Dermatophyte Infections
Dermatophyte infections are caused by fungi that penetrate the hair, nails, and stratum corneum of the skin. Symptoms of fungal infections, regardless of location, are usually pruritus or stinging. Although transmission of infection may occur through direct contact, indirect transmission is more common with exposure to dermatophyte-laden caps, pillow cases, towels, and clothing, as well as baths, showers, pool decks, and gymnasium floors.
Tinea Capitis
Tinea capitis (scalp infection) is seen primarily in preadolescent children 4 to 12 years old. Rarely, healthy adults and occasionally immunosuppressed individuals develop this infection. In the United States, tinea capitis is caused usually by Trichophyton tonsurans. Within well-defined scaly patches of the scalp, broken hairs, flush with the scalp up to a few millimeters in length, are seen. In contrast to seborrheic dermatitis, lymphadenopathy is usually present (1). The most severe complication of tinea capitis is kerion formation, in which boggy, inflammatory, pustular plaques of potentially scarring hair loss develop. If this is not treated early and aggressively with antifungals in combination with intralesional or oral corticosteroids, it generally causes a disfiguring permanent scarring in the scalp. Tinea capitis is diagnosed with a positive potassium hydroxide (KOH) preparation (see Yeast Infections) or fungal swab culture (2). With a kerion, the KOH preparation and fungal culture may be negative because of the intense host response.
When the diagnosis of kerion is suspected, treatment should be given as soon as possible in an attempt to prevent irreversible scarring alopecia. This includes selenium sulfide or ketoconazole shampoo to reduce spore shedding and oral griseofulvin to eradicate the fungus. Griseofulvin is not only teratogenic but may also reduce the
P.1915
effectiveness of oral contraceptive pills (OCPs). Young women who are sexually active must be instructed on the use of two forms of birth control when prescribed griseofulvin, and a pregnancy test must also be performed before institution of therapy if there is any question of pregnancy. Common side effects of griseofulvin include mild diarrhea and headache limited to the first several days of treatment. If these symptoms persist more than a few days, dosage reduction or initiation of another antifungal (e.g., fluconazole once weekly treatments for 2 months [3], itraconazole, or terbinafine [4]) may be substituted but it is best to consult, at least by telephone, with a dermatologist because newer drugs do not yet have U.S. Food and Drug Administration (FDA) approval and certain contraindications may exist. After 4 to 6 weeks of therapy, fungal culture is repeated; if results are negative 2 weeks later, treatment is stopped at that time.
Tinea Faciei
Tinea faciei is often misdiagnosed as rosacea or cutaneous lupus. Lesions tend to appear less “ringworm-like” (less sharp and clearly annular) than fungal infections elsewhere on the body. Patients often note that lesions flare with sun exposure, again suggesting diagnoses such as lupus erythematosus and acne rosacea instead of tinea. Lesions vary from erythematous, ill-defined, scaly plaques to the more classic sharply circumscribed plaques with leading edge scale and central clearing. Diagnosis may be made with a positive KOH preparation; however, on the face, false-negative KOH preparations are common with tinea faciei, and diagnosis may require culture or biopsy. Treatment is generally an oral antifungal (e.g., griseofulvin, itraconazole, fluconazole) because topical therapy may fail to clear this infection.
Tinea Corporis
Tinea corporis indicates a tinea infection outside of the head, face, groin, hands, and feet. Classic lesions are annular (ring-like) plaques that show a delicate scale at the advancing margin. KOH preparation from these lesions is usually positive. Treatment usually consists of topical imidazole antifungals (see Chapter 113) for 1 month with systemic therapy reserved for patients with a great number of lesions or unresponsive to prior topical treatment.
Tinea Cruris
Tinea cruris is predominantly seen in men. Lesions are semicircular scaly plaques on the superior medial thighs extending into the inguinal folds and onto the perineum. Diagnosis is based on a positive KOH preparation. Treatment with topical imidazoles (see Chapter 113) for a few to several weeks is usually adequate to control the problem.
Tinea Pedis
Tinea pedis is exceedingly common, eventually affecting up to 80% of men. Patients may have interdigital and plantar involvement with absent or moderate erythema, scale, and focal maceration. Less commonly seen is acute onset “oozing and blistering” on the plantar feet. Occasionally, interdigital tinea pedis with interdigital fissures may provide a point of entry for Streptococcus, which may ascend and cause recurrent streptococcal erysipelas cellulitis of the leg (5). Diagnosis is made with a positive KOH preparation, and treatment may be initiated with topical imidazoles. When plantar involvement is present, topical therapy may be unsuccessful and requires oral therapy for complete clearance. If treatment failure occurs in a patient at risk for leg cellulitis (e.g., history of prior leg erysipelas or cellulitis, venous stasis, or deep or superficial venous thrombosis), oral therapy should be prescribed to decrease the risk of recurrent ascending bacterial streptococcal cellulitis (6).
Tinea Manum
Tinea manum (tinea of the palmar skin) is uncommon. When seen, it often manifests as “two feet, one hand” syndrome, with areas of involvement as the name implies. The palm shows diffuse usually noninflammatory scaling, and the KOH preparation or fungal culture is positive. Treatment typically requires systemic therapy, but topical imidazoles (see Chapter 113) may initially be tried for 6 to 8 weeks. If topical therapy is unsuccessful or if nail involvement is present, oral itraconazole or terbinafine may be prescribed.
Tinea Unguium (Onychomycosis)
Tinea unguium of the toenails is very common, whereas fingernail infection is relatively rare. Although the incidence of tinea unguium is from 2% to 13% of the general population, the prevalence in the older male population is much higher. Tinea unguium represents approximately 30% of all mycotic infections of the skin and nails. Changes include white discoloration, subungual crumbly debris, and thickening of the nails. Patients are typically asymptomatic unless the toenails become ingrown or secondary bacterial infection occurs. Treatment is notoriously difficult. Although topical therapy is an option (e.g., Penlac Nail Lacquer, Mycocide NS [OTC], Fungi-Nail [OTC]), it generally is only useful in reducing the extent of infection with resultant improvement in the appearance of the nails. True cure rates with topical therapy are generally about 10%.
P.1916
When patients desiring systemic therapy understand the expense, potential side effects, and required laboratory studies (baseline liver function test[s], generally repeated monthly when dosing is continuous), itraconazole or terbinafine may be used. Cure rates several months after completion of a 3-month course of therapy vary from 50% to more than 70%. Because these drugs are retained in the nail for many months after drug discontinuance, patients should not be evaluated until several months after completion of therapy. If they are not clear, another 3-month course of therapy may be initiated. An alternative dosing regimen has been described for terbinafine therapy which shows promise. Investigators studying 59 consecutive patients receiving one week in duration “pulse” dosing at various intervals found a greater than 60% cure rate when the pulsing interval was 3 months or less, i.e., similar to the response seen with 3 months of daily therapy. The optimal regimen (to minimize medication required, yet yield this 60% cure rate) was 4 pulses of terbinafine 250 milligrams per day for 7 days every 3 months. This regimen reduces both drug exposure and expense, i.e., 28 tablets versus 90 tablets ingested; hopefully, these results will be confirmed in randomized, double-blind, placebo controlled trials in the near future (7). After completion of systemic therapy, discarding old footwear or replacement of shoe insoles, as well as ongoing topical pro-phylactic antifungal preparations may help reduce recurrence rates.
Yeast Infections
Candidiasis
Candida albicans and other Candida species are yeast-like fungi that most often cause superficial cutaneous infections; however, in immunocompromised patients, Candida may cause systemic infections, including septicemia. Candida infection presents most often as a diaper rash in infants, summertime inframammary rash in women, vaginitis in premenopausal women, oral candidiasis in endogenously or exogenously immunosuppressed patients, and buttock and perineal rash in incontinent patients. The cutaneous changes are similar in most areas and appear as erythematous, slick, shiny patches with an irregular border of delicate scale and often satellite papules and pustules. The diagnosis can be confirmed with a KOH preparation or a swab culture.
Candidiasis may be treated with topical nystatin cream or an imidazole cream (see Chapter 113). Topicals should be applied two times a day and are continued for 1 to 2 weeks after clearing is seen. For infections unresponsive to topical therapy and when benefit outweighs risks, expense, and required testing, oral itraconazole or fluconazole for 10 to 14 days may be used. Pretreatment liver function tests are prudent in patients with multiple medical problems, and all patients should be instructed to report any signs or symptoms of hepatotoxicity during treatment. Topical nystatin powder or simple body powder may be helpful in preventing recurrences.
Tinea Versicolor
Tinea versicolor is a chronically recurring superficial yeast infection of the skin caused by Pityrosporum orbiculare, also known as Malassezia furfur. Tinea versicolor is seen most often in teens and young adults. It is common year-round in tropical climates and during the warm months in temperate climates.
Tinea versicolor appears as round to oval, scaly hypopigmented, hyperpigmented, or salmon colored macules that coalesce to form large confluent patches over the upper trunk and shoulders and, less often, on the face, scalp, genitalia, arms, and thighs. Although usually asymptomatic, some patients may have significant pruritus, particularly when perspiring during and after exercising. Diagnosis is made with a positive KOH preparation showing pseudohyphae and spores (Fig. 117.1). A simple and usually effective 5-day therapy is daily ketoconazole shampoo (prescription Nizoral 2% or over-the-counter Nizoral AD 1%) applied undiluted as a lotion and left on for 5 minutes before being rinsed. Once-weekly applications may be useful in preventing recurrences. Although not yet an FDA-approved indication, oral itraconazole 200 mg daily for 1 week in a controlled trial appears effective (8); however, recurrence is common.
In contrast to the superficial “epidermal” fungal infections mentioned above, deep fungal infections of the skin involve the underlying dermis. Excluding sporotrichosis,
P.1917
cutaneous infection usually results from seeding of the skin from a distant visceral organ infection (e.g., pulmonary). Table 117.1summarizes some of the more common deep fungal infections.
|
FIGURE 117.1. Short hyphae and spores of Malassezia furfur seen in tinea versicolor (potassium hydroxide preparation, ×400). |
||||||||||||||||||||||||||||||||||||||||
|
TABLE 117.1 Selected Deep Fungal Infections |
||||||||||||||||||||||||||||||||||||||||
|
||||||||||||||||||||||||||||||||||||||||
Potassium Hydroxide Wet Mount Preparation
Dermatophyte and yeast infections of the skin are diagnosed with microscopic examination of surface skin scale. For this examination, scale is scraped from the advancing margin of an active lesion using a no. 15 surgical blade held at a slightly less than 90-degree angle to the skin surface. The scale is placed on a glass slide, one to two drops of KOH 20% added, and a coverslip applied. This is gently heated with a low flame, avoiding boiling, which, if it occurs, will result in crystallization and invalidation of the procedure. With light microscopy, the slide is scanned with the 10× objective and then examined more closely with the 40× objective. Dermatophyte hyphae are seen as refractile rod-shaped filaments of uniform width with characteristic branching (Fig. 117.2A). These hyphae traverse several normal cells and therefore can be distinguished from cell membranes. In contrast, Candida and Pityrosporum appear as nonbranching pseudohyphae and clusters of budding spores (Fig. 117.2B). Occasionally, Candida may show branching hyphae.
Fungal Culture
When the diagnosis of a fungal infection is strongly suspected despite a negative KOH preparation, when KOH examination is not available, and when the identification of a specific dermatophyte is important, a fungal culture should be done. Depending on the site of suspected infection, scale is taken from the advancing margin of the skin lesion, under the nail, or the scalp. The latter sample should also include several “broken off” hairs extracted with tweezers or forceps. Specimens may be placed
P.1918
between two glass slides, taped together, and sent in a sterile cup to the laboratory. Alternatively, particularly when the patient is not able to hold still and using a no. 15 blade may be dangerous, a culturette swab firmly rubbed over the area may be used.
|
FIGURE 117.2. A: Hyphae of tinea (potassium hydroxide preparation, ×400). B: Pseudohyphae of Candida (potassium hydroxide preparation, ×400). (Courtesy of William G. Merz, PhD.) |
Localized Viral Infections of the Skin
Warts
Warts, also known as verrucae, are benign proliferations of the epidermis caused by human papilloma virus (HPV) infection. Warts are most common in children and immunocompromised patients. Three clinical features of all forms of warts include disruption of normal skin lines, surface pinpoint black dots (thrombosed capillaries), and appearance at sites of contact or trauma.
Common warts (verrucae vulgaris) may be noted initially as smooth, skin-colored, <1-mm papules that gradually enlarge to several millimeters with a rough, finely papulated, or hyperkeratotic (warty) surface. Warts may coalesce to form large plaques. Common warts are most often found on the hands.
Flat warts (verrucae plana) are skin-colored to pink flat-topped papules usually less than a few millimeters in diameter. They occur most commonly on the dorsal aspect of the hands, face, and, in women, the legs.
Genital warts (condylomata acuminata) begin as minute flat papules that often become verrucous on the external genitalia, vagina, cervix, perirectal, and/or anal canal. This HPV infection of the cervix or anorectal area predisposes to intraepithelial neoplasia. Immunosuppression, for example, from immunosuppressive therapy in an organ transplant recipient to a patient infected with human im-munodeficiency virus (HIV), may increase the risk of anal intraepithelial neoplasia when genital warts are present.
Plantar warts (verrucae plantaris) appear as circumscribed, thickened, barely elevated papules with surface callous. Extensive infection with HPV may manifest as warts covering the entire heel or plantar aspect of the foot. Plantar warts are often confused with corns or clavi. Warts can be distinguished from corns by paring the surface with a no. 15 surgical blade as the typical minute black dots (thrombosed capillaries) should become visible. In contrast, paring of corns reveals a central core that is easily removed with the paring blade.
Treatment
Two precepts should be remembered when treating warts: There are no guarantees in the success of any treatment and the lesions themselves are benign and should not be treated with modalities that result in harm or scarring, such as ionizing irradiation, deep surgical excision, or deep destructive therapies (extending into the dermis).
Treatment of common, flat, and plantar warts is typically daily self-application of topical 17% salicylic acid solution (e.g., Occlusal or Duofilm) or a 40% salicylic acid patch (MediPlast), all available over the counter. Before application, the wart may be soaked in warm water for several minutes and then filed to remove the white macerated surface with a nail file or pumice stone (available in pharmacies). Because of the risk of infection transmission, whatever instrument is used it must not be used elsewhere or by others. If after 6 weeks of daily therapy the wart is still present, weekly or biweekly liquid nitrogen cryotherapy may be started. Patients should be warned that although liquid nitrogen should not cause scarring, it may cause blistering and, upon healing, permanent depigmentation of the skin, particularly important with face and hand warts, and, rarely, superficial nerve damage (usually on the lateral surface of the digits). If after several cryotherapy sessions warts are still present, other options should be
P.1919
considered, such as “watchful waiting,” laser vaporization, and curette and desiccation. Patients should be warned that these latter treatments may cause scarring.
Initial treatment of condyloma acuminatum may be administered by the patient. Two options are available. Podofilox 0.5% (Condylox gel or solution) is a patient-applied podophyllin derivative that is applied two times a day for 3 consecutive days each week. After several weeks of treatment, clearance rates are 30% to 50%. Another patient-applied medication is imiquimod 5% cream (Aldara). This agent causes local endogenous cytokine release that is believed to lead to a host effected clearance of HPV. Imiquimod cream is applied three times per week for up to 4 months. Both of these medications require a prescription. If these medications are ineffective, liquid nitrogen cryotherapy may be used in the same manner as outlined for other warts. Additional alternative therapies, which may be considered by a consulting dermatologist, include laser vaporization, curette and desiccation, and scalpel excision.
Molluscum Contagiosum
Molluscum contagiosum is common in young children and HIV-infected patients. Lesions are caused by the pox virus, a DNA virus. The lesions are umbilicated, skin-colored to whitish, 1- to 4-mm papules, typically on the neck, trunk, genital, and eyelid areas. The central umbilicated depression contains molluscum bodies, which are enlarged degrading keratinocytes, packed with viral material. The diagnosis is made by obtaining a curette of the molluscum for KOH preparation. With light microscopy, the round, homogeneous, 25-µm molluscum bodies are easily seen.
In children, simple nonthreatening treatments are best. Scotch tape stripping (tape quickly and firmly applied and immediately removed a dozen times) once to twice daily for several weeks may suffice by unroofing the lesion and stimulating a host response through the mild local trauma. Alternatively, topical salicylic acid 17% preparations (as for warts; see above) or topical tretinoin (Retin-A 0.025% gel) applied directly to the lesion twice a day may be tried for 6 weeks. If lesions persist, either curettage or liquid nitrogen cryotherapy may be used, remembering that the latter may cause permanent depigmentation.
Herpes Infection
Herpes Simplex
Herpes simplex virus (HSV) infection may be caused by HSV type I or II, typically with type I causing herpes labialis and type II causingherpes genitalis. HSV is commonly present in asymptomatic individuals. For example, a study of randomly selected patients in a family medicine clinic found 56% seropositivity for HSV I, 23% seropositivity for HSV II, 12% seropositivity for both HSV I and II, and 33% seronegativity (9). Active infection results in a recurrent localized clustered (herpetic) blistering of the skin. After a primary infection has occurred, the virus remains dormant in the cranial nerve or dorsal root nerve ganglia innervating the region of cutaneous infection. Lesions may recur at any time, often being triggered by sun exposure, illness, menses, local trauma, and physical and psychologic stress. Transmission occurs through direct contact with an infected person actively shedding virus. The virus may live on fomites, but unlike HPV, HSV quickly dies on drying (30 minutes), making fomite transmission unlikely.
Primary herpes infection in the oral cavity causes the painful febrile illness acute herpetic gingivostomatitis (see Chapter 112). After healing the virus remains latent, and subsequent reactivation causes herpes labialis, manifest as clustered vesicles on or about the lips. Notably, most patients with recurrent herpes labialis have no history of primary acute herpetic gingivostomatitis or herpetic infection elsewhere and therefore are presumed to have had an asymptomatic primary oral infection. Lesions heal in approximately 1 to 2 weeks, with a typical sequence of rupture, crusting, and desquamation. The lesions are infectious as long as the skin is not intact. The importance of asymptomatic viral shedding in viral transmission, as is known to occur with genital herpes and with exceptionally high frequency in patients with acquired immunodeficiency syndrome (AIDS), is not known, although in one prospective study of couples with one infected partner, 70% of partner infections occurred during periods of asymptomatic shedding (10). Genital herpes, the most common cause of genital ulcers, is discussed in Chap-ter 37.
Herpes simplex infection may occur anywhere on the body; a common site in health care workers is on the finger (herpetic whitlow), acquired through exposure to a patient with active herpes infection. Viral transmission has been reported to occur through vinyl gloves, so one is wise to double glove if touching herpes lesions is required during an examination or in the provision of care.
Chronic herpetic infections in immunocompromised patients appear as chronic punched-out ulcers that may be solitary or multiple. The expanded AIDS surveillance case definition for AIDS diagnosis includes a chronic herpes simplex ulcer present for 1 month or longer in a patient infected with HIV.
Fortunately, cutaneous complications of HSV infection are rare. These complications include cutaneous dissemination in patients with generalized atopic dermatitis and recurrent erythema multiforme as a hypersensitivity response. A history of the latter is an indication for ongoing prophylactic antiviral therapy (see Chapters 102, 112, and 118).
P.1920
Ocular complications include herpetic keratitis, a primary or secondary infection that involves the cornea of the eye and is best managed emergently by an ophthalmologist because of the potential for permanent corneal scarring and loss of vision. Albeit rare, the most common systemic complication is Bell palsy (11). Other serious and systemic complications that are rare complications of HSV include acute ascending necrotizing myelopathy and necrotizing lymphadenitis associated with herpes genitalis (12) and recurrent lymphocytic meningitis (13).
Treatment
Although no treatment is necessary for recurrent facial HSV, an FDA-approved regimen of valacyclovir, 2 g twice a day, may abort or reduce the duration of lesions when taken at the first signs of recurrence (i.e., optimally, with the onset of premonitory dysesthesia in individuals who experience this symptom). Antiviral prophylaxis (e.g., valacyclovir 500 mg daily) should be given when HSV recurrences may complicate any facial cutaneous surgery, oral surgery, or other dental work. Prophylaxis may also be welcomed by patients when recurrences may be anticipated, such as ski trips (oral antiviral and topical high SPF sunscreen), or important ceremonial social events (14).
Novel treatments appear to have promise for HSV. In a randomized, double-blind, placebo-controlled, pilot study, stannous fluoride 0.4% gel applied twice daily at the onset of prodromal symptoms prevented blisters from developing in most individuals, and in those who developed lesions, it decreased their duration significantly (15). Also, aspirin initiated at the onset of recurrent HSV, at a dose of 125 mg, decrease the duration of lesions by almost 50%, whereas a dose of aspirin of 250 mg/day did not show this benefit (16).
Herpes Zoster (Shingles)
Herpes zoster represents a reactivation of the varicella–zoster virus. After initial varicella (chickenpox) infection, the virus resides in a dorsal root or cranial nerve ganglia. At any point thereafter, latent virus may be reactivated and produce multiple erythematous plaques surmounted by clustered vesicles, in a dermatomal or zosteriform distribution. In an immunocompetent patient, lesions begin with vesicles that become turbid in 3 days, dry and crust in 7 to 10 days, and clear within 2 to 3 weeks. New lesions may continue to appear for up to 1 week. Herpes zoster affects a thoracic dermatome in 50%, a cervical dermatome in 20%, the trigeminal dermatome in 15%, and a lumbosacral dermatome in 10% of patients. Of patients with herpes zoster, two thirds are older than 50 years of age and about 10% are younger than 20 years of age (17).
Often, patients who have herpes zoster develop a prodrome of pain in the affected dermatome. Occasionally, this painful prodrome is misdiagnosed as an acute painful disease such as pleurisy, myocardial infarction, cholecystitis, appendicitis, renal colic, or a ruptured intervertebral disk. Rarely, patients may experience acute segmental neuralgia with a concurrent rise in varicella virus antibodies without developing skin lesions. This is called zoster sine herpete.
There are several very significant potential complications of zoster. When the trigeminal dermatome is affected, involvement of the second branch may be associated with involvement of the eye. Affected patients should be evaluated emergently by an ophthalmologist because keratitis, uveitis, secondary glaucoma, iridocyclitis, or rarely panophthalmitis may develop. Ramsay-Hunt syndrome is the constellation of herpes zoster affecting the facial and auditory nerves, causing facial palsy with cutaneous zoster of the external ear or tympanic membrane with associated tinnitus, vertigo, and/or hearing deficit. Among all patients with herpes zoster, motor nerve involvement occurs in only 5%. The incidence is probably understated because mild or partial deficits likely go undetected. Weakness or paralysis usually begins within weeks of the onset of the rash and may involve the muscle groups outside of the affected dermatome. Full recovery from this weakness or paralysis occurs spontaneously in only about half of patients who are so affected (18). Meningoencephalitis may develop with cranial nerve herpes zoster in immunocompromised patients, most often in association with cutaneous dissemination. Granulomatous angiitis of cerebral arteries is an unusual complication of ophthalmic zoster that may lead to a syndrome of delayed contralateral hemiplegia occurring weeks to a few months after an episode of zoster. Such patients are usually diagnosed as having a typical cerebrovascular accident, but arteriograms reveal segmental narrowing or occlusion of cerebral arteries ipsilateral to the site of the ophthalmic zoster. Finally, disseminated herpes zoster, defined as more than 20 vesicles at a distance from the primary dermatome, occurs almost exclusively in immunocompromised patients. Such patients should be hospitalized for intravenous acyclovir therapy and isolated as appropriate to protect those not immune to the virus. Approximately 10% of patients with disseminated cutaneous lesions develop widespread often fatal visceral infection, particularly of the lungs, liver, and brain.
The presumptive diagnosis of herpes zoster is made clinically. A Tzanck smear, done when there is doubt about the diagnosis, shows multinucleated giant cells (see page 1921). Such a positive smear confirms that the eruption is herpes zoster or herpes simplex and rules out other blistering disorders such as impetigo, erythema multiforme, and pemphigus, which occasionally may be confused with herpes infection. Herpes simplex can occur in a dermatomal pattern, so any case of “recurrent” herpes zoster should be cultured because the correct diagnosis is more likely recurrent dermatomal HSV infection. It is important to
P.1921
confirm this infection because recurrent zoster (as opposed to HSV) raises the possibility of an associated illness causing immunosuppression and should prompt further evaluation of immune function.
The early treatment of acute herpes zoster reduces the severity, shortens the duration of the infection, and potentially reduces the incidence of post herpetic neuralgia. Kost and Straus (19) put forth a useful algorithm for treatment and prevention of acute herpes zoster and postherpetic neuralgia (PHN). Antiviral therapy affects the course of disease if initiated within 48 to 72 hours of its onset. A 1-week course of an oral antiviral (e.g., acyclovir [Zovirax] 800 mg five times a day, valacyclovir [Valtrex] 1,000 mg three times a day, famciclovir [Famvir] 500 mg three times a day) is used in immunocompetent patients. Acyclovir has been shown to reduce zoster-associated acute pain and new lesion formation, and both valacyclovir and famciclovir reduce acute pain and speed healing (20,21).
Topical therapy will ease the pain from open lesions. Wet to damp dressings promote drying of the lesions, and a topical ointment (e.g., plain petrolatum or antibiotic ointment with caution given the potential development of allergic contact dermatitis if Neosporin or bacitracin are used) generously applied promotes healing, prevents secondary infection, and reduces the pain caused by air contacting the denuded skin. If acute neuralgia is present, nonsteroidal anti-inflammatory drugs, amitriptyline, or narcotics may be needed to provide comfort. These must be used with caution, particularly in persons living alone, those on multiple medications, and the elderly.
In hospitalized patients with even routine, nondisseminated zoster, contact and respiratory precautions should be instituted. With the advent of polymerase chain reaction technology, it has been shown that viral shedding does occur in patients with herpes zoster; in one report, detectable varicella zoster virus was found at distant sites within an otherwise healthy affected patient's room, including the surface of the room air conditioner filter, consistent with aerosolized spread (22).
PHN, or pain after the cutaneous lesions have resolved, is most commonly seen in patients older than 50 years. Other predictors of the development of PHN include a greater number of health care encounters in the 6 months before zoster, baseline conditions causing immunosuppression, treatment with steroids in the 6 months before zoster, and zoster associated prodromal symptoms, discomfort severe enough to interfere with daily living, and prolonged time to crusting of skin lesions (23). Both valacyclovir and famciclovir have been shown to reduce the incidence and duration of PHN (20,21). Its been estimated that six patients need to be treated with antivirals to prevent one case of PHN (24). The utility of supplemental corticosteroids in the prevention of PHN remains controversial (25,26) and therefore is not recommended. A small study found that amitriptyline 10 to 25 mg nightly initiated at the time of diagnosis of acute zoster reduced the incidence of PHN by 50% (27). If larger studies ultimately show this same benefit, amitriptyline (with appropriate caution; see Chapters 12and 24) would seem to be an ideal treatment for persons with painful acute herpes zoster.
Once developed, treatment of PHN may be very difficult. Some success has been reported with topical capsaicin cream (Zostrix 0.025% and Zostrix HP 0.075%), applied four times a day. Capsaicin depletes substance P in peripheral sensory nerves and may alleviate pain. Not infrequently, there is a delay of several weeks before an effect is appreciated. Patients must be cautioned that about four applications are needed to fully deplete the substance contributing to pain (substance P), so the first few applications (typically, three) when substance P is being released produce local burning and stinging. However, with subsequent consistent applications, the pain should not recur. Alternatively or in conjunction with capsaicin, anesthetic over the counter LidoDerm topical patches and over the counter ELA-Max cream may be tried. Unfortunately, both are quite expensive for long-term use. For some patients, systemic treatment with amitriptyline (as opposed to prevention) is appropriate initial therapy for PHN. Oral amitriptyline in dosages of 12.5 to 150 mg/day (27) may decrease the discomfort of PHN (see Chapters 12 and 24). Gabapentin studied over a 2-month treatment period in a multicenter, double-blind, randomized, placebo-controlled study also was found to be effective in reducing pain and sleep disturbance and improving mood and quality of life (28). PHN most often remits spontaneously within 6 months; however, when this is not the case and the pain cannot be controlled, referral to a pain specialist is appropriate. Although still investigational (29), intrathecal methylprednisolone may prove to be helpful for intractable PHN.
Tzanck Smear
The sensitivity of a Tzanck smear in detecting herpetic changes is greatest when a specimen is taken from the intact vesicle. A chosen vesicle is unroofed, and the base is firmly scraped with a no. 15 surgical blade and smeared onto a glass slide. When vesicles are not present, an early crusted papule is sampled by removing the surface crust and scraping the base. Immediate tissue smear staining is performed with the commercially available Tzanck stain (Dif-Quik Stain, Baxter Scientific Products, McGraw Park, IL), which is a three-step immediate stain. Alternatively, a Giemsa stain may be done by combining 0.5 mL water with 0.5 mL Giemsa tissue stain in a small syringe and flooding over the specimen and then thoroughly rinsing with tap water after 30 seconds. Although the slide may be viewed directly, covering with mounting medium and a coverslip greatly improves resolution. The slide is searched for giant
P.1922
cells containing multiple syncytial nuclei (nuclei that mold together in a jigsaw puzzle-like fashion) (Fig. 117.3). The Tzanck smear preparation should be positive when performed on lesions of herpes simplex, varicella, and herpes zoster eruptions (Fig. 117.3). If the Tzanck smear is nondiagnostic, biopsy of a papule, vesicle, or crusted papule for routine histopathology (results available in 2 to 4 days) should reveal diagnostic herpetic changes of balloon cells and multinucleated giant cells.
|
FIGURE 117.3. Tzanck smear: gentle scraping from the base of a vesicle and stained with Wright or Giemsa stain. Multinucleated cells from herpes simplex are shown (×400). |
Infestations
Scabies
Human scabies is caused by infestation with the mite Sarcoptes scabiei var. hominis. Infestation causes an intense intractable pruritus that is classically most disturbing at night, when competing external stimuli are minimal. The signs and symptoms of scabies infestation are caused by the host's immune response to the mite and its eggs and feces. Generally, this response is delayed, so patients become itchy approximately 10 days to 2 weeks after exposure and infestation. Scabies is seen most often in children, and the pathognomonic lesions are burrows, which are thread-like linear ridges a few millimeters in length with a minute black dot at one end. Burrows occur most often on the hands, wrists, soles, waist, penis, nipples, axillae, and gluteal cleft. Depending on the duration of infestation, patients may have few to innumerable scratches, excoriations, crusts, and eczematous papules and plaques. Less often, small nodules may develop, tending to favor the scrotum, axillae, and buttocks.
Scabies infestation is confirmed by identifying the mite, eggs, or feces in the superficial skin. This often can be done by scraping the black dot at one end of a burrow using a no. 15 surgical blade. If a black dot is not seen, both ends of the burrow are scraped. The sample is prepared on a glass slide with a drop of mineral oil and a coverslip and then viewed with light microscopy. The mite is an approximately 0.2 mm with eight short legs; eggs are smaller and oval and feces are still smaller round pellets.
Patients and family members should be treated with an overnight application of prescription lindane lotion (Kwell lotion, 30 mL per single application) or permethrin cream (Elimite cream, 30 g per single application, 60-g tube). Either is applied from the neck down, using an old toothbrush to get under the finger and toenails and showered off 8 to 12 hours later. After this is completed, patients often require emollients and a mid-potency corticosteroid (e.g., triamcinolone 0.1% ointment) after using the scabicides to suppress the “hyperreactivity” caused by the mites (see Chapter 113). Although both lindane and permethrin are neurotoxins, systemic absorption of lindane is greater (30) so it should be avoided in infants, pregnant and lactating women, and patients with seizure disorders. It should also be avoided when enhanced systemic absorption is possible, such as in patients with extensive secondary excoriations and dermatitis or with widespread skin diseases (e.g., generalized atopic dermatitis, widespread psoriasis). All bed clothing, linens, unwashed clothing, and stuffed animals should be washed and dried in a hot dryer. The latter is necessary, because it is the temperature of the hot dryer that kills the mite. Alternatively, the mites and eggs may be killed by placing the items in airtight plastic bags for 2 weeks.
An alternative treatment now available in this country in patients resistant to topical scabicidal therapy is ivermectin (3-mg tablets) (31,32). If used, the Centers for Disease Control and Prevention (CDC) recommends a dose of ivermectin 0.2 mg/kg (e.g., a single dose of four tablets for a 60-kg adult), repeated in 2 weeks as an alternative to topical permethrin cream (33).
Pediculosis
Infestation with the human louse (Pediculus humanus capitis and corporis, Phthirus pubis) affects different areas of the body and is calledpediculosis capitis, corporis, and pubis. Pediculosis capitis is most common in children. Patients with lice often have intense pruritus, scalp and posterior neck excoriations, and often secondary bacterial infection with pustules, crusting, and adenopathy. Pediculosis corporis is seen most often in patients exposed to others who, like themselves, are unable to maintain good hygiene. Pediculosis pubis (pubic lice) is usually a sexually transmitted disorder.
Patients with pediculosis usually have nits firmly attached to head, body, or pubic hairs (Fig. 117.4). Nits are less than 1-mm-long “shells” that may or may not still
P.1923
contain an egg. Lice hatch from these eggs and are visible, being less than 2 mm long with three pairs of legs that terminate in sharp claws. They are found in the hair or adjacent skin and, specifically in pediculosis corporis, in the seams of clothing. Treatment should be initiated with pyrethrin shampoo (RID, OTC), lindane shampoo or lotion (Kwell), or malathion lotion (Ovide) for pediculosis capitis and pubis (note, Ovide is only labeled for scalp treatment and is contraindicated in neonates and infants) and lindane lotion for pediculosis corporis. The shampoos are left on for 5 to 10 minutes and then washed off; the lotions are left on overnight. Because no pediculicides are 100% ovicidal, nits that potentially contain living eggs and will remain attached to the hair after treatment must be removed with a fine-tooth comb after undiluted white vinegar is applied to the hair for 15 minutes. Close contacts should be treated in a similar fashion, and bed clothing and linens and unwashed clothes should be washed and put through a hot dryer cycle to destroy the lice and eggs. Alternatively, these items may be sealed in an airtight plastic bag for 2 weeks.
|
FIGURE 117.4. Pediculus humanus var. capitis (head louse). A: Gross appearance of nits on the hair shaft. B: Microscopic appearance (×100). (Courtesy of Reed and Carnrick, Kenilworth, NJ.) |
Specific References*
For annotated General References and resources related to this chapter, visit http://www.hopkinsbayview.org/PAMreferences.
P.1924