Verruca vulgaris (VV) lesions represent infection by the human papilloma virus (HPV), a type of DNA virus. While the term verruca vulgaris is used to describe common warts, verruca plantaris refers to plantar warts and verruca plana refers specifically to flat warts. To date, more than 100 different HPV types have been identified; common warts are most associated with infections of HPV types 1, 2, and 4. While the majority of verruca vulgaris lesions are benign and self-resolve, they can be cosmetically unappealing and occasionally painful to patients. Treatment of these lesions is quite challenging for they are often refractory to repeated exposures to many therapeutic modalities.

Human papilloma viruses are a type of DNA virus. HPV can only complete its full life cycle when infecting squamous epithelial cells, particularly proliferating basal epithelial cells. Once the virus infects these proliferating basal epithelial cells, cell proliferation is upregulated. The epidermis then becomes thickened and hyperkeratotic through increased cellular division.

Verruca vulgaris typically present as hyperkeratotic, rough, exophytic, round papules (Fig. 10-1A). These papules often have pinpoint black dots, which result from thrombosed capillary loops (Fig. 10-1B). The most common locations include the fingers, dorsum of the hands, and other sites exposed to trauma. Verruca vulgaris can be spread by autoinoculation; there may therefore be a linear arrangement of lesions as a result of this phenomenon. The majority of lesions are asymptomatic, although the lesions can be quite painful, particularly when located on the soles of the feet. HPV infects fully differentiated squamous epithelium, resulting in the massively thickened epidermis and stratum corneum that characterizes the cutaneous lesions. In some cases, VV can form a cutaneous horn which may be indistinguishable from an actinic keratosis, such as that shown in Figure 10-2.

There is no current medication to “cure” HPV. Rather, current therapies focus on destroying the verrucous lesions or inducing an immune response against those cells infected with HPV. Because about 40% to 65% of warts resolve spontaneously in 2 years, providing no initial treatment is both reasonable and cost-effective. If warts are symptomatic, enlarging, spreading, or persistent, there are several treatment modalities to consider.

Verruca vulgaris lesions can be quite refractory to therapy. The HPV infects keratinocytes at the base of the lesions. Thus, interventions are often unsuccessful, as they treat the lesions from the outside-in. Patients should be counseled that it will take many treatments spread over several months (usually one visit per 3 to 4 weeks) to treat these lesions and that there is no “cure” for warts. Additionally, patients should be instructed that warts can be passed from one person to another by direct physical contact and sometimes by sharing an object that has been touched by someone infected with HPV (such as gym mats and floors of showering facilities). Trauma, excess hand moisture, nail biting, and swimming pools can all increase the transmission of warts.

Herpes simplex virus is a common, ubiquitous infection. In fact, nearly 90% of the world’s population between the ages of 20 and 40 are thought to have been exposed to HSV-1, as measured by positive antibodies. HSV-1 infections are most common on the lips and mouth; however, HSV-1 can also be the cause of genital herpes in approximately 10% to 20% of cases. HSV-1 infections can be primary, latent, and/or recurrent. The majority of affected patients are in the latent phase. Thus, while the majority of the population may have been previously exposed to HSV-1, a much smaller proportion has a clinical outbreak of HSV-1 at any given time.

Transmission of HSV-1 can occur during symptomatic outbreaks or during asymptomatic latent periods. HSV-1 is most commonly spread through contaminated saliva or other secretions. The HSV-1 virus infects localized keratinocytes, and replicates locally. It can then spread up the nerve to the dorsal root ganglion, where it becomes latent. The virus can then be reactivated by multiple stimuli and result in recurrent infections.

Primary HSV-1 infections typically develop a few days after exposure to the virus. These initial outbreaks are usually symptomatic, with systemic symptoms such as fever, malaise, and lymphadenopathy developing 2 to 3 days before any cutaneous lesions. Primary HSV-1 infections commonly manifest as gingivostomatitis or pharyngitis with mononucleosis-like symptoms. The outbreak consists of multiple grouped “herpetiform” vesicles on an erythematous base (Fig. 10-4A). The lesions then crust and resolve over several weeks. In contrast to recurrent aphthous stomatitis (“canker sores”), HSV infections typically affect keratinized surfaces of the mouth such as the gingivae and hard palate; aphthous stomatitis tends to occur on the buccal mucosa and underside of the tongue.

Following the primary infection, HSV-1 infections can become latent. During this latent phase, the virus is localized to the dorsal root ganglion, where it is dormant. No clinical lesions or symptoms are present during this phase. The virus is then reactivated and spreads down the nerve to cause a clinical eruption. Reactivation can be caused by stress, sunlight, fever, sickness, or may occur spontaneously.

Recurrent outbreaks are often preceded by symptoms of burning and tingling in the lips, which may begin 1 to 2 days before the cutaneous outbreak. These symptoms are presumably related to the virus spreading down the nerve. Cutaneous lesions associated with recurrent HSV-1 are typically localized to the vermillion border of the lips and are characterized by small grouped vesicles on an erythematous base. The majority of these recurrent outbreaks are not associated with systemic symptoms, although lymphadenopathy and fatigue may occur. Recurrent outbreaks are typically milder and resolve quicker than primary infections, with the outbreak lasting approximately 1 week.

Recurrent flares of erythema multiforme (EM) are nearly always associated with flares of herpes simplex. As described in the case, patients’ EM will flare in conjunction with reactivation of HSV (Figs. 10-4A,B). Appropriate oral therapy for HSV will also suppress the EM flare.

Primary HSV infections are often severe and symptomatic and most patients are treated with antiviral therapy. A systematic review of acyclovir for treating primary herpetic gingivostomatitis found only weak evidence that acyclovir effectively reduces the number of oral lesions and prevents the development of new extraoral lesions. Patients with recurrent HSV may be treated with topical agents, such as 1% penciclovir or 5% acyclovir ointment, with limited expectations of useful effects. Oral therapy with acyclovir (dosed 5 times per day) or valacyclovir (dosed twice daily) is also an option for severe cases. Currently, no oral agents are Food and Drug Administration (FDA) approved for the treatment of primary oral HSV, though several dosing regimens have been reported in the literature. Mild, asymptomatic HSV-1 outbreaks require no therapy. However, topical agents and oral therapy can potentially abort or shorten an outbreak if given at the first sign of an infection, such as tingling in the lips. Therapy regimens are summarized in Table 10-1.

Finally, for patients with significant, frequent, recurrent outbreaks (including recurrent EM), suppressive therapy with either oral acyclovir or valacyclovir given on a low-dose daily basis is a therapeutic option. The dosing schedules for suppressive and episodic outbreaks are FDA-approved.

Primary HSV-1 infections can be quite painful and severe. They are self-limited infections, with symptoms resolving over 4 to 6 weeks. Unfortunately, the virus travels retrograde up the nerves and becomes latent, with the potential to reactivate.

Recurrent HSV-1 infections tend to be less severe and shorter than primary infections. However, they can be painful and occasionally associated with systemic symptoms such as lymphadenopathy. These outbreaks typically last 1 week, but can be potentially shortened or aborted with early antiviral therapy.

Genital herpes is most commonly caused by infection with the herpes simplex virus type 2 (HSV-2). While HSV-2 infections preferentially affect the genitalia, approximately 10% to 20% of genital herpes outbreaks are caused by HSV-1. In some cases HSV-2 may be the cause of oral herpes as HSV-2 infection is spread via sexual contact. As a result, HSV-2 infections before adolescence are rare.

HSV-2 infections are spread through close intimate contact. The virus then integrates into keratinocytes and spreads in a retrograde fashion to a dorsal root ganglion where it becomes eventually becomes latent.