38.3 Viral Cutaneous Infections: Herpes Simplex, Zoster & Molluscum Contagiosum

Herpes Simplex Virus Infections (HSV-1 & HSV-2)

Herpes simplex viruses (HSV-1 and HSV-2) are double-stranded DNA viruses belonging to the Herpesviridae family. They are characterized by neurovirulence, primary mucocutaneous infection, and the establishment of lifelong latency within sensory nerve ganglia with episodic reactivations.

Virology, Pathogenesis & Latency

• Transmission: Occurs via direct contact with active mucocutaneous lesions or through asymptomatic viral shedding in bodily secretions (saliva, genital secretions) from an infected host.
• Establishment of Latency: Following initial mucosal or cutaneous inoculation and local epidermal replication, viral particles enter unmyelinated sensory nerve endings and ascend along sensory axons via retrograde intra-axonal transport to the sensory neuron cell bodies located in sensory ganglia:
  • Trigeminal Ganglion (CN V): Primary reservoir of latency for HSV-1 (responsible for recurrent orofacial herpes);
  • Sacral Dorsal Root Ganglia (S2 to S4): Primary reservoir of latency for HSV-2 (responsible for recurrent genital herpes), though HSV-1 increasingly establishes sacral latency following orogenital contact.
• Reactivation: Latent viral genomes persist as non-integrated episomal circular DNA in sensory neurons. Physical or emotional stimuli—ultraviolet radiation, fever, psychological stress, tissue trauma, surgical manipulation, immunosuppression, or hormonal fluctuations during menses—trigger viral reactivation. Viral particles travel down sensory nerves via anterograde intra-axonal transport back to the epithelial surface, producing recurrent cutaneous vesicles or asymptomatic shedding.

Clinical Manifestations of HSV

                     HERPES SIMPLEX CLINICAL MANIFESTATIONS

  Syndrome            Primary Features                   Evidence-Based Therapy
  ─────────────────────────────────────────────────────────────────────────────
  Orofacial Herpes    Prodrome (tingling/burning) ────>  Oral Valacyclovir 2,000 mg
  (Herpes Labialis)   Grouped clear vesicles on an       BID for 1 single day
                      erythematous base at vermilion     (Initiate at earliest prodrome)
                      border; crusts in 7-10 days.
  ─────────────────────────────────────────────────────────────────────────────
  Primary Genital     Severe bilateral painful ulcers,   Oral Valacyclovir 1,000 mg
  Herpes              tender inguinal lymphadenopathy,   PO BID for 7 to 10 days
                      dysuria, fever, malaise (2-3 wk).  (or Acyclovir 400 mg TID)
  ─────────────────────────────────────────────────────────────────────────────
  Recurrent Genital   Milder unilateral lesions (4-6 d); Oral Valacyclovir 500 mg BID
  Herpes              neuralgic prodrome in buttocks     for 3 days (patient-initiated)
                      or thighs.                         OR Daily suppressive therapy
  ─────────────────────────────────────────────────────────────────────────────
  Herpetic Whitlow    Painful grouped vesicles on pulp   Oral Valacyclovir 1,000 mg TID
                      of terminal digit; mistaken for    SURGICAL INCISION STRICTLY
                      felon/paronychia.                  CONTRAINDICATED!
  ─────────────────────────────────────────────────────────────────────────────
  Eczema Herpeticum   Widespread punched-out umbilicated Prompt systemic IV or oral
  (Kaposi Eruption)   vesicles on atopic dermatitis;     Acyclovir / Valacyclovir;
                      high fever; MEDICAL EMERGENCY!     monitor for secondary sepsis.

1. Orofacial Herpes (Herpes Labialis / "Cold Sores")

• Over 80% to 90% are caused by HSV-1. Infection begins with a localized sensory prodrome of tingling, burning, pruritus, or hyperesthesia lasting 6 to 24 hours.
• The eruptive phase features a cluster of painful, uniform, grouped vesicles on an erythematous base located at the cutaneous vermilion border of the lip.
• The thin-walled vesicles rapidly rupture, ulcerate, exude serous exudate, and form yellowish crusts that resolve completely in 7 to 10 days without scarring.
• Treatment of Herpes Labialis:
  • First-Line Oral Episodic Regimen: Oral Valacyclovir 2,000 mg (2 g) PO twice daily (12 hours apart) for 1 single day (total 4 grams).
  • Timing: Must be self-initiated by the patient at the very first onset of prodromal tingling to achieve maximal therapeutic benefit.
  • Alternative Oral: Famciclovir 1,500 mg PO as a single dose.
  • Topical Limitations: Topical antiviral creams (acyclovir 5% cream, docosanol 10% OTC) reduce episode duration by only 10 to 18 hours (~0.5 day) and are significantly inferior to oral valacyclovir.

2. Genital Herpes Simplex

• Primary Genital Episode:
  • Characterized by widespread, bilateral, multiple, exquisitely painful vesicular and ulcerative lesions on the labia, penis, perineum, or perianal skin.
  • Accompanied by severe dysuria, vaginal/urethral discharge, marked bilateral tender inguinal lymphadenopathy, and prominent systemic symptoms (fever, headache, myalgias) lasting 2 to 3 weeks.
  • Regimen: Oral Valacyclovir 1,000 mg PO BID for 7 to 10 days (extend if lesions are not fully healed) or Oral Acyclovir 400 mg PO TID for 7 to 10 days.
• Recurrent Genital Episodes:
  • Manifest as localized, unilateral, milder clusters of vesicles that heal rapidly within 4 to 6 days.
  • Episodic Therapy: Patient-initiated within 24 hours of prodrome: Oral Valacyclovir 500 mg PO BID for 3 days or 1,000 mg PO daily for 5 days.
  • Daily Suppressive Therapy: Indicated for patients with frequent recurrences (≥6 episodes per year), severe psychosocial distress, or to minimize viral transmission to an uninfected partner:
    • Oral Valacyclovir 500 mg PO once daily (increase to 1,000 mg daily in patients with >9 recurrences per year);
    • Alternative: Oral Acyclovir 400 mg PO BID;
    • Clinical Impact: Daily suppressive therapy reduces symptomatic clinical outbreaks by 70% to 80% and decreases heterosexual partner transmission by approximately 50% (combined with consistent condom use).

3. Special Clinical Variants of HSV

• Herpetic Whitlow:
  • Painful, vesicular infection involving the distal volar pulp or paronychial folds of a finger or thumb.
  • Occurs in healthcare personnel (dental workers, respiratory therapists) exposed to infected oral secretions (HSV-1), or in young children with primary herpetic gingivostomatitis who suck their fingers. In adults, it is often caused by digital-genital contact (HSV-2).
  • Presents with intense throbbing pain, localized erythema, edema, and deep-seated, clear or turbid grouped vesicles.

  • [!CAUTION] SURGICAL CONTRAINDICATION: Herpetic whitlow is frequently misdiagnosed as a bacterial paronychia or deep digital space felon. SURGICAL INCISION AND DRAINAGE IS STRICTLY CONTRAINDICATED! Incision fails to release pus, leads to delayed wound healing, introduces severe secondary bacterial superinfection, and increases the risk of autoinoculation. Management is strictly medical with oral valacyclovir 1,000 mg PO TID for 7 to 10 days and dry protective dressings.

• Eczema Herpeticum (Kaposi Varicelliform Eruption):
  • Severe, widespread, disseminated cutaneous HSV infection occurring in individuals with pre-existing skin barrier dysfunction, most commonly atopic dermatitis.
  • Manifests as an extensive, explosive eruption of uniform, "punched-out," monomorphic, umbilicated vesicles and shallow erosions clustered in areas of active or inactive eczema (especially the face, neck, and upper trunk), accompanied by high fever, malaise, and regional lymphadenopathy.
  • Represents a dermatologic emergency carrying a significant risk of secondary staphylococcal bacteremia, ocular dissemination, and death. Requires prompt hospitalization, IV or high-dose oral acyclovir/valacyclovir, and empiric antistaphylococcal coverage.

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Herpes Zoster (Shingles)

Herpes zoster (shingles) is a localized, neurocutaneous disease caused by the reactivation of endogenous Varicella-Zoster Virus (VZV) that has remained dormant within cranial nerve sensory ganglia or spinal dorsal root ganglia following primary varicella infection (chickenpox).

Pathophysiology & Risk Factors

• Mechanism: Declining VZV-specific cell-mediated immunity allows latent virus in dorsal root ganglia to replicate, producing acute ganglionitis and neuronal necrosis. Infectious virions travel down the sensory nerve axon to the corresponding cutaneous dermatome.
• Risk Factors: The primary risk factor is advancing age (incidence rises sharply after age 50, with a lifetime risk approaching 30% to 50% by age 85). Other major risk factors include immunosuppression (organ transplantation, hematologic malignancies, chemotherapy, HIV infection with CD4 <200), chronic systemic corticosteroids, autoimmune diseases, and physical trauma.

Clinical Presentation & Staging

1. Pre-eruptive Dermatomal Prodrome (Days 1 to 5):
   • Burning, lancinating, throbbing, shooting, or electric shock-like neuropathic pain, hyperesthesia, paresthesias, and tactile allodynia localized strictly within a single unilateral dermatome.
   • Systemic symptoms (low-grade fever, malaise, headache) occur in 20% of patients.
   • Diagnostic Trap: Dermatomal pain preceding the rash frequently mimics acute visceral emergencies: thoracic zoster mimics myocardial infarction or acute pleurisy; lower thoracic/lumbar zoster mimics acute cholecystitis, appendicitis, or renal colic; lumbosacral zoster mimics acute sciatica or lumbar disc herniation.
2. Acute Eruptive Phase (Days 3 to 10):
   • Erythematous macules and papules erupt rapidly, evolving within 24 hours into grouped, clear, tense vesicles on an erythematous base.
   • Cardinal Feature: The rash is strictly unilateral and distributed in a dermatomal band, respecting the anatomical midline of the body. The most common sites are thoracic dermatomes (T3 to L2, >50% of cases), followed by cranial nerve dermatomes (predominantly the ophthalmic V1 division of the trigeminal nerve) and cervical dermatomes.
   • Over 3 to 5 days, vesicles become pustular, umbilicated, and turbid, then rupture to form crusts by day 7 to 10.
3. Crusting & Resolution (Weeks 2 to 4):
   • Lesions are completely crusted and no longer infectious within 10 to 14 days, with complete cutaneous healing occurring over 2 to 4 weeks, often leaving transient hypopigmentation, hyperpigmentation, or scarring.

• Disseminated Herpes Zoster:
  • Defined as more than 20 discrete vesicular lesions occurring outside the primary and immediately adjacent dermatomes, or zoster with visceral organ involvement (pneumonitis, hepatitis, encephalitis).
  • Occurs almost exclusively in severely immunocompromised hosts. Demands immediate inpatient hospital admission, intravenous acyclovir (10 mg/kg IV every 8 hours), and combined airborne and contact isolation.

Antiviral Management of Acute Herpes Zoster

                      ACUTE HERPES ZOSTER THERAPY

  Drug            Standard Dose               Renal Adjustment (CrCl <50 mL/min)
  ─────────────────────────────────────────────────────────────────────────────
  VALACYCLOVIR    1,000 mg PO TID for 7 days  CrCl 30-49: 1,000 mg PO q12h
  (Preferred)                                 CrCl 10-29: 1,000 mg PO q24h
                                              CrCl <10:   500 mg PO q24h
  ─────────────────────────────────────────────────────────────────────────────
  FAMCICLOVIR     500 mg PO TID for 7 days    CrCl 40-59: 500 mg PO q12h
                                              CrCl 20-39: 500 mg PO q24h
                                              CrCl <20:   250 mg PO q24h
  ─────────────────────────────────────────────────────────────────────────────
  ACYCLOVIR       800 mg PO 5 times daily     CrCl 10-25: 800 mg PO q8h
                  for 7 days                  CrCl <10:   800 mg PO q12h

• Therapeutic Window: Antiviral therapy should ideally be initiated within 72 hours of rash onset. Oral antivirals accelerate cutaneous healing, halt the formation of new vesicles, shorten the duration of viral shedding, and reduce the intensity and duration of acute pain.
• Treating Beyond 72 Hours: Antiviral therapy is still strongly indicated beyond 72 hours if:
  1. New vesicles are actively continuing to form (indicating persistent ongoing viral replication);
  2. The patient is ≥50 years of age with ongoing severe pain or extensive cutaneous involvement;
  3. The patient is immunocompromised;
  4. The infection involves the eye (Herpes Zoster Ophthalmicus) or ear (Ramsay Hunt syndrome).
• Renal Dosing & Neurotoxicity Warning: Acyclovir and its prodrug valacyclovir are eliminated primarily by renal glomerular filtration and tubular secretion. Failure to adjust dosages in patients with renal impairment results in acyclovir-induced neurotoxicity (manifesting as tremors, confusion, visual hallucinations, myoclonus, encephalopathy, and coma) and acute crystal nephropathy (due to intratubular crystal precipitation; prevented by maintaining aggressive oral or IV hydration).

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Critical Complications of Herpes Zoster

1. Herpes Zoster Ophthalmicus (HZO)

• Anatomy: Reactivation of VZV in the ophthalmic division (V1) of the trigeminal nerve, accounting for 10% to 15% of all zoster cases.
• The Hutchinson Sign: The presence of grouped herpetic vesicles on the tip, side, or root of the nose (ala nasi). The cutaneous tip of the nose is innervated by the external nasal branch of the nasociliary nerve, which also provides sensory innervation to the cornea, ciliary body, and iris. Crucial Board Pearl: A positive Hutchinson sign predicts intraocular corneal involvement in over 75% to 80% of patients!
• Ocular Pathology: Epithelial keratitis, anterior uveitis/iritis, stromal keratitis, secondary glaucoma, scleritis, optic neuritis, and permanent visual loss.
• Slit-Lamp Examination: Fluorescein staining reveals classic dendritic pseudodendrites—mucous plaques with tapered, blunt ends and lack of terminal bulbar bulbs (which differentiates them from the delicate, true branching dendrites with terminal bulbs characteristic of HSV keratitis).
• Management Pathway:
  1. Immediate SAME-DAY Ophthalmology Consultation;
  2. Oral Valacyclovir 1,000 mg PO TID for 7 to 10 days initiated immediately;
  3. Urgent slit-lamp biomicroscopy and intraocular pressure measurement;
  4. Strict Warning: Topical ophthalmic corticosteroids must NEVER be prescribed by primary care clinicians without direct in-person ophthalmology evaluation, as steroids cause fulminant corneal melting and perforation in active viral epithelial disease.

2. Ramsay Hunt Syndrome (Herpes Zoster Oticus)

• Anatomy: Reactivation of latent VZV within the geniculate ganglion of the facial nerve (Cranial Nerve VII), frequently involving adjacent fibers of the vestibulocochlear nerve (CN VIII).
• The Classical Diagnostic Triad:
  1. Ipsilateral lower motor neuron facial nerve palsy (complete unilateral facial paralysis: inability to close the eye, loss of nasolabial fold, forehead weakness, oral drooping);
  2. Severe, agonizing otalgia (deep ear pain);
  3. Painful vesicular eruption located on the external auditory canal, pinna, concha of the auricle, or anterior two-thirds of the tongue and soft palate.
• Associated Manifestations: Sensorineural hearing loss, vertigo, nausea/vomiting, nystagmus, tinnitus, and loss of taste (dysgeusia).
• Management:
  • High-dose Oral Valacyclovir 1,000 mg PO TID for 7 to 10 days;
  • PLUS Oral Prednisone (60 mg daily for 5 days, followed by a 5-day taper to 10 mg daily; total 10 to 14 days) to reduce acute edema and ischemia of the facial nerve within the rigid bony fallopian canal;
  • Aggressive corneal eye protection (artificial tears by day, lubricating ophthalmic ointment and moisture chambers/protective eye taping by night) to prevent exposure keratitis;
  • Prognosis: Complete facial nerve functional recovery occurs in only 50% to 60% of Ramsay Hunt cases (substantially worse than the ~85-90% recovery rate seen in idiopathic Bell's palsy).

3. Post-Herpetic Neuralgia (PHN)

• Definition: Clinically significant, debilitating neuropathic pain that persists for >90 days (3 months) after the onset of the acute herpes zoster rash.
• Pathophysiology: Severe inflammatory axonal injury and continuous firing of damaged sensory nociceptive neurons in the dorsal root ganglion, combined with central sensitization in the spinal cord dorsal horn.
• Clinical Presentation: Constant deep burning, aching, or throbbing pain, paroxysms of lancinating or electric shock-like sensations, and profound tactile allodynia (where light, non-painful touch—such as clothing brushing the skin or a gentle breeze—provokes agonizing, excruciating pain).
• Risk Factors: Age ≥50 years (the single most potent predictor; >50% incidence in patients >80 years of age), severe prodromal pain, severe acute rash density, and ophthalmic (V1) distribution.
• First-Line Pharmacologic Management of PHN:
  • Gabapentinoids:
    • Gabapentin: Initiate at 300 mg PO at bedtime; titrate upward gradually by 300 mg every 3 to 5 days to a therapeutic target of 1,800 to 3,600 mg/day divided TID. Doses must be reduced in renal insufficiency;
    • Pregabalin: Initiate at 75 mg PO BID; titrate to 150 mg BID within 1 week, up to maximum 300 mg BID.
  • Topical Lidocaine 5% Patch: Apply up to 3 patches simultaneously over the area of maximal intact painful allodynic skin for 12 hours on, 12 hours off daily. Excellent first-line choice for localized allodynia, providing rapid relief with zero systemic adverse effects.
  • Tricyclic Antidepressants (TCAs): Nortriptyline or Amitriptyline 10 to 25 mg PO at bedtime, slowly titrated up to 75 to 100 mg at bedtime. Nortriptyline is preferred over amitriptyline due to fewer sedating and anticholinergic adverse effects. Caution: Avoid in elderly patients with pre-existing cardiac conduction disease (arrhythmias, QT prolongation), glaucoma, urinary retention, or severe fall risk.
  • Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs): Duloxetine 60 mg PO once daily (titrate up to 120 mg/day).
  • Topical Capsaicin: High-concentration (8%) capsaicin dermal patch (in-office application) or low-concentration cream (0.025-0.075% applied QID); depletes substance P from local nociceptors.

Prevention: Recombinant Zoster Vaccine (Shingrix)

• Vaccine Composition: A non-live, recombinant subunit vaccine containing VZV glycoprotein E combined with the AS01B adjuvant suspension system.
• ACIP & CDC Recommendations:
  • Recommended as a 2-dose series (dose 2 administered intramuscularly 2 to 6 months after dose 1);
  • Indicated for ALL immunocompetent adults aged ≥50 years, regardless of whether they have a prior history of chickenpox, prior episode of shingles, or prior receipt of the historic live-attenuated zoster vaccine (Zostavax);
  • Indicated for immunocompromised adults aged ≥19 years who are or will be at increased risk of zoster;
  • Efficacy: Provides >90% efficacy in preventing herpes zoster and post-herpetic neuralgia across all age cohorts, with sustained efficacy documented beyond 10 years;
  • Note: The live-attenuated vaccine (Zostavax) was permanently discontinued in the United States in November 2020.

Molluscum Contagiosum

Molluscum contagiosum is a common, benign, superficial cutaneous viral infection caused by the Molluscum Contagiosum Virus (MCV), a large, double-stranded DNA virus of the Poxviridae family.

Virology & Histopathology

• Cellular Tropism: MCV replicates exclusively within the cytoplasm of epidermal keratinocytes. It does not establish latency, produce systemic viremia, or invade the dermis.
• Histopathology: Characteristic Henderson-Paterson bodies (molluscum bodies)—large, dense, intracytoplasmic, eosinophilic-to-basophilic inclusion bodies that displace the host keratinocyte nucleus to the cell periphery within the stratum spinosum and corneum.

Transmission & Epidemiology

• Modes of Transmission: Direct skin-to-skin contact, autoinoculation via scratching (producing linear arrangements of lesions along excoriation tracks, known as the pseudo-Koebner phenomenon), and indirect transmission via fomites (shared bath towels, washcloths, clothing, wrestling mats, contaminated pool toys).
• Two Primary Affected Demographics:
  1. Pediatric Population (Ages 1 to 10 years): The most frequent clinical demographic. Lesions are located predominantly on the trunk, intertriginous flexures (axillae, antecubital fossae, popliteal fossae), face, and extremities;
  2. Young Adults (Sexually Active): Transmitted as a sexually transmitted infection (STI). Lesions are clustered on the groin, pubic region, lower abdomen, upper inner thighs, and genitalia.
• Immunocompromised Host Presentation: In patients with advanced HIV/AIDS (CD4 count <200 cells/mcL), hematologic malignancy, or profound T-cell immunosuppression, molluscum presents with atypical, extensive disease: giant mollusca (>1 cm in diameter), extensive facial distribution, or hundreds of widespread, disfiguring, recalcitrant lesions that fail standard therapies.

Clinical Presentation & The "BOTE" Sign

• Physical Exam Findings:
  • Discrete, smooth, firm, dome-shaped, flesh-colored, pink, or translucent pearly papules measuring 1 to 5 mm in diameter.
  • Hallmark Finding: Central umbilication featuring a small dimple or pit on the summit of the papule.
  • Gentle lateral compression of a mature papule expresses a central, solid, white, curd-like or cheesy core consisting of compacted keratin and millions of infectious virions.
• Molluscum Dermatitis: Up to 30% of children develop a localized, intensely pruritic, eczematous dermatitis surrounding molluscum papules, which is an inflammatory reaction to viral antigens rather than secondary bacterial infection.
• The BOTE Sign ("Beginning Of The End"):
  • Individual molluscum papules frequently become markedly erythematous, swollen, fluctuant, and crusted, appearing clinically "infected."
  • Clinical Pearl: This inflammatory flare indicates that the host's cell-mediated immune system has successfully recognized the poxvirus antigens and is actively clearing the lesion! It is known clinically as the BOTE sign ("beginning of the end"). Clinicians must reassure parents that this erythema represents natural immune-mediated resolution rather than secondary bacterial cellulitis; antibiotics are strictly unnecessary.

Evidence-Based Management Strategy

                  MOLLUSCUM CONTAGIOSUM MANAGEMENT

  Patient Category       Clinical Strategy          Rationale & Interventions
  ─────────────────────────────────────────────────────────────────────────────
  Pediatric Uncomplicated WATCHFUL WAITING &         • Benign, self-limiting
  (Most children)        OBSERVATION                • Resolves spontaneously in 6-18 mo
                         (First-line standard)      • Avoid pain, fear, & scarring of
                                                    destructive procedures
                                                    • Counsel: do not share towels
  ─────────────────────────────────────────────────────────────────────────────
  Symptomatic / Active   DESTRUCTIVE or CHEMICAL    • Indicated for disfigurement,
  Therapy Desired        PROCEDURES                 severe pruritus, or transmission
                         (Shared decision-making)   • Options: Cantharidin 0.7%,
                                                    Cryotherapy, Curettage
  ─────────────────────────────────────────────────────────────────────────────
  Adult Genital Lesions  ACTIVE INTERVENTION +      • Cryotherapy / cantharidin to prevent
  (Sexually transmitted) COMPREHENSIVE STI          sexual transmission to partners
                         SCREENING                  • Order HIV, Syphilis (RPR),
                                                    Gonorrhea & Chlamydia NAAT

1. Watchful Waiting (First-Line Standard of Care in Children):
   • In immunocompetent children, molluscum contagiosum is entirely self-limiting, with spontaneous complete resolution typically occurring within 6 to 18 months (occasionally lasting up to 3 to 5 years).
   • Because active destructive therapies (cryotherapy, curettage) cause significant pain, emotional trauma in young children, and carry risks of permanent scarring or post-inflammatory hypopigmentation, observation, watchful waiting, and parental reassurance are strongly recommended as first-line management.
   • Counsel parents to avoid sharing towels or bath sponges, keep lesions covered with loose clothing or bandages during contact sports, and discourage picking or scratching to prevent autoinoculation.
2. Active Treatment Options (for symptomatic, cosmetically distressing, extensive, or sexually transmitted lesions):
   • Cantharidin (0.7% topical solution): In-office application of a tiny droplet of cantharidin directly to the central umbilication using the blunt wooden end of a cotton-tipped applicator, avoiding surrounding normal skin. The area is washed off with soap and water after 2 to 6 hours. Cantharidin causes intraepidermal acantholysis and blistering, sloughing the molluscum body without scarring. Application is completely painless, making it well-suited for pediatric patients, though localized blistering and dyspigmentation occur.
   • Cryotherapy: Application of liquid nitrogen with a cotton swab or spray for 5 to 10 seconds per lesion until a 1-mm freeze halo appears. Highly effective, but painful and carries a risk of permanent post-inflammatory hypopigmentation (especially in darker skin types).
   • Curettage: Physical enucleation of the central core using a sharp dermal curette, preceded by topical lidocaine-prilocaine (EMLA) cream. Produces rapid immediate clearance, with a minor risk of pinpoint scarring.
   • Topical Chemical Agents: Potassium hydroxide 10% solution, podophyllotoxin, or FDA-approved Berdazimer 10.3% topical gel (a novel nitric oxide-releasing agent applied once daily for 12 weeks).
   • Adult Genital Molluscum: Patients presenting with genital or suprapubic lesions should undergo active treatment to prevent sexual transmission and must receive a comprehensive STI screening including serologic testing for HIV and syphilis, as well as nucleic acid amplification testing (NAAT) for Chlamydia trachomatis and Neisseria gonorrhoeae.