feature prominent abdominal pain.
Initially, the patient's bowel movements increase in frequency: the stool loses its fecal character, becoming watery, whitish, or light yellow, with no foul odor. Profuse, repeated vomiting soon develops, provoked by abdominal palpation. Body temperature usually remains normal (36.6 °C) or drops to hypothermia (e.g., 35.6 °C). Fever is not characteristic.
As fluid loss increases, the typical facial appearance of the patient (facies cholerica) develops: pinched features, sunken eyes with dark circles around them. Signs of severe dehydration (grades II–IV) develop:
- Pallor, dryness, and a marbled skin tone, acrocyanosis;
- Decreased skin turgor;
- Drop in blood pressure down to unmeasurable levels, weak pulse;
- Tonic cramps in the extremities (the patient may assume a forced lateral position);
- Lethargy, adynamia, and aphonia (whispering speech);
- A sharp decrease in urine output down to prolonged anuria (10–12 hours).
Laboratory diagnostics
Blood tests reveal signs of hemoconcentration: marked leukocytosis, elevated hematocrit (up to 60%), decompensated metabolic acidosis, hypokalemia, and hypochloremia.
The primary method for confirming the diagnosis is bacteriological. Stool and vomit samples are collected for testing (three times, every 4 hours). If the patient has no stool, a sample is collected using a rectal swab. Inoculation is performed on peptone water, alkaline agar, as well as Endo and Ploskirev media (Form 30).
As an additional method on days 5–7 of the disease, serological diagnostics can be used. However, medical tactics and the clinical diagnosis are established even before receiving the bacteriological culture results.
Treatment Management
Any patient with diarrhea arriving from an endemic region is subject to mandatory emergency hospitalization in an isolation ward of an infectious diseases hospital.
The main principle of treatment is immediate rehydration with polyionic solutions (e.g., Trisol):
- Stage I (Initial Rehydration): The goal is to replenish the volume deficit within 2 hours. The solution must be preheated to 38–40 °C. The volume is 9–10% of body weight. The first 2 liters are administered intravenously by rapid push infusion, after which the rate is reduced to 70–100 mL/min.
- Stage II (Correction of Ongoing Losses): Every 2 hours, the physician measures the volume of excreted fluid (stool, vomit) and infuses the exact equivalent volume of saline solution. Infusion is stopped only upon stable restoration of diuresis and the predominance of urine volume over stool volume over the last 6–12 hours.
After vomiting ceases, parenteral therapy is supplemented with oral rehydration solutions. Antibacterial therapy (e.g., ciprofloxacin 0.5 g twice daily for 5 days) aims at systemic eradication of the pathogen.
Discharge and Follow-up
The discharge criteria are complete clinical recovery and negative bacteriological culture results. Eradication monitoring begins 2 days after discontinuation of antibiotics (daily triple stool culture and a single duodenal content culture are performed).
After discharge, the convalescent is registered at the infectious diseases clinic (IDC) for 1 year. The bacteriological monitoring schedule is:
- Month 1: Once every 10 days;
- Next 5 months: Once a month;
- Subsequent 6 months: Once every 3 months.
If the pathogen is isolated again (bacterial carriage), a repeated course of antibacterial therapy strictly in a hospital setting is indicated.
Briefly: answers to topical questions
What is the pathogenetic mechanism of action of cholera toxin (choleragen) that leads to secretory diarrhea?
Secretory diarrhea in cholera is caused by a dual mechanism: activation of isotonic fluid secretion and blockade of electrolyte reabsorption.
The pathogenesis of toxin action includes the following stages:
- Toxin Structure (Choleragen) — the B pentamer binds to the cell, while subunit A dissociates into an enzymatic (A1) and a linking (A2) part.
- Cellular Action — subunit A1 inactivates the Gs protein, causing sustained activation of the adenylate cyclase enzyme in enterocytes.
- Accumulation of Mediators — cAMP synthesis increases sharply, triggering active secretion of water and ions into the intestinal lumen (at a rate of about 1 L/h).
- Blockade of Absorption — simultaneously, cGMP synthesis is suppressed, which turns off the function of the sodium pump.
As a result, a massive loss of electrolytes (sodium, potassium, bicarbonates) and water occurs, which is not compensated by reabsorption.
The clinical presentation of severe cholera can be remembered by the rule of the "Four As": Aphonia (whispering speech), Anuria (lack of urine), Adynamia (extreme lethargy), and Acrocyanosis.
Class and exam questions
Can a diagnosis be made before bacteriological culture results are available?
Yes. A presumptive diagnosis ("Cholera, severe course") is formulated based on clinical and epidemiological data for the immediate initiation of life-saving therapy.
Why should solutions be preheated before infusion?
Polyionic solutions must be heated to 38–40 °C to prevent the worsening of hypothermia (which frequently accompanies shock) and to improve microcirculation.
When is intravenous infusion stopped?
Continuous infusion is discontinued when diuresis is stably restored and the volume of excreted urine exceeds the volume of stool over the past 6–12 hours.
What else to study on this topic
- Pathogenesis of decompensated metabolic acidosis and hypokalemia in diarrheal syndrome.
- Characteristics of El Tor and Bengal strains, as well as NAG vibrios.
- Differential diagnosis of cholera with salmonellosis, shigellosis, and acute foodborne toxic infections.
- Complications of massive infusion therapy (cardiac arrhythmias, retrosternal pain).
- ICD-10 classification of intestinal infections (categories A00-A09).
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