Mechanisms of development
The pathogenesis of shigellosis begins within the first hours after infection. It is important to understand that inflammatory and dystrophic changes affect not only the large intestine, but also the stomach, small intestine, and even the oral mucosa. At the same time, involvement of the upper gastrointestinal tract is often latent (impairing digestion, absorption, and motility), which requires attention when selecting pathogenetic therapy.
The key link is the migration of polymorphonuclear leukocytes to the site of Shigella invasion. This process triggers exudative inflammation, the severity of which ranges from catarrhal to diphtheritic and ulcerative-necrotic. Exudation is precisely what underlies the diarrheal syndrome in typical forms of the disease.
It is worth noting that shigellosis rarely becomes a generalized infection: the pathological process typically does not penetrate deeper than the lamina propria. Bacteremia is possible only as a brief episode (e.g., in S. dysenteriae infection in 7% of cases).
Clinical forms and variants
Domestic classification divides shigellosis into acute, chronic, and carrier states (although ICD-10 does not account for this division).
Acute forms are subdivided into:
- Colitic variant: a classical scenario with strict correlation between intoxication and involvement of the distal large intestine. It manifests with crampy abdominal pain (especially in the left iliac region), tenesmus, and scanty stool with mucus and blood.
- Gastroenteritic and gastroenterocolitic variants: often associated with the foodborne transmission route. Characterized by a short incubation period, abrupt onset with vomiting and watery diarrhea, and a risk of dehydration.
Symptom dynamics
In the colitic variant, the disease may manifest typically (simultaneous onset of intoxication and dyspepsia) or in a "flu-like" manner, where general toxic symptoms outpace intestinal ones. During convalescence, fever subsides faster than intestinal function recovers.
The gastroenterocolitic variant develops rapidly (within 6–24 hours). In the first hours, watery diarrhea without impurities is observed, and by the end of the day, typical colitic syndrome with mucus and blood in the stool joins. Severe cases can be complicated by exicosis, convulsions, and shock.
Briefly: answers to topical questions
What toxins (endo- and exotoxins) are released by bacteria of the genus Shigella during pathogenesis?
During pathogenesis, bacteria of the genus Shigella produce exotoxins and endotoxin (lipopolysaccharide).
- Shiga toxin (Shigella dysenteriae serotype 1) is an exotoxin with pronounced cyto-, neuro-, and enteroactivity, as well as hemolytic properties; it irreversibly blocks protein synthesis in cells. It enters the bloodstream, causing damage to the endothelium and renal glomeruli.
- Shiga-like toxins (other Shigella species) are produced in smaller amounts, and their action is restricted to the intestinal wall.
- Endotoxin (lipopolysaccharide) provides bacterial protection against low pH and bile, and in the human body, it causes endotoxemia and the manifestation of intoxication syndrome.
What stages of intracellular parasitism (adhesion, invasion, multiplication) do Shigella undergo in epithelial cells?
Shigella sequentially go through the stages of approaching cell membranes, adhesion, colonization, invasion into epithelial cells, and intracellular multiplication (most pronounced in colonocytes).
- Adhesion and colonization — preceded by Shigella approaching cell membranes via hydrophobic and/or electrostatic attraction, followed by adhesion and colonization.
- Invasion — penetration into epithelial cells. The main pathway occurs via M cells with subsequent penetration into intact epithelial cells through their basolateral membranes. The direct pathway occurs through ligand-receptor internalization of Shigella by the apical membranes of epithelial cells.
- Intracellular stage — intracellular multiplication of Shigella. Phagocytosis of Shigella also occurs; the pathological process continues provided that phagocytosis reactions are incomplete.
Class and exam questions
What is the main difference between lesions in shigellosis and salmonellosis?
In shigellosis, the pathological process usually does not extend beyond the lamina propria of the intestinal mucosa, whereas salmonellosis tends toward deeper penetration and generalization.
Why is the term "dysentery" considered obsolete?
It denotes only a symptom — spastic hemocolitis, which can occur not only in shigellosis but also in other intestinal infections.
What is the mechanism of diarrhea in the colitic variant of shigellosis?
The main mechanism is exudation caused by the massive efflux of polymorphonuclear leukocytes into the mucous membrane.
What else to study on this topic
- Development of local and humoral immunity in shigellosis
- Features of the chronic course and carrier state
- Principles of pathogenetic therapy for latent gastrointestinal disorders
- Criteria for assessing the severity of exicosis in the gastroenteritic variant
- Mechanisms of development of hypovolemic and toxic-infectious shock
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