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Summary Table

Category	Details
Risk Factors	Children aged 1 to 10, sexually active young adults, immunocompromised patients (particularly HIV/AIDS with CD4 < 200 cells/mcL), atopic dermatitis, contact sports (wrestling), shared towels or fomites
Etiology	Molluscum Contagiosum Virus (MCV), a double-stranded DNA poxvirus; the largest known DNA virus infecting humans
Patient Presentation	Painless, non-pruritic (or mildly pruritic) skin-colored bumps that have been present for weeks to months; parents often describe "little bumps with a dot in the center"
Classic Physical Exam	Dome-shaped, flesh-colored to pearly papules (2 to 5 mm) with a central umbilication (dell); waxy or pearly surface; lesions may be surrounded by an eczematous halo ("molluscum dermatitis"); white, cheesy core expressible from the center
Key Diagnostic Results	Clinical diagnosis in most cases; biopsy shows Henderson-Patterson bodies (large eosinophilic intracytoplasmic inclusion bodies); dermoscopy reveals a central white-yellow amorphous structure with surrounding crown vessels
Management	Observation (self-limited in immunocompetent); destructive therapies: cryotherapy, curettage; topical agents: cantharidin, podophyllotoxin, imiquimod 5%; in immunocompromised patients, optimize antiretroviral therapy (ART) and consider cidofovir
Keywords	"Umbilicated papules," "central dell," "flesh-colored dome-shaped papules," "Henderson-Patterson bodies," "molluscum bodies," "poxvirus," "waxy papule with central dimple"

1. Pathophysiology

Molluscum contagiosum is caused by the Molluscum Contagiosum Virus (MCV), a member of the Poxviridae family. MCV is the largest double-stranded DNA virus known to infect humans. There are four subtypes (MCV-1 through MCV-4), with MCV-1 being the most common overall and in children, and MCV-2 being more frequently associated with sexually transmitted infections in adults.

The virus infects keratinocytes in the epidermis and replicates exclusively within the cytoplasm of host cells, never integrating into the host genome. As the virus replicates, it produces large intracytoplasmic inclusion bodies that push the cell nucleus to the periphery. These inclusions are the Henderson-Patterson bodies (also called molluscum bodies), which are pathognomonic on histology. The progressive accumulation of viral particles causes the keratinocytes to enlarge dramatically and eventually rupture, releasing the waxy, caseous core that is clinically visible.

A key concept is that MCV encodes immune evasion proteins that suppress local innate and adaptive immune responses. The virus produces chemokine homologs and inhibitors of apoptosis, NF-kB signaling, and MHC class I antigen presentation. This is why lesions persist for months despite being superficial, and why the host does not mount an immediate inflammatory response. The central umbilication seen clinically corresponds to the area where virus-laden keratinocytes degenerate and form a crater-like depression filled with viral debris. This feature directly reflects the underlying epidermal pathology and is the single most recognizable clinical clue.

In immunocompromised patients, particularly those with HIV/AIDS and a CD4 count below 200 cells/mcL, the virus replicates unchecked due to impaired T-cell-mediated immunity. This results in hundreds of lesions, larger papules (sometimes exceeding 1 cm, termed "giant molluscum"), and resistance to standard treatments. The resolution of lesions in these patients often correlates with immune reconstitution following initiation of ART.

2. Classification and Clinical Manifestation

Classification	Description	Typical Patient	Characteristic Features
Childhood molluscum	Most common form; MCV-1 predominant	Children aged 1 to 10	Lesions on the face, trunk, extremities, and axillae; spread through direct skin contact, fomites, and shared bathing
Sexually transmitted molluscum	MCV-2 predominant	Sexually active young adults (15 to 29 years)	Lesions localized to the genital region, inner thighs, lower abdomen, and perineum; classified as a sexually transmitted infection
Immunocompromised molluscum	Extensive, refractory disease	HIV/AIDS (CD4 < 200), organ transplant recipients, patients on immunosuppressive therapy	Hundreds of lesions, giant molluscum (>1 cm), involvement of the face (especially periorbital), poor response to destructive therapy, resolution with immune reconstitution
Molluscum dermatitis	Eczematous reaction surrounding lesions	Any patient, more common in those with atopic dermatitis	Erythematous, scaly, pruritic halo around individual papules; represents a local hypersensitivity reaction to viral antigens; may be confused with eczema or contact dermatitis
Inflamed/BOTE molluscum	"Beginning of the end" phenomenon	Any immunocompetent patient	Lesions become erythematous, swollen, and tender before spontaneous resolution; this indicates the host immune system is mounting a response; often mistaken for bacterial superinfection

3. Diagnostic Workup

Test	Role	Expected Findings
Clinical examination	Best initial test	Dome-shaped, flesh-colored, umbilicated papules in characteristic distribution
Dermoscopy	Adjunct to clinical exam	Central white-yellow amorphous structure (corresponding to the molluscum body), polylobular pattern, surrounding "crown" or "red corona" vessels
Skin biopsy with histopathology	Most accurate / confirmatory test (rarely needed)	Henderson-Patterson bodies: large, eosinophilic, intracytoplasmic inclusion bodies within markedly enlarged keratinocytes; cup-shaped invagination of the epidermis
Wright or Giemsa stain of expressed material	Rapid confirmation if clinical doubt exists	Large, round, intracytoplasmic inclusion bodies visible in the expressed cheesy core
HIV testing	Indicated in adults with extensive or atypical disease	Should be ordered in any adult with widespread facial molluscum or >50 lesions without a clear cause of immunosuppression

Diagnostic reasoning. In the vast majority of cases, molluscum contagiosum is a clinical diagnosis. The combination of multiple dome-shaped papules with a visible central umbilication in a child or young adult is sufficient to make the diagnosis without any laboratory testing. Dermoscopy can be helpful in confirming ambiguous cases, as the polylobular central structure is highly characteristic.

Biopsy is reserved for atypical presentations where the clinical picture overlaps with other conditions. This is particularly relevant in immunocompromised patients, where disseminated cryptococcosis and histoplasmosis can produce umbilicated papules that closely mimic molluscum. If an HIV-positive patient presents with widespread umbilicated papules and systemic symptoms (fever, weight loss, meningeal signs), biopsy with appropriate stains (GMS, mucicarmine for Cryptococcus; GMS, Wright for Histoplasma) is essential to exclude these life-threatening infections.

An important clinical pearl: if an adult presents with genital molluscum, screen for other sexually transmitted infections (chlamydia, gonorrhea, syphilis, HIV), as co-infection is common. If an adult presents with widespread facial molluscum without known immunosuppression, HIV testing is the next step.

4. Management and Treatment

Setting	Treatment	Details
Immunocompetent children (few lesions)	Observation / watchful waiting	Self-limited; resolves spontaneously in 6 to 12 months (may take up to 2 to 4 years); first-line per AAP and many guidelines
Immunocompetent with bothersome or numerous lesions	Cryotherapy with liquid nitrogen	Applied for 6 to 10 seconds per lesion; may require repeat sessions every 2 to 3 weeks
	Curettage	Physical removal with a small curette; rapid and effective; may use topical EMLA (lidocaine 2.5% / prilocaine 2.5%) for pain control, applied 30 to 60 minutes prior
	Cantharidin 0.7% (office-applied)	Applied by clinician; causes blistering at the site within 24 hours; the blister lifts the infected epidermis; washed off 2 to 6 hours after application; not used on the face or genital area
Topical home-based therapy	Imiquimod 5% cream	Applied 3 times per week for up to 16 weeks; stimulates local TLR-7-mediated innate immune response; off-label for molluscum but widely used
	Podophyllotoxin 0.5% solution	Applied twice daily for 3 consecutive days, followed by 4 days off; repeated for up to 4 cycles; contraindicated in pregnancy (teratogenic)
	Potassium hydroxide (KOH) 10% solution	Applied once to twice daily until inflammation develops; available over the counter in some regions; more commonly used in resource-limited settings
Immunocompromised patients	ART initiation or optimization	Immune reconstitution is the cornerstone of treatment in HIV-positive patients; lesions frequently resolve once CD4 count improves above 200 cells/mcL
	Topical cidofovir 1 to 3% cream	Applied once to twice daily for refractory lesions in immunocompromised patients; inhibits viral DNA polymerase
	Combination destructive therapy	Cryotherapy or curettage in combination with ART optimization for persistent lesions

Management reasoning. The most important concept for exam purposes is that observation is the first-line approach in immunocompetent children with limited disease. Parents often request treatment, but the condition is benign and self-resolving. Intervention is indicated when lesions are symptomatic, cosmetically distressing, or located in areas prone to autoinoculation (e.g., periocular, genital).

When treatment is pursued, physical destruction (cryotherapy or curettage) offers the most immediate results. Cantharidin is a popular in-office option because it is painless at application and well-tolerated in children, though the delayed blistering reaction must be explained to parents.

For immunocompromised patients, the treatment paradigm shifts entirely. Destructive therapy alone is insufficient because the underlying immune defect allows continuous viral replication. The cornerstone of management is restoring immune function, most commonly through ART in HIV-positive patients. Topical cidofovir is reserved for refractory cases.

Contraindications to note: podophyllotoxin is absolutely contraindicated in pregnancy. Imiquimod should be used with caution on mucosal surfaces due to the risk of severe local inflammation. Cantharidin should not be applied to the face, genitals, or perianal area due to the risk of scarring and severe blister formation.

5. Differential Diagnosis and Distractors

Differential	Why It Looks Similar	Key Discriminator
Disseminated Cryptococcosis	Produces umbilicated, flesh-colored papules on the face in immunocompromised patients, nearly identical to molluscum	Patient is systemically ill (fever, headache, meningeal signs); serum cryptococcal antigen is positive; India ink preparation of CSF shows encapsulated yeast; biopsy with mucicarmine stain shows organisms
Disseminated Histoplasmosis	Produces papular or umbilicated skin lesions in immunocompromised patients, especially in endemic regions	Patient has systemic symptoms (fever, hepatosplenomegaly, pancytopenia); Histoplasma urinary antigen is positive; biopsy shows intracellular yeast within macrophages on GMS stain
Verruca vulgaris (common warts)	Flesh-colored papular lesions in children and young adults	Warts have a rough, verrucous (hyperkeratotic) surface with thrombosed capillaries ("black dots"); no central umbilication; caused by HPV
Condylomata acuminata (genital warts)	Genital papular/papillomatous lesions in sexually active patients	Lesions are cauliflower-like, soft, and pedunculated rather than dome-shaped with umbilication; caused by HPV types 6 and 11
Basal cell carcinoma	Pearly, dome-shaped papule with telangiectasia	Usually a solitary lesion in a sun-exposed area of an older adult; rolled borders, telangiectatic surface vessels; central ulceration rather than umbilication
Keratoacanthoma	Dome-shaped nodule with a central crater	Rapidly growing solitary nodule with a central keratin plug ("volcano-like"); lesion is typically 1 to 2 cm; occurs in sun-exposed skin of older adults
Folliculitis	Multiple small papules/pustules on the trunk or extremities	Lesions are pustular and centered on hair follicles; tender and erythematous; no central umbilication; culture grows Staphylococcus aureus or other pathogens
Juvenile xanthogranuloma	Flesh-colored to yellowish papules in young children	Lesions are yellow-orange, firm, and non-umbilicated; biopsy shows Touton giant cells; associated with neurofibromatosis type 1

6. Traps and High-Yield Pearls

The most common way students lose points on molluscum contagiosum questions is by failing to recognize the condition in an immunocompromised patient and instead selecting a disseminated fungal infection, or vice versa. When a vignette describes an HIV-positive patient with a very low CD4 count and widespread umbilicated facial papules, students often default to molluscum because of the classic morphology. However, if the vignette includes systemic symptoms (fever, weight loss, headache, meningeal signs, hepatosplenomegaly, or pancytopenia), the answer shifts to disseminated cryptococcosis or histoplasmosis, and the next step is biopsy with appropriate stains, not observation. The discriminator is always whether the patient is systemically ill or has isolated skin findings.

A second common trap involves the "inflamed molluscum" scenario. A child with known molluscum returns because several lesions have become red, swollen, and tender. Students are tempted to choose antibiotics for bacterial superinfection. In most cases, this is the "beginning of the end" (BOTE) reaction, where the host immune system is finally recognizing and attacking the virus. The appropriate answer is reassurance and observation unless there is purulent drainage, warmth, or spreading cellulitis.

The third pearl is about management sequencing. For immunocompetent children, the first-line answer is almost always observation. Students who pick cryotherapy or curettage as first-line are penalized. Physical destruction is reserved for cases where lesions are persistent, symptomatic, or in cosmetically or functionally sensitive areas.

Finally, remember that Henderson-Patterson bodies are pathognomonic and represent the histologic gold standard. If a question describes intracytoplasmic eosinophilic inclusion bodies that push the nucleus to the periphery, the answer is molluscum contagiosum regardless of the clinical context provided.

The core competency being tested is the ability to integrate the clinical morphology (umbilicated papules), the patient context (immunocompetent vs. immunocompromised), and the appropriate management response (observation vs. active treatment vs. systemic workup) into a single coherent clinical decision.

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