Viral Skin Infections
Herpes zoster, also called shingles, is an infection caused by the varicella-zoster virus, a member of a group of DNA viruses. The viruses causing chickenpox and herpes zoster are indistinguish-able, hence the name varicella-zoster virus. The disease is charac-terized by a painful vesicular eruption along the area of distribution of the sensory nerves from one or more posterior ganglia. It is as-sumed that herpes zoster represents a reactivation of latent vari-cella virus infection and reflects lowered immunity. After a case of chickenpox runs its course, it is thought that the varicella-zoster viruses responsible for the outbreak lie dormant inside nerve cells near the brain and spinal cord. Later, when these la-tent viruses are reactivated, they travel by way of the peripheral nerves to the skin, where the viruses multiply and create a red rash of small, fluid-filled blisters. About 10% of adults get shingles during their lifetimes, usually after age 50 years. There is an in-creased frequency of herpes zoster infections among patients with weakened immune systems and cancers, especially leukemias and lymphomas (Odom et al., 2000).
The eruption is usually accompanied or preceded by pain, which may radiate over the entire region supplied by the affected nerves. The pain may be burning, lancinating (ie, tearing or sharply cut-ting), stabbing, or aching. Some patients have no pain, but itch-ing and tenderness may occur over the area. Sometimes, malaise and gastrointestinal disturbances precede the eruption. Thepatches of grouped vesicles appear on the red and swollen skin. The early vesicles, which contain serum, later may become puru-lent, rupture, and form crusts. The inflammation is usually uni-lateral, involving the thoracic, cervical, or cranial nerves in a bandlike configuration. The blisters are usually confined to a nar-row region of the face or trunk (Fig. 56-2). The clinical course varies from 1 to 3 weeks. If an ophthalmic nerve is involved, the patient may have eye pain. Inflammation and a rash on the trunk may cause pain with the slightest touch. The healing time varies from 7 to 26 days.
Herpes zoster in healthy adults is usually localized and benign. However, in immunosuppressed patients, the disease may be se-vere and the clinical course acutely disabling.
The goals of herpes zoster management are to relieve the pain and to reduce or avoid complications, which include infection, scar-ring, and postherpetic neuralgia and eye complications. Pain is controlled with analgesics, because adequate pain control during the acute phase helps prevent persistent pain patterns. Systemic corticosteroids may be prescribed for patients older than age 50 years to reduce the incidence and duration of postherpetic neuralgia (ie, persistent pain of the affected nerve after healing). Healing usually occurs sooner in those who have been treated with corticosteroids. Triamcinolone (Aristocort, Kenacort, Kenalog) injected subcutaneously under painful areas is effective as an anti-inflammatory agent.
There is evidence that infection is arrested if oral antiviral agents such as acyclovir (Zovirax), valacyclovir (Valtrex), or fam-ciclovir (Famvir) are administered within 24 hours of the initial eruption. Intravenous acyclovir, if started early, is effective in sig-nificantly reducing the pain and halting the progression of the disease. In older patients, the pain from herpes zoster may persist as postherpetic neuralgia for months after the skin lesions dis-appear (Hall, 2000).
Ophthalmic herpes zoster occurs when an eye is involved. This is considered an ophthalmic emergency, and the patient should be referred to an ophthalmologist immediately to prevent the possi-ble sequelae of keratitis, uveitis, ulceration, and blindness.
People who have been exposed to varicella (ie, chicken pox) by primary infection or by vaccination are not at risk for infec-tion after exposure to patients with herpes zoster.
The nurse assesses the patient’s discomfort and response to med-ication and collaborates with the physician to make necessary ad-justments to the treatment regimen. The patient is taught how to apply wet dressings or medication to the lesions and to follow proper hand hygiene techniques to avoid spreading the virus.
Diversionary activities and relaxation techniques are encour-aged to ensure restful sleep and to alleviate discomfort. A care-giver may be required to assist with dressings, particularly if the patient is elderly and unable to apply them. Relatives, neighbors, or a home care nurse may need to help with dressing changes and food preparation for patients who cannot care for themselves or prepare nourishing meals.
Herpes simplex is a common skin infection. There are two types of the causative virus, which are identified by viral typing. Generally, herpes simplex type 1 occurs on the mouth and type 2 in the genital area, but both viral types can be found in both locations. About 85% of adults worldwide are seropositive for herpes type 1. The prevalence of type 2 is lower; type 2 usually appears at the onset of sexual activity. Serologic testing shows that many more people are infected than have a history of clinical disease.
Herpes simplex is classified as a true primary infection, a non-primary initial episode, or a recurrent episode. True primary in-fection is the initial exposure to the virus. A nonprimary initial episode is the initial episode of type 1 or type 2 in a person pre-viously infected with the other type. Recurrent episodes are sub-sequent episodes of the same viral type.
Orolabial herpes, also called fever blisters or cold sores, consists of erythematous-based clusters of grouped vesicles on the lips. A prodrome of tingling or burning with pain may precede the ap-pearance of the vesicles by up to 24 hours. Certain triggers, such as sunlight exposure or increased stress, may cause recurrent episodes. Fewer than 1% of people with primary orolabial herpes infections develop herpetic gingivostomatitis. This complication occurs more in children and young adults. The onset is often ac-companied by high fever, regional lymphadenopathy, and gener-alized malaise. Another complication of orolabial herpes is the development of erythema multiforme, an acute inflammation of the skin and mucous membranes with characteristic lesions that have the appearance of targets.
Genital herpes, or type 2 herpes simplex, manifests with a broad spectrum of clinical signs. Minor infections may produce no symptoms at all; severe primary infections with type 1 can cause systemic flulike illness. Lesions appear as grouped vesicles on an erythematous base initially involving the vagina, rectum, or penis. New lesions can continue to appear for 7 to 14 days. Lesions are symmetric and usually cause regional lymphadenopathy. Fever and flulike symptoms are common. Typical recurrences begin with a prodrome of burning, tingling, or itching about 24 hours before the vesicles appear. As the vesicles rupture, erosions and ulcerations begin to appear. Severe infections can cause extensive erosions of the vaginal or anal canal.
Herpes simplex infections are confirmed in several ways. Gener-ally, the appearance of the skin eruption is strongly suggestive. Viral cultures and rapid assays are available, and the type of test used depends on lesion morphology. Acute vesicular lesions are more likely to react positively to the rapid assay, whereas older, crusted patches are better diagnosed with viral culture. In all cases, it is imperative to obtain enough viral cells for testing, and careful collection methods are therefore important. All crusts should be gently removed or vesicles gently unroofed. A sterile cotton swab premoistened in viral culture preservative is used to swab the base of the vesicle to obtain a specimen for analysis.
Eczema herpeticum is a condition in which patients with eczema contract herpes that spreads throughout the eczematous areas. The same type of spread of herpes can occur in severe seborrhea, scabies, and other chronic skin conditions.
Herpes Whitlow is an infection of the pulp of a fingertip with herpes type 1 or 2. There is tenderness and erythema of the lateral fold of the cuticle. Deep-seated vesicles appear within 24 hours.
Most cases of neonatal infection with herpes occur during de-livery by contact of the infant with the mother’s active ulcera-tions. Rarely, in mothers who have primary infections during pregnancy, intrauterine neonatal infections occur. Fetal anom-alies include skin lesions, microcephaly, encephalitis, and intra-cerebral calcifications.
In many patients, recurrent orolabial herpes represents more of a nuisance than a disease. Because sun exposure is a common trig-ger, those with recurrent orolabial herpes should use a sunscreen liberally on the lips and face. Topical treatment with drying agents may accelerate healing. In more severe outbreaks or in pa-tients who have identified a trigger, intermittent treatment with 200 mg of acyclovir administered five times each day for 5 days is often started as soon as the earliest symptoms occur.
Treatment of genital herpes depends on the severity, the fre-quency, and the psychological impact of recurrences and on the infectious status of the sexual partner. For people who have mild or rare outbreaks, no treatment may be required. For those who have more severe outbreaks, but for whom outbreaks are still in-frequent, intermittent treatment as described for oral lesions can be used. Because intermittent treatment reduces the duration of the infection by only 24 to 36 hours, it should be initiated as early as possible.
Patients who have more than six recurrences per year may benefit from suppressive therapy. Use of acyclovir, valacyclovir, or famciclovir suppresses 85% of recurrences, and 20% of pa-tients are free of recurrences during suppressive therapy. Sup-pressive therapy also reduces viral shedding by almost 95%, making the person less contagious. Treatment with suppressive doses of oral antiviral medications prevents recurrent erythema multiforme.
Eczema herpeticum is managed with oral or intravenous acyclovir.
Management of genital herpes in pregnancy is controversial. Routine prenatal cultures do not predict shedding at the time of delivery. The use of scalp electrodes during delivery should be avoided because they increase the risk for infection in the new-born. Because the risk for neonatal herpes is greater in women with their initial episode during pregnancy, suppression therapy should be started in these women to reduce outbreaks during the third trimester. All women with active lesions at the time of de-livery undergo cesarean section.
In immunocompromised patients, suppression therapy should be considered. In severe infections of the hospitalized pa-tient, intravenous acyclovir is prescribed.
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