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Boy’s papule develops lymphangitic streak


A baffled mother brings her 14-year-old son for evaluation of an asymptomatic bump that appeared on the side of his right third finger 1 week ago.


A baffled mother brings her 14-year-old son for evaluation of an asymptomatic bump that appeared on the side of his right third finger 1 week ago. Within the past 24 hours, he developed a long, pruritic, nontender red streak extending from the finger lesion to the upper arm. 

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DERMCASE diagnosis: Infected verruca vulgaris (common wart)

Because of the patient’s history of acute onset of an unusual appearing lesion on his right finger and nontender lymphangitis, a bacterial culture and a small shave biopsy were taken from the crusted hemorrhagic papule, and he was started on oral cephalexin. The culture subsequently grew Staphylococcus aureus, and the biopsy showed changes typical of a common wart. The lymphangitis improved within 24 hours and resolved the following day. The plan was to start topical treatment for the wart the following week. Although the wart may have been present for weeks or months, it was suspected that incidental trauma might have resulted in bleeding into a subtle wart and secondary infection.

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Verruca vulgaris (common wart) presents as a benign, skin-colored, scaly superficial tumor. Lesions result from human papillomavirus (HPV) infection of the skin and mucous membranes. In children, common warts most commonly develop on the fingers, hands, and feet, although any site can be affected.


A recent study showed that 33% of school-aged children are infected with cutaneous warts.1 Young age and non-Caucasian skin types were associated with increased chances of clearance of cutaneous warts.2 However, consistent epidemiological data is limited because most studies focus on specific population subsets.3

Clinical presentation

Common warts are typically painless exophytic papules with rough scaly surfaces that vary from small papules at dry sites (eg, extensor surfaces of the extremities) to confluent cauliflower-like plaques in moist intertriginous areas. Trauma can result in prominent thrombosed vessels resulting in purple-black discoloration and hemorrhagic crusts and vesicles.4 Common warts can emerge on the elbows and knees in addition to the dorsal surfaces of the fingers, hands, and feet.5

Pathophysiology and etiology

Although over 120 HPV genotypes have been identified and many may be associated with verruca vulgaris, HPV-2 and HPV-4 are the most frequent culprits.6 Transmission of warts can be attributed to direct contact with an HPV-infected person or from a contaminated surface. Human papillomavirus enters epithelial cells through a minor abrasion of the skin surface and attaches to surface receptors.4 Viral infection causes metaplasia of the basal keratinocytes, abnormal keratohyaline granules, epidermal acanthosis, papillomatisis, and hyperkeratosis of the horny layer.5 These histologic changes correlate with localized thickening of the epidermis and the typical clinical lesions. Unfortunately, persistence of the virus after treatment leads to regrowth of a wart.

Differential diagnosis

With the lymphangitic streak suggesting infection and the morphological presentation of the acute hemorrhagic papule on the patient’s finger, a number of diagnoses were considered. They included verruca with secondary bacterial infection/cellulitis, or cat scratch disease, and atypical mycobacterial infection. Less likely diagnoses included herpetic whitlow, foreign body reaction, and arthropod bite.

Verruca vulgaris usually can be diagnosed based on history and morphologic features. When the diagnosis is unclear, a biopsy can be obtained. This patient’s biopsy showed typical histologic features.

Additionally, the presence of warts can be confirmed by identifying the typical features of thrombosed vessels within papillae and a white halo on dermoscopy. In special settings, polymerase chain reaction can be used to identify the specific HPV genotype.


Approximately 67% of warts are self-limited and resolve without treatment in 3 to 5 years.6,7 Functional T-cell and natural killer cell cytotoxicity rid the epidermis of HPV induced warts.8 If the warts cause physical or psychological discomfort, there are a variety of treatment options that include liquid nitrogen cryotherapy, salicylic acid, intralesional bleomycin, intralesional 5-fluorouracil, excision, and laser. However, many treatments are painful and may result in scarring, and have not been demonstrated to be effective in evidenced-based studies. As a consequence, conservative treatment with topical salicylic acid and observation may be most appropriate.4



1. de Koning MN, Quint KD, Bruggink SC, et al. High prevalence of cutaneous warts in elementary school children and the ubiquitous presence of wart-associated human papillomavirus on clinically normal skin. Br J Dermatol. 2015;172(1):196-201.

2. Bruggink SC, Eekhof JA, Egberts PF, van Blijswijk SC, Assendelft WJ, Gussekloo J. Natural course of cutaneous warts among primary schoolchildren: a prospective cohort study. Ann Fam Med. 2013;11(5):437-441.

3. Benton, EC. Skin infections III: The epidemiology of human cutaneous papillomavirus infections. In: Williams HC, Strachan DP, eds. The Challenge of Dermato-Epidemiology. Boca Raton, FL: CRC Press; 1997.

4. Leung L. Treating common warts–options and evidence. Aust Fam Physician. 2010;39(12):933-937.

5. Cubie HA. Diseases associated with human papillomavirus infection. Virology. 2013;445(1-2):21-34.

6. Cohen, Bernard. Pediatric Dermatology. 3rd ed. London: Elsevier Mosby; 2005:121-126.

7. Bosch FX, Broker TR, Forman D, et al. Comprehensive control of human papillomavirus infections and related diseases. Vaccine. 2013;31 suppl 7:H1-H31.

8. Leiding JW, Holland SM. Warts and all: human papillomavirus in primary immunodeficiencies. J Allergy Clin Immunol. 2012;130(5):1030-1048.


Ms Alexander is a third-year medical student at Howard University College of Medicine, Washington, DC. Dr Cohen, section editor for Dermcase, is professor of pediatrics and dermatology, Johns Hopkins University School of Medicine, Baltimore, Maryland. The author and section editor have nothing to disclose in regard to affiliations with or financial interests in any organizations that may have an interest in any part of this article. Vignettes are based on real cases that have been modified to focus on key teaching points. Images also may be edited or substituted for teaching purposes.

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