Human papilloma virus (HPV); over 200 types; can cause warts at any site; transmission is skin-to-skin contact or fomites via break in skin; spreads by autoinoculation and survival via immune system evasion; verruca in anogenital area and oropharynx in infants under 1 year of age most commonly acquired vertically and perinatally but sexual abuse should be excluded. Where did my child get it? And when? Time and place of acquisition are almost never obvious. HPV infection in childhood is very common, rarely serious, and usually self-limited. Often acquired from close friends and siblings with whom patients have frequent contact. Does it scar? Not usually, they are epidermal tumors. Some treatment modalities such as cryotherapy, carbon dioxide laser, and surgical removal have a higher risk of scarring and warts often recur in the scars. Will it spread and how? Yes. Both locally and via autoinoculation to distant locations; touching/picking and touching other areas can spread the virus. Persistence of HPV virus in apparently unaffected skin is common. Is it contagious? Yes, skin-to-skin contact and via fomites; damp surfaces, ie, gym floors, shower, and poolside. Wearing water shoes in the shower and avoiding activities where skin-to-skin contact is common such as wrestling may reduce the risk of acquisition. Should we separate siblings to prevent spread? Contact is inevitable so would probably anticipate spread to close contacts and resolution in a timely fashion for this rite of passage of childhood. 10.2. Palmar warts. 10.3. Plantar warts. Where and when did my child get this? Skin-to-skin contact with another child, swimming pool or bath with another infected child, incubation is 2 to 8 weeks; most common source are siblings and close friends. Does it scar? Potentially whether treated or not (it is a pox virus), much more likely when treated especially with aggressive destructive treatments (ie, liquid nitrogen). Will it spread and how? Yes. Both locally and via autoinoculation by scratching or skin-to-skin contact. Persistence of MCV virus in apparently unaffected skin is common. Is it contagious? Yes; generally contagious to other children who have not yet developed immunity—not to other adults; occasionally adults who escaped infection during childhood will acquire molluscum from their children or through sexual exposure. If we do nothing, what will happen? It may go away on its own, it may spread, and worst-case scenario, it lasts for two or so years, will usually remain asymptomatic and rarely become infected and scar; as a consequence, treatment (especially aggressive destructive measures that may result in scarring) is often not recommended. 10.4. Molluscum. 10.5. Molluscum, dermatoscopic view.
CHAPTER
10
LUMPS AND BUMPS
Warts
Synonyms
Verruca vulgaris: “common” warts; verruca plantaris: plantar warts; verruca plana: flat warts; condylomata acuminata: verruca acuminate, genital warts, anogenital warts, and venereal warts.
Inheritance
None.
Prenatal Diagnosis
None.
Incidence
Verruca vulgaris, plantaris, planus; very common, M = F; condyloma acuminata; 20% to 40% of sexually active women, F > M.
Age at Presentation
Verruca vulgaris: School-aged children to young adulthood, most common in 7 to 17 years of age; condyloma may be seen at birth and up to 3 years of age following perinatal exposure.
Pathogenesis
Key Features
Differential Diagnosis
Laboratory Data
Not necessary, diagnosis is clinical. However, if condylomata lata is considered then screening for syphilis, along with HIV.
Management
Prognosis
~60% of verrucae vulgaris resolve without treatment in 2 years, 80% by 4 years; verrucae plantaris are more likely to be treatment refractory, ~50% resolve regardless of treatment or not; verrucae planus can resolve spontaneously <2 years.
PEARL/WHAT PARENTS ASK
Skin
|
Associated Findings 
Molluscum Contagiosum
Synonyms
Molluscum, mollusca, and water warts.
Inheritance
None.
Prenatal Diagnosis
None.
Incidence
Common and rising; estimated incidence 2% to 10%.
Age at Presentation
School-aged children; <8 years most common and another peak in sexually active adolescents.
Pathogenesis
Molluscum contagiosum virus (MCV, types 1-4), majority are type 1; type 2 is often sexually transmitted, also associated with immunosuppression (HIV and hereditary immunodeficiency); transmission is via skin to skin contact, rarely fomites; spread by autoinoculation and survival via immune system evasion; worse in atopic dermatitis/eczema.
Key Features
Differential Diagnosis
Nevi, verrucae, condyloma acuminata, acne, juvenile xanthogranuloma (JXG), pyogenic granuloma, varicella, acrochordons, and milia; in HIV/immunosuppressed and if eruptive or large consider disseminated cryptococcosis/coccidioidomycosis.
Laboratory Data
Clinical diagnosis; biopsy is diagnostic if clinically suspicious, rarely necessary.
Management
Treatment is not usually necessary. Parent education before electing to treat is most important, weight risk vs. benefit; cantharidin (0.7%-0.9%) treated in office and washed off in 2 to 6 hours, applied at 3- to 4-week intervals, can be quite traumatic particularly and blister-forming, no evidence that it is better than placebo; 5% imiquimod cream applied 3 to 5 times per week by parent, curettage, cryotherapy, topical tretinoin, salicylic acid, alpha-hydroxy acids, tape stripping, oral cimetidine; all have no evidence they are better than placebo and may result in itching, pain, scarring, and spreading of lesions.
Prognosis
Good; spontaneous resolution likely within a few weeks to years, scarring possible particularly if destructive therapy (cryotherapy); 60% within 18 months, ~80% by 2 years regardless of treatment; molluscum dermatitis can develop associated with MC lesions, leads to scratching and autoinoculation but also can precede regression; secondary bacterial infection/impetiginization; if immunosuppressed then can develop persistent/giant lesions.
PEARL/WHAT PARENTS ASK
Skin
|
Associated Findings 
Pilomatricoma (PMX)
Synonyms
Calcifying epithelioma of Malherbe, pilomatrixoma, and trichomatricoma.
Inheritance
None.
Prenatal Diagnosis
None.
Incidence
Common; F > M.
Age at Presentation
First to second decade; 40% occur before age 10 years; rare familial association.
Pathogenesis
Benign tumor derived from hair matrix cells; keratinization, calcification, and ossification may occur.
Key Features
Differential Diagnosis
Epidermoid cyst, dermoid cyst, branchial cleft remnants, preauricular cleft/sinus, dermatofibroma (DF), other adnexal tumors, foreign body reaction, and osteoma.
Laboratory Data
Biopsy is diagnostic; lobules and nests of epithelial cells, basophilic cells, and eosinophilic shadow or “ghost” cells.
Management
Surgical excision or observation.
Prognosis
Good; excision is curative, occasional spontaneous regression, and rare malignancy.
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