Principles of treatment for acute intestinal infections

Pathogen characteristics

The causative agent of typhoid fever is the typhoid bacillus — Salmonella typhi, belonging to the family Enterobacteriaceae. It is a motile, flagellated bacterium that does not form spores or capsules, and is Gram-negative.

Salmonella typhi is pathogenic only to humans. As a lymphotropic facultative intracellular parasite, it is capable of persisting in macrophages and transforming into L-forms. The optimal temperature for reproduction is 37°C, and the bacterium grows well on bile-containing nutrient media.

The antigenic structure of the pathogen is represented by:

• O-antigen: thermostable somatic (O-polysaccharide part of the endotoxin).
• Vi-antigen: superficial somatic.
• H-antigen: thermolabile flagellar.

Stability in the external environment

The typhoid bacillus has high environmental stability and is able to survive throughout the winter period. It survives in water for up to 3 months, in ice for 2 months, and on fruits and vegetables from 5 to 10 days.

At the same time, the pathogen is sensitive to high temperatures—it is killed instantly by boiling. Standard disinfectants (3% chloramine solution, corrosive sublimate 1:1000, 5% phenol solution, 3% lysol) destroy the bacteria within 2–3 minutes.

Epidemiology

Typhoid fever is a typical anthroponosis. Sources of infection include sick individuals, convalescents, and bacterial carriers. The pathogen is excreted primarily in feces and urine, contaminating water, food, and household items.

The mechanism of transmission is fecal-oral, realized via waterborne, foodborne, and contact-household routes. Susceptibility to infection among the non-immune population is universal. The incidence is predominantly sporadic in nature and is sustained by bacterial carriers (nearly 80% of infections occur from chronic carriers).

Following the infection, a stable, usually lifelong immunity is formed, although cases of re-infection are known.

Pathogenesis

The development of the infectious process includes several key stages:

1. Penetration: infection occurs orally (infectious dose 10⁷–10⁹ cells). Some bacteria die in the stomach, while the rest reach the alkaline environment of the small intestine.
2. Invasion: the pathogen penetrates the lymphoid formations of the gastrointestinal tract (solitary follicles, Peyer's patches), causing their sensitization and granulomatous inflammation.
3. Lymphogenic dissemination: spread to regional lymph nodes with their subsequent inflammation.
4. Bacteremia and endotoxemia: upon incomplete phagocytosis, the pathogen enters the bloodstream.
5. Hematogenous seeding: bacteria enter the organs of the reticuloendothelial system (liver, spleen, bone marrow), forming secondary foci.
6. Secondary bacteremia: re-entry of bacteria into the bloodstream and invasion into the sensitized lymphoid formations of the intestine, leading to necrosis.
7. Excretion: the pathogen is eliminated into the external environment.

Clinical presentation

The main clinical symptoms of typhoid fever include:

• Prolonged fever.
• Pronounced intoxication, which can lead to the development of encephalopathy.
• Hepatosplenomegaly (enlargement of the liver and spleen).
• Appearance of a characteristic roseolous rash.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Clinical classification and periods of the disease
• Main syndromes determining the severity of the course
• Complications of typhoid fever and the pathogenesis of their development
• Laboratory diagnostic methods (bacteriological and immunological)
• Principles of diet therapy, etiotropic and pathogenetic treatment
• Prophylaxis, dispensary follow-up, and sanitary-epidemiological surveillance

Other topics in the "Acute Intestinal Infections" section

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