Infectious Diseases of the Skin

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[edit] Infectious Diseases of the Skin

Bert G. Tavelli

[edit] BACTERIAL INFECTIONS

[edit] Impetigo

Impetigo is characterized by erythematous macules that evolve into vesicopustules, which quickly rupture to form the hallmark honey-colored crusts, usually on exposed skin of the face and extremities. Caused by Staphylococcus aureus or Streptococcus pyogenes, or both, it is typically seen in children, in whom it is highly contagious. Lesions may burn or itch, but constitutional symptoms are usually absent. Other forms of impetigo include a rare bullous type, mediated by toxins produced by group II S. aureus (which in its most severe form results in staphylococcal scalded skin syndrome), and impetiginized eczema, in which honey-colored crusts and pustules representing staphylococcal or streptococcal superinfection develop on dermatitic skin (see Plate 14 ).

[edit] Management.

Small areas of superficial involvement respond to local cleansing with antibiotic soaps and topical treatment with mupirocin (Bactroban) ointment, applied three times daily until clear. Widespread and bullous lesions are best treated systemically with a penicillinase-resistant antibiotic. In penicillin-allergic patients, clindamycin or erythromycin may be substituted. In recurrent cases, positive nasal swab cultures indicate a carrier state, which responds to twice daily mupirocin ointment application.

[edit] Erysipelas and Cellulitis

Both erysipelas and cellulitis are caused by rapidly spreading infection with streptococcal or, less commonly, staphylococcal organisms. In erysipelas, more superficial skin and lymphatics are affected, resulting in raised, red, warm plaques with sharply demarcated borders and a brawny (orange-peel) appearance. The face is most commonly affected, and vesicles and bullae also may be seen ( Plate 74 ). In cellulitis, deeper tissues and subcutaneous fat are involved, most often on the lower extremities ( Plate 75 ), and the plaques are less well marginated or distinct. Local dermatitis, tinea pedis, trauma, surgical wounds, and stasis ulcers predispose to infection. Both erysipelas and cellulitis can be associated with fever, chills, local pain, lymphangitis, regional lymphadenopathy, and systemic toxicity with tachycardia and hypotension. Tissue culture is usually unnecessary and yields are low, but blood cultures should be obtained with extensive infection or marked toxicity.

[edit] Management.

Treatment consists of systemic antibiotic therapy and support. Penicillin is usually adequate, but erythromycin, clindamycin, or cephalosporins may be used. Attention should be given to predisposing conditions to prevent recurrences, and prophylactic antibiotics (e.g., erythromycin 250 mg twice a day) in susceptible individuals help prevent chronic lymphedema, which is a condition causing progressive woody induration of the legs.

[edit] Necrotizing Fasciitis

In some cases, a combination of anaerobic and aerobic bacteria, including staphylococci and streptococci, causes an infection of the subcutaneous tissues called necrotizing fasciitis. Usually induced by trauma or extension of an antecedent infection, it rapidly spreads to cause bright red, edematous, tender plaques, associated with superficial gangrene, and marked systemic symptoms. This serious often fatal infection requires hospitalization, surgical exploration, and broad-spectrum antibiotics.

[edit] Ecthyma.

Ecthyma is caused by streptococcal and staphylococcal infection, often in patients with poor hygiene or at sites of trauma, especially of the lower extremities. Multiple, discrete vesicopustules quickly enlarge and rupture to form purulent ulcers with overlying necrotic crust. Lesions often scar and spread if untreated but respond quickly to appropriate systemic antibiotics.

[edit] Erythrasma.

Erythrasma is a superficial skin infection occurring in skin folds and toe webs, caused by the diphtheroid Corynebacterium minutissimum. Asymptomatic flat, dry, brown patches develop, which resemble tinea but can be distinguished by negative potassium hydroxide (KOH) examination and by their bright ``coral red fluorescence under Wood's light examination. Topical application of 2% erythromycin or 1% clindamycin for 5 to 7 days is rapidly effective.

[edit] Folliculitis, Furuncles, and Carbuncles.

Folliculitis occurs around hair follicles, caused by occlusion of the ostium with accompanying superficial inflammation and infection. Precipitating factors include trauma, chronic friction, occlusive clothing and chemicals, and excessive sweating or exposure to water. With deeper involvement an inflammatory nodule, or furuncle, is formed, and multiple furuncles can coalesce to form a carbuncle, usually on the posterior neck. S. aureus is the cause in most cases. Simple folliculitis can be treated with chlorhexidine gluconate wash plus topical antibiotics. Recurrent folliculitis or furuncles respond to systemic antibiotics.

``Hot tub folliculitis results from exposure to inadequately disinfected pools or spas contaminated by Pseudomonas aeruginosa. One to 2 days after exposure, pinpoint follicular pustules surrounded by large, bright red macules appear (Fig. 91-1), which resolve without treatment. Systemic infection is rare, but treatment with oral ciprofloxacin may be warranted in cases of widespread or highly symptomatic infection and in health care workers.

Figure 91-1 Hot tub folliculitis. Note discrete pustules on an erythematous base distributed on the trunk.

[edit] Tinea Pedis

Tinea pedis, or athlete's foot, is the most common dermatophytosis. It can present acutely as a blistering eruption with vesicles, pustules, fissures, and marked inflammation (Figs. 91-2 and 91-3). Lesions may burn or itch fiercely, and secondary bacterial infection is frequent. A more common chronic form presents either as maceration and fissuring in toe webs, or as dry, reddish scaly patches around the foot, often in a ``moccasin distribution. Topical treatment is usually sufficient for localized involvement, along with elimination of concominant hyperhidrosis and use of occlusive footwear. Highly inflamed, widespread, or resistant infection requires systemic treatment (see Management section).

Figure 91-2 Tinea pedis, vesicular inflammatory type. Note small vesicles and erosions.

Figure 91-3 Tinea pedis, chronic form. Note the moccasin distribution of scaling and slight erythema.

[edit] Tinea Cruris

Raised, red, scaling, occasionally vesicular plaques, which can expand to involve the thigh, pubic, and perianal skin characterize tinea involvement of the groin area (jock itch). Candidiasis, psoriasis, and erythrasma must be considered in the differential diagnosis, although unlike candidiasis, the penis and scrotum are generally spared. Topical treatment for 3 to 4 weeks is effective for most cases, along with attempts to minimize the chafing and excess moisture that precipitate infection.

[edit] Tinea Corporis

Fungal involvement of the trunk and extremities most often begins as one or more slightly raised, reddish, scaly patches, which slowly enlarge while clearing centrally (see Plate 17 ). These annular lesions represent classic ``ringworm, but tinea corporis also may be vesiculopustular, eczematous, or nodular. Furthermore, all annular lesions are not ringworm: sarcoidosis, granuloma annulare, urticaria, and gyrate erythema, to name a few, can present as annular lesions. Tinea faciale is a variant that is frequently difficult to recognize ( Plate 76 ). Superficial, localized infection is usually cured with topical treatment applied twice a day for 2 to 4 weeks. Deeper or more inflamed areas require systemic treatment.

[edit] Tinea Capitis

Scalp ringworm occurs most often in urban children but is also seen in adults. It can present as one or more scaly plaques with short stalks of broken hair, resembling seborrheic dermatitis, or more commonly as smooth, alopecic plaques with pinpoint hair stubs, broken off at scalp level (``black dot type), which can mimic alopecia areata. Occasionally, lesions are highly inflamed, resulting in an indurated, tender, boggy mass exuding pus called a kerion. Toxic symptoms and adenopathy may be present, and scarring alopecia can result if not treated. These lesions are often misdiagnosed as bacterial infections.

Treatment with systemic antifungals is required, along with aggressive local care and consideration of concomitant treatment with prednisone in the case of kerions.

[edit] Onychomycosis

See Chapter 92 for disorders of the nails.

[edit] Management.

Numerous topical agents are available for treating superficial fungal infections.^[1] The imidazoles, such as clotrimazole (Lotrimin AF), oxiconazole (Oxistat), and econazole (Spectazole) provide good broad-spectrum coverage against dermatophytes and Candida. They are used twice daily until infection is clear. Topical steroids, including those containing antifungals (Lotrisone), blunt local host defenses, may exacerbate infection, and lead to atrophy in occluded skin areas. They have no real place in the treatment of superficial fungal infections.

The emergence of three superior antifungal agents has recently supplanted griseofulvin and ketoconazole for systemic use^[2](Table 91-1). These agents provide better efficacy, shorter treatment times, and improved safety profiles. Itraconazole (Sporanox) provides the best broad-spectrum coverage; in the absence of several important drug interactions, itraconazole is safe and well tolerated. The pulse regimen improves compliance and is the preferred approach. A baseline liver profile should be considered. Terbinafine (Lamisil) has no significant drug interactions, but requires baseline and ongoing monitoring for possible hematologic effects and does not cover candida or most nondermatophyte molds. Fluconazole (Diflucan) is not approved for treatment of dermatomycoses. Its main use is for candidal skin infections.

Table 91-1 A Comparison of New Medications for Dermatomycoses

✢Pulse packs are two 100 mg tablets twice a day for 7 days, then 21 days off.

[edit] Candidiasis

Cutaneous candidiasis is usually caused by C. albicans and may be associated with underlying conditions such as diabetes mellitus, immunosuppression, or use of systemic antibiotics. Moisture, heat, and maceration greatly predispose to infection, which preferentially involves skin folds of the axillae, groin, breasts, and corners of the mouth (perleche). Infection is characterized by burning, beefy red erythema with scale and adjacent (``satellite) pustules ( Plate 77 ).

Candidal involvement of the nail unit presents most commonly with chronic redness, pain, and swelling of nail folds (paronychia). It greatly favors those exposed to constant wet work, including food industry and health care workers.

[edit] Management.

KOH examination and cultures, including bacterial, are necessary for a rational approach to treatment. Most superficial infections respond to twice daily topical applications of nystatin or an imidazole cream, along with attention to any predisposing conditions. Severe, resistant, or paronychial infections require systemic treatment with one of the newer triazole agents (fluconazole or itraconazole).

[edit] VIRAL INFECTIONS

[edit] Human Papillomavirus Infection

Long considered benign and uninteresting, infection with human papillomavirus (HPV) has gained considerable importance, emerging as the second most common sexually transmitted disease in the United States and linked to development of genitourinary tract carcinomas. To date more than 60 specific subtypes of HPV have been identified. Although many of these subtypes have been loosely associated with a particular body region, for most purposes these associations are not clinically relevant.

[edit] Common Warts.

Common warts (verrucae vulgares) are quite polymorphous on skin. They begin tiny and smooth, but progress over weeks to months to become typical, raised, keratotic, and often cauliflower-like papules. Common warts occur most often on the extremities but can be found anywhere on the skin in persons of all ages (see Plate 2 ).

Planar, or flat warts, occur primarily on the face, hands, and pretibial surfaces as tiny, slightly raised, flesh-colored papules. They can be numerous and refractory to treatment.

Palmar and plantar warts present as thick, endophytic papules or plaques, often multiple, which may be exquisitely painful when located over pressure points. These warts may be distinguished from a callus, which they resemble, by the appearance of tiny black dots (sclerosed vessels), or by bleeding points after paring (Fig. 91-4).

Figure 91-4 Plantar wart (verruca). Note the pinpoint thromboses after the lesion is pared.

[edit] Genital Warts.

An enlarging body of evidence documented the explosive rise in incidence of genital HPV infection and its recognition as a sexually transmitted disease (Fig. 91-5). Most important is the association of certain HPV types, including 16, 18, and 31, with the development of intraepithelial neoplasia of the uterine cervix. Recognition of genital HPV infection by the primary care practitioner is vital.

Figure 91-5 Condylomata. Verrucoid pigmented lesions on the penis.

Genital warts, or condyloma accuminata, present as single or multiple papillary or fingerlike proliferations that may coalesce to form large, moist, cauliflower-like tumors on mucosal or nonmucosal skin. Presence on the vulva is an important indicator of vaginal or cervical involvement. Subclinical infection is common, and attempts at elucidation using acetic acid soaks are limited by frequent false positives.

Bowenoid papulosis is a clinicopathologic variant of HPV infection, in which multiple, smooth, slightly raised papules, ranging from flesh-colored to reddish-brown, develop on genital skin. These lesions show squamous cell carcinoma in situ on biopsy and are usually caused by HPV 16, one of the oncogenic subtypes. An affected female, or female sexual partner of an affected male, should be referred to a gynecologist.

[edit] Management.

Because many warts regress spontaneously, some patients, especially children, may not require treatment. For common warts, topical application of keratolytics, such as salicylic acid (Occlusal), or salicylic and lactic acid in flexible collodion (Duofilm), is useful when applied directly to the wart at bedtime. Cryotherapy with liquid nitrogen for 10 to 20 seconds is also effective.

Flat warts often respond to cryotherapy, but subsequent pigment alteration occurs easily, especially on the face of darker-skinned individuals. Patients also should be advised to avoid shaving or scrubbing affected areas.

Palmar and plantar warts can be refractory, and aggressive treatment with keratolytics and liquid nitrogen is the usual initial approach. Surgical excision and laser ablation are treatments of last resort. %There are numerous approaches to treating genital warts^[3]; none are superior and all have only modest efficacy and substantial rates of recurrence. Moist genital lesions respond to topical treatment with 25% to 40% podophyllin, applied weekly until lesions resolve. Treated areas are washed after 3 to 6 hours as tolerated. Podophyllin is toxic and can be a severe irritant and thus should not be dispensed. Podofilox 0.5% solution or gel (Condylox) is available by prescription for home use and is less irritating and more potent than podophyllin. It is applied twice daily for 3 consecutive days followed by 4 days off, repeating this cycle for up to 8 weeks. Imiquimod (Aldara) is a local immune-response modifier, applied at home 3 times a week for up to 16 weeks. Like Condylox, Aldara may be an effective, although expensive, alternative. Liquid nitrogen continues to be a reliable, efficacious, and cost-effective treatment.

Referral to a dermatologist should be considered for additional treatment modalities, and for evaluation of persistent lesions, especially of the mouth, genital and periungual areas, where occult squamous cell carcinoma is a concern.

[edit] Herpesvirus Infections

[edit] Herpes Simplex Virus.

Herpes simplex virus (HSV) (see Plates) infection is an acute, self-limited eruption that is characterized by groups of small vesicles on an erythematous base. After infection by direct inoculation from another individual, the virus replicates within the skin where it involves the sensory nerves. The viral capsid is subsequently transported to the nerve root ganglion where it remains latent, with the potential for reactivation and reinfection at any time. Both the HSV-1 and HSV-2 subtypes can involve nearly any mucocutaneous site.

[edit] Oral-Facial Infection.

Gingivostomatitis and pharyngitis are the most frequent primary HSV-1 infections, occurring primarily in children. Lesions develop anywhere in the mouth, on the lips, or on the face. Numerous rapidly evolving vesicles rupture to form painful, necrotic ulcers, associated with fever, malaise, anorexia, and cervical adenopathy. Infection lasts 1 to 3 weeks and heals without scarring. Recurrences present most frequently as herpes labialis (fever blisters, cold sores) where prodromal stinging or burning is quickly followed by one or more typical painful vesicles, usually located on the lips. Viral shedding lasts until the lesions have crusted over, approximately 5 to 7 days. Fever and ultraviolet (UV) light may precipitate the recurrences.

[edit] Genital Infection.

Primary genital herpes, usually caused by HSV-2, is characterized by bilaterally distributed groups of vesicles. The infection may also involve the cervix and urethra, with accompanying fever, headache, and malaise. Local symptoms include pain, itching, dysuria, and tender inguinal adenopathy. Viral shedding may persist for 10 to 12 days or more, and the complete course lasts 3 to 4 weeks.

Recurrences vary considerably in severity and duration. Prodromal tingling or burning commonly precedes the eruption, which is unilateral, and usually without adenopathy. Lesions can be painful, but the course is milder than primary disease and lasts 7 to 10 days. Recurrence rates also vary greatly, averaging three to four recurrences per year, and patients should be reassured that these tend to become milder and less frequent over time. Unfortunately, asymptomatic shedding, also called subclinical reactivation, likely occurs in all persons infected with HSV, and results in transmission of infection despite the lack of physical evidence of active disease.

[edit] Herpetic Whitlow.

HSV infection of the finger is characterized by redness, swelling, and painful vesicles or pustules resembling bacterial infection. Systemic symptoms and localized adenopathy accompany primary infection, but recurrences are infrequent.

[edit] Herpetic Eye Infection.

See Chapter 108 for herpetic eye infection.

[edit] Eczema Herpeticum.

Eczema herpeticum occurs in patients with an underlying skin problem, such as atopic dermatitis or Darier's disease, which causes altered skin integrity and thereby allows widespread superinfection with HSV. Diffuse vesiculopustular, eroded, and crusted lesions are accompanied by fever, pain, and adenopathy. Referral to a dermatologist should be considered.

[edit] Laboratory Evaluation.

Most HSV infections can be diagnosed by the clinical presentation. When in doubt, the quickest and least expensive confirmatory test is the Tzanck smear (see Chapter 88 ), which like all tests for HSV should be taken from intact vesicles or fresh erosions.

Most laboratories now perform fluorescent antibody tests on specimens sent for culture, with initial results in 24 hours. These tests are highly specific but not very sensitive. Negative samples are then submitted for standard cultures, requiring 3 to 7 days. The polymerase chain reaction assay is rapid, highly sensitive and can distinguish HSV from varicella-zoster virus infection but is more costly and less readily available. It should be used when rapid diagnosis is required.

Serologic tests are unreliable in documenting acute HSV infection but can help demonstrate the presence of a previous infection and are useful in identifying asymptomatic infection in patients undergoing immunosuppressive regimens who should receive prophylactic treatment.

[edit] Management.^[4]

Most acute primary oral-facial or genital HSV infections can be safely treated with acyclovir, 400 mg orally 3 times a day for 7 to 14 days. Significant improvement in the rate of healing and the resolution of symptoms can be achieved, especially if initiated early (within 12 to 36 hours), but treatment has no effect on the development of recurrences.

The benefits of oral acyclovir for acute recurrent disease are less dramatic, but long-term daily therapy to suppress frequent recurrences is safe and effective. Initial doses of 400 mg twice a day can be tapered as tolerated, with periodic drug holidays to reassess the need to continue. Long-term suppressive therapy does not eliminate ganglionic latency, and reactivation occurs when treatment is stopped.

Two new oral antiviral agents have demonstrated superior pharmacokinetics vs. acyclovir, allowing less frequent dosing while achieving higher serum drug concentrations. Valacyclovir (Valtrex) is taken as 1 gm twice a day for 10 days with initial infection and 1 gram twice a day for 5 days with recurrences, or 500 mg each day for suppression. The dose for famciclovir (Famvir) is 125 mg twice daily for recurrences.

Topical acyclovir ointment has minimal effect on typical primary or recurrent HSV infection but has been used adjunctively for chronic disease. Intravenous acyclovir is generally reserved for immunocompromised patients and those with CNS involvement, but it can be used in severely ill patients with first-episode HSV infection. Other adjunctive therapies include analgesics, sitz baths, and topical xylocaine ointment or viscous xylocaine mouthwash.

[edit] Prevention.

Because of frequent asymptomatic shedding, it is suggested that all patients with HSV-2, whether on oral antiviral therapy or not, should use condoms at all times, and abstain totally from sex during recurrences. Sunscreen agents to block UV-activated recurrent labial HSV are useful.

[edit] Herpes Zoster Virus.

Herpes zoster (shingles) ( Plate 78 ) is an acute vesicular eruption caused by reactivation of latent virus from a previous varicella infection. Reactivation can occur at any time and may be triggered by illness, immunosuppression, debilitation, and advancing age. The eruption is unilateral and follows the dermatome of the affected ganglion, although involvement of adjacent dermatomes is common.

[edit] History.

A prodrome of 1 to 4 days or more is common, consisting of tingling, itch, or pain and tenderness, often accompanied by systemic symptoms. The pain can be severe, suggesting acute myocardial infarction or acute abdomen in thoracic or lumbar dermatomes. Following the prodrome, an eruption develops that consists of several or multiple groups of vesicles on an erythematous base. Vesicles umbilicate, become purulent, rupture and ulcerate, and over 10 to 14 days, progress to crusting and complete healing.

Infection may involve motor neurons as well, usually of the same dermatome, and can lead to nerve palsies, weakness, and urinary retention. Zoster in the ophthalmic distribution can lead to severe ocular complications. Dissemination of infection also can occur, primarily in immunocompromised individuals and those with certain underlying malignancies.

The most common sequela of zoster is postherpetic neuralgia, in which pain in the involved region may persist for months or rarely years. It occurs in 10% to 15% of patients and is more common in those over 60 years of age. Scarring may be seen, especially after severe infection.

[edit] Laboratory Evaluation.

See diagnosis section for HSV.

[edit] Management.

Pain control is the mainstay of treatment in zoster and should include narcotic analgesics when indicated. In younger and middle-aged patients, who tend to have milder disease courses, pain control and attention to possible secondary infection may be all that is necessary.

Acyclovir attenuates the course and symptoms of herpes zoster. For optimal effect, therapy must be initiated early at a usual adult dose of 800 mg taken orally five times a day. It is still considered safe at these doses, but gastrointestinal intolerance is greater; CNS effects, such as confusion and lethargy, can occur; and the patient should be well hydrated. In patients with reduced renal function, lower doses are required. The newer agents valacyclovir (Valtrex), at 1 gram three times a day or famciclovir (Famvir), at 500 mg three times a day, each for 7 days, are safe and excellent alternatives with more sane dosing schedules.

Unfortunately, antivirals have no effect on subsequent pain. Concurrent treatment with prednisone has traditionally been given to reduce the incidence of postherpetic neuralgia and is typically reserved for persons over age 55. The usual adult dose is 60 mg/day for 7 days tapered over 2 to 3 weeks. Its use is controversial, however, and must be weighed against known risks and side effects.

[edit] Molluscum Contagiosum.

Molluscum contagiosum ( Plate 79 ) is a benign papular eruption caused by a poxvirus. It is characterized by multiple, 2 to 5 mm, dome-shaped, flesh-colored papules with distinctive central umbilication from which caseous material can be expressed. After an average incubation period of 2 to 3 months, lesions develop primarily on the face, trunk, and extremities in children and on thighs, abdomen, buttocks, and genital areas in adults. The mode of transmission can be sexual, nonsexual, or by fomites. Autoinoculation is also possible, causing linear lesions and distant spread.

Diagnosis is usually clinical, but molluscum contagiosum can be mistaken for many lesions, including warts, nevi, adnexal tumors, and keratoacanthomas. Giant or widespread lesions should alert the practitioner to possible immunodeficiency.

Without treatment, the lesions can persist for months or years, but they respond to cryotherapy, light curettage, or any sufficiently destructive or irritating technique.

[edit] INFESTATIONS

[edit] Pediculosis

Three forms of lice infest humans: head lice (pediculosis capitis), body lice (pediculosis corporis) and pubic or ``crab lice (Phthirus pubis). All are obligate blood-sucking ectoparasites, which produce eggs (nits) that attach firmly to the base of the human's hair shafts or to clothing. Adult lice appear as tiny rust-colored spots after feeding, but diagnosis is made more easily by finding nits, especially with the aid of a hand magnifier or microscope.

Head lice infestation occurs only on scalp hair, particularly the nape of the neck, where intense pruritus may lead to secondary excoriations and furunculosis.

Body lice are similar in appearance, but unlike head lice can be vectors for systemic diseases, such as typhus. Females lay eggs in clothing along seams, a good place to check in suspected individuals ( Plate 80 ). Transmission occurs by contact with infested skin, clothing, or bedding. Widespread pruritic dermatitis can result, along with excoriations and secondary infection from scratching.

Pubic lice are usually contracted from sexual contact, but clothing or linen are possible sources. In addition to the genital area, skin, hair of the face, eyelashes, trunk, and axillae can be involved.

[edit] Management.

Control of all types of louse infestation includes attention to affected clothing, bed sheets, towels, combs and brushes, and measures to limit spread to others. Hot water laundering, dry cleaning, and use of a disinfectant (e.g., Lysol) for combs and brushes are effective measures, as is isolation of fomites for 1 to 2 weeks.

Treatment of head lice in adults is best accomplished with 1% lindane shampoo (Kwell) applied to hair for 10 minutes and then thoroughly washed off, or 1% permethrin (Nix), applied as a cream rinse after shampooing, left on for 10 minutes, and then rinsed. Nonprescription products containing pyrethrins and piperonyl butoxide (Rid) are also quite effective. All of the treatments probably should be repeated in 1 week, and nits should be dislodged with tweezers or a fine-toothed comb.

Body and pubic lice are treated by application of 1% lindane (Kwell) lotion or shampoo for not more than 8 to 10 hours, then completely washed off. Over-the-counter regimens (Rid) are also effective.

Close contacts should be treated in all types of pediculosis. Lindane can be neurotoxic and should be avoided in patients with widespread dermatitis, pregnant or nursing women, and children less than 3 years of age.

[edit] Scabies

Scabies ( Plate 81 ) is caused by infestation with the itch mite Sarcoptes scabiei, resulting in intensely pruritic vesicles, faint red papules, or short linear burrows ( Plate 82 ). Sites of predilection include finger webs, wrists, axillae, and elbows, with sparing above the neck except in infants. Typical red papules on the glans penis are nearly pathognomonic ( Plate 83 ). Keratotic, crusted scabies (Norwegian scabies) is a variant seen mostly in institutionalized or immunosuppressed patients, in which widespread, crusted lesions teeming with mites are not accompanied by pruritus.

Because the differential diagnosis for scabies includes nearly all pruritic dermatoses, a slide prepared from scrapings of multiple suspected lesions should be prepared to demonstrate mites or ova (Fig. 91-6). Treatment of the nonpregnant adult is usually with 5% permethrin cream (Elimite), or 1% lindane, now somewhat less effective since resistance has emerged. Both are applied from the neck down (30 gm or 1 oz), washed off after 8 to 10 hours, then repeated once after 5 days. As described with pediculosis, infested clothing and bedding and close contacts should be treated simultaneously. Patients should be reminded that posttreatment hypersensitivity and pruritus can persist for several weeks.

Figure 91-6 Scabies. KOH preparation demonstrating scabetic mites and eggs.

[edit] REFERENCES