DR8.4 | Viral Wart Recognition — Summary & Reflection

KEY TAKEAWAYS

Viral warts are caused by HPV, which infects basal keratinocytes and drives them to proliferate, producing hyperkeratotic lesions with interrupted skin lines and black dots (thrombosed capillaries); the histological hallmark is the koilocyte, and warts spread by autoinoculation along trauma lines (Koebner phenomenon) with no ganglion latency. The four types are verruca vulgaris (rough exophytic papule, hands/periungual), verruca plantaris (inward-growing, painful on direct pressure, soles; mosaic variant), verruca plana (flat, multiple, face/hands, often linear), and filiform (thread-like, perioral/eyelid). The crucial everyday differential is the plantar wart versus the corn — corns let skin lines run through, lack black dots, and hurt on lateral pressure — and the wart versus the smooth, umbilicated molluscum. There is no systemic antiviral for HPV: management is watchful waiting (many self-resolve) or destructive/keratolytic treatment (salicylic acid, cryotherapy first-line; electrocautery, laser, intralesional agents, imiquimod for resistant lesions), with counselling to avoid scratching and to expect possible recurrence.

REFLECT

Think of a wart you have seen — perhaps a painful lump on a sole that someone had been treating as a corn, or a child's hand covered in rough papules. Could you, at the time, have used the paring test to read the skin lines and black dots and settle the diagnosis? Consider how you would explain to a parent that their child's warts are likely to clear on their own, why picking them spreads them, and why recurrence after treatment is common. Reflecting on a real lesion, and on how you would counsel the patient, turns the recognition rules — interrupted skin lines, black dots, the corn-versus-wart distinction — into a practical bedside habit you will use often.