verruca vulgaris

**Etiology/Pathogenesis:** Human papillomavirus (HPV) is a non-enveloped, circular dsDNA virus. It infects basal keratinocytes through microabrasions. Verruca vulgaris is most often due to HPV 1, 2, 4, 27, and 57. Viral E6 and E7 proteins drive proliferation. In high-risk HPV types (16, 18), E6 inactivates p53 and E7 inactivates Rb. Those high-risk types are NOT the usual cause of common warts. They cause cervical, anal, and oropharyngeal cancers. Low-risk types such as 6 and 11 cause condylomata acuminata.

**Transmission:** Direct skin contact, fomites (e.g., pool decks, communal showers), and autoinoculation. Trauma and nail biting or picking promote spread (Koebner/isomorphic phenomenon). Immunosuppressed patients (HIV, transplant recipients) have more extensive, recalcitrant warts.

**Clinical presentation:** Firm, rough, flesh-colored to gray-brown, exophytic papules with a verrucous (cauliflower-like) surface. They are common on the hands, fingers, knees, and periungual areas. Thrombosed capillaries appear as black dots (pinpoint bleeding on paring). Skin lines are interrupted, which distinguishes warts from calluses and corns. Variants include: - Plantar warts (HPV 1): endophytic, painful with walking, and found on pressure points - Flat warts / verruca plana (HPV 3, 10): smooth, flat-topped papules on the face, dorsal hands, and shaving areas - Filiform warts: finger-like projections on the face or eyelids - Mosaic warts: confluent plantar plaques

**Histology:** Acanthosis, hyperkeratosis, parakeratosis, and papillomatosis. Koilocytes (keratinocytes with perinuclear halo and raisinoid, pyknotic nuclei) are found in the granular and upper spinous layers. The granular layer is prominent (hypergranulosis). Dilated, thrombosed capillaries are present in the dermal papillae.

**Diagnosis:** Usually clinical. Biopsy is reserved for atypical or refractory lesions and for suspected squamous cell carcinoma, especially in immunosuppressed patients.

**Management:** Spontaneous regression occurs in about 2/3 of cases within 2 years, mediated by cell-mediated immunity. Options include: - Topical salicylic acid (keratolytic) - Cryotherapy with liquid nitrogen - Cantharidin - Duct tape occlusion (limited evidence) - Imiquimod (TLR-7 agonist) - Intralesional Candida antigen or immunotherapy - 5-FU - Laser or surgical destruction (curettage, electrodesiccation) - Intralesional bleomycin for refractory cases

**Boards pearls:** - Koilocytes plus papillomatosis and hyperkeratosis point to HPV. - Common warts are NOT caused by the oncogenic HPV 16/18. - Warts that spread along scratch lines illustrate the Koebner phenomenon. - Molluscum contagiosum is a distinguishing pox virus lesion with a central umbilication and Henderson-Patterson bodies. - The HPV vaccine (Gardasil 9) covers types 6, 11, 16, 18, 31, 33, 45, 52, and 58. It does not target the usual common wart types. - Anogenital warts in a young child should prompt consideration of sexual abuse, though vertical or autoinoculated transmission is possible.