Which virulence factor of Shigella is responsible for invasion of intestinal epithelial cells and is encoded by a plasmid?

Explanation

## Shigella Virulence Factors **Key Point:** Shigella's ability to invade and damage intestinal epithelium depends on plasmid-encoded virulence factors, not chromosomal genes alone. ### Invasion Plasmid Antigen (Ipa) The Ipa proteins (IpaA, IpaB, IpaC, IpaD) are the primary virulence determinants that enable Shigella to: 1. Invade non-phagocytic intestinal epithelial cells 2. Trigger actin polymerization and cell membrane ruffling 3. Escape the phagolysosome and replicate intracellularly 4. Spread to adjacent cells via actin-propelled movement **High-Yield:** Loss of the virulence plasmid (pINV) renders Shigella non-invasive and avirulent — it becomes a harmless commensal. ### Comparison of Shigella Virulence Factors | Factor | Encoded by | Function | Effect | |--------|-----------|----------|--------| | **Ipa proteins** | Plasmid (pINV) | Cell invasion, intracellular survival | Essential for pathogenesis | | **Shiga toxin** | Chromosome (Shigella dysenteriae type 1 only) | Protein synthesis inhibition | Hemolytic uremic syndrome (HUS) | | **LPS endotoxin** | Chromosome | Systemic inflammatory response | Fever, shock | | **Flagella** | Chromosome | Motility | Not present in Shigella (non-motile) | **Clinical Pearl:** Shigella is a non-motile, gram-negative rod that lacks flagella — this is why it relies on plasmid-encoded invasion mechanisms rather than flagellar-assisted penetration. **Mnemonic:** **IPA = Invasion Plasmid Antigen** — remember that Shigella's invasiveness is plasmid-dependent, not chromosomal.