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DR11.1-2 | HIV Dermatology — Practice Quiz
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A 28-year-old HIV-positive man presents with thick, white, non-removable plaques on the lateral borders of his tongue. He is not on antifungals. Smear shows no pseudohyphae. The MOST likely diagnosis is:
Correct. Oral hairy leukoplakia (OHL) is EBV-driven, appears on the lateral tongue, cannot be wiped off (unlike thrush), and KOH/smear is negative for candida. It is a marker of advancing HIV disease.
Oral hairy leukoplakia is caused by EBV (Epstein-Barr virus), appears on lateral tongue as corrugated white plaques that cannot be removed, and does not respond to antifungals. It signals significant immunosuppression (CD4 typically <300 cells/μL).
The lateral tongue location, inability to scrape off the lesion, and negative smear for pseudohyphae point away from candidiasis or lichen planus. Oral hairy leukoplakia caused by EBV is the correct answer.
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A 34-year-old woman with known HIV and a CD4 count of 80 cells/μL develops vascular, friable papules on her forearm. Biopsy shows lobular capillary proliferation with plump endothelial cells and neutrophilic infiltrate. The causative organism is:
Correct. Bacillary angiomatosis is caused by Bartonella species (henselae/quintana). The lobular proliferation with neutrophilic infiltrate and bacterial clumps on Warthin-Starry stain distinguishes it from Kaposi sarcoma.
Bacillary angiomatosis is caused by Bartonella henselae or B. quintana, occurs at CD4 <100 cells/μL, and mimics Kaposi sarcoma clinically. Histology shows lobular capillary proliferation with neutrophilic infiltrate and clumps of bacteria. HHV-8 causes Kaposi sarcoma, not bacillary angiomatosis.
Although this lesion resembles Kaposi sarcoma, the histology with neutrophilic infiltrate and lobular capillary proliferation indicates bacillary angiomatosis caused by Bartonella, not HHV-8 (Kaposi).
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A newly diagnosed HIV patient has CD4 count 380 cells/μL. He presents with greasy, erythematous scaling over the nasolabial folds, eyebrows and scalp. The MOST appropriate first-line topical treatment is:
Correct. Seborrhoeic dermatitis in HIV is driven by Malassezia; antifungal-steroid combinations are first-line for facial/scalp involvement.
Seborrhoeic dermatitis is the most common inflammatory dermatosis in HIV, can occur even at relatively preserved CD4 counts (often CD4 200–500), and is driven by Malassezia overgrowth. First-line treatment combines an antifungal (ketoconazole shampoo/cream) with a low-potency topical corticosteroid.
Seborrhoeic dermatitis has a fungal (Malassezia) component; an antifungal is essential. Topical steroid alone addresses inflammation but not the fungal driver.
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A patient with HIV on antiretroviral therapy develops intensely itchy, symmetrically distributed follicular papules on the trunk and proximal limbs. CD4 is 210 cells/μL. Histology shows eosinophilic infiltrate around hair follicles. Diagnosis is:
Correct. HIV-associated eosinophilic folliculitis is characterised by pruritic follicular papules and histological eosinophilic infiltration around follicles, typically at CD4 100–300 cells/μL.
HIV-associated eosinophilic folliculitis presents as pruritic follicular papules with peripheral blood and tissue eosinophilia, typically at CD4 100–300 cells/μL. Pruritic papular eruption (PPE) also occurs in HIV but shows non-specific chronic inflammation without the eosinophilic follicular infiltrate on histology.
The eosinophilic follicular infiltrate on histology specifically points to eosinophilic folliculitis, not PPE (non-specific infiltrate) or scabies (mites/eggs in stratum corneum).
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A patient with advanced HIV (CD4 40 cells/μL) has purple-brown plaques on the lower limb, hard palate and trunk. Biopsy shows spindle cell proliferation with slit-like vascular spaces. The causative virus is:
Correct. Kaposi sarcoma is caused by HHV-8. The clinical features (purple-brown lesions, palate, CD4 <100) and histology (spindle cells, slit-like vascularity) are classic.
Kaposi sarcoma in HIV is caused by HHV-8 (KSHV — Kaposi sarcoma herpesvirus). It presents as purple-brown patches/plaques/nodules, involves skin and viscera, and classically at CD4 <200 cells/μL. Histology: spindle cells + slit-like vascular channels. ART is the cornerstone; chemotherapy for advanced visceral disease.
EBV causes OHL and lymphomas; Bartonella causes bacillary angiomatosis (neutrophilic infiltrate, not spindle cells). KS = HHV-8.
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A patient started on nevirapine-based ART develops a maculopapular rash covering 15% BSA on day 12, without mucosal involvement, blistering, fever, or hepatic symptoms. The BEST initial management is:
Correct. A mild morbilliform rash without red flags can be watched on nevirapine with antihistamines. Premature discontinuation risks ART resistance. Monitor for escalation to SJS/TEN or DRESS.
A mild, isolated morbilliform rash from nevirapine (no mucosal involvement, no blistering, no systemic features) can be managed conservatively — continue nevirapine, antihistamines, and close monitoring. The critical decision point is the presence of red flags: mucosal involvement, blistering, skin tenderness, fever, hepatitis, or eosinophilia → stop immediately.
Immediate drug stoppage is appropriate only for SEVERE reactions (mucosal involvement, blistering, hepatitis, DRESS). A mild morbilliform rash without red flags warrants watchful continuation with antihistamines.
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A patient being initiated on abacavir as part of ART develops fever, rash, gastrointestinal symptoms and malaise on day 9. He is from South Asia. Before initiating abacavir, which test should ideally have been performed?
Correct. HLA-B*57:01 screening is recommended before abacavir to prevent the potentially life-threatening abacavir hypersensitivity reaction. Abacavir must NEVER be rechallenged after HSR.
Abacavir hypersensitivity reaction (HSR) is strongly associated with the HLA-B*57:01 allele. Routine HLA-B*57:01 screening before abacavir initiation virtually eliminates immunologically confirmed HSR. HLA-B*15:02 is associated with carbamazepine/phenytoin-induced SJS in South-East Asian populations, not abacavir.
HLA-B*15:02 predicts carbamazepine/phenytoin-SJS in South-East Asians — not relevant to abacavir. The abacavir HSR marker is HLA-B*57:01.
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A patient on zidovudine for 18 months develops longitudinal darkening of the nails and hyperpigmentation over the knuckles and oral mucosa. CD4 is 350 cells/μL. HIV viral load is undetectable. The MOST likely cause of the pigmentation is:
Correct. Zidovudine-induced pigmentation is a well-recognised side effect causing longitudinal melanonychia and mucocutaneous hyperpigmentation; management is reassurance (cosmetic, not pathological).
Zidovudine (AZT) commonly causes nail hyperpigmentation (longitudinal melanonychia), and mucocutaneous hyperpigmentation of knuckles, tongue, and oral mucosa — typically appearing months after initiation. With undetectable viral load and stable CD4, ART-related pigmentation is the most parsimonious explanation.
Kaposi sarcoma would not cause diffuse longitudinal nail darkening and mucosal hyperpigmentation uniformly. Addison's disease is possible in HIV but less likely with undetectable viral load. The AZT-pigmentation pattern is the first explanation to consider.
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A patient with HIV develops new skin lesions appearing on previous KS sites 3 weeks after starting ART. CD4 has risen from 45 to 160 cells/μL. Viral load has dropped. The MOST likely explanation for the worsening lesions is:
Correct. Paradoxical IRIS on KS: rising CD4, suppressed viral load, yet worsening Kaposi lesions — the reconstituted immune system is reacting to HHV-8/KS antigens. Continue ART; add corticosteroids for life-threatening IRIS.
IRIS occurs in the weeks to months after ART initiation as the recovering immune system mounts an inflammatory response to pre-existing opportunistic pathogens or tumours. Paradoxical KS worsening is a well-documented IRIS manifestation. CD4 rise + VL suppression despite worsening lesions is the diagnostic clue. Management: continue ART; consider corticosteroids in severe IRIS.
ART failure would show rising viral load and falling CD4 — the opposite of what is seen here. This is classic IRIS: immune recovery unmasking or paradoxically worsening an existing condition.
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A patient on nevirapine develops widespread blistering involving 35% BSA with mucosal erosions and skin pain on day 18 of therapy. The CORRECT immediate management is:
Correct. 35% BSA detachment = TEN. Nevirapine must be stopped immediately and permanently. Switch ART (protease inhibitor or integrase inhibitor-based). Burns-unit supportive care is essential.
BSA detachment >30% = TEN (toxic epidermal necrolysis) — a dermatological emergency with mortality 30–50%. Blistering >10% with mucosal involvement = at minimum SJS-TEN overlap. Nevirapine is a major culprit. Immediate steps: stop the offending drug permanently (never rechallenge), switch to a non-NNRTI ART regimen, admit to burns unit or ICU, supportive care (IV fluids, wound care, nutritional support, ophthalmology). Systemic steroids are controversial; IVIG may be used.
Dose reduction is never an option for SJS/TEN. Stopping all ART is also wrong — HIV must be controlled. Stop the offending NNRTI and switch to a safer regimen while providing burns-level supportive care.
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