## Virulence Factors of S. pneumoniae ### Correct Virulence Factors (Options 0–2) **Key Point:** S. pneumoniae possesses multiple redundant virulence mechanisms that work synergistically to evade immunity and cause tissue damage. | Virulence Factor | Mechanism | Clinical Significance | | --- | --- | --- | | **Polysaccharide capsule** | Inhibits complement deposition (C3b) and opsonization; prevents phagocytosis | Unencapsulated strains are avirulent; serotype determines invasiveness | | **Pneumolysin** | Oxygen-labile cholesterol-dependent cytolysin; creates pores in host cell membranes | Causes epithelial damage, triggers inflammation, enables bacterial spread | | **Hyaluronate** | Molecular mimicry of host hyaluronic acid in connective tissue | Evades innate immune recognition; poor immunogenicity | ### Why M Protein is NOT a Primary Virulence Factor in S. pneumoniae (Option 3) **High-Yield:** M protein is the signature adhesin and virulence factor of *Streptococcus pyogenes* (Group A Streptococcus), NOT S. pneumoniae. **Clinical Pearl:** S. pneumoniae uses **choline-binding proteins (CBPs)** and **pneumococcal surface proteins (PspA, PspC)** as primary adhesins for respiratory epithelial colonization. These proteins bind to choline residues on teichoic acids and facilitate attachment. **Warning:** Confusing M protein (GAS) with pneumococcal adhesins is a common trap. S. pneumoniae does NOT produce M protein. ### Summary of Pneumococcal Adhesins - **PspA (pneumococcal surface protein A):** binds respiratory epithelium; inhibits complement - **PspC:** binds to platelet-activating factor (PAF) receptor - **Choline-binding proteins:** interact with host cell receptors via choline moieties **Mnemonic: CAP-PL** — **C**apsule, **A**dhesins (PspA/PspC), **P**neumolysin, **P**rotein virulence factors, **L**ipoteichoic acid (LTA) triggers inflammation.
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