Classification and microbiological properties
The genus is named after the Japanese bacteriologist K. Shiga and includes four main species that differ in antigenic structure (O-antigen) and biochemical activity:
- S. dysenteriae (12 serovars) is the least stable, but most dangerous species.
- S. flexneri (9 serovars, divided into subserovars).
- S. boydii (18 serovars).
- S. sonnei (1 serovar, divided into chemovars) is the most biochemically active, capable of slowly fermenting lactose.
Morphologically, they are small ($0.5–0.7 \times 2–3$ µm) Gram-negative rods. They are non-motile, non-spore-forming, and unencapsulated. The bacteria are undemanding regarding nutrient media, producing turbidity in liquid media and small smooth colonies on solid media. S. sonnei is characterized by colony dissociation (S- and R-forms).
Unlike Escherichia and Salmonella, Shigella species are "silent" bacteria. They do not release gas during glucose fermentation, do not produce hydrogen sulfide, and (with the exception of a late reaction in S. sonnei) do not ferment lactose.
Pathogenicity factors and mechanism of invasion
The ability of shigellae to invade cells is controlled by a large invasion plasmid. In S. sonnei, its mass is 120 MDa (and it encodes the K-antigen), while in other species it is 140 MDa. The plasmid ensures the functioning of the secretion system (TTCC) and the synthesis of ipa BCD effector proteins.
The invasion process is strictly restricted to the large intestine because ipa BCD proteins are degraded by small intestinal enzymes. The bacteria penetrate through M cells, are engulfed by macrophages, and induce their death (apoptosis). This triggers inflammation due to cytokine release (IL-1, IL-8). Shigellae then invade enterocytes from the basolateral side, multiply intracellularly, and spread between cells, destroying the epithelium.
Toxins and disease progression
Upon the death of shigellae, toxins are released into the environment. S. dysenteriae serovar 1 produces a potent Shiga toxin (ST), while other species produce less concentrated Shiga-like toxins (SL-T).
The toxin binds to Gb3 receptors on the endothelium and irreversibly blocks protein synthesis at the ribosomes (60S). In the case of S. dysenteriae, a massive release of toxin into the bloodstream leads to vascular and glomerular damage in the kidneys, which can cause a severe complication — hemolytic uremic syndrome (HUS).
The infectious process itself (shigellosis) presents as colitis with bloody diarrhea. Bacteremia (circulation of bacteria in the blood) does not occur. Different species have characteristic routes of transmission: S. flexneri is more commonly waterborne, S. sonnei is foodborne (where they can even multiply, e.g., in milk), and S. dysenteriae is transmitted via contact-household routes.
Diagnostics and prevention
The basis of shigellosis diagnosis is bacteriological culture. The material used consists of feces (mucoid-purulent-bloody flakes). In acute disease, direct inoculation onto differential lactose media is performed; for carrier screening, an enrichment medium (selenite broth) is used. The laboratory technician's goal is to find lactose-negative colonies and identify them.
Treatment includes the use of specific bacteriophages and antibiotics (only after susceptibility testing). Prevention is non-specific: strict sanitary control of water and food, and personal hygiene.
Briefly: answers to topical questions
What antigens are included in the antigenic structure of shigellae?
- Somatic O-antigen (O-antigen) is the basis of shigella classification, determining their serovar.
- Surface K-antigen (K-antigen) is a surface antigen possessed by the phase 1 antigen in the species S. sonnei.
What specific differential diagnostic media are used for primary stool inoculation for shigellosis?
- Solid lactose-containing differential media (media) are used for direct stool inoculation in overt disease.
- Ploskirev medium (Ploskirev medium) is a medium specifically indicated in sources, where lactose differentiates shigellae/salmonellae, which form colorless colonies, from E. coli, which forms dark red colonies.
- Selenite broth (selenite broth) is not a differential diagnostic medium for primary inoculation, but an enrichment medium; it is used when searching for carriers with subsequent subculturing onto solid media.
What type of immunity is formed after recovering from shigellosis?
- Post-infectious immunity (post-infectious immunity) develops after recovering from the disease and is short-lived (from 6 months to 1 year).
- Species- and type-specificity (species- and type-specificity) is a characteristic feature of defense where repeated infections with shigellae of the same species and serotype are required to build robust immunity.
Class and exam questions
How do Shigella species fundamentally differ from Salmonella species biochemically?
Shigella species do not produce gas during glucose fermentation and do not generate hydrogen sulfide ($H_2S$), whereas Salmonella species actively produce hydrogen sulfide and gas.
Why do shigellae affect only the large intestine?
Their invasion proteins (ipa BCD) are sensitive to trypsin and are destroyed in the small intestine, remaining active only in the distal parts of the GI tract.
Which species of Shigella causes the most severe forms of the disease?
S. dysenteriae serovar 1. It produces true Shiga toxin in large quantities, which can lead to kidney damage (HUS).
What else to study on this topic
- Structure and functions of the shigella invasion plasmid
- Features of S- and R-dissociation in S. sonnei
- Differential diagnostics of enteric infection pathogens (Escherichia, Shigella, Salmonella)
- Molecular mechanism of Shiga toxin action on the eukaryotic cell
- Mechanisms of intestinal mucosal local immunity formation
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