Cutaneous manifestations of human immunodeficiency virus

Created 2009.

Learning objectives

• Identify cutaneous complications of human immunodeficiency virus infection

Clinical features

Human immunodeficiency virus (HIV) type 1 (usual kind) and type 2 (West African kind) nearly always results in skin changes. Recognising that atypical or severe cutaneous infections and other skin conditions may be related to underlying HIV infection allows initiation of early retroviral treatment and reduces the risk of transmission. It is estimated that there are at least 30 million infected individuals worldwide (2005).

Infection may arise through sexual intercourse, injection (especially illicit drug use), transplacentally or by breastfeeding.

HIV affects the skin because of the depletion of CD4+ cells (helper T lymphocytes), facilitated by initial infection via Langerhans cells in mucosal tissue. Viraemia appears within a few days and is initially controlled by specific immune response including CD8+ cells (cytotoxic T lymphocytes) and soluble cytokines.

Cutaneous manifestations are numerous. Detailed descriptions are found elsewhere in the course or on other online resources. In general, the presentations resemble more typical infections or dermatoses but are more florid, persistent and resistant to treatment.

Primary HIV viraemia:

• Morbilliform eruption on trunk and limbs

Viral infections:

• Recurrent or chronic herpes zoster
• Hyperkeratotic and proliferative viral warts
• Oral hairy leukoplakia (Epstein-Barr virus)
• Persistent ulcerated herpes simplex
• Molluscum contagiosum
• Cytomegalovirus infection (perineal ulcers)

Bacterial infections:

• Staphylococcus aureus: folliculitis, impetigo, furunculosis, abscess
• Mycobacterial infections
• Bacillary angiomatosis (Bartonella quintana)
• Syphilis (ulcers increase HIV transmission)

Fungal infections:

• Mucocutaneous candidiasis
• Dermatophytosis
• Pityriasis versicolor
• Seborrhoeic dermatitis
• Cutaneous cryptococcosis
• Cutaneous histoplasmosis
• Blasomycosis
• Coccidioidomycosis

Arthropods:

• Norwegian scabies
• Demodex folliculitis

Tumours:

• Kaposi sarcoma (proliferation of endothelial cells induced by human herpesvirus type 8)
• B-cell non-Hodkin lymphoma
• Papillomavirus-associated neoplasia
• Aggressive melanoma

Dermatoses:

• Xerosis and ichthyosis
• Pruritus
• Psoriasis
• Eosinophilic folliculitis
• Pruritic papular eruption
• Aphthosis
• Atopic dermatitis
• Urticaria
• Vasculitis

Hair and nail problems:

• Diffuse alopecia
• Hypertrichosis
• Beau's lines
• Pigmented nails (zidovudine effect)

Drug eruptions:

• Morbilliform eruption especially with trimethoprim + sulphamethoxazole
• Fixed drug eruption
• Erythroderma
• Lipodystrophy (lipoatrophy and lipohypertrophy) due to protease inhibitors, associated with hyperlipidaemia, insulin resistance and hyperglycaemia

Investigations

HIV infection is diagnosed by positive ELISA screen confirmed by Western blot, immunofluorescent assay or viral load assay. Viral load assays are used to evaluate the effectiveness of antiviral treatment. PCR and viral culture are sensitive but expensive and difficult to perform.

The ratio of CD4+/CD8+ T cells is decreased.

Suspected infections can be identified and cultured in the usual way. Histopathology may be necessary.

Management

Infections nearly always require oral treatment.

• HSV and HZV: aciclovir, valaciclovir, famciclovir
• EBV: aciclovir, ganciclovir, foscarnet
• CMV, HPV, molluscum contagiosum: imiquimod cream, AZT, cidofovir
• Candidiasis: oral azole
• Dermatophytosis: oral terbinafine
• Bacillary angiomatosis: erythromycin

Kaposi sarcoma is treated by localised destruction, systemic chemotherapy, interferon and antiretrovirals.

Refer the patient to an infectious disease expert for antiretroviral therapy.

Activity

Describe the effects and complications of antiretroviral therapy.