Dermatologic Virology

Anita Satyaprakash MD

Parisa Ravanfar MD, MBA, MS

Stephen K. Tyring MD, PhD

Viral diseases of the skin are exceedingly common. The various clinical entities are distinct and because we have no specific antiviral drug for many diseases, the treatment varies for each entity. The following viral diseases are discussed here:

Herpes simplex virus 1 and 2
Varicella-zoster virus
Human herpesvirus 6
Human herpesvirus 7
Human papillomaviruses
Molluscum contagiosum virus
Measles (rubeola)
German measles (rubella)
Erythema infectiosum
Coxsackievirus infections
Herpangina
Hand, foot, and mouth disease
Echovirus exanthema

Herpes Simplex Virus 1

Herpes simplex virus 1 (HSV-1) is the usual cause of herpes labialis as well as the cause of up to 50% of first-episode genital herpes infections. Approximately 90% of people between 20 to 40 years of age have antibodies against HSV-1. The primary infection typically occurs early in life, with viral latency established in the neural ganglia. Reactivation can occur due to several different triggers, including immunosuppression, respiratory tract viral infection, or any febrile disease, physical trauma, psychological stress, or sun exposure. Transmission of HSV-1 occurs with viral shedding during the asymptomatic and symptomatic periods through direct contact with infected secretions (i.e., saliva).

Presentation and Characteristics

True primary infection occurs when a patient is seronegative for HSV types 1 and 2 prior to the episode. Nonprimary initial episodes occur when the first symptomatic episode occurs later than the initial infection and tend to be less severe. Asymptomatic primary infection is the rule. During symptomatic episodes, 60% of patients experience prodromal symptoms such as burning, itching, or tingling. Systemic symptoms such as fever, chills, fatigue, and muscle aches may also accompany primary infection. The mouth and lips are the most common areas of primary infection (Figs. 23-1 and 23-2). Lesions start as papules on an erythematous base that become vesicular, progress to ulcers, then crust, and eventually heal, generally within 72 to 96 hours. Symptomatic primary episodes tend to be followed by less severe recurrences; however, some patients may never experience a second episode. Recurrent episodes often present as three to five vesicles at the vermilion border of the lip, which last at least 48 hours. Other locations include the palate, chin, and oral mucosa. Recurrent labial herpes affects approximately one third of the US population, with patients typically experiencing one to six episodes annually.

Treatment

Oral acyclovir, famciclovir (the prodrug of penciclovir), and valacyclovir are effective for the treatment of herpes labialis. Different doses are recommended depending on whether the patient is presenting with his or her primary episode, a recurrent episode, or qualifies for suppressive therapy (Table 23-1). The use of suppressive therapy requires periodic reevaluation, generally within a year, in order to assess its necessity. Topical therapies that may be used are acyclovir 5% cream five times daily for 4 days and penciclovir 1% cream every 2 hours (while awake) for 4 days.

Herpes Simplex Virus 2

Herpes simplex virus 2 (HSV-2) is one of the most widespread sexually transmitted diseases (STDs) in the world. It causes 70% of primary genital herpes and over 95% of recurrent genital herpes (Fig. 23-3). In the United States, the prevalence of genital herpes is 40 to 60 million, and the incidence is 500,000 to 1,000,000 cases per year, with approximately 22% of the general population being seropositive for HSV-2. Similar to HSV-1, HSV-2 causes primary, latent, and recurrent infections, and is transmitted during both asymptomatic and symptomatic phases, typically through sexual contact. Genital herpes infections caused by HSV-2 tend to be more severe than those caused by HSV-1, are more likely to have recurrent episodes, and have a greater frequency of subclinical viral shedding. HSV-2 can also cause neonatal herpes, with the highest risk occurring when the mother has primary genital herpes during delivery. In addition to cutaneous lesions, the infected neonate may develop multiorgan involvement, which carries a high mortality rate.

FIGURE 23-1 ▪ Herpes simplex on the arm (A), chin (B), and true primary infection on the lips and mouth (interoral) (C). (Courtesy of Dermik Laboratories, Inc.)

FIGURE 23-2 ▪ (A) Recurrent herpes simplex on the chin with secondary bacterial infection. (B) Recurrent herpes simplex on the thumb. (Courtesy of Dermik Laboratories, Inc.)

TABLE 23-1 ▪ Treatments for Herpes Labialis

First Clinical Episode of Herpes Labialis	Intermittent Episodic Therapy for Recurrent Herpes Labialis	Suppressive Therapy for Recurrent Herpes Labialis
Acyclovir 400 mg PO 5 times daily for 7-10 days	Acyclovir 400 mg PO 5 times daily for 5 days	Acyclovir 400 mg PO b.i.d.
Famciclovir 500 mg PO b.i.d. for 7 days	Famciclovir 1.5 g PO once	Famciclovir 500 mg PO b.i.d.
Valacyclovir 1 g PO b.i.d. for 1 day	Valacyclovir 1 g PO BID for 1 day	Valacyclovir 500 mg PO q.d.

FIGURE 23-3 ▪ Recurrent herpes simplex on the penis. (Courtesy of Dermik Laboratories, Inc.)

Presentation and Characteristics

Up to 90% of patients infected with HSV-2 become infected via asymptomatic viral shedding. Genital herpes infection is typically asymptomatic, because the lesions may be painless and inapparent. The first clinically recognized lesions of genital herpes may be either true primary or a first-episode, nonprimary. True primary genital herpes usually develops after 2 to 14 days of HSV exposure. There may be widespread vesicles and ulcers on the genitalia with inguinal adenopathy, and the patient may complain of discharge, dysuria, fever, lethargy, myalgias, and photophobia. The most common site of involvement in women is the cervix, although the classic painful clinical presentation is mostly that of vaginal and vulvar lesions.

More than half of patients with the first recognized signs and symptoms of genital herpes have a nonprimary first episode, which occurs when the initial infection is asymptomatic. This may occur weeks, months, or even years after initial HSV infection. A strong immune response may prevent the infection from becoming clinically recognizable. The initial immune response does attenuate the severity of first-episode nonprimary genital herpes. Lesions are often less extensive, and systemic symptoms are less common and severe compared to that of true primary genital herpes.

Treatment

Because there is no cure for genital herpes, therapy is aimed at controlling the signs and symptoms of an outbreak. In 2006, the Centers for Disease Control and Prevention (CDC) made therapeutic recommendations for individuals with a first clinical episode of genital herpes; for episodic development of genital herpes; and for suppressive therapy for recurrent genital herpes (Table 23-2). Pharmacologic therapies for genital herpes include

acyclovir,
valacyclovir,
famciclovir,
cidofovir,
foscarnet (especially in immunocompromised HIV patients), and
penciclovir.

Varicella-Zoster Virus

Varicella-zoster virus (VZV) causes primary varicella (chickenpox) and herpes zoster (shingles), which is a reactivation of the primary varicella infection. Primary varicella is usually a self-limited disease in immunocompetent children. Prior to the availability of the varicella vaccine, there were more than 11,000 hospitalizations each year in the United States due to complications of varicella infection in children who were often otherwise healthy. Susceptible adults typically develop more extensive skin lesions, more frequent complications, and more severe constitutional symptoms, such as prolonged fever.

Following primary VZV infection, the virus resides in a latent state in the sensory ganglia. With aging or a weakened immune system, the VZV may reactivate as shingles, which is also known as herpes zoster. With the highest incidence of all neurologic diseases, herpes zoster occurs annually in more than 1,000,000 people in the United States and has a lifetime incidence of 20%. Since childhood varicella vaccination was introduced in the United States in 1995, the incidence of shingles has increased. This is presumably due to the lack of subclinical immune boosting that generally results from the wild-type virus in the environment.

Presentation and Characteristics

Two weeks after exposure, primary varicella may start with 2 to 3 days of prodromal symptoms such as low-grade fever, chills, headache, malaise, nausea, and vomiting. The rash appears as crops of small red macules on the face and scalp, which then spreads to the trunk with sparing of the distal
upper and lower extremities. Over 12 hours, the macules progress to 1- to 3-mm papules, vesicles, and then pustules. Crusting occurs within a few days, and complete healing occurs in approximately 1 month. Lesions are generally found to be in different stages of healing in the same skin region.

TABLE 23-2 ▪ Treatments for Genital Herpes

First Clinical Episode of Genital Herpes	Intermittent Episodic Therapy for Recurrent Genital Herpes	Suppressive Therapy for Recurrent Genital Herpes
Acyclovir 400 mg PO t.i.d. for 7-10 days	Acyclovir 400 mg PO t.i.d. for 5 days	Acyclovir 400 mg PO b.i.d.
Acyclovir 200 mg PO 5 times a day for 7-10 days	Acyclovir 800 mg PO t.i.d. for 2 days	Famciclovir 250 mg PO b.i.d.
Famciclovir 250 mg PO t.i.d. for 7-10 days	Acyclovir 800 mg PO b.i.d. for 5 days	Valacyclovir 500 mg PO q.d. (≤9 outbreaks/year)
Valacyclovir 1 g PO b.i.d. for 7-10 days	Famciclovir 125 mg PO b.i.d. for 5 days
Famciclovir 1 g PO b.i.d. for 1 day	Valacyclovir 1 g PO q.d. (>9 outbreaks/year) Valacyclovir 500 mg PO b.i.d. for 3 days Valacyclovir 1 g PO q.d. for 5 days

More than 90% of patients with herpes zoster have a prodrome of intense pain in the involved single sensory ganglion (dermatome) preceding the zoster rash (Fig. 23-4

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