Verrucae, or warts (Figure 53-4), are common benign papillomas caused by DNA-containing papillomaviruses. Although warts vary in appearance depending on their location, the histologic characteristics of all lesions are similar. A wart is actually an exaggeration of normal skin composition, with the stratum corneum being irregularly thickened. The human papillomaviruses, the subgroup of papovaviruses that causes human warts, are not found in other animals and invade only the skin and mucous membranes of humans.

Warts may resolve spontaneously if immunity to the virus develops, but the immune response can be delayed for years and is not reliably activated in every case. In 95% of cases, untreated warts will resolve within 5 years,2 but they may multiply into hundreds of lesions and can involve any body site. Current surgical treatment may be directed at removal of the wart by laser. Liquid nitrogen or acid chemicals, cryotherapy, and salicylic acid paint or plasters have also been effective medical treatments. Topical blistering agents, immunomodulators, and intralesional injections of various agents may also be effective treatment modalities.

Herpes simplex virus (HSV) infections of the skin and mucous membranes are common (Figure 53-5). Two types of herpesviruses infect humans: type 1 and type 2. Most HSV-1 infections occur above the waist.³ HSV-1 may result when external infection is spread to the other parts of the body through the occupational hazards that exist in professions such as dentistry and medicine and some athletics. HSV-2 is responsible for most infections in the genital region.³

Herpesvirus lesions usually begin with a burning or tingling sensation. Vesicles and erythema follow and progress to pustules, ulcers, and crusts before healing. The lesion is most common on the lips, face, and mouth. Pain is common, and healing takes place in 10 to 14 days.4 After the initial infection, the herpesvirus persists in latent form in the trigeminal nerve and other ganglia. Recurrent lesions are common and may be precipitated by stress, sunlight exposure, menses, or injury.^5,6 The vast majority of patients have at least 1 episode of herpesvirus reactivation, and some individuals may have 10 or more outbreaks per year. Recently, concern has arisen over the identification of infectious viral shedding in the absence of symptomatic lesions.⁵

Herpes zoster (shingles) is an acute localized inflammatory disease of a dermatomal segment of the skin (Figure 53-6). It is caused by the same herpesvirus that causes chickenpox (varicella-zoster virus). It is believed to be the result of reactivation of a latent varicella-zoster virus that has been present in the sensory dorsal ganglia since childhood infection. During an attack of shingles, the reactivated virus travels from the ganglia to the skin of the corresponding dermatome.

The clinical manifestations of shingles include the eruption of vesicles with erythematous bases that are restricted to skin areas supplied by sensory neurons of a single or associated group of dorsal root ganglia. Eruptions generally follow a unilateral dermatomal distribution and most often occur on the thorax, trunk, and face. In immunosuppressed persons, the lesions may extend beyond the dermatome. New crops of vesicles erupt for 3 to 5 days along the nerve pathway.3 Lesions are deeper and more confluent than those of chickenpox. The vesicles dry, form crusts, and eventually fall off. Lesions usually clear in 2 to 3 weeks.³ Severe pain and paresthesias are common. In the elderly, herpes-zoster virus is a particularly serious condition that may be long lasting. Pain reports from elderly individuals indicate an increased severity and lengthy episodes of up to 1 year.³ Systemic treatment with acyclovir, famciclovir, or valacyclovir should be initiated as soon as possible, preferably within the first 48 to 72 hours.

Postherpetic neuralgia is the most important complication occurring in people older than 50 years.³ Eye involvement can result in permanent blindness.

Management of shingles includes oral antiviral drugs; acyclovir (Zovirax) is one example. Topical agents such as Burow compresses or aqueous alcohol shake lotions may also be used. Pain medication may be indicated in severe cases. Systemic corticosteroids have also been effective in healthy persons older than 50 years with severe pain, but their use remains controversial. High doses of interferon, an antiviral glycoprotein, have been used in persons with cancer when the herpetic lesions are limited to the dermatome.7

Additionally, vaccination is becoming an important tool in preventing herpes zoster (e.g., Zostavax).

The clinical signs of superficial fungal infection vary depending on the physical location and the host’s response to the invading organism. Often fungal infections are manifested as erythematous macules or plaques with peripheral scaling and some central clearing. Vesicular lesions often accompany the dry scaling on the feet. Because of the variability of signs and symptoms, superficial dermatophytosis must be considered when evaluating even a weeping, crusted area more suggestive of eczema or impetigo. Dermatophyte infection of the nails, or onychomycosis, is usually seen as a white or yellow opaque discoloration that often progresses to a thickened, crumbed, or deformed nail (Figure 53-8).

Impetigo is an acute, contagious skin disease characterized by the formation of vesicles, pustules, and yellowish crusts (Figure 53-10). The most common cause of infection of the skin, impetigo is caused by staphylococci or streptococci. Approximately 5% of the population each year sustains staphylococcus infections of a severity sufficient to require medical attention.⁸ Approximately 20% of adults are chronic carriers of the bacterium Staphylococcus aureus, and another 60% are intermittent carriers.⁸ The bacterium is carried in the nasal area and may pass onto the skin and produce disease. Staphylococcal infections are a special problem for hospitalized patients, who may become infected from the infected hospital staff.

Seborrheic dermatitis (Figure 53-12) is a papulosquamous skin disease manifested by various degrees of scaling and erythema in areas of high oil gland concentration such as the scalp, eyebrows, glabellae, eyelids, nasolabial folds, pinna and posterior sulcus of the ears, sternum, axillae, umbilicus, and anogenital area. Common manifestations of this disease are cradle cap in newborns and dandruff in adolescents and adults.

Psoriasis is a common chronic skin disease characterized by papules and plaques with an overlying silvery scale. The specific cause of psoriasis is unknown, but it appears to be a multifactorial inherited condition in which minor aberrations of the immune system promote inflammation and hyperproliferation within the skin. The disease may affect, with varying degrees of severity, people of all ages. Lesions can appear on any area of the body; however, they seem to have a predilection for the knees, elbows, lower part of the back, scalp, and nails (Figure 53-13). Disease progression is unpredictable, and the patient may periodically experience spontaneous exacerbations or remission.

Lichen planus is a relatively common, chronic, pruritic disease involving inflammation and papular eruption of the skin and mucous membranes. Idiopathic lichen planus is of unknown cause but can be stimulated by a variety of drugs and chemicals in susceptible persons. The characteristic lesion is a shiny, white-topped, purplish, polygonal papule. Lesions appear on the wrists, ankles, and trunk (Figure 53-14). Mucous membrane lesions are white and lacy and may become bullous. Pruritus is severe, and new lesions develop as a result of scratching (Koebner phenomenon). Nails are affected in approximately 10% of people with lichen planus.⁹

Pityriasis rosea is a rash of unknown origin that primarily affects young adults. The incidence is highest in the spring and fall seasons. It has been speculated to be viral in origin, but to date no virus has been isolated. The characteristic lesion is a macule or papule with surrounding erythema. The lesion spreads with central clearing, much like tinea corporis. This initial lesion is a solitary lesion, called the herald patch, and is usually located on the trunk or neck. As the lesion enlarges and begins to fade away (2 to 10 days), successive crops of lesions appear on the trunk and neck.10 The extremities, face, and scalp may be involved, and mild to severe pruritus may occur. The disease is self-limiting and usually disappears within 2 to 10 weeks.¹⁰ Treatment is palliative and includes topical steroids, antihistamines, and colloid baths. Systemic corticosteroids may be indicated in severe cases. Systemic antibiotics, especially erythromycin, may also shorten the course.

Acne, an extremely common disease of the pilosebaceous unit, affects up to 90% of all individuals and produces unsightly lesions and sometimes permanent scarring and disfigurement11 (Figure 53-15). Etiologically, acne involves multiple factors such as sex hormones, heredity, bacterial flora of the skin, stress, mechanical occlusion, and cosmetics’ use. Acne arises when sludging of sebaceous oils and deposition of loose epithelial cells cause an obstruction of the follicular canal. Continued oil production and bacterial growth in this obstructed follicle may cause rupture of the wall or sebaceous gland and result in an inflamed lesion.

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