Cryptococcus neoformans meningitis in AIDS patients has a characteristically gelatinous appearance on autopsy. The specific reason for the absence of inflammatory response despite high fungal burden is:
- A Melanin production in the capsule absorbing reactive oxygen species
- B Polysaccharide capsule of GXM (glucuronoxylomannan) suppressing TNF-alpha, IL-12, and neutrophil function ✓
- C Urease production alkalinizing phagolysosome pH
- D Phospholipase B degrading phagosome membranes
Explanation
The massive polysaccharide capsule (GXM, ~90% of capsule by mass) of Cryptococcus neoformans is shed into surrounding tissue and CSF; soluble GXM suppresses macrophage TNF-alpha production, inhibits IL-12, promotes IL-10 (anti-inflammatory), and impairs neutrophil chemotaxis; this explains the paucity of inflammatory cells ('soap bubble' lesions in cryptococcoma, gelatinous exudate on autopsy). Melanin produced by laccase uses catecholamines as substrate and helps resist oxidative killing, but capsule is the primary immune evasion. Urease alkalinization is a minor virulence factor. Phospholipase B enhances pulmonary invasion.
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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