The insidious damage to the immune system by the human immunodeficiency virus results in increasing susceptibility to opportunistic viral infections. These can be localised,
widespread, confined to the skin, or systemic. They can cause mild though disfiguring lesions such as molluscum contagiosum (MCV), or lead to life-threatening infections
such as human papillomavirus (HPV-induced squamous cell carcinoma. Southern African Journal of HIV Medicine Vol. 6 (1) 2005: pp. 12-1

Dlova, N

Mosam, A

English

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MARCH 2005                                             THE SOUTHERN AFRICAN JOURNAL OF HIV MEDICINE  12CUTANEOUS MANIFESTATIONS OFHIV/AIDS: PART 2DERMATOLOGYThe insidious damage to the immune system by the humanimmunodeficiency virus results in increasing susceptibilityto opportunistic viral infections. These can be localised,widespread, confined to the skin, or systemic. They cancause mild though disfiguring lesions such as molluscumcontagiosum (MCV), or lead to life-threatening infectionssuch as human papillomavirus (HPV-induced squamouscell carcinoma.Viral opportunistic infections represent activation ofsubclinical infection (e.g. HPV, MCV) or reactivation oflatent infection, e.g. herpes simplex virus (HSV 1 and 2) orvaricella zoster virus (VZV). The incidence of opportunisticviral infections has diminished remarkably with the adventof highly active antiretroviral therapy (HAART).HERPES SIMPLEX VIRUS 1 AND 2 INFECTIONSChronic herpetic infection was recognised early as a sign ofchronic immunosuppression and as a marker for thepresence of HIV infection, particularly in young adults.There is a sharp rise in the incidence of HSV infection withCD4 counts below 50. Herpes simplex infection is socommon in our patients that we can almost assume thatmost wet-crusted lesions are herpetic until provenotherwise.  A typical presentations are the rule.  With moreadvanced HIV disease, lesions tend to be subacute orchronic and indolent and response to oral antiviral therapytends to be less prompt. The presence of mucocutaneousherpes simplex infection for more than 1 month isclassified as an AIDS- defining illness. In 65% of patientswith recurrent erythema multiforme there is a history ofherpes labialis or genitalis. This usually precedes theerythema multiforme by several days to weeks andoccasionally may coincide with the herpes lesions.With increasing immunocompromise, recurrent HSVinfection may become persistent and progressive. Thelesions are typically painful and occur at the typical sites –perioral, anogenital and digital (Fig. 1). They enlarge anddeepen into painful ulcers (Fig. 2). When diagnosis is indoubt, a tzanck smear or viral culture of blister fluid of anearly lesion (< 72 hours) is recommended; this usually takesabout 1 - 5 days. Viral culture is the easiest way to make adiagnosis and can differentiate HSV 1 from HSV 2, butlesions must be in an early stage. If lesions are atypical orhave been present for some time, other diagnosticmodalities such as biopsy or polymerase chain reaction(PCR) may be considered. Variations in clinical manifestations can occur as a result ofthe location of the lesions. Genital HSV infection canmanifest as oedema, ulcers, crusts, fissures, erythematousNcoza Dlova, MB ChB, FCDerm (SA)Anisa Mosam, MB ChB, MMed, FCDerm (SA)Department of Dermatology, Nelson R Mandela School of Medicine, University of KwaZulu-Natal, DurbanVIRAL INFECTIONSFig. 1. Herpes simplex infection in a patient with early HIV infection.Fig. 2. Herpes simplex ulcerating penile lesions.MARCH HIV ISSUE 1-16  4/16/05  9:37 AM  Page 12THE SOUTHERN AFRICAN JOURNAL OF HIV MEDICINE                                            MARCH 2005  13patches, pustules or fleeting irritations. HSV infection in theanal region may resemble a traumatic lesion, while inguinalcrease lesions can result in ‘kissing’ or adjacent lesions.Virtually all patients who have had symptomatic primarygenital disease caused by HSV 2 will experience bothsymptomatic recurrence and asymptomatic shedding.However, no matter what the viral type and how infrequentthe recurrences, asymptomatic viral shedding is a featureof HSV disease. Physicians are therefore obliged to warnpatients of these facts and to advise appropriateprophylactic measures. The lower the CD4 cell count thegreater the likelihood of shedding.HSV infection is treated with aciclovir 400 mg tid,famciclovir 125 mg bid or valaciclovir 500 mg bid for 5 - 14 days. Recurrences are common, but prophylactic therapy isdiscouraged as the condition is not life-threatening andresistant strains which are very difficult to treat maydevelop after prolonged prophylaxis. If suppressive therapyis required, aciclovir 200 - 400 mg bid for up to 1 year hasbeen advocated in cases with very frequent relapses. Early administration, preferably in the prodromal phase, iscritical and maximises the value of treatment.Cytomegalovirus can induce lesions similar to HSV and skinbiopsy may be necessary to differentiate between the twoconditions.Foscarnet and cidofovir are administered intravenously forinfections caused by aciclovir-resistant HSV. Imiquimod 5%cream has been used as topical treatment for cutaneousherpetic infections including those caused by aciclovir-resistant HSV strains.VARICELLA ZOSTER VIRUS (VZV)Herpes zoster (shingles)Varicella zoster virus causes herpes zoster or shingles.Primary VZV infection presents as chickenpox, usually inchildhood, and can then reactivate as  herpes zoster in laterlife. HIV-related zoster may be recurrent, haemorrhagic,multidermatomal, disseminated or ulcerated (Fig. 3).The head, neck and trunk are commonly affected. The initialextent and severity of the herpes zoster infection, severityof pain, and cranial (Fig. 4) and cervical dermatomalinvolvement are often associated with a poorer outcome.Disseminated herpes zoster (Fig. 5), defined as cutaneousinvolvement of more than three contiguous dermatomes,more than 20 lesions scattered outside the initialdermatome or systemic infection (hepatitis, encephalitis,pneumonitis), may also develop more commonly inimmunosuppressed patients.Latent VZV infection can present with a clinical pattern ofscattered vesicles in the absence of dermatomal herpeszoster.Treatment with oral antivirals within 72 hours (or if  lesionshave been present for more than 72 hours, in the presenceof new active lesions) is usually effective. Early treatmentaccelerates healing of skin lesions, decreases the durationof acute pain and may decrease the frequency of post-herpetic neuralgia (PHN).Fig. 3. Herpes zoster.Fig. 4. Post-herpetic scarring (PHN).Fig. 5. Disseminated zoster.MARCH HIV ISSUE 1-16  4/18/05  11:28 AM  Page 13MARCH 2005                                             THE SOUTHERN AFRICAN JOURNAL OF HIV MEDICINE  14Treatment is with aciclovir 800 mg po 5 times a day for 7days or valaciclovir 1 g 3 times a day for 7 days orfamciclovir 500 mg three times a day for seven days.  Thelesions are painful and attention should be given toadequate analgesia, e.g. paracetamol-codeine. Strongeranalgesics may be required for the acute attack but shouldbe avoided later.It is important to look out for PHN, which is a commoncomplication of HIV-related zoster and manifests as pain inthe area of the lesions once they have cleared. It should betreated with analgesics with or without amitryptilinenocturnally.VARICELLA (CHICKENPOX)In chickenpox, the rash presents as a vesicular eruption onan erythematous base which may become pustular andcrusted (Fig. 6). The rash tends to involve the face and trunkmore than the limbs. In HIV it tends to become more denseand more extensive, may ulcerate and may involve systemicorgans. Chickenpox may be confused with disseminatedHSV infection or disseminated zoster. Especially in children,it may be an extensive mucocutaneous disease withrepeated new crops of vesicles, which may necrotise andbecome haemorrhagic. If left untreated this has a highmortality in immune-suppressed individuals.  Even thoughthe diagnosis is usually made on clinical findings alone,when in doubt isolation of virus on viral culture fromvesicular skin lesions confirms the diagnosis. Cytologicalexamination of fluid or scraping from the base of a vesicleor pustule (tzanck smear) shows both giant andmultinucleated epidermal cells, but cannot differentiatefrom herpes zoster or HSV infection. The followingcomplications may occur and are seen more frequently inimmunocompromised individuals: hepatitis, pneumonitis,encephalitis, and less commonly arthritis, carditis, nephritisand orchitis.Varicella-zoster immunoglobulin may reduce the severityof chickenpox if given within 72 hours of exposure. Oralaciclovir, valaciclovir or famciclovir are effective and mayreduce the severity of the infection and recurrence.Symptomatic treatment of pruritus can be achieved withthe use of systemic antihistamines. Treatment of bacterialsecondary skin infection with the use of antibiotics may berequired. Secondary bacterial infections such asstaphylococcal pneumonia can be life threatening.Disseminated varicella in the immunocompromised host istreated with intravenous acyclovir.MOLLUSCUM CONTAGIOSUMMolluscum contagiosum is a common infection in HIV andtypically presents with umbilicated flash-coloured, dome-shaped lesions (Fig. 7). In most cases molluscumcontagiosum is self-limiting, and in adults it is most oftensexually transmitted. It is seen more frequently in thepaediatric population. In AIDS patients, molluscumcontagiosum lesions can be widespread, attain immensesize (giant molluscum) (Fig. 8) and have unusual locations.Fig. 6. Chickenpox.Fig. 7. Molluscum contagiosum. Fig. 8. Giant molluscum contagiosum.MARCH HIV ISSUE 1-16  4/17/05  10:26 AM  Page 14THE SOUTHERN AFRICAN JOURNAL OF HIV MEDICINE                                            MARCH 2005  15The extent and size of the lesions is often related to thedegree of immune compromise. In HIV-infected individualsit tends to be progressive and recurrent and veryrecalcitrant to therapy. Local treatment includes potassiumhydroxide, silver nitrate, trichloroacetic acid or liquidnitrogen. Patients may need repeated applications.Cryotherapy, electrocautery and imiquimod 5% cream maybe tried though the latter is expensive. There is oftencomplete resolution of lesions in those patients whorecieve HAART. Diagnosis can be confirmed by biopsy, andif there is reason to suspect another diagnosis, thespecimen can be sent for fungal culture and histology. Inmore severely immune suppressed individuals, thedifferential diagnosis includes cryptococcosis andhistoplasmosis. Systemic illness associated with variablemorphology of lesions should alert the clinician. CYTOMEGALOVIRUSAlthough ulcers can occur anywhere, lesions are commonly seen as perianal ulceration (Fig. 9) and may be mistaken forgenital herpes ulceration. The most common sites ofinfection are adrenal gland (75%), lungs (58%),gastrointestinal tract (30%), and central nervous system(20%). Biopsy of the skin lesion for histology and culturewill help to differentiate it from HSV.  HUMAN PAPILLOMAVIRUS INFECTIONSVerruca vulgarisHuman papillomaviruses commonly produce skin lesionsduring the course of HIV disease. In contrast to otheropportunistic viral infections, the incidence of HPVFig. 9. Cytomegalovirus.Fig. 12. Verruca planar (epidermodysplasia verruciformis-likelesions, shins).Fig. 11. Verruca planar (epidermodysplasia verruciformis-likelesions, face).Fig. 10. Verruca vulgaris.MARCH HIV ISSUE 1-16  4/16/05  9:38 AM  Page 15MARCH 2005                                             THE SOUTHERN AFRICAN JOURNAL OF HIV MEDICINE  16infections may actually increase despite patients being onHAART. A variety of skin lesions may be seen, ranging fromverruca vulgaris (Fig. 10), which can enlarge and becomeconfluent, to an unusual pattern of extensive verruca planaand pityriasis versicolor-like warts which may resembleepidermodysplasia verruciformis (Figs 11 and 12). Theselesions tend to be unresponsive to therapy. Treatmentmodalities include use of cryotherapy, electrocautery,surgical excision and use of imiquimod.Genital wartsHPV 6 and 11 tend to infect mucosal areas causingcondylomata acuminata, which can be  large (Figs 13 and14). In the immune-compromised individual condylomasare more common, more extensive and resistant totreatment. They are often associated with vulvarintraepithelial neoplasia and squamous carcinoma, andcervical and anal intraepithelial neoplasia. Diagnosis isusually made by recognition but biopsies should beperformed if lesions look atypical, or if the warts areresistant to conventional treatment or becomehyperpigmented, indurated, fixed or ulcerated. Applypodophyllin 25% to anogenital warts weekly (not inpregnancy). Wash off after 4 hours to prevent irritation.Alternatively apply 80% trichloroacetic acid in waterweekly. Cautery, liquid nitrogen or laser therapy may berequired but recurrences do occur. Fig. 14. Condyloma acuminatum.Part 1 of the article 'Cutaneous manifestations ofHIV/AIDS', which appeared on pp. 12 - 17 of theNovember 2004 issue of the Southern African Journal ofHIV Medicine, contained a sentence that could bemisleading. On p. 15 (left-hand column) the dosage ofamphotericin B for treating the acute stage ofhistoplasmosis is given as 15 mg/kg. The dosage is in fact0.7 mg/kg/d. In response to a reader query, the authors have alsoclarified the dosage of fluconazole. On p. 13 (right-handcolumn) it was stated that when oesophageal candidiasisis suspected, fluconazole 100 mg/d should be given for 5days. The treatment for oral candidiasis that is notresponsive to topical treatments is 100 mg fluconazoleonce per day. If oesophageal candidiasis is suspected(dysphagia with oral candida) the dosage is 200 mgfluconazole daily for 2 - 3 weeks.ERRATUMFig. 13. Condyloma acuminatum.MARCH HIV ISSUE 1-16  4/17/05  10:27 AM  Page 16

Cutaneous manifestation of HIV/AIDS: Part 2

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Cutaneous manifestation of HIV/AIDS: Part 2

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