Epidemiology


Etiology


  • Caused by Molluscum Contagiosum Virus (MCV), a member of the poxvirus family.
  • Transmission: direct skin-to-skin contact, autoinoculation (scratching), fomites, or sexual contact (adults).
  • Risk Factors:
    • Children (especially school-aged, due to close contact and swimming pools).
    • Atopic dermatitis (AD) due to impaired skin barrier facilitating spread.
    • Immunocompromised state (especially HIV with CD4 < 200).

Pathophysiology


Clinical features


  • Morphology: Flesh-colored, pearly, dome-shaped papules with characteristic central umbilication. c
  • Predilection sites:
    • In children: face, trunk, and extremities (e.g., axilla, antecubital and popliteal fossa)
    • In adults: lower abdomen, groin, genitalia, and proximal thighs

Diagnostics


  • Dx is typically made clinically based on the pathognomonic appearance of the lesions.
  • Histology is diagnostic and shows characteristic large, intracytoplasmic eosinophilic inclusion bodies, known as Henderson-Paterson bodies or molluscum bodies, within keratinocytes.
  • The epidermis shows cup-shaped, inverted lobular hyperplasia.

Treatment

  • First-line (Healthy Children)Reassurance & observation (spontaneous resolution typically occurs within 6–12 months). c
  • Active Intervention (Indicated for severe pruritus, rapidly spreading lesions, cosmetic concern, or sexual transmission in adults):
    • Physical: Cryotherapy (liquid nitrogen), curettage.
    • Chemical: Cantharidin (topical blistering agent; avoid on face due to scarring risk), podophyllotoxin, or salicylic acid.
    • Immunotherapy: Topical imiquimod.
  • Immunocompromised/HIVInitiate ART to restore CD4 count, which leads to clearance.