Classification and Microbiological Properties
The genus is named after the Japanese bacteriologist K. Shiga and includes four main species, which differ in antigenic structure (O-antigen) and biochemical activity:
- S. dysenteriae (12 serovars) — the least stable in the environment, but the most virulent species.
- S. flexneri (9 serovars, subdivided into subserovars).
- S. boydii (18 serovars).
- S. sonnei (1 serovar, divided into chemovars) — the most biochemically active species, capable of slow lactose fermentation.
Morphologically, these are small ($0.5–0.7 \times 2–3$ µm) Gram-negative rods. They are non-motile, sporeless, and non-encapsulated. They are non-fastidious regarding nutrient media, producing uniform 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 produce gas during glucose fermentation, do not produce hydrogen sulfide, and (with the exception of delayed reactions in S. sonnei) do not ferment lactose.
Pathogenicity Factors and Invasion Mechanism
The ability of Shigella to invade host cells is controlled by a large invasion plasmid (120 MDa in S. sonnei, encoding the K-antigen; 140 MDa in other species). This plasmid encodes the type III secretion system (TTCC) and the synthesis of ipa BCD effector proteins.
The invasion process is strictly restricted to the large intestine because the ipa BCD proteins are degraded by small intestinal enzymes. Bacteria cross the mucosal barrier via M cells, are engulfed by macrophages, and induce macrophage apoptosis. This triggers a strong inflammatory response driven by cytokines (IL-1, IL-8). Subsequently, Shigella invade enterocytes from the basolateral side, multiply intracellularly, and spread laterally between cells, destroying the epithelial lining.
Toxins and Disease Pathogenesis
Upon bacterial lysis, toxins are released into the extracellular environment. S. dysenteriae serovar 1 produces a potent Shiga toxin (ST), whereas other species produce less potent Shiga-like toxins (SL-T).
The toxin binds to Gb3 receptors on endothelial cells and irreversibly inhibits protein synthesis by targeting the 60S ribosomal subunit. In S. dysenteriae infections, massive systemic release of the toxin leads to endothelial damage and glomerular microangiopathy, resulting in a severe complication: hemolytic uremic syndrome (HUS).
The clinical infection (shigellosis) manifests as colitis with bloody diarrhea. Bacteremia is generally absent. Different species show distinct primary transmission routes: S. flexneri is frequently waterborne, S. sonnei is foodborne (they can multiply in foods such as milk), and S. dysenteriae is transmitted primarily via the fecal-oral route (person-to-person contact).
Diagnosis and Prevention
The diagnostic gold standard for shigellosis is stool culture. The preferred specimen consists of mucus-pus-blood flecks from the stool. In acute cases, direct plating onto differential lactose-containing media is performed; for carrier screening, an enrichment broth (e.g., selenite broth) is used. The primary objective is to isolate lactose-negative colonies and confirm their identity.
Treatment involves targeted bacteriophages and antibiotics (guided by susceptibility testing). Prevention is primarily non-specific: strict sanitary control of water and food supplies, and proper personal hygiene.