Molluscum Contagiosum

Etiology & Epidemiology

• MCV-1 is the most common worldwide, responsible for virtually all infections in young children.
• MCV-2 predominates in HIV-infected patients (causing ~60% of HIV-associated MC).

• Young children (peak ages 1-4 years) - community/contact spread
• Sexually active young adults (ages 20-29) - STI route
• Immunosuppressed individuals - especially HIV/AIDS (between 10-30% of untreated AIDS patients get MC)

Pathogenesis

1. Entry and replication: The virus infects epidermal keratinocytes following direct skin-to-skin contact. It does not enter the dermis under normal conditions.
2. Immune evasion - NF-κB inhibition: MC virus protein MC005 inhibits NF-κB activation by targeting NEMO-regulated IKK activation. This suppresses innate immune signaling, allowing the virus to persist for months without triggering a prompt inflammatory response.
3. Epidermal hyperplasia: Infected cells undergo ballooning degeneration and proliferate, forming a lobulated endophytic mass. As cytoplasmic viral factories grow, they compress the nucleus to the periphery, forming the pathognomonic Henderson-Patterson bodies (molluscum bodies) - large, eosinophilic, cytoplasmic inclusions visible on H&E staining.
4. Role of host immunity in resolution: When cell-mediated immunity eventually overcomes the virus, an inflammatory response is mounted - lesions become inflamed and ultimately involute spontaneously (12-18 months typically). In patients with atopic dermatitis (AD), abnormal cutaneous immunity facilitates infection, and children with AD are 4x more likely to have >50 lesions. In AIDS patients with CD4 <100, there is essentially no immune clearance, leading to hundreds of lesions and giant forms.
5. Cannot be cultured in tissue culture or animal models, complicating research.

Clinical Features

Fig. Molluscum contagiosum - characteristic lesions with central umbilication. (Andrews' Diseases of the Skin)

Typical Lesion

• Small (3-5 mm), smooth, firm, dome-shaped, pearly/flesh-colored papule
• Central umbilication is pathognomonic - may contain a white cheesy core (caseous plug)
• Early lesions: <1 mm; "giant" lesions: >1 cm
• Appear in clusters of 5-20 (or more)
• Painless; rarely pruritic unless inflamed
• Incubation period: 2-8 weeks

Distribution by Population

Inflammatory Variants

• Molluscum dermatitis (40% of children): Eczematous reaction surrounding individual lesions - especially in atopic individuals
• Inflamed MC (20% of children): Erythema, swelling, pustulation of individual lesions; known as the "BOTE sign" (Beginning Of The End) - signals impending spontaneous resolution
• Giannotti-Crosti-like reaction: Monomorphic papules on extensor surfaces sparing the trunk - can mimic sudden rapid spread
• Eyelid/conjunctival involvement: associated follicular conjunctivitis or keratitis

HIV-Associated MC

• Facial predominance (cheeks, neck, eyelids)
• Giant lesions, confluent plaques, possible disfigurement
• Mucosal involvement (oral/genital) indicates very advanced AIDS (CD4 <50)

Histopathology

Fig. (A) Skin lesions, arrows. (B) Epidermis filled with molluscum bodies (Henderson-Patterson bodies) - 100x magnification. (Medical Microbiology 9e)

• Lobulated epidermal hyperplasia with a central crater
• Henderson-Patterson bodies (molluscum bodies): Large eosinophilic intracytoplasmic inclusions in keratinocytes; they compress the nucleus and progressively enlarge as cells move toward the surface
• Can be seen on biopsy or by expressing the caseous core and staining with Wright, Giemsa, or Gram stain

Diagnosis

• Primarily clinical - the central umbilication of dome-shaped pearly papules is characteristic
• Light cryotherapy can highlight the round umbilical opening
• Microscopy: Expressed core squashed between two slides, stained - oval Henderson-Patterson bodies visible
• Differential includes: Cryptococcus, histoplasmosis, coccidioidomycosis (in immunocompromised), keratoacanthoma, desmoplastic trichilemmoma, condyloma acuminatum (in intergluteal region)

Treatment

Observation (Watchful Waiting)

• First-line for immunocompetent young children with numerous lesions
• Individual lesions last 2-4 months each; total infection duration: 12-18 months
• Aggressive treatment risks scarring and emotional trauma in young children

Physical/Destructive Methods

Topical Agents

Immunomodulatory

Analgesia Before Procedures

• EMLA (lidocaine-prilocaine) cream applied 1 hour prior to painful procedures - but use with caution due to reports of systemic toxicity in children

HIV-Associated MC

• Initiation of antiretroviral therapy (ART) is the primary treatment - immune reconstitution leads to resolution
• Note: Immune Reconstitution Inflammatory Syndrome (IRIS) can cause paradoxical flare of MC after starting ART
• Local destructive measures (cryotherapy/curettage) are used adjunctively

Genital MC in Adults

• Cryotherapy or curettage is very effective
• Neither imiquimod nor podophyllotoxin has been shown to be effective

Recent Evidence

• Andrews' Diseases of the Skin: Clinical Dermatology, Chapter 19
• Medical Microbiology 9e, Chapter 44
• Pfenninger and Fowler's Procedures for Primary Care, Chapter 12