## Diphtheria Toxin and Pseudomembrane Formation ### Mechanism of Toxin Action **Key Point:** Diphtheria toxin is an A–B exotoxin produced only by lysogenized strains of *C. diphtheriae* carrying the β-phage encoding the *tox* gene. The toxin causes: 1. Local tissue necrosis and fibrin deposition → pseudomembrane (gray-white, adherent, bleeds if removed) 2. Systemic effects: inhibition of protein synthesis via inactivation of elongation factor 2 (EF-2) ### Pseudomembrane Characteristics | Feature | Details | |---------|----------| | **Composition** | Dead epithelial cells, fibrin, RBCs, WBCs | | **Appearance** | Gray-white, leathery, firmly adherent | | **Location** | Throat, nasopharynx, larynx, trachea | | **Removal** | Bleeds profusely (high vascularity underneath) | | **Caused by** | Local toxin action + inflammatory response | **High-Yield:** The pseudomembrane is pathognomonic for diphtheria and is the hallmark clinical sign. Its formation is entirely dependent on diphtheria toxin production. ### Why Toxin, Not Structure? - **LPS** (endotoxin) is absent in gram-positive bacteria; *C. diphtheriae* is gram-positive and lacks an outer membrane. - **Teichoic acid** is a structural component involved in cell wall integrity, not toxin production. - **Pili-associated adhesin** aids colonization but does not cause tissue necrosis or pseudomembrane formation. **Clinical Pearl:** Only toxigenic strains (lysogenized with β-phage) cause diphtheria; non-toxigenic strains cause only mild pharyngitis.
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