Cutaneous Manifestations of HIV



Cutaneous manifestations of human immunodeficiency virus (HIV) disease may result from HIV infection itself or from opportunistic disorders secondary to the decline in immunocompetence from the disease.[1] Cutaneous disorders may be the initial signs of HIV-related immunosuppression. Recognizing HIV-related skin changes may lead to the diagnosis of HIV infection in the early stages, allowing initiation of appropriate antiretroviral therapy. Many associated skin diseases are more severe in this group. With the use of antiretroviral therapy, the incidence of some of these skin disorders has declined, but the incidence of drug reactions and other noninfectious skin eruptions has been enhanced.[2]

A variety of neoplastic, infectious, and noninfectious diseases can produce cutaneous manifestations throughout the course of HIV disease. These manifestations may occur more frequently than in persons without HIV infection and may be less responsive to usual treatment modalities.

For other discussions of HIV infection, see HIV Disease, Pediatric HIV Infection, and Antiretroviral Therapy for HIV Infection.

For patient education information, see the Immune System Center, Sexually Transmitted Diseases Center, Teeth and Mouth Center, and Yeast and Fungal Infections Center, as well as HIV/AIDS, Canker Sores, Candidiasis (Yeast Infection), and Syphilis.

Manifestations by HIV Disease Stage

During acute primary HIV infection, a transient, generalized, morbilliform eruption may develop on the trunk and the arms. In the early asymptomatic stage of HIV disease, which may last from a few years to a decade or longer, no signs of infection other than lymphadenopathy are present. In a survey of 165 children in India with HIV infection, cutaneous manifestations were evident in 100 (61%) of them. Papular pruritic eruptions were evident in 16%, the most common condition, with highest prevalence in severe CD4 category.[3]

Kaposi sarcoma can occur prior to the onset of immunosuppression. With the onset of immunosuppression, nonspecific skin changes occur, such as common disorders with atypical clinical features, including recurrent varicella zoster, numerous hyperkeratotic warts, treatment-resistant seborrheic dermatitis, and oral hairy leukoplakia. However, Kaposi sarcoma of skin and/or oral cavity may develop in HIV patients with well-controlled HIV disease and may be a significant factor in their morbidity and mortality.[4]

In the later stages of HIV disease, chronic herpes simplex virus (HSV), molluscum contagiosum (MC), and cytomegalovirus (CMV) infections appear. An autopsy analysis of HIV-seropositive patients revealed that 72% had opportunistic viral infections; most patients were infected with CMV and HSV. The prevalence of clinically apparent MC infection varies from 5-18% in different series. Mycobacterial infections and mucocutaneous candidiasis occur.

A 42-month prospective study by Smith et al in 912 HIV-1–infected patients found that condylomata acuminata and verrucae are observed early, and their frequency does not increase as the disease progresses, whereas the incidence of HSV infections, MC, and oral hairy leukoplakia increases as the disease advances.[5, 6]

Verrucous herpes infection, leprosy, condylomalike molluscum contagiosum, and AIDS-associated pigmented or nonpigmented erythroderma may be seen in early HIV disease or as part of immune restoration syndrome after the initiation of antiretroviral therapy.[7, 8, 9, 10, 11] Leishmaniasis and miliary tuberculosis may be a concern in advanced HIV disease.[12, 13, 14] Diffuse or disseminated leishmaniasis may occur with HIV disease,[15, 16] including in association with the immune reconstitution inflammatory syndrome.[16]

Manifestations in HIV-Infected Children

Mucocutaneous candidiasis, including recurrent and widespread diaper dermatitis and chronic paronychia, is a common cutaneous manifestation in children with HIV infection. The most common cutaneous infections in children with HIV disease are impetigo and cellulitis caused by Staphylococcus aureus.

Other cutaneous manifestations of HIV infection in the pediatric age group are as follows:


Kaposi sarcoma (KS) was the first reported malignancy associated with HIV infection and was first documented in 1981 from reports in New York, Los Angeles, and San Francisco.[17] The worldwide prevalence of KS in patients with AIDS may approach 34%; in the United States; however, the prevalence of KS in patients with HIV disease is less than 5%. Most of the patients are homosexual men, although all patients who acquire HIV infection through sexual contact are at somewhat increased risk. One should also be aware of mimickers of KS, including acroangiodermatitis.[18]

Since the advent of highly active antiretroviral therapy (HAART), the incidence of non–AIDS-defining cutaneous cancers—in particular, basal cell carcinoma—among HIV-infected persons has exceeded that of AIDS-defining cutaneous cancers such as KS. In a prospective study, Crum-Cianflone et al found that 6% of HIV-infected persons developed a cutaneous malignancy over a mean follow-up period of 7.5 years.[19]

The development of cutaneous non–AIDS-defining cancers in this cohort proved to be associated with the traditional risk factors of increasing age and lighter skin color, rather than with CD4 lymphocyte counts, HIV RNA levels, or receipt of HAART.[19]

KS remains the most common HIV-associated malignancy in sub-Saharan Africa.[20] Pediatric KS is distinct, and lymph node involvement is a common manifestation.

AIDS-related B-cell non-Hodgkin lymphomas may cause skin nodules.

HIV-infected patients may also develop cutaneous T-cell lymphoma.[21] Amazingly, they had higher survival and lower mortality than those non–HIV-infected persons, possibly because of antiretroviral therapy restoring immune functions.

Anal carcinoma and cervical intraepithelial neoplasia are papillomavirus-associated tumors associated with HIV disease. These tumors tend to be more progressive and aggressive. An increase in squamous cell carcinoma of the anal mucosa has been reported, especially in young homosexual men with HIV infection.

Intraoral or multiple squamous cell carcinoma, Bowen disease, and metastatic basal cell carcinoma have occasionally been reported in patients infected with HIV.

Malignant melanoma appears to be more aggressive in patients with HIV. One study reported shorter disease-free and overall survival rates in patients with melanoma who had HIV disease, compared with those who did not have HIV.[22]

Children with AIDS have a higher risk of developing leiomyosarcoma, although the incidence is still low in this population.

Kaposi sarcoma

KS is an abnormally vascularized tumorlike lesion affecting skin, lymph nodes, and viscera. It is believed to be a proliferation of endothelial cells induced by human herpesvirus type 8. KS is promoted by various angiogenic and proinflammatory factors, including HIV-Tat. In addition, the latency-associated nuclear antigen type 1 (LANA-1) protein is highly expressed in spindle cells, which is considered important in the maintenance of human herpesvirus type 8–associated malignancies.

KS begins as pink macules that become disseminated and palpable. Purplish or brown macules and plaques may become nodular (see the images below). Mucosal involvement is common. KS demonstrates more aggressive clinical progression in patients infected with HIV than in other populations with the disease. It may develop in HIV patients with well-controlled HIV disease.[4]

View Image

Kaposi sarcoma in a man with HIV infection.

View Image

Kaposi sarcoma in a man with HIV infection.

Viral Infections

In patients infected with HIV, several viruses of the Herpesviridae family may lead to cutaneous disease, including chronic perianal and perioral herpetic ulcers caused by herpes simplex virus (HSV), recurrent typical dermatomal zoster caused by herpes zoster virus (HZV), and disseminated cytomegalovirus (CMV) infection.

Herpes simplex and herpes zoster viruses

Recurrent oral and anogenital HSV infection is common in patients infected with HIV, and it may lead to chronic ulcerations. In pediatric patients, HSV stomatitis is more common than varicella-zoster virus (VZV) and may become chronic and ulcerative. Patients with VZV may develop chronic ecthymatous VZV (see the image below).

View Image

Old herpes zoster and Kaposi sarcoma in a patient with HIV disease.

Acute disseminated HZV infection and the following atypical manifestations have also been described:

According to Leibovitz et al, chronic VZV infections associated with HIV-1 infection begin as vesicles and progress into necrotic, nonhealing ulcers.[23, 24] Chronic VZV infection may mimic basal cell carcinoma.[22]

Epstein-Barr virus

Epstein-Barr virus (EBV) has been implicated in the pathogenesis of oral hairy leukoplakia, which may develop in patients infected with HIV, particularly men. Oral hairy leukoplakia is characterized by filiform white papules localized on the sides of the tongue. This condition has no malignant potential, but it may be the initial sign of progressive immunosuppression. White plaques may be confused with oral candidiasis, lichen planus, and geographic tongue.


CMV is a DNA virus in the Herpesviridae family. Ulcers in the perineal region are the most common presentation of CMV infection in patients infected with HIV-1. The concurrent involvement of other infectious agents, such as HSV, in the same lesions confounds the role of CMV in cutaneous lesions. HSV is proposed to be the initiating infection leading to ulcer formation, with CMV secondarily localizing in the granulation tissue.

Nonspecific maculopapular eruptions similar to those affecting patients with EBV or papulovesicular, nodular, purpuric, and ulcerative lesions of CMV infection are observed in patients who are immunocompromised. However, cutaneous lesions are rarely observed in patients infected with HIV.

CMV infection of the eccrine ducts resulting in squamous metaplasia has been described in a patient with HIV.

Diagnosing skin CMV infection in individuals infected with HIV is important. The presence of CMV infection is considered a poor prognostic sign in HIV disease.


Widespread or recalcitrant warts may be observed on the oral mucosa, the face, the perianal region, and the female genital tract in patients infected with HIV. The perianal and cervical lesions may be difficult to treat. Large plantar warts caused by human papillomoavirus–66 (HPV-66) and an epidermodysplasia verruciformislike eruption, which is believed to be associated with HPV infection, have also been reported in patients infected with HIV.[25]

Molluscum contagiosum

The molluscum contagiosum (MC) virus is a DNA virus in the Poxviridae family. It replicates in the cytoplasm of epidermal cells. MC lesions are small papules with central umbilication (see the images below).

View Image

Young man with HIV disease and molluscum contagiosum on the lateral part of the eyebrow.

View Image

Molluscum contagiosum on the penile shaft in a patient with HIV disease.

In HIV infection, MC may be widespread and atypical. The lesions may be observed on unusual sites, such as the face, neck, and scalp, and the lesions may be of unusual morphology and size.[26] Such unusual forms include solitary, endophytic, aggregated, inflamed, and giant MCs. MCs mimicking sebaceous nevus of Jadassohn, ecthyma, and giant condylomata acuminata have been reported.

Superficial Fungal Infections

Recurrent and persistent mucocutaneous candidiasis is common in patients with HIV infection. In the United States, recurrent vaginal candidiasis is the most common presentation of HIV infection in women.

In adults, generalized dermatophytosis, or tinea capitis, which is typically caused by Trichophyton rubrum, may suggest HIV infection. Bournerias et al reported tinea capitis from Microsporum canis in 2 patients infected with HIV.[27]

Pityriasis versicolor may be persistent and recurrent in patients with HIV infection.

Deep Fungal Infections

Rarely, cutaneous cryptococcosis may be observed in patients with HIV infection.[28] Clinical manifestations include the following:

Cutaneous histoplasmosis may lead to red papules, a cellulitislike eruption, ulcerations, acneiform papules, or molluscumlike lesions in patients infected with HIV.[29, 30]

North American blastomycosis may present as a disseminated maculopapular eruption in HIV disease.

Systemic coccidioidomycosis may disseminate to the skin, usually as hemorrhagic papules or nodules. A positive culture/staining from pus and cutaneous lesions may be used to document the cryptococcosis.[31]

Bacterial infections

Impetigo and folliculitis may be recurrent and persistent in HIV disease, particularly in children. Disseminated furunculosis, gingivitis, gangrenous stomatitis, and abscess formation can occur in patients with HIV infection. Bacillary angiomatosis, which is caused by Bartonella henselae and rarely by Bartonella quintana, usually manifests as red papules and nodules.[32] . Antiretroviral therapy may be complicated by bacillary angiomatosis from B quintana as an immune reconstitution inflammatory syndrome and a Jarisch-Herxheimer reaction.[33]

Mycobacterial infections

Mycobacterium tuberculosis; M avium-intracellulare complex (MAC); and, rarely, M kansasii may present as acneiform papules and indurated crusted plaques.

MAC, a common opportunistic pathogen among patients with AIDS, usually causes disseminated disease involving the lungs, lymph nodes, and gastrointestinal tract. Primary cutaneous infections with MAC are extremely rare; most cutaneous lesions are caused by dissemination. Cutaneous manifestations thus far reported include the following:

Localized skin involvement resembling sporotrichosis is unusual. Primary cutaneous MAC infection manifesting as sporotrichosislike lesions was described in a patient with AIDS.[34]

The possibility of coinfections, which may be multiple, should be kept in mind. Coinfection with B quintana, MAC, and CMV has been reported in an AIDS patient.[35]

In patients with HIV, M haemophilum can also present as violaceous draining nodules and superficial ulcers on the extremities, trunk, head, and genitalia.


Co-infection with syphilis (as well as other sexually transmitted diseases) may be found in HIV-infected patients, particularly those who are homosexual or bisexual or who use illicit drugs. Syphilitic ulcers are believed to increase HIV transmission.

Most cases of syphilis that occur in HIV disease are clinically and serologically typical,[36] but some are not.[37] A high rate of reinfection was noted in one French study, with less severe cutaneous manifestations.[36] However, syphilis seroconversion may be delayed, and standard serologic tests that aid in diagnosing syphilis may be unreliable. Also, in primary syphilis, presentation with multiple ulcers is more common in HIV-infected patients. Rapid progression of secondary syphilis to tertiary syphilis and syphilis maligna has been reported in patients infected with HIV.

Appropriate serologic follow-up to ensure an adequate response to treatment is important in patients infected with HIV.

Staphylococcus aureus infection

Patients with HIV have been found to have increased rates of cutaneous colonization by Staphylococcus aureus, and in patients with advanced disease, sepsis and deep tissue infection can be common. Methicillin-resistant S aureus (MRSA) soft-tissue infection is an increasing problem.[38]

Parasitic Infestations

Atypical or Norwegian scabies, which is characterized by widespread hyperkeratotic, scaly maculopapular eruptions or crusted plaques, can occur in patients with HIV infection.

Atypical disseminated leishmaniasis has been reported in an HIV-infected patient.[39]

Demodex folliculorum folliculitis may lead to a pruritic papular eruption (PPE) on the face and the upper part of the trunk in patients with HIV disease.

Papulosquamous Dermatoses of AIDS

Generalized dry skin syndrome is frequently observed in patients with HIV infection. Xerosis may be the initial clinical manifestation of AIDS and is often a cause of pruritus. In the United States, pruritus has been reported in 4.5% of patients with AIDS.

Seborrheic dermatitis may be the initial cutaneous manifestation of HIV disease. According to Mathes et al, seborrheic dermatitislike eruptions are observed in 83% of patients with AIDS.[40] The eruption, which is characterized by widespread inflammatory and hyperkeratotic lesions, may progress to erythroderma in some patients. Seborrheic dermatitis may be increased in patients with AIDS-associated dementia or CNS disease.

The immune alterations caused by HIV infection may lead to psoriasis and Reiter syndrome. In some instances, preexisting psoriasis may become more severe with disseminated plaques and pustules.

The typical skin lesions of pityriasis rosea may accompany HIV disease.

Acquired ichthyosis may begin on the lower extremities and disseminate in advanced HIV disease. Acquired ichthyosis may be a marker of concomitant infection with HIV-1 and human lymphotropic virus II in persons who use intravenous drugs and have profound helper T-cell depletion.[41]

Eosinophilic folliculitis manifests as an idiopathic, highly pruritic, papulopustular eruption of sterile pustules involving the face, neck, trunk, and extremities.

Pruritic papular eruption (PPE) is a common cutaneous manifestation in patients infected with HIV. It manifests as small, itchy, red or skin-colored papules on the head, neck, and upper part of the trunk. The cause is not known. According to Boonchai et al, 81.25% of patients with PPE have advanced immunosuppression.[42] (See the image below.)

View Image

Dull red, violaceous, maculopapular lesions on the upper part of the trunk in a 49-year-old man with primary HIV-1 infection.

Hair and Nail Disorders

Diffuse alopecia or alopecia areata may be associated with HIV disease and may be inflammatory and permanent. The apoptotic follicular stem cell population in higher proportion may represent a hair cycle disturbance in patients with diffuse alopecia related to HIV-1 infection.[43]

Beau lines, telogen effluvium, and pallor of the nail beds are the general effects of the chronic illness. Elongation of the eyelashes and softening and straightening of the scalp hair may be observed in HIV disease, and proximal subungual onychomycosis is also usually a sign of HIV disease. The frequency of onychomycosis may be higher in men than in women.

Generalized alopecia can occur in patients with HIV who are treated with indinavir, an antiretroviral protease inhibitor.[44] Zidovudine is associated with longitudinal, transverse, or diffuse melanin pigmentation of the nails; however, nail pigmentation has also been observed in patients with HIV who have never taken zidovudine.

Drug Eruptions

Drug eruptions have been reported as the most common cause of erythroderma in patients infected with HIV. A study identified 177 cases of Steven-Johnson syndrome/toxic epidermal necrolysis from 2000-2010 and found a high proportion of the patients were infected with HIV in sub-Saharan Africa, with a high frequency of antiretroviral drugs as the cause.[45] This elevated incidence of HIV patients with an adverse cutaneous drug eruption, including toxic epidermal necrolysis, may be due to a loss of skin-protective CD4+ CD25+ regulatory T cells.[46]

As many as 65-70% of patients treated with trimethoprim-sulfamethoxazole for Pneumocystis jiroveci pneumonia experience morbilliform eruptions within 7 days of starting the therapy. Reddish macules and papules may be generalized and can become permanent after the discontinuation of the therapy.

Sulfonamides may cause the following:

Toxic epidermal necrolysis has been reported with the following agents in patients with HIV:

Fixed drug eruption has been reported in 2 patients receiving saquinavir, an HIV-1 protease inhibitor.

Photosensitivity and Drug-Induced Pigmentation

A study by Vin-Christian et al found that photosensitivity in HIV-infected patients appears to be a manifestation of advanced disease.[47] Most of the patients in that study were sensitive to ultraviolet B (UV-B) light; however, the patients who were most severely affected were sensitive to both UV-B and UV-A light.[47]

Photo-induced lichenoid drug reactions may occur in HIV-infected patients, particularly those with dark skin. In addition, HIV-infected patients may experience drug-induced pigmentation of skin exposed to light.

Miscellaneous Dermatologic Disorders

The following dermatologic conditions may be associated with HIV disease:

Thrombocytopenic purpura, vitiligo, alopecia areata, sicca syndrome, pemphigoid, and other autoimmune blistering diseases have been reported in association with HIV disease.

Atopic disease may be reactivated by HIV disease. Atopic eczema may be severe in children infected with HIV. Increased serum IgE levels have been found in these children; however, increased IgE levels were not correlated with atopic symptoms.[51]

Urticaria may occur primarily or as a drug eruption in HIV disease. Cold urticaria has also been associated with HIV disease.[52]

Differential Diagnosis

The differential diagnosis includes the following:

Other problems to be considered in HIV-infected patients with dermatologic conditions include the following:


Histopathologic examination is useful to diagnose cutaneous manifestations of HIV disease with atypical clinical features and Kaposi sarcoma (KS). Routine hematoxylin and eosin and periodic acid-Schiff stainings may demonstrate multinuclear cells with intracytoplasmic inclusions of herpes simplex virus infection. Other special stains may identify additional pathogens, or they may confirm malignancies, such as KS. Histologic assessment of the CXCL12 axis may be a useful biomarker for diagnosing KS and assessing its progression.[59]

Imaging studies may be helpful in evaluating extracutaneous manifestations of KS, lymphoma, and systemic infections.


Viral infections

For herpes simplex virus (HSV) and herpes zoster virus (HZV) infections in HIV-infected patients, the treatment of choice is acyclovir and other members of this drug class. These agents are activated by viral thymidine kinase. In some disseminated cases, the virus may be resistant to acyclovir because of the deficiency in viral thymidine kinase activity.

Prolonged therapy and chronic suppressive therapy with subtherapeutic doses have also been implicated in the development of acyclovir resistance. In the presence of acyclovir resistance, other viral therapies, including cidofovir, foscarnet, and vidarabine, may be necessary.

Treatment is usually not necessary for patients with oral hairy leukoplakia. If the patient is experiencing significant discomfort, systemic (1200 mg/day) and topical acyclovir, ganciclovir, or foscarnet may be recommended.

In most cases of molluscum contagiosum, imiquimod (Aldara) is curative. Resolution with zidovudine therapy has been reported in HIV-associated molluscum contagiosum. There are isolated reports of the efficacy of cidofovir in several viral infections (eg, molluscum contagiosum,[60] warts,[25] CMV infection) that are frequently observed in HIV-infected patients infected with HIV, but extensive studies of the safety and the efficacy of cidofovir have not been conducted to date.

Ablation and curettage may be useful in the treatment of molluscum contagiosum.

Noninfectious and nonmalignant cutaneous manifestations of HIV infection

For xerosis, emollients and dry skin care regimens are effective. For seborrheic dermatitis, coal tar, sulfur, and salicylic acid shampoos; topical corticosteroids; topical tacrolimus; and 2% ketoconazole cream may be effective.

For psoriasis and Reiter syndrome, ultraviolet B (UV-B) and psoralen with UV-A (PUVA) may be useful. Systemic corticosteroids, methotrexate, and cyclosporine may increase the immune suppression and must be considered only with careful monitoring. Zidovudine is also reported to be useful in the treatment of HIV-associated psoriasis.

For pruritic papular eruption, topical steroids, UV-B, PUVA, and pentoxifylline[61] have been reported to be effective. Eosinophilic folliculitis may respond to UV-B,[62] isotretinoin, or zidovudine treatment. For severe aphthous stomatitis, tacrolimus is reported to be effective.

Kaposi sarcoma

For patients with limited disease, local therapy with liquid nitrogen, alitretinoin, or intralesional vincristine may be effective. Surgery, radiotherapy, and systemic chemotherapy—usually with a single agent (eg, vinblastine, vincristine, bleomycin, doxorubicin, etoposide)—may be useful in the treatment of KS; however, systemic chemotherapy has not been shown to improve the long-term survival rates. Patients who recover immune response withantiretroviral therapy have had remission of KS.

Interferon (IFN)-alpha and IFN-beta photodynamic therapy and systemic hyperthermia have also been used. Cryotherapy, laser irradiation, and electrodesiccation can be useful for localized solitary lesions of KS.

Miscellaneous conditions

Mucocutaneous candidiasis is usually difficult to treat; oral azole treatment may be required. Generalized dermatophytosis may be resistant to topical antifungal creams and may require systemic antifungal therapy. Bacillary angiomatosis usually responds to oral erythromycin.


Overall care for patients with HIV should be provided by a primary care practitioner with expertise in managing the disease. Infectious disease consultants are typically involved in the care of these patients. Patients confronting this chronic and debilitating disease may require additional support services.

The following are other specialists that may be consulted:

What are the cutaneous manifestations of HIV disease?What are the cutaneous manifestations of HIV by disease stage?What are the cutaneous manifestations of HIV disease in children?Which malignancies cause cutaneous manifestations of HIV infection?How are the cutaneous manifestations of Kaposi sarcoma (KS) in HIV characterized?Which viral infections are associated with cutaneous manifestations of HIV disease?What are the possible cutaneous complications of herpes simplex and herpes zoster viruses in HIV disease?What are atypical cutaneous manifestations of herpes zoster virus (HSV) in HIV disease?What are the signs and symptoms of oral hairy leukoplakia in HIV disease?How are the cutaneous manifestations of cytomegalovirus (CMV) in HIV disease characterized?How are warts characterized in HIV disease?What are the cutaneous manifestations of molluscum contagiosum (MC) virus in HIV disease?What are the cutaneous manifestations of superficial fungal infections in HIV disease?What are the cutaneous manifestations of deep fungal infections in HIV disease?Which bacterial infections are associated with cutaneous manifestations of HIV disease?What are the cutaneous manifestations of mycobacterial infections in HIV disease?What are the cutaneous manifestations of syphilis in HIV disease?What are the cutaneous manifestations of staphylococcus aureus infection in HIV disease?Which parasitic infestations are associated with cutaneous manifestations of HIV disease?What are the cutaneous manifestations of papulosquamous dermatoses in HIV disease?Which hair and nail disorders are associated with HIV disease?What is the role of drug eruptions in the development of HIV infection?What are the cutaneous manifestations of sulfonamide use in HIV disease?Which medications may cause toxic epidermal necrolysis in HIV disease?What are photo-induced drug reactions in HIV disease?Which dermatologic conditions are associated with HIV disease?Which conditions are included in the differential diagnoses of cutaneous HIV disease?What is the role of histology in the diagnosis of cutaneous manifestations of HIV infection?What is the role of imaging studies in the diagnosis of cutaneous manifestations of HIV infection?How are HSV and HZV treated in HIV disease?How are noninfectious and nonmalignant cutaneous manifestations of HIV disease treated?How is Kaposi sarcoma (KS) treated in HIV disease?How are cutaneous manifestations of HIV disease treated?Which specialist consultations are beneficial to patients with cutaneous manifestations of HIV infection?


Robert A Schwartz, MD, MPH, Professor and Head of Dermatology, Professor of Pathology, Professor of Pediatrics, Professor of Medicine, Rutgers New Jersey Medical School

Disclosure: Nothing to disclose.


Anna Zalewska, MD, PhD, Professor of Dermatology and Venereology, Psychodermatology Department, Chair of Clinical Immunology and Microbiology, Medical University of Lodz, Poland

Disclosure: Nothing to disclose.

Emel Erdal, MD, Associate Professor of Dermatology, Mesa Hospital, Turkey

Disclosure: Nothing to disclose.

Specialty Editors

David F Butler, MD, Former Section Chief of Dermatology, Central Texas Veterans Healthcare System; Professor of Dermatology, Texas A&M University College of Medicine; Founding Chair, Department of Dermatology, Scott and White Clinic

Disclosure: Nothing to disclose.

Julia R Nunley, MD, Professor, Program Director, Dermatology Residency, Department of Dermatology, Virginia Commonwealth University Medical Center

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: American Board of Dermatology<br/>Co-Editor for the text Dermatological Manifestations of Kidney Disease .

Chief Editor

William D James, MD, Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

Disclosure: Received income in an amount equal to or greater than $250 from: Elsevier; WebMD.


The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author Randa M Hamadeh, MD, to the development and writing of the source article.


  1. Cedeno-Laurent F, Gómez-Flores M, Mendez N, Ancer-Rodríguez J, Bryant JL, Gaspari AA, et al. New insights into HIV-1-primary skin disorders. J Int AIDS Soc. 2011 Jan 24. 14:5. [View Abstract]
  2. Altman K, Vanness E, Westergaard RP. Cutaneous manifestations of human immunodeficiency virus: a clinical update. Curr Infect Dis Rep. 2015 Mar. 17(3):464. [View Abstract]
  3. Britto GR, Augustine M. Mucocutaneous manifestations of human immunodeficiency virus (HIV) infection in children in relation to the degree of immunosuppression. Int J Dermatol. 2019 Mar 29. [View Abstract]
  4. Hwang A, Iskandar AS, Kerr WT, Farrell S, Plaxe SC, Dasanu CA. Clinico-epidemiologic characteristics and patterns of care in Kaposi's sarcoma: Data from a single-institution series. J Oncol Pharm Pract. 2019 Apr 2. 1078155219838614. [View Abstract]
  5. Smith KJ, Skelton HG, Yeager J, Ledsky R, McCarthy W, Baxter D, et al. Cutaneous findings in HIV-1-positive patients: a 42-month prospective study. Military Medical Consortium for the Advancement of Retroviral Research (MMCARR). J Am Acad Dermatol. 1994 Nov. 31(5 Pt 1):746-54. [View Abstract]
  6. Zampogna JC, Flowers FP. Persistent verrucous varicella as the initial manifestation of HIV infection. J Am Acad Dermatol. 2001 Feb. 44(2 Suppl):391-4. [View Abstract]
  7. Janniger CK, Gascon P, Schwartz RA, Hennessey NP, Lambert WC. Erythroderma as the initial presentation of the acquired immunodeficiency syndrome. Dermatologica. 1991. 183(2):143-5. [View Abstract]
  8. Wiederkehr M, Schwartz RA. Giant proliferative molluscum contagiosum. Acta Derm Venerol (Ljubjlana). 2002;11:101-104.
  9. Pignataro P, Rocha Ada S, Nery JA, Miranda A, Sales AM, Ferrreira H, et al. Leprosy and AIDS: two cases of increasing inflammatory reactions at the start of highly active antiretroviral therapy. Eur J Clin Microbiol Infect Dis. 2004 May. 23(5):408-11. [View Abstract]
  10. Tzung TY, Yang CY, Chao SC, Lee JY. Cutaneous manifestations of human immunodeficiency virus infection in Taiwan. Kaohsiung J Med Sci. 2004 May. 20(5):216-24. [View Abstract]
  11. Itin PH, Gilli L. Molluscum contagiosum mimicking sebaceous nevus of Jadassohn, ecthyma and giant condylomata acuminata in HIV-infected patients. Dermatology. 1994. 189(4):396-8. [View Abstract]
  12. Puig L, Pradinaud R. Leishmania and HIV co-infection: dermatological manifestations. Ann Trop Med Parasitol. 2003 Oct. 97 Suppl 1:107-14. [View Abstract]
  13. High WA, Evans CC, Hoang MP. Cutaneous miliary tuberculosis in two patients with HIV infection. J Am Acad Dermatol. 2004 May. 50(5 Suppl):S110-3. [View Abstract]
  14. Diatta BA, Diallo M, Diadie S, Faye B, Ndiaye M, Hakim H, et al. [Cutaneous leishmaniasis due to Leishmania infantum associated with HIV]. Ann Dermatol Venereol. 2016 May 3. [View Abstract]
  15. Chiewchanvit S, Tovanabutra N, Jariyapan N, Bates MD, Mahanupab P, Chuamanochan M, et al. Chronic generalized fibrotic skin lesions from disseminated leishmaniasis caused by Leishmania martiniquensis in two HIV-infected patients from northern Thailand. Br J Dermatol. 2015 Mar 30. [View Abstract]
  16. Sinha S, Fernández G, Kapila R, Lambert WC, Schwartz RA. Diffuse cutaneous leishmaniasis associated with the immune reconstitution inflammatory syndrome. Int J Dermatol. 2008 Dec. 47(12):1263-70. [View Abstract]
  17. Borkovic SP, Schwartz RA. Kaposi's sarcoma presenting in the homosexual man -- a new and striking phenomenon!. Ariz Med. 1981 Dec. 38(12):902-4. [View Abstract]
  18. Goorney BP, Newsham J, Fitzgerald D, Motta L. Acroangiodermatitis mimicking Kaposi's sarcoma in an HIV-positive man. Int J STD AIDS. 2018 Jan 1. 956462417750709. [View Abstract]
  19. Crum-Cianflone N, Hullsiek KH, Satter E, Marconi V, Weintrob A, Ganesan A, et al. Cutaneous malignancies among HIV-infected persons. Arch Intern Med. 2009 Jun 22. 169(12):1130-8. [View Abstract]
  20. Cox CM, El-Mallawany NK, Kabue M, Kovarik C, et al. Clinical Characteristics and Outcomes of HIV-Infected Children Diagnosed With Kaposi Sarcoma in Malawi and Botswana. Pediatr Blood Cancer. 2013 Mar 11. [View Abstract]
  21. Wang J, Liang R, Hao C, Liu X, Zhang N, Duan X, et al. Survival outcomes of primary cutaneous T-cell lymphoma in HIV-infected patients: a national population-based study. J Investig Med. 2018 Jan 12. [View Abstract]
  22. Tsao H, Tahan SR, Johnson RA. Chronic varicella zoster infection mimicking a basal cell carcinoma in an AIDS patient. J Am Acad Dermatol. 1997 May. 36(5 Pt 2):831-3. [View Abstract]
  23. Leibovitz E, Cooper D, Giurgiutiu D, Coman G, Straus I, Orlow SJ, et al. Varicella-zoster virus infection in Romanian children infected with the human immunodeficiency virus. Pediatrics. 1993 Dec. 92(6):838-42. [View Abstract]
  24. Leibovitz E, Kaul A, Rigaud M, Bebenroth D, Krasinski K, Borkowsky W. Chronic varicella zoster in a child infected with human immunodeficiency virus: case report and review of the literature. Cutis. 1992 Jan. 49(1):27-31. [View Abstract]
  25. Davis MD, Gostout BS, McGovern RM, Persing DH, Schut RL, Pittelkow MR. Large plantar wart caused by human papillomavirus-66 and resolution by topical cidofovir therapy. J Am Acad Dermatol. 2000 Aug. 43(2 Pt 2):340-3. [View Abstract]
  26. Kolokotronis A, Antoniades D, Katsoulidis E, Kioses V. Facial and perioral molluscum contagiosum as a manifestation of HIV infection. Aust Dent J. 2000 Mar. 45(1):49-52. [View Abstract]
  27. Bournerias I, De Chauvin MF, Datry A, Chambrette I, Carriere J, Devidas A, et al. Unusual Microsporum canis infections in adult HIV patients. J Am Acad Dermatol. 1996 Nov. 35(5 Pt 2):808-10. [View Abstract]
  28. Dharmshale SN, Patil SA, Gohil A, Chowdhary A, Oberoi C. Disseminated crytococcosis with extensive cutaneous involvement in AIDS. Indian J Med Microbiol. 2006 Jul. 24(3):228-30. [View Abstract]
  29. K Ramdial P, Mosam A, Dlova NC, B Satar N, Aboobaker J, Singh SM. Disseminated cutaneous histoplasmosis in patients infected with human immunodeficiency virus. J Cutan Pathol. 2002 Apr. 29(4):215-25. [View Abstract]
  30. Chande C, Menon S, Gohil A, Lilani S, Bade J, Mohammad S, et al. Cutaneous histoplasmosis in AIDS. Indian J Med Microbiol. 2010 Oct-Dec. 28(4):404-6. [View Abstract]
  31. Chetchotisakd P, Anunnatsiri S, Nithichanon A, Lertmemongkolchai G. Cryptococcosis in anti-interferon-gamma autoantibodies-positive patients: a different clinical manifestation from HIV-infected patients. Jpn J Infect Dis. 2016 May 9. [View Abstract]
  32. Plettenberg A, Lorenzen T, Burtsche BT, Rasokat H, Kaliebe T, Albrecht H, et al. Bacillary angiomatosis in HIV-infected patients--an epidemiological and clinical study. Dermatology. 2000. 201(4):326-31. [View Abstract]
  33. DallaPiazza M, Akiyama MJ. The First Report of Bartonella quintana Immune Reconstitution Inflammatory Syndrome Complicated by Jarisch-Herxheimer Reaction. J Int Assoc Provid AIDS Care. 2017 Jan 1. 2325957417702484. [View Abstract]
  34. Kayal JD, McCall CO. Sporotrichoid cutaneous Mycobacterium avium complex infection. J Am Acad Dermatol. 2002 Nov. 47(5 Suppl):S249-50. [View Abstract]
  35. Rovery C, Rolain JM, Lepidi H, Zandotti C, Moreau J, Brouqui P. Bartonella quintana coinfection with Mycobacterium avium complex and CMV in an AIDS patient: case presentation. BMC Infect Dis. 2006 May 29. 6:89. [View Abstract]
  36. Courjon J, Hubiche T, Dupin N, Grange PA, Del Giudice P. Clinical Aspects of Syphilis Reinfection in HIV-Infected Patients. Dermatology. 2015 Mar 24. [View Abstract]
  37. Balagula Y, Mattei PL, Wisco OJ, Erdag G, Chien AL. The great imitator revisited: the spectrum of atypical cutaneous manifestations of secondary syphilis. Int J Dermatol. 2014 Dec. 53(12):1434-41. [View Abstract]
  38. Rodgers S, Leslie KS. Skin infections in HIV-infected individuals in the era of HAART. Curr Opin Infect Dis. 2011 Apr. 24(2):124-9. [View Abstract]
  39. Boumis E, Chinello P, Della Rocca C, Paglia MG, Proietti MF, Petrosillo N. Atypical disseminated leishmaniasis resembling post-kala-azar dermal leishmaniasis in an HIV-infected patient. Int J STD AIDS. 2006 May. 17(5):351-3. [View Abstract]
  40. Mathes LE, Hayes KA, Kociba G. Evidence that high-dosage zidovudine at time of retrovirus exposure reduces antiviral efficacy. Antimicrob Agents Chemother. 1996 Sep. 40(9):2183-6. [View Abstract]
  41. Kaplan MH, Sadick NS, McNutt NS, Talmor M, Coronesi M, Hall WW. Acquired ichthyosis in concomitant HIV-1 and HTLV-II infection: a new association with intravenous drug abuse. J Am Acad Dermatol. 1993 Nov. 29(5 Pt 1):701-8. [View Abstract]
  42. Boonchai W, Laohasrisakul R, Manonukul J, Kulthanan K. Pruritic papular eruption in HIV seropositive patients: a cutaneous marker for immunosuppression. Int J Dermatol. 1999 May. 38(5):348-50. [View Abstract]
  43. Barcaui CB, Gonçalves da Silva AM, Sotto MN, Genser B. Stem cell apoptosis in HIV-1 alopecia. J Cutan Pathol. 2006 Oct. 33(10):667-71. [View Abstract]
  44. Harry TC, Matthews M, Salvary I. Indinavir use: associated reversible hair loss and mood disturbance. Int J STD AIDS. 2000 Jul. 11(7):474-6. [View Abstract]
  45. Saka B, Barro-Traore F, Atadokpede FA, et al. Stevens-Johnson syndrome and toxic epidermal necrolysis in sub-Saharan Africa: a multicentric study in four countries. Int J Dermatol. 2013 Jan 20. [View Abstract]
  46. Yang C, Mosam A, Mankahla A, Dlova N, Saavedra A. HIV infection predisposes skin to toxic epidermal necrolysis via depletion of skin-directed CD4+ T cells. J Am Acad Dermatol. 2014 Mar 12. [View Abstract]
  47. Vin-Christian K, Epstein JH, Maurer TA, McCalmont TH, Berger TG. Photosensitivity in HIV-infected individuals. J Dermatol. 2000 Jun. 27(6):361-9. [View Abstract]
  48. Ingen-Housz-Oro S, Sbidian E, Ortonne N, et al. HIV-Related CD8+ Cutaneous Pseudolymphoma: Efficacy of Methotrexate. Dermatology. 2013 Jan 22. [View Abstract]
  49. Martinelli C, Azzi A, Buffini G, Comin CE, Leoncini F. Cutaneous vasculitis due to human parvovirus B19 in an HIV-infected patient: report of a case. AIDS. 1997 Dec. 11(15):1891-3. [View Abstract]
  50. Rachline A, Lariven S, Descamps V, Grossin M, Bouvet E. Leucocytoclastic vasculitis and indinavir. Br J Dermatol. 2000 Nov. 143(5):1112-3. [View Abstract]
  51. Ellaurie M, Rubinstein A, Rosenstreich DL. IgE levels in pediatric HIV-1 infection. Ann Allergy Asthma Immunol. 1995 Oct. 75(4):332-6. [View Abstract]
  52. Yu RC, Evans B, Cream JJ. Cold urticaria, raised IgE and HIV infection. J R Soc Med. 1995 May. 88(5):294P-295P. [View Abstract]
  53. Handler NS, Handler MZ, Stephany MP, Handler GA, Schwartz RA. Porphyria cutanea tarda: an intriguing genetic disease and marker. Int J Dermatol. 2017 Mar 21. [View Abstract]
  54. Molinero J, Vilata JJ, Nagore E, Obón L, Grau C, Aliaga A. Ashy dermatosis in an HIV antibody-positive patient. Acta Derm Venereol. 2000 Jan-Feb. 80(1):78-9. [View Abstract]
  55. Kanitakis J, Carbonnel E, Delmonte S, Livrozet JM, Faure M, Claudy A. Multiple eruptive dermatofibromas in a patient with HIV infection: case report and literature review. J Cutan Pathol. 2000 Jan. 27(1):54-6. [View Abstract]
  56. García-Patos V, Repiso T, Rodríguez-Cano L, Castells A. Ofuji papuloerythroderma in a patient with the acquired immunodeficiency syndrome. Dermatology. 1996. 192(2):164-6. [View Abstract]
  57. Duvic M, Reisman M, Finley V, Rapini R, DiLuzio NR, Mansell PW. Glucan-induced keratoderma in acquired immunodeficiency syndrome. Arch Dermatol. 1987 Jun. 123(6):751-6. [View Abstract]
  58. Kanitakis J, Misery L, Nicolas JF, Lyonnet S, Chouvet B, Haftek M, et al. Disseminated superficial porokeratosis in a patient with AIDS. Br J Dermatol. 1994 Aug. 131(2):284-9. [View Abstract]
  59. Desnoyer A, Dupin N, Assoumou L, Carlotti A, Gaudin F, Deback C, et al. Expression pattern of the CXCL12/CXCR4-CXCR7 trio in Kaposi's sarcoma skin lesions. Br J Dermatol. 2016 May 13. [View Abstract]
  60. Meadows KP, Tyring SK, Pavia AT, Rallis TM. Resolution of recalcitrant molluscum contagiosum virus lesions in human immunodeficiency virus-infected patients treated with cidofovir. Arch Dermatol. 1997 Aug. 133(8):987-90. [View Abstract]
  61. Berman B, Flores F, Burke G 3rd. Efficacy of pentoxifylline in the treatment of pruritic papular eruption of HIV-infected persons. J Am Acad Dermatol. 1998 Jun. 38(6 Pt 1):955-9. [View Abstract]
  62. Misago N, Narisawa Y, Matsubara S, Hayashi S. HIV-associated eosinophilic pustular folliculitis: successful treatment of a Japanese patient with UVB phototherapy. J Dermatol. 1998 Mar. 25(3):178-84. [View Abstract]

Kaposi sarcoma in a man with HIV infection.

Kaposi sarcoma in a man with HIV infection.

Old herpes zoster and Kaposi sarcoma in a patient with HIV disease.

Young man with HIV disease and molluscum contagiosum on the lateral part of the eyebrow.

Molluscum contagiosum on the penile shaft in a patient with HIV disease.

Dull red, violaceous, maculopapular lesions on the upper part of the trunk in a 49-year-old man with primary HIV-1 infection.

Dull red, violaceous, maculopapular lesions on the upper part of the trunk in a 49-year-old man with primary HIV-1 infection.

Kaposi sarcoma in a man with HIV infection.

Kaposi sarcoma in a man with HIV infection.

Young man with HIV disease and molluscum contagiosum on the lateral part of the eyebrow.

Molluscum contagiosum on the penile shaft in a patient with HIV disease.

Old herpes zoster and Kaposi sarcoma in a patient with HIV disease.