Pathogen characteristics
Bacterial dysentery is caused by microorganisms of the genus Shigella, belonging to the family Enterobacteriaceae. These are Gram-negative, non-motile bacteria (lacking flagella) capable of parasitizing within macroorganism cells.
The most critical indicator of their virulence is invasiveness — the ability to penetrate, multiply, and parasitize within the cells of the colonic mucosa and macrophages of the lamina propria. This process is mediated by specialized invasin proteins.
The criteria for differentiating Shigella species include their antigenic structure (O- and K-antigens), toxin-producing capacity, and biochemical activity. Interestingly, an inverse relationship exists between biochemical activity and pathogenicity: the higher the activity, the lower the pathogenicity of the pathogen.
Sources and mechanism of transmission
The transmission mechanism of the infection is the classic fecal-oral route. The primary reservoir and source of the pathogen are infected humans.
From an epidemiological perspective, patients with mild, mild/subclinical, or subclinical forms (bacterial carriers), as well as (to a lesser extent) patients with a chronic course, are of the greatest importance. They often remain undetected, continue to visit public places, and spread the pathogen. Flies serve as an important factor in the mechanical vectoring of the pathogen.
Mass outbreaks of dysentery occur when two key factors combine:
- The presence of undetected sources of infection within a community or workplace.
- Gross violations of sanitary and hygienic standards in the food industry or unsatisfactory conditions of water supply systems.
Species-specific transmission routes
A dominant transmission route has historically formed for each Shigella species. This is due to the peculiarities of their survival in the external environment and the required infectious dose.
| Pathogen species | Predominant transmission route |
|---|---|
| Shigella sonnei (subgroup D) | Foodborne |
| Shigella flexneri (subgroup B) and Boydii (subgroup C) | Waterborne |
| Shigella dysenteriae (subgroup A, including the Grigoriev-Shiga bacillus) | Contact-mediated |
Susceptibility and immunity
Susceptibility of the non-immune population to shigellosis is absolute (universal). Sometimes the entry of even single microbial cells into the gastrointestinal tract is sufficient for disease development. The infectious dose strictly depends on the species: for S. dysenteriae, it is minimal (only 3–5 bacteria), whereas for S. flexneri, it is 10–200 cells.
Post-infection immunity is extremely short-lived (lasting up to one year). It has strict type and species specificity, making reinfection with other serotypes possible. Intestinal local immunity plays the primary protective role in shigellosis. The incidence is characterized by pronounced summer-autumn seasonality, which coincides with the period of activation of infection transmission routes.
Epidemiological significance of toxin production and invasion
The pathogenesis of the infection is closely related to the properties of the pathogen. Upon entering the gastrointestinal tract, some of the bacteria die, releasing endotoxin and causing initial toxemia.
Surviving Shigella cells adhere to cells and penetrate into epithelial cells (colonocytes). The main route of invasion occurs via M cells of the lymphoid tissue, followed by penetration into intact epithelial cells through their basolateral membranes. Inside the cells, Shigella multiply, causing cell destruction (cytopathic effect) and massive inflammation due to the synthesis of interleukins (IL-1β, IL-8, TNF-α).
Shigella also produce exotoxins with entero-, cyto-, and neurotoxic properties. Shiga toxin, produced by Shigella dysenteriae, is the most dangerous. Its cyto-, neuro-, and enteroactivity exceeds that of Flexner and Sonne Shigella exotoxins by 1000 times. With the foodborne transmission route (typical for Sonne), toxins can accumulate directly in food products, which triggers a hypersecretory mechanism of diarrhea and leads to gastroenteritic clinical variants of the disease.
Briefly: answers to topical questions
What types of bacterial carrier states are distinguished in the epidemiology of shigellosis?
In the epidemiology of shigellosis, convalescent, subclinical, and transient bacterial carrier states are distinguished.
- Convalescent carrier state — occurs in patients immediately after recovering from acute shigellosis.
- Subclinical carrier state — Shigella are excreted by individuals without clinical manifestations of the disease at present and in the preceding 3 months, in the absence of changes in the mucosa of the distal colon.
- Transient carrier state — refers to one of the atypical clinical forms of the infection.
What are the survival factors of Shigella in the external environment, and at what temperature do they die?
Shigella possess relative resistance to environmental factors, but rapidly die at high temperatures.
The bacteria persist for a long time in water and on household items (up to 2–3 weeks), and survive in frozen and dried states for up to several months. Pathogens are highly sensitive to direct sunlight, UV radiation, and disinfectants.
Temperature regime for destruction:
- at temperatures above 60°C, Shigella die within 10 minutes;
- boiling results in instant death.
It should be noted that thermoresistant strains of S. flexneri and S. sonnei exist, which are capable of surviving at 59°C.
Mnemonic: Sonne likes to eat (foodborne), Flexner likes to drink (waterborne), and Dysentery (Grigoriev-Shiga) is transmitted via dirty hands (contact-mediated).
Class and exam questions
Who is the main source of infection in shigellosis?
The greatest danger is posed by individuals with mild, mild/subclinical, and subclinical forms (bacterial carriers), as they are not isolated and continue to actively spread the bacteria.
Does lasting immunity develop after having dysentery?
No, immunity is short-lived (lasting up to 1 year) and has strict species and type specificity. The local immunity of the intestinal wall plays the main protective role.
Does the infectious dose depend on the Shigella species?
Yes, only 3–5 bacteria are sufficient to infect with Shigella dysenteriae, whereas Shigella flexneri requires from 10 to 200 microbial cells.
Why does Shigella sonnei more frequently cause foodborne outbreaks?
This is due to the historically formed dominant transmission route for this serotype, in which exotoxins can accumulate directly in contaminated food products before consumption.
What else to study on this topic
- Clinical presentation of spastic hemocolitis
- Russian classification of Shigella (Stutzer-Schmitz, Ludge-Sachs, Newcastle)
- Molecular mechanisms of Shiga toxin action
- The role of phagocytosis and incomplete reactions in the pathogenesis of shigellosis
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