Molluscum Contagiosum

Slide 1 · Molluscum Contagiosum

Virology · clinical morphology · dermatopathology · diagnosis

Central depression

Waxy core

Epidermis

Dermis

Schematic: exaggerated vertical scale

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning objectives

Identify the causal poxvirus and principal routes of transmission.

Recognize the typical umbilicated papule and its distribution.

Explain the cup-shaped hyperplasia and cytoplasmic molluscum bodies.

Select an appropriate diagnostic and clinical-management approach.

Slide 3 · Definition: A self-limited epidermal viral infection

Molluscum contagiosum is a common, benign infection of the skin caused by a poxvirus.

The hallmark lesion is a discrete, dome-shaped papule with central umbilication.

Its defining histologic feature is the intracytoplasmic molluscum body.

Most infections ultimately resolve spontaneously in immunocompetent people.

Slide 4 · Three diagnostic anchors

Clinical architecture: Firm, smooth, centrally umbilicated papule.

Epidermal architecture: Crateriform or cup-shaped epithelial hyperplasia.

Cytopathic feature: Large, eosinophilic or pale-blue cytoplasmic inclusion.

These three observations connect surface morphology to viral replication.

Central depression

Waxy core

Epidermis

Dermis

Schematic: Exaggerated vertical scale

Slide 5 · What kind of cutaneous infection is this?

Molluscum contagiosum

Verruca vulgaris

Impetigo

Poxvirus infection

Human papillomavirus infection

Superficial bacterial infection

Smooth umbilicated papule

Rough, papillomatous wart

Pustules and honey-colored crust

Cytoplasmic molluscum bodies

Nuclear-associated koilocytosis

Subcorneal neutrophilic pustule

Slide 6 · Etiologic agent: Molluscum contagiosum virus

The pathogen is a member of the poxvirus group.

Infection produces characteristic cytopathic inclusions in epidermal keratinocytes.

The viral disease is distinct from HPV-associated cutaneous verrucae.

Large, brick-shaped poxvirus

Dumbbell-shaped DNA core

Schematic—not an electron micrograph

Slide 7 · Poxvirus virion architecture

Virions are characteristically brick-shaped.

A dumbbell-shaped DNA core is present.

Robbins gives a maximal dimension of approximately 300 nm.

This unusually large viral particle should not be confused with a molluscum body.

Large, brick-shaped poxvirus

Dumbbell-shaped DNA core

Schematic—not an electron micrograph

Slide 8 · Virus and inclusion: Different scales

Virion: Approximately 300 nm at its largest dimension.

Molluscum body: Up to approximately 35 µm in diameter.

The large inclusion contains numerous smaller viral particles.

An inclusion body is a host-cell cytopathic structure, not a single virion.

Virions

Accumulation

Molluscum body

Conceptual sequence

Slide 9 · Four MCV types

MCV-1, MCV-2, MCV-3, and MCV-4.

MCV-1 is reported as the most prevalent type.

MCV-2 is described as more commonly associated with sexual transmission.

Routine recognition of a lesion does not require clinical viral typing.

Slide 10 · Epidermis as the site of disease

The dominant tissue response is proliferation of infected epidermal keratinocytes.

Dermatopathology descriptions emphasize follicular infundibular epithelium.

The epithelial focus produces a central crater and virus-rich core.

This localization explains why a classic lesion is a superficial papule.

Central crater

Lobulated epidermal proliferation

Schematic—not a histologic specimen

Slide 11 · Direct skin contact transmits infection

Skin-to-skin contact is a major mode of transmission.

Close contact is common in childhood settings.

Adults may acquire infection through intimate or sexual contact.

The infectious material is associated with visible lesions.

Infected lesion

Direct contact

New lesion

Conceptual sequence

Slide 12 · Shared objects may transmit infection

Robbins mentions shared towels as a route in children.

CDC also identifies clothing, toys, and shared pool equipment as possible fomites.

Object-mediated transmission does not require a genital exposure.

Avoiding shared personal items is a practical preventive intervention.

Slide 13 · Autoinoculation spreads lesions on one host

Scratching or rubbing an infected papule transfers viral material.

New lesions can appear at adjacent or distant skin sites.

Shaving and other hair-removal practices may disseminate lesions.

Linear clusters can reflect repeated local inoculation.

Existing papule

Scratch or shave

New skin sites

Conceptual sequence

Slide 14 · Transmission changes with clinical context

Setting

Typical exposure

Distribution clue

Young child

Direct contact; shared objects

Trunk and limbs

Sexually active adult

Intimate skin contact

Genital and adjacent skin

Any age

Autoinoculation

Groups or linear clusters

Slide 15 · Childhood infection predominates

Young children are a major affected population.

Robbins Chapter 22 cites ages 2–12 years; CDC highlights ages 1–10 years.

These are descriptive ranges from different sources, not diagnostic criteria.

Nonsexual contact is the usual pediatric transmission setting.

Slide 16 · Molluscum in adults

Anogenital lesions in adults often reflect sexual exposure.

Relevant sites include genitals, lower abdomen, buttocks, and inner thighs.

The presence of molluscum does not identify a precise time of acquisition.

Distribution and history guide an appropriate sexual-health assessment.

Slide 17 · Incubation and visible disease

An average incubation period of about six weeks.

Clinical lesions may not be visible immediately after exposure.

A reported recent exposure cannot establish exact transmission timing.

The infection is recognized when characteristic papules appear.

Slide 18 · Typical lesion: Pearly, dome-shaped papule

Papules are firm and often skin-colored or pink.

A smooth dome-shaped surface contrasts with the rough surface of warts.

The central pit may be obvious or subtle.

Most uncomplicated papules are painless.

Central depression

Waxy core

Epidermis

Dermis

Schematic: Exaggerated vertical scale

Slide 19 · Central umbilication is a structural clue

Umbilication is a depression at the center of the raised papule.

It corresponds to the central opening of the crateriform epithelial lesion.

A white, curd-like core may lie within the depression.

Umbilication is highly suggestive but is not itself an exclusive diagnosis.

Central depression

Waxy core

Epidermis

Dermis

Schematic: Exaggerated vertical scale

Slide 20 · The expressible white core

The central material may be waxy, cheesy, or curd-like.

Identifying molluscum bodies in a Giemsa-stained smear.

Expression is a diagnostic observation, not recommended patient self-treatment.

Squeezing and scraping can cause injury, secondary infection, or spread.

Slide 21 · Most papules are only a few millimeters wide

Robbins Chapter 25: Typically 0.2–0.4 cm in diameter.

Robbins Chapter 22: Often 1–5 mm in diameter.

CDC: Average lesion size approximately 2–5 mm.

These descriptions overlap and should not be treated as hard cutoffs.

Slide 22 · Giant molluscum is an unusual presentation

Rare lesions approaching 2 cm in diameter.

Atypical or unusually extensive lesions deserve a broader differential diagnosis.

Marked immune compromise is associated with larger and more numerous papules.

Biopsy can be useful when morphology is not clinically convincing.

Slide 23 · Color is variable; Morphology is more specific

Papules may be pearly white, pink, or similar in color to surrounding skin.

Inflammation may produce redness or swelling.

Do not rely on a single color description across skin phototypes.

Seek a central pit, lesion grouping, and characteristic surface architecture.

Slide 24 · Common anatomical sites

The trunk and anogenital skin.

The childhood discussion also includes arms and legs.

CDC describes widespread cutaneous sites; Palms and soles are unusual.

Site distribution must be interpreted together with age and exposure.

Slide 25 · Anogenital and mucosal lesions

Molluscum may occur on skin and mucosal surfaces.

Adults with genital lesions may have sexually transmitted infection.

Genital papules require careful exclusion of other causes of genital lesions.

Morphology and distribution, rather than assumptions about behavior, guide work-up.

Slide 26 · Pruritus can accompany infection

Papules are often painless but may itch.

Scratching increases the opportunity for autoinoculation.

It also disrupts the barrier and predisposes to bacterial infection.

Associated itchy dermatitis may be more symptomatic than the papule itself.

Slide 27 · Molluscum-associated dermatitis

Eczematous skin can develop around molluscum lesions.

The surrounding skin may become dry, pink, and itchy.

This reaction may obscure a previously classic papule.

Recognizing the viral lesion prevents mistaking all inflammation for bacterial infection.

Slide 28 · Inflammation does not always mean bacterial infection

A lesion may become inflamed, erythematous, or crusted as it resolves.

Secondary bacterial infection is a different process after barrier disruption.

Interpret tenderness, purulence, and surrounding inflammation in context.

Do not equate every red papule with impetigo.

Slide 29 · Secondary bacterial infection is an important complication

Scratching or rupturing papules can introduce bacteria.

Impetiginization changes the clinical appearance and may require separate care.

Immunocompromised patients can experience more consequential infections.

Infection prevention includes avoiding picking and keeping lesions covered.

Slide 30 · Natural history: Often spontaneous clearance

In immunocompetent individuals, molluscum usually resolves without treatment.

CDC reports that lesions commonly clear in 6–12 months.

Persistence for several years is possible in some patients.

Observation is a valid management strategy for uncomplicated disease.

Slide 31 · Resolution and the risk of scarring

Unmanipulated lesions generally resolve without scarring.

Traumatic curettage or squeezing can produce skin injury.

The choice to treat balances discomfort and spread against treatment harms.

Scarring risk is particularly important when evaluating cosmetic concerns.

Slide 32 · Immunosuppression changes disease severity

People with impaired immune function may develop many more lesions.

Lesions can be larger and persist longer than usual.

The facial region is a recognized site in severe immune deficiency.

Extensive or atypical infection should prompt assessment of immune context.

Slide 33 · Clinicopathologic correspondence

The raised dome reflects localized epithelial hyperplasia.

The central pit corresponds to crateriform epithelial architecture.

The pale core consists of keratinocytes containing viral cytoplasmic inclusions.

Visible morphology can therefore predict microscopic architecture.

Epidermal growth

Central crater

Umbilicated papule

Conceptual sequence

Slide 34 · Low-power histology: A cup-like lesion

The epidermis grows downward and around the central crater.

Cup-like verrucous epidermal hyperplasia.

The surface opening corresponds to the clinical umbilication.

A low-power view establishes lesion architecture before cellular analysis.

Central crater

Lobulated epidermal proliferation

Schematic—not a histologic specimen

Slide 35 · Epidermal lobules converge on a crater

Prominent keratinocyte proliferation produces a lobulated architecture.

The crater contains upper epithelial cells and viral material.

DermNet describes marked follicular infundibular hyperplasia.

Atypical inflammation or rupture can partially conceal this architecture.

Central crater

Lobulated epidermal proliferation

Schematic—not a histologic specimen

Slide 36 · High-power histology: Cytoplasmic inclusions

Numerous enlarged inclusion-bearing cells occupy the lesional epithelium.

Their cytoplasm becomes filled with dense, homogenous viral material.

A small residual nucleus is pushed toward the cell periphery.

These Henderson–Patterson or molluscum bodies establish the diagnosis.

Cytoplasmic inclusion

Peripheral nucleus

Schematic—not a histologic specimen

Slide 37 · Molluscum bodies are intracellular

The inclusion is within the keratinocyte cytoplasm—not its nucleus.

The inclusion is ellipsoid and homogeneous on routine H&E.

A peripheral crescent of nuclear material may remain visible.

This intracytoplasmic location distinguishes molluscum from HPV koilocytosis.

Cytoplasmic inclusion

Peripheral nucleus

Schematic—not a histologic specimen

Slide 38 · Dimensions of the diagnostic inclusion

Molluscum bodies may reach approximately 35 µm.

The inclusion is much larger than a single 300-nm virion.

The large size reflects accumulation of numerous virions in a keratinocyte.

The inclusion, rather than virus size on light microscopy, enables diagnosis.

Cytoplasmic inclusion

Peripheral nucleus

Schematic—not a histologic specimen

Slide 39 · H&E appearance changes with maturation

In the stratum granulosum, the inclusions are eosinophilic.

In the stratum corneum, inclusions may acquire a pale-blue hue.

The variation depends on the epidermal level being examined.

Review both mid-epidermal and cornified lesional layers.

Stratum corneum

Pale blue inclusions

Stratum granulosum

Eosinophilic inclusions

Lower epidermis

Keratinocyte maturation

Interpretation of Robbins H&E description

Slide 40 · Eosinophilic and pale-blue inclusions are one process

An H&E hue change is expected as infected cells move toward the surface.

Do not assign separate diagnoses based only on the two colors.

Interpret the inclusion in the context of epithelial maturation.

The surrounding crateriform lesion provides an essential architectural clue.

Stratum corneum

Pale blue inclusions

Stratum granulosum

Eosinophilic inclusions

Lower epidermis

Keratinocyte maturation

Interpretation of Robbins H&E description

Slide 41 · A molluscum body contains numerous virions

The large intracytoplasmic inclusion represents virus-rich material.

Robbins specifically states that numerous virions are found within the bodies.

Electron microscopy is unnecessary when characteristic inclusions are evident.

The visible inclusion is a cytopathic correlate of active infection.

Keratinocyte infection

Viral accumulation

Inclusion body

Conceptual sequence

Slide 42 · Linking microscopy back to the central core

The central pit overlies a zone rich in infected keratinocytes.

The curd-like material is derived from this altered epithelium.

Cytologic sampling of the core may reveal the defining inclusions.

Clinical, cytologic, and histologic observations are mutually reinforcing.

Central depression

Waxy core

Epidermis

Dermis

Schematic: Exaggerated vertical scale

Slide 43 · Clinical recognition is usually sufficient

Typical dome-shaped, centrally depressed papules suggest the diagnosis.

Lesion distribution and epidemiologic setting strengthen recognition.

Routine biopsy is unnecessary when the clinical appearance is characteristic.

Atypical lesions warrant reconsideration of the differential.

Slide 44 · When histology becomes valuable

Unusually large, persistent, or morphologically atypical papules.

Severe immune compromise with an expanded diagnostic differential.

Lesions clinically resembling verruca or a keratinocytic neoplasm.

A disrupted or inflamed lesion in which viral bodies may be focal.

Slide 45 · Giemsa smear can identify viral cytopathy

Expressing the central curd-like core for cytology.

A Giemsa-stained preparation may reveal molluscum bodies.

This method samples the inclusion-rich central lesion material.

It is a diagnostic technique, not a recommendation for home lesion expression.

Slide 46 · Biopsy interpretation: A four-step sequence

First identify epidermal crateriform or cup-shaped hyperplasia.

Next locate the inclusion-rich portion of the lesional epithelium.

Verify homogeneous cytoplasmic bodies with compressed peripheral nuclei.

Finally assess rupture, inflammation, or secondary surface infection.

Architecture

Cytoplasm

Nuclei

Complications

Conceptual sequence

Slide 47 · Special stains usually add little

H&E morphology generally makes the diagnosis.

DermNet notes that the characteristic inclusions limit special-stain utility.

Lendrum phloxine–tartrazine staining is a described specialist technique.

Ancillary work-up is targeted to alternative diagnoses rather than routine cases.

Slide 48 · Molluscum versus verruca vulgaris

Feature

Molluscum contagiosum

Verruca vulgaris

Etiology

Poxvirus

Human papillomavirus

Surface

Smooth; umbilicated

Rough; papillomatous

Architecture

Central cup or crater

Papillary epidermal proliferation

Viral cytopathy

Cytoplasmic bodies

Koilocytes with perinuclear halos

Slide 49 · HPV koilocytes are not molluscum bodies

HPV cytopathy involves perinuclear clearing and nuclear alteration.

Molluscum features dense, large inclusions in the cytoplasm.

Molluscum lesions form a central cup rather than primarily radiating papillae.

Cell-level and low-power findings should agree before signing out.

Cytoplasmic inclusion

Peripheral nucleus

Schematic—not a histologic specimen

Slide 50 · Molluscum versus superficial impetigo

Finding

Molluscum contagiosum

Impetigo

Primary agent

Poxvirus

Commonly Staphylococcus aureus

Clinical lesion

Umbilicated firm papule

Pustule → erosion → honey crust

Microscopy

Viral inclusions in keratinocytes

Subcorneal neutrophilic pustule

Complication

May become secondarily infected

Primary bacterial infection

Slide 51 · Molluscum versus superficial dermatophytosis

Finding

Molluscum

Dermatophytosis

Lesion

Umbilicated papule

Often annular/scaly plaque

Site of microbe

Epidermal epithelial cells

Cornified layer, hair, or nails

Diagnostic finding

Cytoplasmic viral bodies

Fungal hyphae in keratin

Helpful study

Clinical features or H&E

KOH / PAS depending on setting

Slide 52 · Rupture and inflammation may mask viral bodies

Follicular rupture can generate suppuration and marked inflammation.

Inclusion-bearing epithelial cells may be sparse in the most inflamed region.

Examine less-disrupted epithelium and adjacent sections if necessary.

A heavy infiltrate alone should not overturn characteristic viral morphology.

Slide 53 · A structured approach to an umbilicated papule

Confirm whether the surface truly contains a central pit and waxy core.

Assess distribution, age, exposure history, and immune status.

Look for morphology inconsistent with molluscum: Rough surface, pustule, scale.

Biopsy or alternate studies are appropriate if diagnosis remains uncertain.

Morphology

Context

Differential

Confirm if atypical

Conceptual sequence

Slide 54 · Observation versus active therapy

Uncomplicated infection in an immunocompetent patient often resolves.

Treatment may be considered for symptomatic, extensive, or genital disease.

Explain that procedures can cause irritation, pain, or scarring.

Shared decision-making weighs transmission, appearance, symptoms, and burden.

Slide 55 · Avoid unnecessary traumatic extraction

Scraping and squeezing can disrupt skin and promote inoculation elsewhere.

Office-based destruction must not be equated with home manipulation.

Mechanical removal can produce post-procedural pain and scar formation.

Counsel against picking and against unverified online remedies.

Slide 56 · Clinician-performed procedures: Risks and tradeoffs

Cryotherapy, curettage, and laser treatment are options in selected patients.

They require clinician judgment and often local anesthesia.

Pain, irritation, and potential scarring can outweigh benefits in mild disease.

These modalities are not interchangeable with observation in low-risk children.

Slide 57 · FDA-approved cantharidin (United States)

In 2023, the FDA approved topical cantharidin (Ycanth) for molluscum.

The U.S. Indication includes adults and children aged 2 years or older.

Administration is by a healthcare provider, not unsupervised home extraction.

This is supplemental treatment information, not part of the Robbins morphology text.

Slide 58 · FDA-approved berdazimer gel (United States)

FDA approved berdazimer (Zelsuvmi) in January 2024.

The U.S. Indication includes patients 1 year of age or older.

Berdazimer is a topical nitric-oxide–releasing treatment applied to lesions.

Regulatory age cutoffs refer to U.S. Prescribing information, not diagnostic criteria.

Slide 59 · Management in immunocompromised patients

Disseminated or persistent lesions may resist standard local therapy.

Optimizing underlying immune function is a major management consideration.

Concurrent bacterial infection and atypical lesions require separate assessment.

Coordinate care with clinicians managing the underlying immunosuppression.

Slide 60 · Preventing spread at home

Cover lesions where feasible and maintain hand hygiene.

Avoid scratching, shaving across lesions, and sharing towels or clothing.

Do not squeeze out the contents or attempt home removal.

Explain that exposure and autoinoculation can produce new lesions over time.

Slide 61 · School, daycare, and swimming

CDC does not recommend excluding children solely because of molluscum.

Covering lesions reduces opportunities for contact transmission.

Shared objects, rather than pool water itself, are a more likely pool-associated route.

Open or secondarily infected sores require appropriate protection and evaluation.

Slide 62 · Case 1: Multiple papules in a school-aged child

A child has several firm, pearly papules on the trunk and upper arm.

Each papule has a central depression; The child is otherwise well.

What etiologic agent and route of transmission are most likely?

Explain why immediate destructive therapy may not be necessary.

Central depression

Waxy core

Epidermis

Dermis

Schematic: Exaggerated vertical scale

Slide 63 · Case 1: Clinicopathologic reasoning

Diagnosis: Uncomplicated molluscum contagiosum.

Agent: Cutaneous poxvirus; Typical exposure is direct contact or fomites.

Morphology: Central umbilication corresponds to crateriform epidermal growth.

Approach: Counsel, observe where appropriate, and reduce autoinoculation.

Slide 64 · Case 2: Inclusion-rich epidermal biopsy

A small papule is biopsied after uncertainty about a viral wart.

Histology shows cup-like epidermal hyperplasia and large cytoplasmic bodies.

The inclusions lie in the granular and cornified epidermal layers.

Which microscopic feature decisively distinguishes it from an HPV wart?

Central crater

Lobulated epidermal proliferation

Schematic—not a histologic specimen

Slide 65 · Case 2: The decisive distinction

Molluscum: Homogeneous, large intracytoplasmic viral inclusions.

Verruca: HPV-related koilocytosis with nuclear-associated alterations.

The cup-shaped architecture further supports molluscum contagiosum.

Do not mistake viral inclusions for isolated keratohyalin granules.

Cytoplasmic inclusion

Peripheral nucleus

Schematic—not a histologic specimen

Slide 66 · Case 3: Unusually widespread facial papules

An adult with immune suppression has numerous enlarged facial papules.

Some lesions lack the typical small, neat umbilicated appearance.

Which clinical context should be considered and why might biopsy be useful?

What additional issues affect management and prevention of complications?

Slide 67 · Case 3: Integrate immune context

An immune-deficient state can produce more numerous and larger lesions.

Histologic viral inclusions can resolve uncertain clinical morphology.

Consider an expanded differential rather than diagnosing from site alone.

Management addresses immune status, lesion burden, and secondary infection.

Slide 68 · Synthesis: Three levels of diagnostic evidence

Clinical: Pearly, firm, centrally umbilicated papules.

Histologic: Crateriform epidermal hyperplasia with viral inclusions.

Cytologic: Giemsa-stained material containing molluscum bodies.

Immune status and lesion distribution inform diagnostic confidence and care.

Slide 69 · Five high-yield points

Molluscum contagiosum is a self-limited cutaneous poxvirus infection.

Transmission includes direct contact, shared objects, and autoinoculation.

Look for a smooth dome-shaped papule with central umbilication.

Henderson–Patterson bodies are large intracytoplasmic inclusions.

Observation is often suitable; Atypical or immunocompromised cases need more care.

Slide 70 · Selected sources and image-status note

Primary textbook

Robbins, Cotran & Kumar. Pathologic Basis of Disease. 11th ed. (2026). Chapters 25 and 22.

Supplementary clinical and pathology sources

CDC: Clinical Overview; About Molluscum Contagiosum; Schools and Daycares (2025).

DermNet: Molluscum contagiosum; Molluscum contagiosum pathology.

U.S. FDA: cantharidin (2023) and berdazimer gel (2024) approvals.

All cellular and lesion illustrations are original editable schematics, not authentic clinical photographs or histopathology sections.