Syphilis

Syphilis is a chronic STD caused by Treponema pallidum, involving skin/mucosa and many organs with varied manifestations and latent asymptomatic periods. It is transplacental (congenital syphilis). Mostly sexually transmitted; clinically primary/secondary/secondary/latent stages. Class B notifiable disease under Chinese law.

Common Symptoms

Vesicle; macule; sore throat; depigmentation; Yue Jun; upturned saddle nose; mucous patch

Causes and Pathogenesis

T. pallidum was discovered in 1905 (Spirochaetales, Treponemataceae, Treponema). It is a slender spiral organism 5-20 µm long (avg 6-10) × 0.15 µm wide with 6-12 regular coils, slow regular motility, not stainable by ordinary dyes—seen by dark-field/phase microscopy. In vitro culture is difficult; rabbit testicular inoculation yields treponemes. Immunity: infection induces infection immunity; specific IgM appears at 2 weeks (does not cross placenta); IgG at 4 weeks (crosses). Early syphilis can be reinfected. TP damages tissues releasing cardiolipin antigen; reagin detected by RPR/USR/VDRL turns positive 5-7 weeks after infection or 2-3 weeks after chancre. Environmental resistance: low; loses infectivity at 40°C, killed 56°C/3-5 min/boiling; survives hours on damp objects but not drying; sensitive to soap/disinfectants (70% alcohol, 0.1% phenol, 0.1% mercuric chloride); cold-tolerant. Pathogenesis: treponemes enter intact mucosa/abraded skin, reach local nodes in hours, disseminate hematogenously in 2-3 days—so blood is infectious even before chancre. ID50 is 57 organisms; 500-1000 usually cause disease; time to primary lesion rarely >6 months. After 2-3 weeks (first incubation), chancre appears (primary syphilis). Histology: mononuclear then lymphocyte (T-cell) infiltration peaks day 13, then macrophages; treponemes seen intercellularly. Immunity clears treponemes by day 24 (immunofluorescence) and chancre heals—latent primary syphilis. Untreated survivors multiply; at 6-8 weeks massive spirochetemia causes secondary early syphilis (skin/mucosa/bone/eye/CNS involvement). Antibodies then clear most treponemes, secondary lesions resolve—latent secondary. Relapses occur when immunity falls; 90% in year 1. After 2 years, 30-40% progress to late syphilis with gummas. Late latent = positive serology/PCR without symptoms/visceral disease. Late syphilis involves skin/bone/CV/CNS; some self-cure. Pathology: (1) endarteritis with endothelial swelling/proliferation; (2) perivasculitis with lymphocytes/plasma cells; late gummas with epithelioid/giant cells and necrosis. Chancre: perivascular CD4/CD8 lymphocytes/plasma cells/histiocytes with endothelial proliferation and small-vessel occlusion. Secondary papules: hyperkeratosis, neutrophils in dermal papillae, mononuclear/plasma/lymphocytic perivascular infiltration. Condyloma lata: papillomatous epidermal hyperplasia with central necrosis, perivascular plasma cells (cuffing); treponemes in ~1/3 by silver stain. Tertiary: granulomas of epithelioid cells/macrophages with caseous necrosis; nodular syphilids are dermal (mild necrosis, no large vessels), gummas extend subcutaneously (marked caseation, large-vessel involvement).

Treatment

Drug therapy, supportive therapy

Preventive Measures

Follow treated early syphilis for 2-3 years (every 3 months year 1, every 6 months year 2, end of year 3). Abstain from sex until cured; women avoid pregnancy. Examine sex contacts within 3 months. Seek early care at STD clinics. Health education, screening, isolation, contact tracing.

Department to Visit

It is recommended to visit the STD department; an appointment can be booked on this platform before the visit.

Warm reminder: The above information is for health science reference only and cannot replace professional medical diagnosis. If you have related symptoms, please seek medical attention at a regular hospital promptly.