Viral Infections of the Skin
Virginia P. Arcangelo
Viruses producing skin lesions may be categorized into three groups: herpes viruses, papillomaviruses, and pox viruses. Herpes and papillomaviruses each affect approximately 20% of the adult population in the United States, with an even distribution between the sexes.
Viruses are further classified by family—either the ribonucleic acid family or the deoxyribonucleic acid (DNA) family. Herpes viruses, papillomaviruses, and pox viruses are members of the DNA family.
Viruses are obligate intracellular parasites that consist of a nucleic acid core surrounded by one or more proteins. A host cell is required for viral replication. Several mechanisms exist for viral replication, and different DNA viruses replicate by their own specific mechanism. Pox viruses replicate entirely in the cytoplasm. Herpes viruses replicate their own polymerase, along with several of their own enzymes. Papillomavirus proteins contribute to the initiation of DNA replication.
HERPES VIRUS INFECTIONS
CAUSES
Seven types of herpes viruses are associated with human illness: herpes simplex virus type 1 (HSV-1), herpes simplex virus type 2 (HSV-2), varicella-zoster virus (VZV), Epstein-Barr virus, cytomegalovirus, human herpes virus type 6 (HHV-6), and human herpes virus type 8 (HHV-8).
HSV-1 infection usually involves the face and skin above the waist. HSV-2 is most commonly associated with the genitalia and the skin below the waist. A life-threatening neonatal infection is associated with HSV-2 in a baby whose mother is infected with the virus; the infection is transmitted during vaginal birth. Herpes zoster (shingles) and varicella (chickenpox) are the result of VZV infection. The overall incidence of herpes zoster is 3.2 per 1,000 (Htwe et al., 2007). Risk factors include aging, female gender, recent transplant, human immunodeficiency virus (HIV) infection, and cancer. Infectious mononucleosis is a result of Epstein-Barr virus infection. HHV-6 is associated with a mild childhood illness called roseola. HHV-8 is associated with Kaposi sarcoma, especially in patients with HIV infection. HSV-1 and VZV are discussed in this chapter; HSV-2 is discussed in Chapter 35.
PATHOPHYSIOLOGY
Herpes viruses replicate their own polymerase along with several of their own enzymes. HSV is highly contagious. It is spread by direct contact with skin or mucous membrane. After the primary infection, the virus retreats to the dorsal root ganglion, where it remains latent until it is reactivated by triggers such as stress, viral infections, or sunlight.
Those who have had varicella virus infection are most prone to herpes zoster. After the primary infection resolves, the virus retreats to the dorsal root ganglion, where it remains dormant. Herpes zoster is caused by reactivation of the virus, most often with no apparent cause. There is a migration of virions through the axon to the skin of one or several adjacent axons. In immunocompetent patients, recurrent episodes are uncommon.
DIAGNOSTIC CRITERIA
Infection with HSV-1 and HSV-2 causes vesicular eruptions that are painful and often recurrent. The common incubation period of 4 to 10 days is followed by the eruption of clustered
vesicles on an erythematous base. Distribution of the virus into autonomic and sensory nerve endings allows the virus to remain latent.
vesicles on an erythematous base. Distribution of the virus into autonomic and sensory nerve endings allows the virus to remain latent.
Typically, HSV-1 causes oral or facial infections, with the most common sites being the mouth, pharynx, lips, or face. Primary occurrences usually have intense symptoms. Prodromal symptoms include burning, tingling, or itching; these symptoms may accompany recurrent infection as well. Recurrence of the infection is thought to be precipitated by fatigue, stress, trauma, fever, or ultraviolet radiation. The lesion presents as a single vesicle or group of vesicles that overlie an erythematous base. They become pustules and become crusted or erode. Lesions recur at the site innervated by the dorsal root ganglion inhabited by the virus.
The two different diseases caused by VZV (chickenpox and shingles) have similar symptoms. After an incubation period of 10 to 20 days, chickenpox (primary varicella) manifests with fever and malaise followed by the outbreak of itchy, vesicular lesions on an erythematous base. The outbreak usually begins on the trunk and progresses to the extremities and face. Primary varicella occurs most often in children. Adults infected with primary varicella tend to have more systemic effects, especially if they have preexisting medical conditions.
A reactivation of VZV in the nerve root ganglion is referred to as herpes zoster, or shingles. The infection characteristically begins with neuralgia in the affected dermatome, followed by an outbreak of grouped vesicles on an erythematous base, clustered in a unilateral pattern of the dermatome. In two thirds of infections, the lesions are on the trunk. Additional symptoms include fever, myalgia, and increasing localized pain. The most common presentation of herpes virus infection in the elderly is VZV in the form of herpes zoster. Three fourths of all cases of shingles occur in patients older than age 50. A significant complication of herpes zoster is postherpetic neuralgia, pain in the dermatome site that lasts longer than 6 weeks after resolution of the infection.
INITIATING DRUG THERAPY
Although nonpharmacologic interventions, such as soaks with Burow’s solution, help to relieve symptoms, HSV-1 infection is treated primarily with other topical agents. In the case of severe infection in an immunocompromised patient, treatment may be with systemic drug therapy, which shortens the duration of symptoms; however, there is no treatment to prevent recurrence.
For oral HSV-1 infections (oral herpes), symptoms may or may not respond to viscous lidocaine (Xylocaine) 2% applied to the lesion. A solution of diphenhydramine (Benadryl) elixir and aluminum hydroxide/magnesium hydroxide (Maalox) mixed in a 1:1 proportion can be used as an oral rinse four times a day. Sucking on popsicles also can provide temporary relief.
For primary VZV infections that manifest as chickenpox, systemic therapy is used only in special cases and is not recommended for uncomplicated disease. For VZV infections that manifest as herpes zoster, antiviral agents may help relieve symptoms. Patients should be treated if the rash has been present for fewer than 72 hours or if new lesions are still developing. If therapy starts within 72 hours of the appearance of the lesion, systemic therapy decreases the duration of the rash and the acute pain associated with herpes zoster. In addition, any patient older than age 50 who is immunocompromised should be treated with antiviral agents. The use of antiviral therapy in herpes zoster decreases the symptoms of postherpetic neuralgia from 62 days with placebo to 20 days with acyclovir. Antiviral agents used are acyclovir, famciclovir, and valacyclovir. All antiviral agents have shown to shorten the duration of postherpetic neuralgia, but none prevent it.
Goals of Drug Therapy
In herpes virus infections, the goal of therapy is to reduce the duration of symptoms and suppress pain. The treatment aim is to stop reproduction of the virus.
Topical Antiviral Agents
Two topical agents—acyclovir 5% and penciclovir (Denavir)— are available to treat herpes infections. These agents work by inhibiting viral DNA synthesis (Table 13.1). They may decrease healing time.
Patients usually apply topical acyclovir every 3 hours, six times per day, for 7 days. Penciclovir is applied every 2 hours, during waking hours, for 4 days. Adverse effects include mild skin irritation and pruritus.
Systemic Antiviral Agents
The three first-line systemic agents are acyclovir (Zovirax), famciclovir (Famvir), and valacyclovir (Valtrex), although famciclovir and valacyclovir are more bioavailable than acyclovir. Systemic antivirals are highly effective against herpes virus. In general, antiviral therapy is recommended for adolescents, adults, and high-risk patients, but not usually for healthy children younger than age 12 (see Table 13.1).
Contraindications
Caution should be used in patients with renal disease because antivirals are excreted by the renal system. They are also contraindicated in patients with congestive heart failure and in lactation. Dosage adjustments are made for patients with a creatinine clearance rate less than 25 mL/min.
Adverse Events
Adverse effects include headaches, vertigo, depression, and tremors. Patients may also experience gastrointestinal symptoms and rashes.
Interactions
The effect of antiviral agents is increased in patients taking probenecid, and patients taking zidovudine (Retrovir) may experience drowsiness.
TABLE 13.1 Overview of Antiviral Agents for Herpes Virus Infections | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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