Chlamydia trachomatis causes trachoma (serotypes A-C) and genital infections (D-K). The specific virulence mechanism by which C. trachomatis avoids phagolysosome fusion after entering epithelial cells is:

• A LPS of C. trachomatis activates TLR4 signaling that blocks acidification
• B Elementary body (EB) produces a CAP (clathrin-associated phosphatase) preventing endosome maturation
• C The inclusion membrane protein IncA sequesters SNAREs required for lysosome-phagosome membrane fusion ✓
• D MOMP (major outer membrane protein) mimics CD59 to inhibit complement membrane attack

Explanation

After entry as elementary bodies (EBs), Chlamydia resides within a specialized intracellular vacuole (inclusion) that avoids fusion with lysosomes; the inclusion membrane proteins (Incs), particularly IncA, decorate the inclusion surface and interact with host SNARE proteins; IncA directly binds and sequesters VAMP3/7/8 (v-SNAREs) required for late endosome-lysosome fusion, preventing phagolysosome formation. Chlamydia has non-classical LPS (lacking typical lipid A endotoxicity). No CAP enzyme has been described for Chlamydia. MOMP is the immunodominant surface protein but does not mimic CD59.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.