HIV Infection and the skin

Introduction The Human Immunodeficiency Virus is a retrovirus. Retroviruses are made up of RNA. The HIV virus replicates by using the enzyme reverse transcriptase in order to encode for DNA and the subsequent DNA is then integrated into the host genome.  The main routes of transmission are sexual transmission, sharing of infected needles during intravenous drug abuse, and a smaller group of patients have been infected by blood products for their haemophilia. Vertical transmission can occur during pregnancy and by breast-feeding.  

 

Presentation of sero-conversion

There may be no signs or symptoms of initial infection, and patients may remain without symptoms for several years with no evidence of immunosuppression. Some patients may experience an acute febrile illness which resembles glandular fever and it presents with a macular/papular generalised eruption, fever, sweating, lethargy, arthralgia, myalgia, sore throat, and a lymphadenopathy. Such symptoms are said to be due to an acute sero conversion of the HIV virus. The rash associated with such an illness is maculo-papular, erythematous and primarily truncal.    

 

HIV and the skin More than 90% of HIV infected patients will be afflicted with skin and mucus membrane conditions. Superficial fungal infections are amongst the most common infections in HIV disease. Indeed fungal infections may present unusually in such patients, thereby leading to a suspicion of HIV disease, e.g. oral candidiasis, seborrhoeic dermatitis, and infection with cryptococcus neoformans. Seborrhoeic dermatitis is the most common dermatosis associated with HIV disease. As in non immunocompromised patients it effects the naso labial folds, the eyebrows, and the beard area and the scalp. It is much more severe in the HIV infected patient, and mycology reveals a fungus called malassezia furfur. Fungal nail infections are also more common particularly proximal white onychomycosis.

  

In general the first rash to appear is seborrhoeic dermatitis, followed by herpes zoster and then oral hairy leucoplakia. If the patient survives, he or she may go on to develop muco-cutaneous candidiasis followed by molluscum contagiosum, which may appear at the same time as a pruritus associated with HIV disease. Ulcerating herpes simplex and Kaposi’s sarcoma appear at a relatively late stage in HIV infection and are associated with greater immunosuppression.  

 

The common viral infections are molluscum contagiosum, herpes zoster, herpes simplex, and Kaposi’s sarcoma, which has been found to be caused by herpes simplex virus type 8. Bacillary angiomatosis is a tumour caused by a rickettsia like organism called Bartonella Henselae. It may mimic Kaposi's sarcoma. It responds rapidly to treatment with erythromycin or tetracyclines and therefore is important to diagnose as Kaposi’s sarcoma would not respond to such therapy. Although psoriasis is not more frequently found in patients with HIV disease it is often more severe and joint involvement is more commonly found. It may be a presenting feature of HIV.

 
Anti-retroviral therapy has changed the face of HIV. What was once an invariably fatal disease, associated with a markedly shortened life expectancy, has changed, at least in developed countries, into a chronic condition. Hence many of the cutaneous diseases that were frequently seen in the early days of HIV are now no longer apparent. Kaposi's sarcoma remains relatively uncommon but one should be aware of this diagnosis, as it is still occasionally a presenting feature of undiagnosed HIV infection.  

 

Kaposi’s sarcoma

There are four forms of Kaposi’s sarcoma.

  1. Classic form

  2. Endemic Kaposi’s sarcoma

  3. Immunosuppression related Kaposi’s sarcoma

  4. Aids related Kaposi’s sarcoma

Kaposi’s sarcoma – red-purple nodules on the lower legs

 

  • Classic Kaposi’s sarcoma - seen mainly on the legs of elderly Ashkenazi Jews, Eastern Europeans, or elderly men of Mediterranean extraction. The course of the disease is indolent, with patients dying of unrelated causes. Interestingly, secondary malignancies particularly lymphomas develop in more than one third of cases.

  • African endemic Kaposi’s sarcoma - occurs in two age groups: (i) Young adults with generally benign cutaneous nodular disease, but this type can turn aggressive and become fatal within 5 to 8 years;  (ii) Young children who present with fulminant lymphadenopathy, and this is fatal within 2 to 3 years.

  • Iatrogenic immunosuppressive Kaposi’s sarcoma - seen among organ transplant recipients. This Kaposi’s sarcoma may remit after discontinuation of immunosuppressive therapy.

  • Aids-related Kaposi’s sarcoma - This is the commonest form of Kaposi’s sarcoma seen in Britain. It is thought that this form of Kaposi’s sarcoma is actually sexually transmitted by the human herpes virus type 8 (HHV8). This virus may be found in Kaposi’s sarcoma lesions, blood, semen, bronchial washings, and saliva of HIV positive men. Aids related KS is usually multi focal, and may progress rapidly. The lesion begins as a patch stage which is a small flat dusky red or violet area of skin discolouration. This progresses over weeks and months to raised painless firm nodules and plaques. The commonest involved cutaneous sites are the legs, trunk, arms, face, hard palate, tip of the nose, and penis. Mucocutaneous involvement is a strong predictor of visceral involvement which should prompt an urgent investigation of such involvement, as the untreated medium survival with pulmonary involvement is six months. Indications for treatment include cosmetic control of disfiguring lesions, associated symptoms such as pain and oedema, and problematic oral lesions. Options used include, cryotherapy, intralesional therapy with Bleomycin, Vimblastin or Vincristine, radiation therapy, laser and surgical excision if there are relatively few lesions. Systemic treatments include chemotherapy. Some lesions will resolve with anti-retroviral therapy alone once the patient's immunity improves.