45 HIV: dermatological disorders

Skin conditions are extremely common and may occur at any stage of HIV infection. Pre-existing skin conditions may worsen after its acquisition. Appearance of certain skin conditions should alert physicians to possibility of undiagnosed HIV infection. Immunodeficiency is associated with atypical presentations, severe manifestations, and a poor response to treatment. In general, improved immunity with HAART resolves or improves them.

Skin rash occurs in up to 70% cases. It is often part of an infectious mononucleosis-like illness. Typically symmetrical and non-itchy, extending over the trunk and upper limbs, and macular or maculopapular in appearance, although it can be vesicular, pustular, or urticarial. May be associated with oro-pharyngeal (highly suspicious of seroconversion illness) and genital ulceration. Resolves spontaneously within 1–2 weeks.

1° and recurrent HSV present with genital and orofacial clusters of vesicles that ulcerate, crust, and heal within 2–3 weeks during the early stages of HIV infection. With advanced disease, ulcers become atypical or chronic and may coalesce to form large painful crusted lesions commonly seen peri-anally but may involve the peri-oral and rarely the peri-ungual region. Though dissemination is rare, lesions may be auto-inoculated to distant sites. HSV infection rarely presents with necrotizing folliculitis (difficult to diagnose without biopsy).

Swabs for viral culture and immunofluorescence usually confirm the diagnosis. Polymerase chain reaction (PCR) testing of skin lesions is very sensitive and specific but not widely available. Viral culture can be performed on skin biopsy from the edge of the lesion when swab is not conclusive. Histological examination may provide a rapid diagnosis by demonstrating multinucleated giant epithelial cells.

( Chapter 21, Management p. 268; Chapter 40, Anal diseases p. 470)

Those with no previous exposure to VZV develop chickenpox which may be severe and associated with visceral involvement. Most adults have been infected by VZV and so present with herpes zoster. Usually affects multiple dermatomes, commonly the thoracic and the trigeminal nerves. Vesicular eruption is normally preceded by tingling and a burning sensation. Individuals with more advanced HIV disease tend to have painful bullous haemorrhagic necrotic lesions that may persist for several weeks and heal with severe scarring. Recurrences and dissemination ↑. Disseminated disease is characterized by dermatomal and non-dermatomal eruptions. Rarely VZV presents with chronic widespread ulcers or hyperkeratotic lesions (if infected with aciclovir-resistant VZV).

Clinical diagnosis is usually accurate in typical dermatomal involvement but skin biopsy is required for atypical, chronic ulcerative, and hyper-keratotic lesions.

Prompt treatment with high-dose aciclovir ↓ risk of dissemination and shortens its course. Clinical presentation and degree of immune deficiency determine mode and length of therapy, which is usually continued until lesions start to crust.

Skin care with bathing with water and mild soap is helpful. Analgesics for pain control.

Caused by a pox virus and when widespread is a marker of advanced HIV disease. Lesion is typically a flesh-coloured, 2–3mm domed, umblicated papule with a faint whitish core. Those with relatively preserved immune function may have mollusca on the groin, which may be chronic. With advanced HIV disease, lesions may reach 1cm in size and may be widespread involving the face, trunk, eyelids, and rarely the mucous membranes (conjunctivae and lips). Mollusca are commonly seen on the beard area (related to trauma of shaving) where they are difficult to treat.

Treatment is given for cosmetic reasons as no cure is available. Usual treatment is cryotherapy. Curettage is effective for recalcitrant cases.

Widespread, resistant, and recurrent warts which may have atypical appearances are seen more frequently in those immunosuppressed. Facial involvement, otherwise rare, is well recognized in HIV infection.

Principles of therapy are as for those not infected by HIV. Ablative treatment is used depending on morphology, location, and number.

Staphylococcus aureus nasal carriage is common explaining ↑ rates of infection with this organism. Staph.aureus skin infection presents as:

Superficial infection responds to standard anti-staphylococcal antibiotics (e.g. flucloxacillin 500mg four times daily for 7–10 days).

Deep infection may require abscess drainage and prolonged courses of combined antibiotics based on bacterial sensitivities. Washing the area with antiseptics helps by removing crusts and ↓ bacterial concentration.

Caused by Bartonella henselae and Bartonella quintana, small Gram-negative aerobic fastidious bacilli. In addition, B.henselae causes cat scratch fever and B.quintana causes trench fever. Angiogenic lesions are most often recognized in cutaneous or subcutaneous tissues and can be difficult to differentiate from Kaposi’s sarcoma (KS). B.henselae causes lesions in lymph nodes, liver (peliosis hepatis), and spleen. B.quintana has a predilection for subcutaneous deep soft tissues and bones.

Serological tests are not reliable in HIV infection.

Prolonged course of antibiotics, e.g. erythromycin 500mg four times daily, doxycycline 100mg twice daily, or azithromycin 0.5–1.0g daily, until lesions heal.

1° mycobacterial skin infection is rare. Skin may be involved in up to 10% of disseminated Mycobacterium avium complex infection, typically when the CD4 count is <50cells/μL. Most frequent presentations are chronic sinuses overlying an infected lymph node (scrofuloderma) and chronic skin ulcer. Rare presentations include violaceous nodules, necrotic papules, plaques, panniculitis, and erythema nodosum.

Mycobacterial infection should be considered in any chronic non-healing skin ulcer. Diagnose by demonstration of acid-fast bacilli in smears and by culture. Typical histological feature of caseating granuloma is usually absent.

( Chapter 42, Tuberculosis p. 492; Chapter 46, Mycobacterium avium complex p. 532).

Skin infection with Candida spp occurs in different forms including tinea unguium (leuconychia, nail ridging, flaking, onycholysis, and atrophy), acute paronychia (tender fluctuation of the nailbed), chronic paronychia, and intertrigo (an erosive painful erythematous rash on flexures associated with satellite pustules). Acute candidal paronychia must be differentiated from that caused by HSV infection using appropriate tests.

Very common in HIV infection. May be atypical and extensive and may mimic inflammatory skin conditions such as seborrhoeic dermatitis or psoriasis.

Apart from tinea pedis, which can be treated with topical antifungals, other forms need systemic antifungals such as terbinafine (250mg daily for several weeks) or a triazole (e.g. fluconazole 50mg daily).

Skin involvement occurs in up to 20% of systemic cryptococcal infection. Most common skin manifestation is a nodule or papule with central umbilication resembling molluscum contagiosum, usually on the face. Plaques and tender subcutaneous lesions are rare. Diagnosed by skin biopsy.

Patient should be evaluated for systemic and neurological cryptococcal infection and managed accordingly ( Chapter 43, Meningitis p. 504).

Endemic to Southeast Asia. Caused by Penicillium marneffei. Presents with fever, skin lesions, anaemia, lymphadenopathy, and hepatosplenomegaly. Skin lesions resemble haemorrhagic molluscum contagiosum. Diagnosed by culture of blood, bone marrow, and skin scrapings. Responds well to liposomal amphotericin and itraconazole but relapses are common and long-term prophylaxis with itraconazole is recommended.

Cutaneous histoplasmosis has been reported in up to 10% of patients with systemic infection, which usually occurs in endemic areas. Diagnosis by biopsy of papules, nodules, or ulcers. Treat with liposomal amphotericin or high-dose itraconazole followed by itraconazole maintenance.

In advanced HIV disease crusted (Norwegian) scabies may occur, characterized by widespread scaly erythematous lesions on the face and scalp together with hyperkeratotic lesions on the hands and feet giving the characteristic ‘breadcrumb’ appearance. Highly infectious because of heavy infestation.

( Chapter 26, Management p. 312)

Patients with crusted scabies must be barrier nursed and in addition to topical treatment may be given (ivermectin 200mcg/kg as a single dose). Topical steroids may be needed for eczematous nodules.

Occurs in up to 85% and may be a first indicator of HIV infection. Severity and recurrences ↑ with ↓ CD4 count. Related to infection with Pityrosporum spp, ↑ sebum production, and a genetic predisposition.

Presents as an itchy erythematous rash with a yellow greasy scale, but in severe cases plaques and hyperkeratotic lesions occur. Usually has a butterfly distribution but may involve eyebrows, post-auricular areas, and scalp. May also affect intertriginous areas and chest. Severe cases may resemble psoriasis. Facial lesions must be differentiated from lupus erythematosus and rosacea.

A chronic disease characterized by erythematous plaques or papules covered by silvery adherent scales. May appear for the first time or pre-existing disease may become worse with HIV infection. Psoriatic arthritis ( Chapter 50, Inflammatory arthropathies/Psoriatic arthritis p. 556) ↑. Several forms of psoriasis may coexist.

Seen in up to 30%. Severity and frequency ↑ as CD4 count ↓. Xerosis (dry skin) is a common complaint and may be associated with an itchy papular scaly rash on the arms and legs. Skin may be damaged as a result of excessive scratching, resulting in excoriation, lichenification, eczematous changes, and discoloration.

Treatment includes topical steroids and emollients.

Pruritus is a common occurrence. 1° follicular, papular, or nodular lesions may be altered by excoriation and lichenification.

Chronic intensely itchy follicular rash affecting face, upper trunk, and extensor surfaces of the arms. Usually seen when CD4 count <200cells/μL. Sterile papular, papulo-pustular, or urticarial papules centred around hair follicles found. May be ↑ IgE with eosinophilia.

Responds best to phototherapy. Emollients for eczematous lesions. Anti-histamines not usually helpful. HAART may produce some improvement.

Diagnosis of exclusion of other causes of pruritus. No 1° lesions. Clinical features 2°to scratching—excoriation, linear lesions, lichenified eczematous changes, and post-inflammatory pigmentation.

Regular emollients, topical steroids for eczematous changes, and anti-histamines.

Yeast overgrowth producing folliculitis through production of fatty acids and scale formation blocking follicular ostea. Presents with chronic or relapsing pruritic follicular-centred papules on the scalp, flexures, upper trunk, and face.

Oral itraconazole (preferred option) 200mg daily for 7 days. If patient has AIDS, maintenance (200mg once or twice daily) or intermittent ‘pulse’ therapy should be considered. Other options are oral fluconazole and 2% ketoconazole cream. Scalp relapses are best treated with intermittent ketoconazole shampoo.

( Chapter 52, Kaposi’s sarcoma p. 567)

Incidence ↓ since the introduction of HAART. Human herpes virus-8 (HHV-8) identified in 1994 as the causative agent. Although the skin is usual site, KS may develop in visceral organs.

Typically, KS lesions appear on the nose and hard palate, but may arise anywhere on the skin. Disease usually has an insidious course with new lesions appearing as existing ones enlarge. Rapidly aggressive disease may occur but is rare. Initially starts as a painless non-pruritic pink or red macule or a papule which gradually darkens to resemble a bruise. It is surrounded by a yellow halo due to extravasated red cells (Plate 22). May be dark and difficult to recognize in black people. KS lesions vary in size from a few millimetres to several centimetres. Extensive plaques with scaling can develop on the legs and may break down, producing local pain and oedema. Lesions on the soles may be particularly troublesome as they interfere with walking. Facial and genital KS is cosmetically unsightly. With treatment, the lesion becomes flat and the colour fades, but some pigmentation persists even in the absence of residual tumour.

Non-pitting oedema is commonly associated with KS, especially affecting the lower limbs. May be due to skin lymphatic involvement or 2° to vasoactive substances produced by KS. Degree of oedema occasionally disproportionate to size of KS lesions (i.e. feature of the disease itself rather than 2° to lymph node enlargement/lymphatic obstruction).

Typical skin KS lesions are diagnosed clinically, but biopsy provides an absolute diagnosis in atypical lesions. Patients with symptoms or signs suggestive of other organ involvement should be evaluated by imaging techniques. Patients with severe oedema may require CT to exclude localized obstruction or accompanying pathology.

( Chapter 52, Kaposi’s sarcoma/Management p. 567)

Treatment for skin KS is for cosmetic reasons and to alleviate symptoms.

( Chapter 52, Non-Hodgkin’s lymphoma p. 570)

Extranodal cutaneous involvement occurs in up to 8% of those with B-cell non-Hodgkin’s lymphoma. Presents with an enlarging violaceous nodule or plaque, which may ulcerate.

Cutaneous T-cell lymphoma presents as a scaly patch or plaque with erythema, hypo- or hyperpigmentation, and atrophy. It may be mis-diagnosed as chronic eczema.

The skin may be involved when lymphoma (usually B-cell) involves an underlying lymph node.

( Chapter 52, Non-Hodgkin’s lymphoma p. 570)

The principles of management of non-Hodgkin’s lymphoma are the same as for lymphoma elsewhere and chemotherapy is usually given.

Cutaneous drug reactions ↑, as does the development of hypersensitivity reactions to previously tolerated drugs. Mild drug eruptions do not always necessitate the cessation of the causative drug, especially if it is the most effective agent and is given for a short time (e.g. co-trimoxazole for Pneumocystis jiroveci (carinii) pneumonia). Desensitization may be possible for essential drugs. Cross-sensitivities may occur, e.g. between dapsone and co-trimoxazole.

Hypersensitivity reactions are common with certain antiretroviral drugs such as nevirapine and abacavir which may cause a fatal reaction. Special attention (with counselling) to patients on these treatments is important to ensure early recognition and prompt action.