secondary syphilis

Secondary syphilis is caused by the spirochete Treponema pallidum after it disseminates from the primary chancre site via blood and lymphatics. Key clinical features include: (1) a symmetric maculopapular rash characteristically involving the palms and soles (a distinguishing feature from many other rashes), (2) condylomata lata—broad, moist, wart-like plaques in warm, moist areas (perineum, vulva) that are highly infectious, (3) generalized lymphadenopathy, (4) mucous patches (painless mucosal erosions), (5) constitutional symptoms like fever, malaise, sore throat, and headache, and (6) patchy alopecia ('moth-eaten' appearance). Diagnosis involves nontreponemal tests (RPR, VDRL) for screening, which correlate with disease activity and can be used to monitor treatment response, followed by confirmatory treponemal tests (FTA-ABS, TPPA) which remain positive for life. Darkfield microscopy of lesion exudate can visualize spirochetes directly. Histopathology shows plasma cell-rich infiltrates with obliterative endarteritis. If untreated, secondary syphilis resolves spontaneously but may progress to a latent phase and eventually tertiary syphilis (gummas, cardiovascular syphilis, neurosyphilis) years later. Treatment is a single intramuscular dose of benzathine penicillin G (2.4 million units); patients with penicillin allergy require desensitization, especially in pregnancy. The Jarisch-Herxheimer reaction—a transient fever, chills, and myalgia occurring within 24 hours of treatment due to release of endotoxin-like substances from dying spirochetes—is a classic complication to distinguish from a true penicillin allergic reaction. Secondary syphilis is highly contagious due to the presence of numerous spirochetes in skin lesions and mucous patches. It is important to test for HIV co-infection and other STIs, and to notify and treat sexual partners.