Interstitial keratitis (IK) due to congenital syphilis presents with corneal stromal vascularization (salmon patch). The mechanism by which Treponema pallidum causes corneal inflammation despite the organism not typically being found in the cornea is:

• A Type II cytotoxic hypersensitivity from anti-treponemal IgG cross-reacting with corneal collagen antigens
• B Type IV (delayed) hypersensitivity reaction where sensitized T-cells respond to treponemal antigens retained in the corneal stroma, causing stromal inflammation and neovascularization ✓
• C Immune complex deposition (type III) from high circulating antigen-antibody complexes in secondary syphilis
• D Direct spirochete invasion of corneal keratocytes detected only by PCR

Explanation

Interstitial keratitis in congenital syphilis is an immunological reaction rather than direct infection of the cornea. Treponema pallidum spirochetes invade various tissues (including corneal stroma) during the fetal period, eliciting T-lymphocyte sensitization. The IK of congenital syphilis typically manifests at age 5-20 years as a delayed hypersensitivity (type IV) response when sensitized T-cells encounter treponemal antigens (spirochete remnants or cross-reactive antigens) within the corneal stroma. This triggers stromal inflammation with progressive vascularization from the limbus. The inflammation is immune-mediated — hence the cornea typically shows no viable organisms. Systemic penicillin treats the infection but topical corticosteroids are needed to suppress the corneal immune response.

Reference: Khurana Comprehensive Ophthalmology, 7th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.