Chlamydia trachomatis serovars L1, L2, L3 cause Lymphogranuloma Venereum (LGV). Which of the following best characterises the pathogenesis that distinguishes LGV from non-LGV chlamydia urogenital infections?
- A LGV serovars infect squamocolumnar junction epithelial cells exclusively, causing more superficial ulceration
- B LGV serovars produce a more cytotoxic MOMP (major outer membrane protein) causing immediate cell lysis
- C LGV serovars are more invasive and replicate within macrophages, spreading to regional lymph nodes causing buboes and systemic disease ✓
- D LGV infection elicits less fibrosis because LGV serovars do not activate TLR-2 on fibroblasts
Explanation
LGV serovars (L1–L3) are biologically more invasive than genital serovars (D–K). Unlike D–K which infect columnar epithelial cells of the urethra/cervix causing mucosal disease (urethritis, cervicitis), LGV serovars infect and replicate within macrophages, which carry them to inguinal lymph nodes via lymphatics. This causes dramatic inguinal lymphadenopathy (groove sign — inguinal and femoral node enlargement separated by Poupart's ligament), bubo formation, and systemic inflammation. Late sequelae include lymphatic obstruction, genital elephantiasis (esthiomene), and rectal stricture (proctocolitis). Diagnosis by nucleic acid amplification test (NAAT) with LGV genotyping; treatment is doxycycline 100 mg twice daily for 21 days (longer than non-LGV chlamydia).
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
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