Answer: D

Verruca vulgaris, also known as the common wart, is a benign cutaneous lesion caused by human papillomavirus (HPV) infection of the skin and mucosa and is most commonly seen in children and adolescents.8 Common warts are caused by a large group of the hundreds of identified HPV genotypes, most frequently types 1, 2, 27, and 57.8 Although warts are asymptomatic in immunocompetent patients, lesions have the potential to undergo malignant transformation in immunosuppressed patients due to impaired cell-mediated immunity and infection clearance.

HPV is a nearly universal infection that is eventually cleared by the immune system of healthy individuals. This ubiquitous infectious agent can give rise to a wide variety of clinical manifestations, including cutaneous or anogenital warts and malignancies of both the male and female reproductive tracts. HPV represents one of the most common causative agents of cutaneous infections in patients of all ages, with the greatest prevalence of verruca vulgaris occurring in primary school-aged children.10 Increased incidence of warts is also reported among immunocompromised patients and handlers of meat or fish, an occupation in which the skin of the hands is continuously exposed to moisture.10,11  

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Verruca vulgaris occurs as a result of viral inoculation of the epidermis through direct skin-to-skin contact or contact with contaminated surfaces.11,12 Individuals are increasingly susceptible to HPV infection if the barrier function of the skin is compromised by disruption or injury. Once the DNA virus has infected the basal epithelial layer, viral proteins use the host’s replication machinery to proliferate within the more superficial layers of the skin, creating benign growth.12 Children regularly spread the virus both through contact with others and autoinoculation, especially when putting their fingers in their mouths, which results in localized expansion of lesions.11 Risk factors involve contact with infected individuals, occupational contact with meat or fish, and immunosuppressed states, including HIV infection or after organ transplantation. Plantar infection may also occur by walking barefoot on contaminated surfaces, such as in communal showers.13

Verruca vulgaris presents as fleshy or pink papules of varying size with a verrucous surface. Common warts can develop on any part of the body, including mucous membranes, palms, and the soles as plantar warts. The most common distribution occurs along the fingers or dorsal surface of the hands.10 Warts caused by HPV serotype 1 have a characteristic presentation, often arising on the plantar surfaces in children aged <12 years.8 Typically, fewer than 4 lesions arise, and resolution usually occurs in <6 months. The pathognomonic feature of HPV on histopathologic examination are koilocytes, which are squamous epithelial cells surrounded by a perinuclear halo.10 The common wart appears largely benign on histologic examination, with prominent keratohyaline granules and dermal hypertrophy, leading to striking acanthosis and papillomatosis.11

The differential diagnosis of HPV includes other benign lesions that may present with a hyperkeratotic or verrucous papule, such as seborrheic keratoses, keratoacanthomas, or fibrokeratomas. Other cutaneous manifestations of viral infections, such as molluscum contagiosum caused by poxvirus, lead to similar skin lesions that are spread through skin-to-skin contact; however, verruca vulgaris lacks the central umbilication seen in poxvirus papules.14 Warts that coalesce along the nail beds may also resemble onychomycosis, so fungi should be cultured to distinguish the diagnosis. Verruca vulgaris may resemble malignant lesions, such as verrucous carcinoma or squamous cell carcinoma, and an excisional biopsy should be performed if the diagnosis is unclear based on clinical presentations alone or lesions are refractory to standard treatments.15

When a patient presents with 1 or multiple well-demarcated, fleshy papules on the fingers, hands, elbows, or knees, the diagnosis of verruca vulgaris traditionally is made based on established diagnostic criteria.16 However, in the case of an atypical lesion that cannot be readily diagnosed on examination, the lesion should be sampled for polymerase chain reaction (PCR) to detect viral DNA or a histopathologic examination should be performed.10 After the diagnosis is established, warts that do not spontaneously regress can be treated with a variety of therapeutic options, supported by limited clinical data. Topical salicylic acid, a keratinolytic agent that eradicates infected cells, is often used as first-line treatment for HPV.15 Other forms of immunotherapy, such as topical dinitrochlorobenzene, or ablation with cryotherapy are only associated with a moderate increase in resolution compared with placebo.15 The 3 available vaccinations against HPV aim to provide protection against the serotypes of the virus with the greatest risk of progression to malignancy of the genital tracts (6, 11, 16, and 18) but do not protect against the most common types associated with cutaneous infection. Some studies suggest that vaccination with the nonavalent HPV vaccine, which provides the greatest coverage, can aid in the treatment of diffuse verruca vulgaris in immunocompromised patients.17

The patient in the case presented was diagnosed with verruca vulgaris. He was treated with cryotherapy and prescribed topical salicylic acid. After several weeks, the patient’s lesions resolved.

Rachel E. Graubard, BSA, and McKenna E. Boyd, BS, are medical students at Baylor College of Medicine, in Houston, Texas. Christopher Rizk, MD, is a dermatologist with Elite Dermatology, in Houston, Texas.


1. Wollina U. Seborrheic keratoses – the most common benign skin tumor of humans. Clinical presentation and an update on pathogenesis and treatment options. Open Access Maced J Med Sci. 2018;6(11):2270-2275.

2. Hafner C, Vogt T. Seborrheic keratosisJ Dtsch Dermatol Ges. 2008;6(8):664-677.

3. Braun RP, Ludwig S, Marghoob A. Differential diagnosis of seborrheic keratosis: clinical and dermoscopic features. J Drugs Dermatol. 2017;16(9):835-842.

4. Hafner C, Vogt T, Hartmann A. FGFR3 mutations in benign skin tumorsCell Cycle. 2006;5(23):2723-2728.

5. Hafner C, Hartmann A, Oers JMMV, et al.FGFR3 mutations in seborrheic keratoses are already present in flat lesions and associated with age and localizationMod Pathol. 2007;20(8):895-903.

6. Braun RP, Rabinovitz H, Krischer J, et al. Dermoscopy of pigmented seborrheic keratosis: a morphological studyArch Dermatol. 2002;138(12):1556-1560.

7. Chakradeo K, Narsinghpura K, Ekladious A. Sign of Leser–TrélatBMJ Case Rep. 2016;2016:bcr2016215316

8. Bruggink SC, Koning MND, Gussekloo J, et al. Cutaneous wart-associated HPV types: prevalence and relation with patient characteristicsJ Clin Virol. 2012;55(3):250-255.

9. Scott M, Nakagawa M, Moscicki AB. Cell-mediated immune response to human papillomavirus infectionClin Vaccine Immunol. 2001;8(2):209-220.

10. Cardoso JC, Calonje E. Cutaneous manifestations of human papillomaviruses, a reviewActa Dermatovenerol Alp Pannonica Adriat. 2011;20(3):145-154.

11. Cubie HA. Diseases associated with human papillomavirus infectionVirology. 2013;445(1-2):21-34.

12. Tyring SK. Human papillomavirus infections: epidemiology, pathogenesis, and host immune responseJ Am Acad Dermatol. 2000;43(1 Pt 2):S18-26.

13. Loo SK, Tang WY. Warts (non-genital). BMJ Clin Evid. 2014;2014:1710.

14. Stulberg DL, Hutchinson AG. Molluscum contagiosum and wartsAm Fam Physician. 2003;67(6):1233-1240.

15. Miller DJ, Strauch RJ. Management of cutaneous warts of the handJ Hand Surg Am. 2015;40(11):2274-2276.

16. Young R, Jolley D, Marks R. Comparison of the use of standardized diagnostic criteria and intuitive clinical Ddiagnosis in the diagnosis of common viral warts (verrucae culgaris). Arch Dermatol. 1998;134(12):1586-1589.

17. Ferguson SB, Gallo ES. Nonavalent human papillomavirus vaccination as a treatment for warts in an immunosuppressed adultJAAD Case Rep. 2017;3(4):367-369.