A 25-year-old immunocompetent patient develops rapidly progressive headache, fever and meningismus. CSF shows: opening pressure 280 mmH2O, turbid appearance, 800 cells/mm3 (90% neutrophils), protein 350 mg/dL, glucose 20 mg/dL (serum glucose 90 mg/dL). India ink is negative. Gram stain shows gram-positive diplococci. Which virulence factor of the causative organism most critically enables evasion of complement-mediated lysis?
- A IgA protease — cleaves secretory IgA to prevent mucosal immunity
- B Pneumolysin — directly activates complement consumption without directing it against the organism
- C Surface-expressed factor H binding protein (fHBP) — recruits factor H to inhibit the alternative pathway convertase
- D Polysaccharide capsule — prevents C3b opsonisation and blocks MAC assembly by sterically hindering complement component access to the bacterial surface ✓
Explanation
The gram-positive diplococci with this CSF profile indicate Streptococcus pneumoniae. The polysaccharide capsule is the primary virulence factor enabling evasion of complement lysis: it sterically masks surface-deposited C3b from interacting with complement receptors on phagocytes and prevents the terminal membrane attack complex (MAC, C5b-9) from accessing the bacterial membrane by its thick hydrophilic nature. The capsule also inhibits alternative pathway activation by reducing the half-life of surface-bound C3bBb convertase. IgA protease is important for mucosal colonisation. Pneumolysin activates complement but consumes it away from the organism. fHBP (factor H binding protein) is a virulence factor of Neisseria meningitidis, not S. pneumoniae.
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.