15.3 HIV-Related Dermatoses, Partner Notification & Anogenital Lichen Sclerosus
Key Takeaways
- Cutaneous manifestations track CD4 T-cell decline in HIV: acute seroconversion presents with morbilliform rash and aphthoid ulcers; moderate decline (CD4 200-500) features florid seborrhoeic dermatitis, multidermatomal zoster, and non-scrapable oral hairy leukoplakia (EBV); severe decline (CD4 <200) triggers Kaposi sarcoma, bacillary angiomatosis, and crusted scabies.
- Bacillary angiomatosis (Bartonella henselae/quintana) mimics Kaposi sarcoma clinically but is distinguished histopathologically by lobular vascular proliferation with neutrophils, leukocytoclasia, and positive Warthin-Starry silver staining; it responds rapidly to oral erythromycin or doxycycline.
- Immune Reconstitution Inflammatory Syndrome (IRIS) represents paradoxical exacerbation of opportunistic infections following cART initiation; combination antiretroviral therapy must be maintained while administering pathogen-targeted antimicrobial and anti-inflammatory therapy.
- Partner notification lookback windows are pathogen-specific: primary syphilis 3 months, secondary or early latent syphilis up to 2 years (IUSTI), gonorrhoea 3 months, and chlamydia 6 months; epidemiological treatment of recent contacts should be considered.
- Anogenital Lichen Sclerosus causes porcelain-white, cigarette-paper atrophic plaques in a figure-of-eight distribution sparing the vaginal mucosa, posing a 4-5% risk of squamous cell carcinoma; first-line therapy is ultra-potent topical corticosteroids (clobetasol propionate 0.05% ointment). In contrast, erosive Lichen Planus characteristically involves the internal vaginal mucosa.
Last updated: September 2026
15.3 HIV-Related Dermatoses, Partner Notification & Anogenital Lichen Sclerosus
Cutaneous Markers and Stage-Defining Dermatoses in HIV Infection
Cutaneous manifestations occur in over 90% of individuals living with human immunodeficiency virus (HIV) across the trajectory of infection. The morphology, clinical severity, and atypicality of skin disorders correlate inversely with the peripheral blood CD4+ T-lymphocyte count, serving as vital sentinel markers of immune depletion.
1. Acute HIV Seroconversion Syndrome (Primary HIV Infection)
Develops 2 to 6 weeks after initial viral inoculation, coinciding with peak viremia and a precipitous transient drop in CD4+ T-cell count:
- Systemic Syndrome: Resembles infectious mononucleosis, presenting with high fever, lethargy, pharyngitis, generalized non-tender lymphadenopathy, arthralgias, and myalgias.
- Cutaneous Exanthem: Symmetrical, non-pruritic, erythematous maculopapular (morbilliform) eruption distributed predominantly over the upper trunk, neck, and face, with occasional palmoplantar involvement. Lesions resolve spontaneously within 1 to 2 weeks.
- Mucosal Ulcerations: Hallmark feature consisting of painful, well-demarcated, shallow aphthoid ulcerations on the oral mucosa, pharynx, esophagus, or anogenital region.
- Diagnostic Confirmation: Standard 4th-generation antibody/antigen combo assays may be indeterminate or antibody-negative during the initial "window period"; diagnosis is confirmed by plasma HIV-1 RNA viral load testing and reactive p24 antigen.
2. Early to Moderate Immune Suppression (CD4 200–500 cells/µL)
- Severe Seborrhoeic Dermatitis: Highly characteristic marker. Unlike classic seborrhoeic dermatitis, in HIV it presents as extensive, refractory, intensely erythematous, inflammatory plaques with greasy yellowish scales, expanding beyond typical seborrhoeic zones to involve the malar face, eyebrows, beard, neck, chest, and intertriginous vaults. The severity mirrors rising Malassezia yeast density and worsening immunosuppression.
- Oral Hairy Leukoplakia (OHL): Driven by opportunistic Epstein-Barr Virus (EBV) lytic replication in tongue squamous epithelium. Presents as asymptomatic, white, corrugated, vertically folded, non-removable plaques along the lateral borders of the tongue. Crucial exam discriminator: Oral hairy leukoplakia CANNOT be scraped off with a tongue depressor or gauze, in sharp contrast to oral pseudomembranous candidiasis (thrush), which scrapes off readily leaving an erythematous bleeding surface.
- Pruritic Papular Eruption (PPE) of HIV / Eosinophilic Folliculitis: Intensely pruritic, chronic, dome-shaped, follicular and non-follicular erythematous papules distributed symmetrically across the trunk and extremities. Characterized histologically by marked perifollicular eosinophilic infiltration and clinically by intractable excoriations and post-inflammatory hyperpigmentation. Improves markedly with combination antiretroviral therapy (cART) and narrowband UVB phototherapy.
- Herpes Zoster (Shingles): Severe, multidermatomal, recurrent, or necrotic varicella-zoster virus reactivation in a young adult is an absolute clinical indication for diagnostic HIV screening.
- Proximal Subungual Onychomycosis (PSO): Rapid invasion of the nail bed from beneath the proximal nail fold caused by Trichophyton rubrum; recognized clinical indicator of HIV-induced cellular immunodeficiency.
3. Severe Immune Suppression (CD4 < 200 cells/µL / AIDS-Defining)
- Kaposi Sarcoma (KS): Low-grade vascular neoplasm driven by Human Herpesvirus 8 (HHV-8 / KSHV). Most common HIV-associated malignancy. Manifests as violaceous, reddish-brown, or purplish macules and patches that progress to indurated plaques and compressible nodules, characteristically oriented along skin cleavage lines (Langer's lines). Prominently affects the tip of the nose, ears, trunk, lower extremities, and oral cavity (especially the hard palate and gingiva). Histopathology shows proliferation of spindle cells forming slit-like vascular channels containing extravasated erythrocytes, hemosiderin pigment, and hyaline globules; immunohistochemistry is positive for HHV-8 LANA-1 and endothelial markers (CD31, CD34, ERG, podoplanin/D2-40). First-line therapy is cART; systemic liposomal doxorubicin is indicated for visceral involvement.
- Bacillary Angiomatosis (BA): Infectious vascular proliferative pseudoneoplasm caused by fastidious Gram-negative bacilli: Bartonella henselae (reservoir: domestic cat / cat flea) and Bartonella quintana (reservoir: human body louse). Clinically mimics Kaposi sarcoma or pyogenic granulomas, presenting with multiple red, violaceous, vascular, compressible, pedunculated or dome-shaped subcutaneous nodules and papules that bleed easily upon contact. May disseminate to bone, liver, and spleen (peliosis hepatis). Distinguishing Histology: Lobular vascular proliferation lined by plump, protuberant ("epithelioid") endothelial cells with a dense neutrophilic infiltrate, nuclear dust (leukocytoclasia), and granular amphophilic clumps of bacteria highlighted by Warthin-Starry silver stain. First-line therapy: Oral Erythromycin 500 mg four times daily or Doxycycline 100 mg twice daily for 3 months (rapidly curative).
- Crusted (Norwegian) Scabies: Caused by massive uncontrolled hyperinfestation with millions of Sarcoptes scabiei var. hominis mites. Presents as thick, adherent, hyperkeratotic, fissured, yellow-gray crusts and psoriasiform plaques over the hands, feet, scalp, and subungual spaces. Pruritus is characteristically minimal or absent due to defective cell-mediated immunity. Highly contagious. Treatment requires multiple oral ivermectin doses (200 µg/kg on days 1, 2, 8, 9, and 15) combined with daily topical 5% permethrin.
- Disseminated Cryptococcosis & Histoplasmosis: Cutaneous lesions present as umbilicated papules mimicking molluscum contagiosum across the face and neck.
4. Immune Reconstitution Inflammatory Syndrome (IRIS)
IRIS is an exaggerated, dysregulated inflammatory reaction occurring within weeks to months after starting or optimizing combination antiretroviral therapy (cART), driven by rapid recovery of pathogen-specific CD4+ T-cell immunity:
- Forms of IRIS: Paradoxical IRIS (worsening of a previously diagnosed and treated infection) and Unmasking IRIS (hyperinflammatory manifestation of a previously occult, undiagnosed opportunistic infection).
- Common Triggers: Mycobacterium tuberculosis, Mycobacterium avium complex, Cryptococcus neoformans, Varicella-Zoster Virus, HSV, and HHV-8 (Kaposi sarcoma flare).
- Clinical Management: Do NOT discontinue cART (cessation allows viral rebound and renewed immune destruction). Provide targeted antimicrobial therapy against the underlying opportunistic pathogen. For moderate to severe disabling inflammatory flares, initiate anti-inflammatory therapy with NSAIDs or systemic corticosteroids (prednisone 0.5–1.0 mg/kg/day with gradual taper).
Master Comparative Breakdown: Kaposi Sarcoma vs. Bacillary Angiomatosis
| Feature | Kaposi Sarcoma (KS) | Bacillary Angiomatosis (BA) |
|---|---|---|
| Etiological Agent | Human Herpesvirus 8 (HHV-8 / KSHV) | Bartonella henselae or Bartonella quintana |
| Clinical Morphology | Violaceous, red-brown patches, plaques, and firm nodules aligned along Langer's lines; hard palate commonly involved | Red, purple, vascular, dome-shaped or pedunculated pyogenic granuloma-like papules/nodules; bleed easily |
| Inflammatory Cellular Infiltrate | Mononuclear infiltrate (lymphocytes, plasma cells, macrophages) | Dense neutrophilic infiltrate with prominent nuclear dust (leukocytoclasia) |
| Vascular Architecture | Dermal proliferation of spindle cells forming jagged, slit-like vascular spaces with extravasated erythrocytes | Lobular proliferation of well-formed capillary vessels lined by plump, protuberant epithelioid endothelial cells |
| Special Stains / Biomarkers | HHV-8 LANA-1 positive (nuclear staining); CD31, CD34, D2-40 positive | Warthin-Starry silver stain positive (reveals clumps of dark extracellular bacteria) |
| First-Line Medical Therapy | Combination antiretroviral therapy (cART); systemic liposomal doxorubicin for visceral disease | Oral Erythromycin 500 mg qid or Doxycycline 100 mg bid for 3 months (curative) |
Partner Notification and STI Contact Tracing Principles
Partner notification (contact tracing) represents an essential public health intervention aimed at breaking the chain of STI transmission, preventing reinfection of the index case, preventing irreversible reproductive sequelae (PID, infertility, ectopic pregnancy), and curbing vertical congenital transmission.
1. Notification Strategies
- Patient Referral: The index patient assumes responsibility for informing sexual partners and encouraging them to attend clinical services. (Supported by clinic-provided notification slips or secure anonymous electronic messaging tools).
- Provider Referral: The healthcare provider or dedicated venereology contact tracer confidentially contacts named sexual partners directly, without ever disclosing the index patient's identity.
- Contract / Conditional Referral: A hybrid agreement where the index patient is given a designated timeframe (e.g., 48–72 hours) to notify partners, after which the healthcare provider steps in to notify untraced partners.
2. European Contact Tracing Lookback Windows
The windows below follow the 2020 IUSTI syphilis and gonorrhoea guidelines and European/UK partner-notification practice. National services may use slightly different periods.
| STI Diagnosis | Lookback Window for Sexual Contacts | Clinical Management of Traced Contacts |
|---|---|---|
| Primary Syphilis | 3 months (incubation period up to 90 days) | Full STI screen at first visit, 6 weeks, and 3–6 months; consider immediate epidemiological treatment with benzathine penicillin G 2.4 MU IM (especially pregnant partners or those unlikely to return) |
| Secondary Syphilis | Commonly 6 months plus symptom duration; extended up to 2 years if there has been clinical relapse (IUSTI) | As above |
| Early Latent Syphilis | Up to 2 years (IUSTI) | As above |
| Late Latent / Unknown Syphilis | Long-term sexual partners, spouses, and children (to exclude vertical congenital transmission) | Full serological screening; treat if seropositive according to clinical stage |
| Neisseria gonorrhoeae | 3 months before symptom onset or diagnosis (IUSTI); UK practice uses 2 weeks for men with symptomatic urethritis | Test for gonorrhoea and other STIs; treat if positive, or treat epidemiologically if the contact may not return |
| Chlamydia trachomatis | 6 months before diagnosis (or the last partner if longer ago); UK practice uses 4 weeks for men with symptomatic urethritis | Test for chlamydia and other STIs; epidemiological treatment with doxycycline 100 mg twice daily for 7 days is commonly offered |
The 60- or 90-day windows found in some sources are US (CDC) conventions.
3. Epidemiological (Presumptive) Treatment
Epidemiological treatment means treating a contact on the day of assessment, before test results are available. IUSTI advises that it should be considered for contacts of early syphilis (especially pregnant partners) unless they can attend reliably for repeat serology, and for gonorrhoea contacts who may not return. It covers the window period, when tests can still be negative, and interrupts onward transmission.
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Anogenital Lichen Sclerosus and Lichen Planus
Inflammatory anogenital dermatoses represent a high-stakes domain in European dermatovenereology, carrying significant risks of scarring, architectural destruction, sexual dysfunction, and malignant transformation.
1. Anogenital Lichen Sclerosus (LS)
Anogenital Lichen Sclerosus is a chronic, progressive, lymphocyte-mediated inflammatory dermatosis with a strong autoimmune underpinning (frequent association with autoimmune thyroiditis, vitiligo, and circulating autoantibodies to extracellular matrix protein 1 [ECM1]):
- Epidemiology: Predominantly affects females (female-to-male ratio ~6:1). Displays a bimodal peak in prepubertal girls and postmenopausal women. In males, it affects uncircumcised boys and adult men (Balanitis Xerotica Obliterans - BXO).
- Female Clinical Morphology: Characterized by glistening, ivory-white or porcelain-white atrophic papules coalescing into sclerotic plaques with a "cigarette-paper" or parchment-like crinkled surface. Lesions classically distribute in a symmetrical "figure-of-eight" or hourglass pattern encircling both the vulva and the perianal region. Accompanying features include follicular plugging ("delling"), purpura/ecchymoses (due to fragile dermal capillary ectasia), and painful fissuring in the interlabial and posterior fourchette folds.
- Architectural Destruction: Progressive disease causes resorption and effacement of the labia minora, encasement and burial of the clitoris (clitoral phimosis), and introital stenosis causing intractable dyspareunia.
- Absolute Diagnostic Discriminator: Lichen sclerosus strictly spares the non-keratinized internal vaginal mucosa! Any inflammatory involvement of the vaginal canal definitively rules out lichen sclerosus and indicates Lichen Planus, pemphigoid, or infection.
- Male Clinical Morphology (BXO): Involves the glans penis, prepuce, and urethral meatus as sclerotic, porcelain-white plaques. Complications include secondary non-retractile phimosis, recurrent balanitis, meatal stenosis with obstructive voiding, and painful erections.
- Histopathology:
- Hyperkeratosis with prominent follicular plugging.
- Atrophy of the stratum spinosum with hydropic/vacuolar degeneration of the basal cell layer.
- Broad, pale, edematous zone of homogenized collagen sclerosis / hyalinization in the upper papillary dermis, entirely devoid of elastic fibers.
- Band-like (lichenoid) lymphocytic infiltrate pushed deep beneath the sclerotic zone.
- Malignancy Risk: Untreated or chronically active lichen sclerosus confers a 4% to 5% lifetime risk of developing invasive squamous cell carcinoma (cSCC) of the vulva or penis. Malignancy develops through an HPV-negative pathway driven by TP53 mutations arising from differentiated vulvar intraepithelial neoplasia (dVIN). Regular long-term specialist surveillance is mandatory.
- European First-Line Treatment:
- Topical Corticosteroid Regimen: Ultra-potent topical corticosteroid (Clobetasol propionate 0.05% ointment) applied on a tapering schedule: once daily at night for 1 month, alternate nights for 1 month, twice weekly for 1 month, followed by long-term intermittent maintenance. Ointment base is mandatory (creams sting and contain sensitizing preservatives).
- Second-Line: Topical calcineurin inhibitors (tacrolimus 0.1% ointment).
- Male BXO: Early therapeutic circumcision is curative in up to 90% to 95% of cases confined to the foreskin.
2. Anogenital Lichen Planus (LP)
Lichen planus is a T-cell-mediated autoimmune disorder targeting basal keratinocytes:
- Erosive Vulvovaginal Lichen Planus: The most severe and destructive anogenital variant. Manifests as painful, fiery-red, denuded erythematous erosions of the vulva bordered by fine, delicate, reticulated, lacy white striae (Wickham striae).
- Vaginal Involvement: Unlike lichen sclerosus, erosive lichen planus characteristically involves the internal non-keratinized vaginal mucosa, causing desquamative vaginitis with copious seropurulent yellow discharge, deep vaginal denudation, and progressive fibrotic synechiae formation leading to complete obliteration of the vaginal canal.
- Vulvovaginal-Gingival Syndrome: Classic severe clinical triad characterized by erosive vulvovaginal lesions accompanied by painful desquamative gingivitis and oral mucosal Wickham striae on the buccal mucosa and tongue.
- Histopathology: Hyperkeratosis, wedge-shaped hypergranulosis, irregular "saw-tooth" acanthosis, liquefaction degeneration of the basal layer, apoptotic basal keratinocytes (Civatte / colloid bodies), and a dense, band-like, lymphocytic infiltrate hugging the dermo-epidermal junction.
- Management: Ultra-potent topical corticosteroids (clobetasol ointment for vulva; hydrocortisone acetate suppositories or budesonide foam for intravaginal erosions); systemic corticosteroids or immunosuppressive agents (methotrexate, mycophenolate mofetil) for severe, scarring, or recalcitrant disease.
Master Differential Table of Inflammatory and Premalignant Vulvar Dermatoses
| Disease Entity | Key Clinical Morphology | Vaginal Canal Involvement | Extragenital Features | Key Histopathological Features | Malignancy Risk | First-Line European Therapy |
|---|---|---|---|---|---|---|
| Anogenital Lichen Sclerosus | Porcelain-white sclerotic plaques; cigarette-paper atrophy; figure-of-eight distribution; resorption of labia | Strictly spared (never involves non-keratinized vagina) | Extragenital white atrophic macules on neck/trunk in 10–15% | Epidermal atrophy; basal vacuolation; broad zone of upper dermal collagen hyalinization | 4–5% lifetime risk of cSCC (via HPV-independent dVIN pathway) | Ultra-potent topical corticosteroid (Clobetasol propionate 0.05% ointment) |
| Erosive Lichen Planus | Fiery-red denuded erosions with delicate peripheral lacy Wickham striae; labial agglutination | Frequently involved (desquamative vaginitis, synechiae, canal stenosis) | Oral desquamative gingivitis; classic cutaneous polygonal violaceous papules | Saw-tooth acanthosis; band-like lymphocytic infiltrate hugging DEJ; Civatte bodies | Low risk (~1–2%) of mucosal cSCC | Ultra-potent topical steroids (vulva) + intravaginal corticosteroid foam/suppositories |
| Lichen Simplex Chronicus | Leathery, hyperkeratotic, lichenified plaques with exaggerated skin markings; severe intractable pruritus | Strictly spared | Concomitant atopic dermatitis, flexural eczema, or neurodermatitis | Marked hyperkeratosis; massive regular acanthosis; elongation of rete ridges; dermal fibrosis | No intrinsic malignant potential | High-potency topical steroids; sedating antihistamines; eliminate itch-scratch cycle |
| Differentiated VIN (dVIN) | Unifocal white, pink, or red roughened plaque or nodule; usually superimposed on background of chronic LS | Strictly spared | None | Atypical enlarged basal keratinocytes with abundant eosinophilic cytoplasm; TP53 mutated | High and rapid progression to invasive cSCC | Complete surgical excision with clear pathological margins |
| Usual VIN (uVIN / HSIL) | Multifocal, pigmented, warty, or verrucous papules/plaques; younger women | Can involve vagina (VaIN) and cervix (CIN) | Perianal and anal intraepithelial neoplasia (AIN) | Full-thickness nuclear atypia, loss of maturation, high mitotic figures; p16 strongly positive (HPV-driven) | Moderate progression to invasive cSCC if untreated | Surgical excision, CO2 laser ablation, or topical Imiquimod 5% cream |
Test Your Knowledge
A 35-year-old HIV-infected man with a CD4 count of 65 cells/µL presents with a 4-week history of multiple rapidly growing, bright red, vascular, dome-shaped nodules on his face and forearms that bleed profusely when traumatized. A punch biopsy of a representative nodule demonstrates a lobular proliferation of capillaries lined by plump, protuberant endothelial cells surrounded by a dense infiltrate of neutrophils with abundant nuclear dust (leukocytoclasia). Clumps of extracellular granular material within the stroma stain strongly positive with Warthin-Starry silver staining. What is the most appropriate first-line antimicrobial therapy?
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Test Your Knowledge
A 42-year-old man who was recently diagnosed with HIV infection presents with asymptomatic white plaques on his tongue. Examination reveals prominent, vertically corrugated, white hyperkeratotic plaques along both lateral borders of the tongue. The examiner attempts to remove the plaque using a wooden tongue depressor and dry gauze, but the lesion firmly adheres and cannot be scraped off. What is the underlying etiological pathogen responsible for this lesion?
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Test Your Knowledge
A 62-year-old postmenopausal woman presents with a 2-year history of progressive vulvar pruritus, soreness, and dyspareunia. Examination reveals symmetrical porcelain-white atrophic plaques with a wrinkled, 'cigarette-paper' surface encircling the vulva and perianal region in a figure-of-eight configuration. The labia minora are largely resorbed, and the clitoral hood is fused. Speculum examination confirms that the non-keratinized vaginal mucosa and cervix are completely normal with no erosions or inflammation. What is the diagnosis, and what is the primary neoplastic risk associated with this condition?
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Test Your Knowledge
A 26-year-old man is diagnosed with primary syphilis after presenting with a penile chancre and an RPR titer of 1:16. He reports having had three sexual partners over the preceding 5 months. According to the European IUSTI syphilis guideline, what is the lookback window for identifying sexual contacts, and what is the recommended management for an identified asymptomatic partner whose last contact was 4 weeks ago?
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