In Salmonella typhi pathogenesis, bacteria survive within macrophages after phagocytosis. Which specific virulence mechanism allows S. typhi to resist phagolysosomal killing in macrophages?

• A Production of catalase and superoxide dismutase neutralizing reactive oxygen species
• B SPI-2 type III secretion system effectors prevent phagosome acidification and fusion with lysosomes ✓
• C Vi capsular antigen inhibits complement-mediated lysis
• D Lipid A modification reduces TLR4 recognition

Explanation

Salmonella Pathogenicity Island 2 (SPI-2) encodes a type III secretion system (T3SS-2) that is activated within the phagosome. SPI-2 effectors (SpiC, SseB-G, SifA) prevent phagosome acidification, inhibit NADPH oxidase recruitment, and block lysosome fusion, creating a unique membrane compartment called the Salmonella-containing vacuole (SCV) in which bacteria survive and replicate intracellularly. SPI-1 T3SS mediates initial invasion. Vi antigen reduces complement opsonization and TLR signaling but is not the mechanism of intracellular survival.

Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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