Taxonomy and morphology
The genus Shigella belongs to the family Enterobacteriaceae. For study purposes, four clinically significant species are distinguished: S. dysenteriae, S. flexneri, S. boydii, and S. sonnei. It is useful to compare each species in a table format, as interspecies differences are most frequently tested on the exam.
Morphologically, shigellae are small gram-negative rods, non-motile (lack flagella), and non-capsulated. They do not form spores. They stain red in Gram staining due to the structure of the cell wall, which features a thin peptidoglycan layer and an outer membrane containing lipopolysaccharide.
Biochemical and cultural properties
Shigellae exhibit weak biochemical activity. Characteristic features include:
- absence of gas production during glucose fermentation;
- absence of hydrogen sulfide (H₂S) production;
- absence of lactose fermentation within 48 hours;
- the exception is S. sonnei, which ferments lactose slowly (after 72 hours).
According to their type of respiration, shigellae are facultative anaerobes. They are undemanding to nutrient media and grow well on simple and bile-containing media. On solid media, they form small, smooth, shiny, translucent colonies (S-forms); in liquid media, they cause diffuse turbidity. Selenite broth is used as an enrichment medium.
A distinctive feature of S. sonnei is dissociation into S- and R-forms (rough colonies), which is associated with the structure of the cell wall lipopolysaccharide: the completeness of the O-specific chain determines the colony type.
Virulence factors
The key characteristic of pathogenesis is invasiveness. Mutants that have lost toxin production but retained invasiveness remain pathogenic; the reverse ratio leads to a loss of virulence.
- Invasion factors are encoded by virulence plasmids and are present in all species; key invasins include the IpaBCD complex.
- Intra- and intercellular spread proteins lyse the eukaryotic cell membrane and ensure the movement of bacteria between enterocytes.
- Shiga toxin is produced by S. dysenteriae; other species produce shiga-like toxins. AB₅ structure: five B subunits form a pore, the A subunit enters the cell and binds to the 60S ribosomal subunit, inhibiting protein synthesis.
- Endotoxin (lipopolysaccharide) protects shigellae from low pH and bile.
The antigenic structure includes O-antigen (somatic, component of LPS) and K-antigen (capsular), which serve as the basis for serological differentiation.
Epidemiology and pathogenesis
Shigelloses are anthroponotic infections. The source is a sick person or a bacterial carrier. The localization of the pathogen is the distal intestine. Transmission factors include hands, flies, food, and feces. Transmission routes vary by species:
- S. dysenteriae — predominantly contact-household;
- S. flexneri — predominantly waterborne;
- S. sonnei — predominantly foodborne (alimentary).
Pathogenesis: penetration through M cells into the submucosal layer → engulfment by macrophages → macrophage apoptosis with the release of interleukin-8 → development of an inflammatory reaction and inflammatory diarrhea. Macrophage death grants access to epithelial cells from the basolateral side, leading to invasion and intercellular spread, which results in the formation of mucosal erosions. When shigellae die, Shiga and shiga-like toxins are released, damaging blood vessels; clinically, this manifests as bloody diarrhea with mucus.
Clinical presentation and immunity
The disease is called shigellosis (bacillary dysentery). The incubation period ranges from 1 to 4 days. Onset is acute: fever, spastic abdominal pain, followed by watery diarrhea progressing to stools with blood and mucus.
Severity depends on the pathogen species and the patient's age. The most severe course is caused by S. dysenteriae (often imported cases); the mildest is caused by S. sonnei. Diarrhea typically resolves within 2–3 days.
In immunity, a leading role is played by secretory IgA, which prevents bacterial adhesion, as well as cytotoxic antibody-dependent activity of intraepithelial lymphocytes.
Laboratory diagnostics, treatment, and prevention
The study material is stool. The primary method is bacteriological; the auxiliary method is serological (detection of antibodies and antigens).
- On MacConkey agar — colorless (lactose-negative) colonies;
- on triple sugar iron agar (TSI, Russell's medium) — alkaline slant, acidic butt without gas and without H₂S;
- additionally — stool smear staining with methylene blue to detect neutrophils as a sign of inflammation.
Treatment is primarily aimed at replenishing fluid and electrolyte losses and maintaining a diet. Bacteriophages may be used. In mild cases, antibiotics are not indicated. In severe forms, fluoroquinolones are prescribed, with trimethoprim/sulfamethoxazole as an alternative. Antiperistaltic drugs are contraindicated as they prolong fever, diarrhea, and pathogen excretion.
Prophylaxis. Specific: Shigellvak vaccine (purified S. sonnei lipopolysaccharide); a number of textbooks indicate the absence of specific prophylaxis, antibiotics are not used for prophylaxis. Non-specific: compliance with sanitary and hygienic standards: sewage treatment, chlorination of drinking water, food control, personal hygiene.
Key points
- The genus Shigella includes 4 species: dysenteriae, flexneri, boydii, sonnei.
- Gram-negative non-motile rods without a capsule, facultative anaerobes.
- S. sonnei ferments lactose after 72 hours and exhibits dissociation into S- and R-forms.
- The main pathogenicity factor is invasiveness; S. dysenteriae produces true Shiga toxin.
- Transmission routes differ: contact-household (dysenteriae), waterborne (flexneri), foodborne (sonnei).
- Pathogenesis: penetration through M cells, macrophage apoptosis, IL-8, inflammatory and bloody diarrhea.
- Diagnostics — bacteriological (MacConkey, selenite broth, TSI); serology is auxiliary.
- Treatment: rehydration; fluoroquinolones for severe forms; antiperistaltics are contraindicated.