## Shigella Virulence Factors **Key Point:** Shigella's pathogenesis depends on plasmid-encoded invasion proteins, not toxin production alone. ### Invasion Plasmid Antigen (Ipa) Proteins The **Ipa proteins** (IpaA, IpaB, IpaC, IpaD) are the primary virulence determinants encoded on a large plasmid (pINV). These proteins: 1. Form a type III secretion system (T3SS) that injects bacterial effectors into host cells 2. Trigger actin polymerization and membrane ruffling 3. Enable bacterial invasion of M cells and epithelial cells 4. Cause cytoskeletal disruption leading to cell lysis and spread ### Distinction from Other Factors | Factor | Role | Specificity | |--------|------|-------------| | **Ipa proteins** | Cell invasion, intracellular spread | Plasmid-encoded, essential for pathogenesis | | **Shiga toxin** | Cytotoxicity, HUS in some strains | Only S. dysenteriae type 1; not universal | | **LPS** | General endotoxin effect | Non-specific to Shigella | | **Flagella** | Motility | Absent in Shigella (non-motile) | **High-Yield:** Shigella is **non-motile** (lacks flagella) despite being a gram-negative rod. The absence of flagella is a key identifying feature. **Clinical Pearl:** The plasmid carrying Ipa genes is essential — plasmid-cured Shigella strains lose virulence entirely and cannot cause dysentery. **Mnemonic:** **IPA = Invasion Plasmid Antigen** — remember this is the *plasmid-encoded* invasion system that makes Shigella pathogenic.
Sign up free to access AI-powered MCQ practice with detailed explanations and adaptive learning.