Epidemiology


Etiology


Pathophysiology


  • Spirochetes invade the body → disseminate systemically within hours → bind to endothelial cells → inflammatory reaction → endarteritis and perivascular inflammatory infiltrates
    • May be obliterating if reactive endothelial hyperproliferation occurs and results in ischemia and necrosis.

Clinical features


Primary syphilis

  • Primary lesion (chancre)
    • Typically starts out as a solitary, raised papule (usually on the genitals)
    • Evolves into a painless, firm ulcer with indurated borders and smooth base
    • Resolves spontaneously within 3–6 weeks, typically without scarring
  • Nontender regional lymphadenopathy (e.g., involvement of the inguinal lymph nodes in genital primary syphilis)

Secondary syphilis

  • Disseminated disease due to the systemic spread of the spirochetes, inducing an immunologic reaction
  • Begins approx. 2–12 weeks after primary infection and typically lasts 2–6 weeks
  • Constitutional symptoms
  • Polymorphic rash
    • Typically disseminated, nonpruritic macular or papular rash
    • Involves trunk and extremities, also the palms and soles L9512.jpg
    • Reddish-brown or copper-colored
  • Condylomata lata
    • Broad-based, wart-like, smooth, white papular erosions
    • Painless
    • Located in the anogenital region, intertriginous folds, and on oral mucosa
  • Additional lesions

Diagnostics


Nontreponemal Tests

  • Examples: RPR, VDRL
  • Antibody: to cardiolipin-cholesterol-lecithin antigen
  • Sensitivity: Lower sensitivity in early infection

Treponemal Tests

  • Examples: FTA-ABS, TP-EIA
  • Antibody: to treponemal antigens
  • Sensitivity: Greater sensitivity in early infection

Treatment