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Chapter Title Cutaneous Manifestations of HIV Carrie L. Kovarik, MD Addy Kekitiinwa, MB, ChB Heidi Schwarzwald, MD, MPH

Objectives Table 1. Cutaneous manifestations of HIV 1. Review the most common cutaneous Cause Manifestations manifestations of human Neoplasia Kaposi sarcoma (HIV) infection. 2. Describe the methods of diagnosis and treatment for each cutaneous . Infectious Herpes zoster virus Superficial fungal infections Key Points Angular 1. Cutaneous are often the first manifestation of HIV noted by patients and Cryptococcus health professionals. Human papillomavirus (verruca vulgaris, 2. Cutaneous lesions occur frequently in both adults verruca plana, condyloma) and children infected with HIV. 3. Diagnosis of several mucocutaneous in the setting of HIV will allow appropriate treatment and prevention of complications. Furunculosis 4. Prompt diagnosis and treatment of cutaneous manifestations can prevent complications and improve quality of life for HIV-infected persons. Other Pruritic papular eruption Seborrheic Overview Many people with human immunodeficiency virus (HIV) infection develop cutaneous lesions. The risk of developing cutaneous manifestations increases with disease progression. As increases, patients may develop multiple diseases at once, changes atypical-appearing skin lesions, or diseases that are refractory to standard treatment. Skin conditions that have been associated with HIV infection are listed in Clinical staging is useful in the initial assessment of a Table 1. patient, at the time the patient enters into long-term HIV care, and for monitoring a patient’s disease progression. Once HIV infection has been confirmed, the diagnosis of The clinical stage of a patient has been shown to be certain mucocutaneous conditions in children (Table 2) related to survival, prognosis, and disease progression. and adults (Table 3) can be used to clinically stage the As shown in Tables 2 and 3, the skin examination plays a patient. The World Health Organization (WHO) clinically significant role in the clinical staging process of patients stages patients as having HIV that is (stage with HIV. Also, the diagnosis of these cutaneous diseases 1) or with mild symptoms (stage 2), advanced symptoms may lead to the early testing and diagnosis of HIV in (stage 3), or severe symptoms (stage 4). children and adults if recognized with other of HIV infection.

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This module focuses on many of the most common and/or significant cutaneous manifestations of HIV; however, other sections cover several mucocutaneous manifestations in depth. To avoid duplication, we will mention them here only briefly.

Viral Skin Disease Cutaneous Infection with Herpes simplex virus (HSV) infection most commonly causes disease in the oral or anogenital region; however, widespread disease may be seen in immunocompromised patients (Figure 1). In adults, a relationship has been + Figure 1. Herpes Simplex Confirmed herpes simplex virus infection on the nose and observed between decreased CD4 cheek of an HIV-infected man. This patient also had similar ulcers on the genitals. lymphocyte counts and an increased incidence of cutaneous HSV. In children, herpes gingivostomatitis can be so severe that it leads to progressive, and painful orolabial, genital, or anorectal poor nutrition and dehydration (Figure 2). Chronic HSV lesions and is one of the criteria for severely symptomatic infection (present for >1 month) may manifest as severe, (WHO Clinical Stage 4) HIV infection (Figure 3).

Table 2. Criteria for recognizing HIV-related mucocutaneous clinical events in children (younger than 15 years)* Clinical Event Clinical Diagnosis Definitive Diagnosis Clinical Stage 2 Pruritic papular Papular lesions with intense pruritus. Clinical diagnosis, exclude other causes, such eruptions as drug eruptions, atopic dermatitis, . Fungal Fungal (painful, red, and swollen nail bed) or Clinical diagnosis, microscopic demonstration infections (painless separation of the nail from the nail bed). of fungal hyphae, or culture of the nail. Proximal white subungual onycho mycosis is uncommon without immunodeficiency. Splits or cracks at the angles of the , usually with Clinical diagnosis or response to surrounding , and not attributable to nutritional . deficiency. Extensive Characteristic warty skin lesions. Variants include flat, Clinical or histologic diagnosis. virus infection plantar, papular, and genital. More than 5% or body surface area or disfiguring. Extensive molluscum Characteristic skin lesions: small flesh-colored, pearly or Clinical or histologic diagnosis. contagiosum pink, dome-shaped or umbilicated . May have surrounding redness. More than 5% or body surface area or disfiguring. Recurrent oral Current event plus at least one previous episode in the Clinical diagnosis. ulceration past 6 mo. Aphthous ulceration, typically with a halo of and yellow–gray pseudomembrane. Herpes zoster Painful with fluid-filled , dermatomal distribution, Clinical diagnosis, microscopic diagnosis can be hemorrhagic on erythematous background, and can with Tzanck smear, or culture. become large and confluent. Should not cross the midline. Can become disseminated. Continued on next page

174 Cutaneous Manifestations of HIV Infection

Table 2. Criteria for recognizing HIV-related mucocutaneous clinical events in children (younger than 15 years)* (concluded) Clinical Event Clinical Diagnosis Definitive Diagnosis Clinical Stage 3 Oral Persistent or recurrent, creamy white to yellow, soft Clinical, microscopic, or culture diagnosis. plaques that can be scraped off, or red patches on the , or lining on the mouth, usually painful or tender (erythematous form). Oral hairy Fine, small linear patches on lateral borders of the tongue, Clinical diagnosis. Acute necrotizing generally bilateral, that do not scrape off. ulcerative Severe , ulcerated gingival papillae, loosening of teeth, Clinical diagnosis. or , or spontaneous , bad odor, and rapid loss or bone acute necrotizing or soft tissue. ulcerative periodontitis Clinical Stage 4 Chronic herpes Severe and progressive painful orolabial, genital, or Clinical diagnosis, microscopic diagnosis simplex infection anorectal, lesions caused by HSV and present for >1 mo. with Tzanck smear, or culture. (HSV) Extrapulmonary Systemic illness, usually with prolonged , night sweats, Positive microscopy showing acid-fast bacilli tuberculosis and weight loss. Clinical features of organs involved, such or culture of Mycobacterium tuberculosis as sterile pyuria, pericarditis, ascites, pleural effusion, from blood or other relevant specimen/tissue , arthritis, orchitis, or skin lesions. except sputum or bronchoalveolar lavage. Biopsy and . Kaposi sarcoma Typical appearance in skin or oropharynx of persistent, Clinical diagnosis, may need histologic initially flat, patches with a pink or purple color. May confirmation. develop into plaques, nodules, or tumors. Disseminated fungal Wide range of clinical presentations in the skin, including Histology, antigen detection, and/or culture infection (cryptococ- papules, nodules, and ulcerations. is needed. cosis, histoplasmosis, ) Disseminated Wide range of clinical presentations in the skin, including Nonspecific clinical symptoms (weight loss, mycobacterial papules, nodules, and ulcerations. fever, ) plus culture of atypical infection, other than mycobacterial species from tissue other tuberculosis than lung. *Adapted from 2006 WHO case definitions of HIV for surveillance and revised clinical staging and immunological classification of HIV-related disease in adults and children.

HSV cutaneous disease presents as small grouped vesicles (or blisters) with redness on the surrounding skin. The spread of HSV infection to other areas of the skin is common and occurs through autoinoculation or sexual contact. The typical clinical course of HSV infection includes the rupture of the blisters over the course of a week, with subsequent healing in 2 weeks; however, this course can be significantly prolonged in the immunocompromised host.

The diagnosis of HSV infection can be reached through clinical examination,

Figure 2. Herpes Simplex Figure 3. Large ulceration on the upper due microscopic identification of virally Herpes simplex virus inrection in an HIV- to herpes simplex virus infection. This patient’s infected girl. Chronic or progressive herpes had been present for more than 3 months. infected from the skin lesions are observed occasionally in cavity with a Tzanck stain, viral culture, HIV-infected children. 175 HIV Curriculum for the Health Professional

Table 3. Criteria for recognizing HIV-related mucocutaneous clinical events in adults and adolescents (15 years and older)* Clinical Event Clinical Diagnosis Definitive Diagnosis Clinical Stage 2 Pruritic papular eruptions See Table 2. See Table 2. Fungal nail infections See Table 2. See Table 2. Angular cheilitis See Table 2. See Table 2. Recurrent oral ulceration See Table 2. See Table 2. Herpes zoster See Table 2. See Table 2. Seborrheic dermatitis Itchy scaly , particularly affected Clinical diagnosis. hair-bearing and oily skin (scalp, axillae, upper trunk, groin). Clinical Stage 3 See Table 2. See Table 2. Oral See Table 2. See Table 2. Acute necrotizing ulcerative See Table 2. See Table 2. gingivitis or stomatitis, or necrotizing ulcerative periodontitis Clinical Stage 4 Chronic herpes simplex infection Severe and progressive painful orolabial, genital, Positive culture or DNA (by polymerase (HSV) (orolabial, genital, or or anorectal, lesions caused by herpes simplex chain reaction) of herpes simplex virus or anorectal) for more than one virus and present for >1 mo. Visceral herpes compatible cytology or histology. month or visceral of any duration simplex requires definitive diagnosis. Extrapulmonary tuberculosis Systemic illness, usually with prolonged fever, Mycobacterium tuberculosis isolation or night sweats, and weight loss. Clinical features compatible histology from appropriate of organs involved, such as sterile pyuria, site or radiologic evidence of miliary pericarditis, ascites, pleural effusion, meningitis, tuberculosis (diffuse uniformly distributed arthritis, orchitis, or skin lesions. small miliary shadows or micronodules on chest x-ray). Kaposi sarcoma See Table 2. See Table 2. Disseminated fungal infection See Table 2. See Table 2. (cryptococcosis, histoplasmosis, coccidioidomycosis) Disseminated mycobacterial See Table 2. See Table 2. infection, other than tuberculosis Atypical disseminated Wide range of clinical presentations. Diagnosis by histology (amastigotes leishmaniasis visualized) or culture from appropriate clinical specimen. *Adapted from 2006 WHO case definitions of HIV for surveillance and revised clinical staging and immunological classification of HIV-related disease in adults and children. immunofluorescent tests, or polymerase (Primary Disease) chain reaction (PCR). Initial infection is treated with In resource-limited settings, where varicella vaccination acyclovir at a dose of 10-20 mg/kg of body weight four is unavailable, chickenpox (primary varicella zoster virus times per day in children and 400 mg three times per [VZV] disease) remains a common childhood illness. day in adults for 7-14 days. Adults have been treated Typically there is a prodromal phase with fever, , with both valacyclovir (1 g twice a day) and famciclovir and . Skin lesions appear as successive crops of (500 mg twice a day) for 7 days. Patients with severe or vesicles (or small blisters) with surrounding redness. The disseminated disease will probably need intravenous lesions are in different stages, including papules, vesicles, acyclovir. Patients taking acyclovir need to be instructed pustules, and crusts (Figure 4). The rash typically starts on to drink plenty of fluids to maintain adequate hydration the face and scalp and spreads toward the feet. Primary VZV to reduce the risk of acyclovir-induced renal failure. infection in HIV-infected children or adults may cause severe

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pre­sent as erythema, impetiginous changes (honey-colored crusting), and persistent ulcerations. The most common responsible for superinfection include and group A . Appropriate therapy is warranted.

Clinical examination, a Tzanck smear, viral culture, immunofluorescent antibody tests, or PCR can be used to diagnose VZV infection. An HIV- infected child who is exposed to chickenpox should receive varicella zoster immune globulin, where available, within 96 h of exposure. Figure 4. The lesions of primary varicella Figure 5. Herpes Zoster infection are in different stages, including papules, Herpes zoster on a child’s leg vesicles, pustules, and crusts. There is a window of opportunity for effective therapy, and it is ideal to administer antiviral therapy within 72 h of disease onset. Immunocompromised children with uncomplicated cases of chickenpox may be treated with acyclovir at a dose of 20 mg/kg by mouth, administered four times per day for 5 days. The maximum dose is 800 mg administered four times daily in children and 800 mg five times daily in adults. Patients with complicated Figure 7. Molluscum contagiosum disease may need intravenous Molluscum contagiosum lesions are pearly or acyclovir. Adequate hydration while flesh-colored, dome-shaped, umbilicated papules, on acyclovir therapy is imperative. ranging from 2 to 5 mm, with a central core.

If a patient is identified as having chickenpox, all efforts should be made to isolate the patient to limit exposure to Figure 6. Herpes zoster in an HIV-infected other children. child, manifesting as grouped vesicles and crusts in a dermatomal pattern. Herpes Zoster or complicated disease, depending on the patient’s level of Patients with HIV infection may also experience reactiva­ immunosuppression. Severe disease may be characterized by tion of latent VZV infection (also known as herpes zoster near-confluent skin lesions and involvement of the mucous or ). One study reported that nearly half of HIV- membranes. Other potential complications of primary infected children with chickenpox will have reactivation VZV infection include hemorrhagic skin lesions, , of disease within 24 months. Herpes zoster is one of the , , bacterial complications, and criteria for mildly symptomatic (WHO Clinical Stage 2) death. Bacter­ial superinfection of cutaneous lesions may HIV infection in children and adults (Figure 5).

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prone to many lesions and to giant lesions larger than 1 cm. Extensive molluscum (involving >5% of body surface area or disfiguring) is one of the criteria for mildly symptomatic (WHO Clinical Stage 2) HIV infection in children (but not adults).

Molluscum contagiosum lesions are pearly or flesh-colored, dome-shaped, umbilicated papules, ranging from 2 to 5 mm, with a central core (Figure 7). Giant lesions often occur on the face, and they can be disfiguring (Figure 8). These lesions can be spread by autoinoculation, sexual contact, or into a linear configuration by Figure 8. Herpes zoster in an HIV-infected Figure 9. often presents as scratching (a phenomenon known as child, manifesting as grouped vesicles and crusts diffuse, round, scaly patches of and may be koebnerization). in a dermatomal pattern. associated with tinea on other parts of the body.

Herpes zoster is characterized by painful, grouped, Diagnosis is either made clinically, by microscopic vesicular lesions that appear in a dermatomal pattern demonstration of virally infected cells within material (Figure 6). Complications include severe painful expressed from lesions, or histologically. Treatment ulcerations, (pain along the course options include curettage, liquid nitrogen, topical of a nerve), herpes keratitis (if eye involvement occurs), , imiquimod, topical acids, or electrodesiccation. and disseminated disease. Herpes zoster lesions can be Despite treatment, the recurrence rate is high. Highly distinguished from other vesicular (blisterlike) eruptions active antiretroviral treatment coupled with increasing because they do not cross the midline. CD4+ lymphocyte cell counts lessens the severity of disease or assists in the resolution of disease. Clinical examination, a Tzanck smear, viral culture, immunofluorescent antibody tests, or PCR can be used to Kaposi Sarcoma diagnose VZV infection. As with primary VZV infection, Kaposi sarcoma (KS) is an HIV-related vascular neoplasm therapy is most effective if introduced within 72 h of that is associated with human herpes virus 8 infection. disease onset. The treatment of choice for herpes zoster Cutaneous KS presents as red, violaceous (purple), or in children is acyclovir 20 mg/kg by mouth, administered brown lesions, which vary from macules or patches to four times per day for 7 days; the maximum dose is 800 papules, nodules, or tumors (Figure 9). KS can present mg administered four times daily. Adults may take up as lesions on the skin or mucous membranes; however, to 800 mg five times daily. Patients who have severe disseminated disease may involve in any organ. The most disease or who cannot take liquids should be treated with common sites of disseminated disease include the skin, acyclovir at a dose of 10-20 mg/kg intravenously every 8 mucosal surfaces, respiratory tract, and lymph nodes, h for 7 days. Adequate hydration is imperative. and extensive disseminated disease is often associated with . Pulmonary and lymph node disease Molluscum Contagiosum may mimic those of tuberculosis. KS is one of the criteria Molluscum contagiosum is caused by a poxvirus and for severely symptomatic (WHO Clinical Stage 4) HIV is commonly found in persons with advanced HIV infection in children and adults. Please see the chapter on infection. In adults, it occurs more commonly with CD4+ opportunistic infections for a more detailed description lymphocyte counts of less than 200 cells/µL. Adults with of KS. CD4+ lymphocyte counts of less than 50 cells/µL are more

178 Cutaneous Manifestations of HIV Infection

Table 4. Superficial bacterial infections Bacterial Causative Organism(s) Clinical Description Impetigo Staphylococcus aureus majority, Streptococcus Small erythematous macule, , or blister pyogenes minority. that eventually erodes and develops a characteristic honey-colored . May be primary or secondary to other skin conditions, such as eczema, scabies, or herpes. Folliculitis Staphylococcus aureus most common cause; Infection or inflammation within the hair other causes include . follicle, manifesting as erythematous perifollicular pustules. Common sites include head, neck, trunk, , buttocks. Furunculosis Staphylococcus aureus most common cause. Infection or inflammation of the skin and soft tissue surrounding the . Lesions are larger than folliculitis. Staphylococcus aureus majority, Streptococcus Localized collection of in the skin or soft pyogenes minority. tissue. May be a complication of untreated . Cellulitis Staphylococcus aureus majority, Streptococcus Inflammation of the skin, characterized by a pyogenes minority. painful, edematous, erythematous expanding (plaque). Paronychia Staphylococcus aureus (acute), (chronic). Inflammation, pain, and tenderness of the folds May be multifactorial or complicated by other of tissue surrounding the fingernail or toenail. organisms, such as gram-negative rods.

Bacterial Skin Disease be dosed in children as 20-25 mg/kg/day divided four Superficial Bacterial Skin Infections times a day (maximum of 1 g/day) for 7 days. Adults may Superficial bacterial skin infections include impetigo, take 250 mg every 6 h for 7 days. folliculitis, cellulitis, skin , furunculosis, and In areas where methicillin-resistant Staphylococcus paronychia (Table 4). Staphylococcus aureus is the cause in most bacterial skin infections, and S. aureus colonization aureus (MRSA) is prevalent, empiric antibiotic coverage is substantially increased in HIV-infected patients. of skin infections should include coverage of this organism. Appropriate coverage will change depending Treatment for bacterial skin infections includes keeping on the setting, but MRSA acquired in the community is the lesions clean with soap and water. Parents should be often sensitive to trimethoprim-sulfamethoxazole and instructed in good handwashing to prevent the spread of clindamycin. MRSA should be suspected if bacterial skin lesions. Staphylococcus aureus often colonizes the nails, infections, such as impetigo or furunculosis, are not nares, and anogenital areas of patients. Antibacterial responsive to first-line antistaphylococcal , creams, such as , should be applied to these such as dicloxacillin. sites twice daily for 3-4 weeks to prevent spread of infection to others cutaneous sites and to household Disseminated Mycobacterial Infections contacts. Antibacterial washes, such as , HIV-infected patients are at risk for disseminated myco­ or vinegar baths (add 1 cup of plain white vinegar to the bacterial infections. Extrapulmonary tuberculosis and bath water) may be used to treat impetigo and folliculitis, disseminated nontuberculoid mycobacterial infections are as well as prevent recurrence of any of these superficial both criteria for severely symptomatic (WHO Clinical Stage bacterial infections. 4) HIV infection in children and adults.

More severe cases of impetigo, folliculitis, or bacterial HIV-infected patients have an increased risk of skin infections can be treated with an oral penicillinase- developing extrapulmonary tuberculosis as CD4 counts resistant penicillin, such as dicloxacillin. Dicloxacillin can decline. The most common forms of extrapulmonary

179 HIV Curriculum for the Health Professional tuberculosis include pleural effusions, , or fluconazole 100-400 mg/day. interacts pericardial disease, meningitis, and miliary disease. with many antiretroviral , so a thorough is a progressive and disseminated drug history should be taken prior to initiating therapy. form of the disease caused by hematogenous dissemina­ Patients should be instructed to take ketoconazole with tion with potential involvement of any , food to prevent stomach upset. including the skin. Young children with HIV and tuber­ culosis are at increased risk of disseminated disease, occurs as , tinea capitis, especially tuberculous meningitis, lymphadenopathy, and or . Tinea corporis is characterized by miliary disease. Please see the chapter on tuberculosis for erythematous, sometimes annular (circular), scaling a more detailed description. lesions with raised borders. Tinea capitis often presents as diffuse, round, scaly patches of hair loss and may Disseminated nontuberculous mycobacterial infections, be associated with tinea on other parts of the body caused by Mycobacterium avium complex, M. kansasii, M. (Figure 10). The lesions may be extensive and refractory chelonae, M. abscessus, or M. genavense, may occur in HIV- to treatment in HIV-infected persons. Fungal nail infected patients with severe immunosuppression or as infections, such as fungal paronychia (chronic, painful, an immune reconstitution syndrome. These disseminated red, and swollen nail beds) or proximal white subungual infections typically cause lymph node, intraabdominal, onychomycosis (a white, thickened, and brittle nail and thoracic disease; however, skin lesions may also be near the proximal nail fold) occur more frequently in present. immunosuppressed patients with HIV infection. Fungal nail infections are criteria for mildly symptomatic (WHO Fungal Skin Disease Clinical Stage 2) HIV infection in children and adults. Superficial Fungal Skin Infections Dermatophytosis is treated with a topical broad-spectrum Fungal skin infections among people with HIV/AIDS antifungal, such as or cream include candidiasis and dermatophytosis. applied to lesions twice daily until the rash resolves. Whitfield’s ointment may also be effective. Tinea corporis In HIV-infected patients, candidiasis commonly mani­ usually responds to topical medications alone, and topical fests as oral disease, such as thrush or angular cheilitis. treatments may also be tried for tinea capitis if the Mucocutaneous candidiasis is one of the most frequently infection is mild, no griseofulvin is available, or patients reported mucocutaneous manifestations of pediatric HIV are taking concomitant hepatotoxic medications. More infection and is often the first manifestation of disease. (Please see the chapter on oral manifestations of HIV infection for a more detailed description.) Candidiasis is also seen frequently in the diaper area and within skin folds as a brightly erythematous (red) rash with well-demarcated borders and satellite lesions (pustules or papules).

Cutaneous candidiasis can be treated topically with 1% aqueous solution of gentian violet applied to lesions three times per day for 3 days or with ointment applied to lesions three times per day until the rash resolves. If there is no response to topical treatment, systemic treatment with ketoconazole or fluconazole can be used. Dosages in children are the following: ketoconazole 3.3-6.6 mg/ kg/day given by mouth, once a day for 2-4 weeks, or fluconazole 3-6 mg/kg/day (maximum, 100- 200 mg) once daily for 14 days. Dosages in adults Figure 10. Tinea capitis often presents as diffuse, round, scaly patches of hair are the following: ketoconazole 200-400 mg/day loss and may be associated with tinea on other parts of the body.

180 Cutaneous Manifestations of HIV Infection severe cases of (Figure 11). Patients with PPE show infections can be treated with evidence of increased immunoglobin E systemic medications such as and eosinophilia. Some studies suggest griseofulvin microsize tablets, 20 that PPE may represent an overexuberant mg/kg per day (or 500 mg/day in reaction to bites. As the name adults) given once daily by mouth. suggests, PPE is pruritic. The rash Patients should be instructed most often presents as symmetric to take griseofulvin with a meal and evenly distributed skin-colored to that is high in fat to enhance hyperpigmented papules on the trunk . Monitor complete and extremities. Before diagnosing a blood count, electrolytes, blood patient with PPE, it is important to urea nitrogen, creatinine, and consider other potential treatable causes liver function test after 4 weeks for the rash, including scabies, atopic of receiving griseofulvin, when dermatitis, folliculitis, a drug eruption, available. Duration of therapy urticaria (), or syphilis. depends on the location of infection. Tinea corporis should Figure 11. Pruritic papular eruption of HIV Between 11% and 45% of HIV-infected be treated for 2-4 weeks; tinea presenting as symmetric and evenly distributed patients will present with PPE. PPE is hyperpigmented and crusted papules on the trunk capitis should be treated for of a severely immunosuppressed patient. believed to be a marker of worsening 4-6 weeks. immunosuppression Itraconazole, and is more commonly ketoconazole, associated with a CD4+ or terbinafine lymphocyte count of less may also be used than 50 cells/µL. PPE for severe tinea can create substantial corporis or fungal morbidity in both children . and adults because it causes significant distress Disseminated to the patient and often Fungal Infections becomes superinfected Disseminated with Staphylococcus aureus. fungal infections, In many regions of the including world, the characteristic cryptococ­cosis and Figure 12. An HIV-infected child with generalized, erythematous, and monomorphous PPE rash has become papules secondary to tuberculosis medications. histoplasmosis, associated with HIV and may occur in severely immuno­­suppressed patients with may be stigmatizing. Treatment of PPE is difficult and HIV infection and cause cutaneous manifestation in 10%- usually requires and topical steroids 20% of these patients. These infections may present with with or without antibiotics. This treatment may be a wide range of skin lesions, including papules, nodules, required for symptomatic relief for months, until the and ulcerations. Disseminated fungal infections are CD4 count recovers with concomitant antiretroviral criteria for severely symptomatic (WHO Clinical Stage medications. -B light may assist with 4) HIV infection in children and adults. Please see the symptomatic treatment. PPE is one of the criteria for chapter on opportunistic infections for a more detailed mildly symptomatic (WHO Clinical Stage 2) HIV infection description. in children and adults.

Other Skin Conditions Drug Eruptions Drug eruptions often occur in patients receiving Pruritic Papular Eruption treatment for HIV infection. Antibiotics that are used Pruritic papular eruption (PPE) is a chronic eruption of in the treatment of HIV patients, including sulfa drugs, papular lesions on the skin whose etiology is unclear

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promote comfort, the patient can be given an oral , such as diphenhydramine HCl 1 mg/ kg every 6 h. In more severe cases, such as eruptions with blisters, skin sloughing, or involvement, the must be discontinued and supportive care should be provided.

Seborrheic Dermatitis Seborrheic dermatitis occurs in up to 85% of adults and children with HIV infection and may be an early sign of HIV. Seborrheic dermatitis is characterized by thick, yellow scaling areas that may have surrounding Figure 13. Mother and child with scabies Figure 14. Norwegian Scabies erythema (redness) and may occur infection manifesting as severely pruritic papules. Norwegian (crusted) scabies in an HIV-infected on the scalp, face, skin folds, and/ boy. Generalized scaling and hyperkeratotic, crusted plaques are present. or diaper area. Older children and adults may also have involvement penicillin, cephalosporins, and dapsone, may cause drug of the nasolabial folds, the skin behind the ears, and the eruptions, ranging from benign maculopapular lesions to eyebrows. fatal reactions. Treatment consists of selenium sulfide or ketoconazole Antiretroviral medications also have many cutaneous shampoo, topical coal tar, or salicylic acid. To decrease side effects. Abacavir, a nucleoside reverse transcriptase inflammation, 1% cream can be applied inhibitor, may cause a potentially fatal hypersensitivity to the affected area three times per day. Hydrocortisone syndrome, which manifests as progressive, multiorgan cream should be used sparingly in the diaper area and on system symptoms, including fever; shortness of breath; the face. ; gastrointestinal side effects including nausea, vomiting, and ; and an erythematous (red) Scabies rash. Nonnucleoside reverse transcriptase inhibitors, Scabies infection in adults and children is characterized most notably nevirapine, are frequently associated with by pruritic papular lesions and/or linear burrows found pruritic, maculopapular skin eruptions. Nonnucleoside most commonly in the webs of the fingers and toes, folds reverse transcriptase inhibitors are also rarely associated of the wrist, antecubital area, axilla, and genitals. Infants with Stevens-Johnson syndrome and toxic epidermal may also have lesions on the palms and soles of the necrolysis, a potentially fatal drug eruption with feet that often become pustular (Figure 13). Scrapings sloughing of the skin and mucous membranes. Protease observed under the microscope may reveal the , , inhibitors may also cause a rash and have been rarely or feces. implicated in Stevens-Johnson syndrome and toxic epidermal necrolysis. Treatment consists of an application of topical lotion, 25%, which is applied from the neck Drug eruptions range in appearance from pink to down, left on the skin overnight, and washed off in the erythematous (red) macules and papules (Figure 12), morning; the process is repeated 1 week later. HIV- scaling papules, hives, mucous membrane erosions, infected patients with advanced disease can experience skin sloughing, or light sensitivity. Most drug eruptions a variant of scabies known as crusted scabies, which is are mild, and the medication can be continued with characterized by generalized scaling and enlarged, crusted eventual spontaneous resolution of the eruption. To plaques (Figure 14). After a patient is treated for scabies,

182 Cutaneous Manifestations of HIV Infection the family should be advised to all clothing and 6. Garmen ME, Tying SK. The cutaneous manifesta­ bedclothes in hot water and them to kill that tions of HIV infection. Dermatol. Clin. 2002;20:193- may live in the cloth. 208. 7. Kline M. Cutaneous and oral manifestations of Clinical Considerations pediatric HIV infection. In PA Pizzo and CM Wilfert (Eds.), Pediatric AIDS: The Challenge of HIV Infection in Patients should be encouraged to complete all medica­ Infants, Children, and Adolescents. 3rd ed. Baltimore: tions as prescribed and to report any lesions that get Williams & Wilkins, 1998. worse or do not heal. Patients should be instructed to 8. Liao CH, Chen MY, Hsieh SM, et al. Discontinuation monitor for the development of bacterial superinfection of secondary prophylaxis in AIDS patients with of lesions. Superinfection, or secondary infection, occurs disseminated non-tuberculous mycobacteria when a primary lesion becomes infected with a secondary infection. J. Microbiol. Immunol. Infect. 2004;37:50- organism, such as a varicella lesion that becomes infected 56. with Staphylococcus aureus. 9. Liautaud B, Pape JW, De Hovitz JA, et al. Pruritic skin lesions. Arch. Dermatol. 1989;125:629-632. Patients should be instructed on how to maintain hygiene 10. Phillips P, Bonner S, Gataric N, et al. Nontuberculous without producing dry skin. They should be instructed mycobacterial immune reconstitution syndrome in to avoid deodorant soaps and to use tepid water when HIV-infected patients: spectrum of disease and long- bathing. Skin should be patted dry without rubbing, and term follow-up. Clin. Infect. Dis. 2005;41:1483-1497. moisturizer should be applied to the skin immediately 11. Piot P (Ed.). AIDS in Africa: A Manual for Physicians. after bathing. Bedridden patients should be turned Geneva, Switzerland: World Health Organization, every 2 h to avoid skin breakdown. Patients should keep 1992. their nails short and smooth and be discouraged from 12. Rigopoulos D, Paparizos V, Katsambas A. Cutaneous scratching lesions. Scratching can lead to open lesions markers of HIV infection. Clin. Dermatol. and secondary infections. If open lesions are present, 2004;22:487-498. patients should be instructed to avoid contact with other 13. Rosatelli JB, Roselino AMF. Hyper-IgE, eosinophilia, areas of the skin to prevent spread of the infection. and immediate cutaneous hypersensitivity to insect antigens in the pruritic papular eruption of References human immunodeficiency virus.Arch. Dermatol. 1. Cohen PR, Grossman ME, Silvers DN. Disseminated 2001;137:672-673. histoplasmosis and human immunodeficiency virus 14. Trent JT, Kirsner RD. Cutaneous manifestations of infection. Int. J. Dermatol. 1991;30:614-622. HIV: a primer. Adv. Skin Wound Care 2004;17:116- 2. Dimino-Emme L, Gurevitch AW. Cutaneous 127. manifestations of disseminated cryptococcosis. J. 15. World Health Organization. Guidelines for the Clinical Am. Acad. Dermatol. 1995;32(5 Pt 2):844-850. Management of HIV Infection in Adults. Geneva, 3. Eisman S. Pruritic papular eruption in HIV. Switzerland: World Health Organization, 1991. Dermatol. Clin. 2006;24:449-457, vi. 16. World Health Organization. TB/HIV: A Clinical 4. El Hachem M, Bernardi S, Pianosi G, et al. Manual. Geneva, Switzerland: World Health Mucocutaneous manifestations in children with HIV Organization, 2004. infection and AIDS. Pediatr. Dermatol. 1998;15:429- 17. World Health Organization. WHO Case Definitions of 434. HIV for Surveillance and Revised Clinical Staging and 5. Ganesh R, Castle D, McGibbon D, et al. Immunological Classification of HIV-Related Disease Staphylococcal carriage and HIV infection. Lancet in Adults and Children. Geneva, Switzerland: World 1989;ii(8662):558. Health Organization, 2006.

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