Infection

Slide 1 · Infection

Cutaneous infections: mechanisms, morphology and clinicopathologic recognition

Viral • bacterial • superficial fungal infections

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning objectives

By the end of this lecture, students should be able to:

Classify selected skin infections by pathogen group and epidermal compartment.

Link pathogen-specific mechanisms to characteristic visible and microscopic lesions.

Distinguish warts, molluscum, impetigo and superficial mycoses using diagnostic clues.

Select an appropriate microscopic or microbiologic approach when required.

Slide 3 · Why does the skin remain vulnerable?

A formidable barrier is continuously exposed to the environment.

Frequent trauma provides opportunities for microbial access to susceptible tissue.

The epidermis is in continuous contact with microorganisms, parasites and insects.

Some infections remain local; Host immune competence helps determine their impact.

The disease pattern depends on the infectious agent and the tissue response.

Slide 4 · From exposure to cutaneous disease

Environmental contact

→

Barrier or host susceptibility

→

Microbial colonization / infection

→

Tissue reaction and lesion

The same exposure may have very different consequences depending on the host and the depth and type of tissue involved.

Slide 5 · Immunocompromise changes the risk

A seemingly trivial skin infection can become dangerous.

That ordinarily limited cutaneous infections can become life-threatening in immunocompromised hosts.

Assessment therefore includes immune status, lesion burden and evidence of extension.

The severity of illness is not determined by lesion size alone.

Slide 6 · Anatomic location helps organize infections

Stratum corneum

Living epidermis

Dermis

Subcutis

Dermatophytes

Predominantly cornified surface

HPV / molluscum

Epidermal epithelial lesions

Impetigo

Superficial intraepidermal pustules

Slide 7 · A practical overview of pathogen groups

Group

Representative lesion

Mechanistic emphasis

Papillomavirus

Verrucae (warts)

Viral-driven epidermal proliferation

Poxvirus

Molluscum contagiosum

Cytoplasmic inclusions within epidermal cells

Bacteria

Impetigo

Neutrophilic pustules and surface crust

Dermatophytes / yeast

Tinea syndromes / versicolor

Involvement of cornified tissue or surface

These are representative skin-predominant infections, not an exhaustive infectious-disease taxonomy.

Slide 8 · Clinical morphology is a diagnostic language

A descriptive lesion pattern can narrow the differential.

Rough papules suggest a proliferative epidermal process.

Umbilicated papules raise suspicion for molluscum contagiosum.

Pustules that rupture into honey-colored crust point toward impetigo.

An expanding scaly border suggests a superficial dermatophyte infection.

Slide 9 · Four patterns: One compact differential

Observed pattern

Priority exemplar

Distinctive tissue clue

Rough, keratotic papule

Verruca vulgaris

Papillomatosis + koilocytosis

Smooth, centrally umbilicated papule

Molluscum

Cytoplasmic molluscum bodies

Crusted erosion or pustule

Impetigo

Subcorneal neutrophilic pustule

Scaly, often annular plaque

Tinea corporis

Hyphae in cornified keratin

Slide 10 · Direct infection versus reactive skin findings

A cutaneous finding does not always mean local microbial proliferation.

Warts, molluscum, impetigo and superficial mycoses represent processes with primary cutaneous manifestations.

An infection elsewhere may provoke a cutaneous immune reaction; The skin finding is then not simply a local focus of microbial growth.

Herpes simplex, herpes zoster, viral exanthems and deep fungal diseases are additional infection-related patterns addressed in other Robbins sections.

Slide 11 · Verrucae are HPV-induced proliferations

The primary lesion is a virally driven epidermal growth.

Human papillomaviruses produce benign-appearing warts at characteristic anatomic sites.

Verrucae are particularly common in children and adolescents, but occur at any age.

The clinical subtypes differ by surface morphology and location.

Histopathology reflects keratinocyte proliferation and viral cytopathic change.

Slide 12 · Transmission of cutaneous warts

Direct contact

→

Epidermal HPV infection

→

Local epidermal proliferation

→

Clinical wart

Autoinoculation can move infection from one cutaneous site to another; Direct person-to-person contact is also described.

Slide 13 · Warts often regress without intervention

Natural history is usually self-limited.

That many verrucae regress spontaneously over approximately 6 months to 2 years.

A persisting papule therefore need not indicate invasive neoplasia.

Clinical context and histology are important for lesions with atypical morphology.

Slide 14 · HPV types are biologically heterogeneous

Not all HPV genotypes have equivalent tissue or oncogenic effects.

More than 150 papillomavirus types are discussed.

Different types are associated with different forms of cutaneous and anogenital warts.

Site, viral genotype and host background jointly affect clinical interpretation.

Slide 15 · Selected HPV genotype associations

HPV types

Association in Robbins

Interpretive point

6, 11

Predominant types in anogenital warts

Typically low-risk associations

16

Genital carcinoma in situ and bowenoid papulosis

High-risk HPV association

5, 8

Epidermodysplasia verruciformis-associated lesions

Unusual host and lesion context

Slide 16 · HPV 6 and 11: Anogenital warts

Anogenital site and verrucous architecture are linked.

Anogenital warts are predominantly associated with HPV types 6 and 11.

Condyloma acuminatum appears as a soft, tan, cauliflower-like growth.

Typical anogenital distribution includes genital and perianal mucocutaneous sites.

Slide 17 · HPV 16 and high-risk intraepithelial lesions

A subset of HPV infections is linked to neoplastic change.

HPV 16 with genital squamous carcinoma in situ and bowenoid papulosis.

Bowenoid papulosis may show carcinoma-in-situ histology despite an often regressive clinical course.

Do not equate ordinary verruca vulgaris with an HPV-associated neoplastic lesion.

Slide 18 · HPV 5 and 8: Unusual host association

Epidermodysplasia verruciformis provides a distinct context.

Patients may develop numerous flat wart-like lesions containing HPV genomes.

Some lesions can progress to squamous cell carcinoma.

This uncommon setting should not be generalized to ordinary self-limited warts.

Slide 19 · Oncogenic HPV mechanism emphasized by Robbins

High-risk HPV

→

E6 viral oncoprotein

→

Loss of p53 function

→

Reduced tumor-suppressor protection

This selected mechanism explains a cancer association in high-risk HPV infection; It does not define the behavior of every cutaneous HPV subtype.

Slide 20 · Low-risk HPV: Altered keratinocyte differentiation

Low-risk HPV E6

→

Interference with Notch signaling

→

Impaired normal maturation

→

Epidermal hyperplasia

Interference with Notch-dependent differentiation as a likely contributor to wart hyperplasia.

Slide 21 · Verruca vulgaris: Prototypical surface pattern

Papillary epidermal hyperplasia

Often a rough, pebble-like papule.

Common on the hands, including dorsal and periungual areas.

Color varies with background skin pigmentation.

Original schematic; Not a clinical image or photomicrograph

Slide 22 · Flat warts differ from common warts

Clinical designation depends on contour and distribution.

Verruca plana tends to form small, slightly elevated, smooth, flat papules.

Typical locations include the face and dorsal surfaces of the hands.

The lack of an obvious rough surface does not exclude HPV infection.

Slide 23 · Palmar / plantar warts versus common warts

Palmar or plantar verrucae

Arise on palms or soles.

Rough, scaly lesions; May resemble a callus.

Can reach approximately 1–2 cm in the source description.

Verruca vulgaris

Commonly occurs on dorsal hands and near nails.

Rough, pebble-like surface.

Frequently small papules measuring about 0.1–1 cm.

Slide 24 · Condyloma acuminatum: Clinical architecture

Exophytic anogenital warts can become sizable.

Lesions are soft, tan, papillary or cauliflower-like masses.

Involvement may include genital, perianal, urethral and rectal locations.

Microscopic changes may be subtler than in common cutaneous verrucae.

Slide 25 · Verrucae: Papillomatous epidermal architecture

Papillary epidermal hyperplasia

Epidermal hyperplasia can be undulant, papillomatous or spire-like.

The proliferating squamous epithelium creates the rough surface.

Architectural changes must be integrated with cellular viral effects.

Original schematic; Not a clinical image or photomicrograph

Slide 26 · Koilocytosis: Cytopathic evidence

Pale perinuclear halo + altered nucleus

Superficial epidermal cells show conspicuous perinuclear pallor.

The halo surrounds an altered infected nucleus.

Koilocytosis supports HPV-associated epithelial change in context.

Original schematic; Not a clinical image or photomicrograph

Slide 27 · Other HPV cytopathic features

The diagnosis is more than a single perinuclear halo.

Prominent condensed keratohyalin granules.

Jagged eosinophilic intracytoplasmic keratin aggregates can occur.

Infected nuclei contain virions demonstrable ultrastructurally.

Condylomata may have less obvious cytopathic alteration than common warts.

Slide 28 · HPV typing is not synonymous with morphology

Molecular detection answers a different question.

In situ hybridization or polymerase chain reaction can determine HPV type.

The routine wart pattern is initially a clinicopathologic diagnosis.

Molecular genotype becomes pertinent when the clinical question concerns viral association or risk context.

Slide 29 · Molluscum: A poxvirus infection of epidermis

The lesion is typically benign and self-limited.

Molluscum contagiosum is caused by a poxvirus, not a papillomavirus.

Person-to-person direct contact is a usual route of spread.

Children and young adults are common affected groups.

The lesion exhibits highly characteristic intracytoplasmic inclusions.

Slide 30 · Poxvirus architecture distinguishes the pathogen

The infectious agent is unusually large for a virus.

A brick-shaped virion with a dumbbell-shaped DNA core.

Its maximal dimension is given as approximately 300 nm.

These ultrastructural features identify the virus family; They are not needed to diagnose a routine papule clinically.

Slide 31 · Clinical hallmark: The umbilicated papule

Morphology can be more decisive than symptoms.

Firm pink or skin-colored papules show a central umbilication.

Lesions may be pruritic and are usually multiple.

The trunk and anogenital areas are common distributions.

Typical papules around 0.2–0.4 cm; Larger lesions are unusual.

Slide 32 · Molluscum: Central umbilication

Central umbilication

Epidermal papule

A depressed center is characteristic of the clinical papule.

A curd-like core may be expressed from the depression.

Surface appearance should be correlated with tissue morphology.

Original schematic; Not a clinical image or photomicrograph

Slide 33 · Histologic configuration: A cup-shaped lesion

Molluscum causes a distinctive growth pattern of epidermis.

The affected epithelium forms a cup-like focus of verrucous hyperplasia.

Keratinocytes accumulate large intracytoplasmic viral inclusions.

The virus-containing structures are concentrated in upper epidermal layers.

Slide 34 · Molluscum bodies: An inclusion signature

Large cytoplasmic viral inclusion

Ellipsoid homogeneous inclusions occupy the cytoplasm.

They may enlarge to approximately 35 μm account.

Numerous viral particles are present within the inclusions.

Original schematic; Not a clinical image or photomicrograph

Slide 35 · Molluscum bodies change staining appearance

Their position in the epidermis affects H&E color.

Eosinophilic inclusions in the stratum granulosum.

At the stratum corneum, the inclusions can acquire a pale blue appearance.

The same diagnostic structure is therefore recognizable in more than one staining state.

Slide 36 · From molluscum lesion to cytologic confirmation

Umbilicated papule

→

Core material obtained

→

Giemsa-stained smear

→

Diagnostic molluscum bodies

The textbook specifically describes a smear of expressed core material as a way to display inclusion bodies.

Slide 37 · Verruca versus molluscum

Feature

Verruca (HPV)

Molluscum (poxvirus)

Surface

Rough / papillomatous in common wart

Often smooth, centrally umbilicated

Architectural clue

Papillary epidermal hyperplasia

Cup-like epidermal hyperplasia

Signature cytopathy

Koilocytosis

Intracytoplasmic molluscum bodies

Molecular group

Human papillomavirus

Poxvirus

Slide 38 · Impetigo is a superficial bacterial infection

Its dominant lesion is pustular and crusted.

Impetigo is highly contagious and classically affects children.

Exposed sites, particularly the face and hands, are frequent locations.

The primary histologic event involves the superficial epidermis.

Deep dermal involvement is generally absent in uncomplicated lesions.

Slide 39 · Contemporary etiology

Historical organisms and present patterns should not be conflated.

Older descriptions linked nonbullous impetigo largely to group A β-hemolytic streptococci.

Bullous impetigo was classically associated with Staphylococcus aureus.

S. Aureus now commonly causes both forms.

Slide 40 · Nonbullous versus bullous impetigo

Feature

Nonbullous (contagiosa)

Bullous form

Typical morphology

Smaller pustules and erosions

Larger fragile blisters / pustules

Clinical context

Often on exposed sites

Especially encountered in children

Agent in Robbins

S. aureus frequently implicated

S. aureus implicated

Basic tissue plane

Very superficial epidermis

Very superficial epidermis

The source distinguishes forms chiefly by lesion size, not by an entirely different infected organ.

Slide 41 · Impetigo lesion evolution

Erythematous macule

→

Superficial pustules

→

Pustular rupture

→

Shallow erosion + crust

Exuded serum, inflammatory cells and debris dry on the surface; New lesions may appear around the edges.

Slide 42 · Why is the crust honey-colored?

A visible sign reflects epidermal exudation.

Bacteria provoke epidermal injury and a local innate inflammatory response.

Pustular contents include serum proteins and neutrophils.

After rupture, serous material and cellular debris dry to form a superficial crust.

The crust is a consequence of tissue reaction, not a pigmented microbial colony.

Slide 43 · Impetigo: Subcorneal pustule

Neutrophil-rich subcorneal pustule

Neutrophils accumulate immediately beneath the stratum corneum.

Serum and inflammatory cells occupy a superficial pustule.

Special stains may demonstrate bacteria in the lesion.

Original schematic; Not a clinical image or photomicrograph

Slide 44 · The bacterial response remains epidermal

Innate immunity can create much of the lesion morphology.

Microbial presence triggers an acute inflammatory response in the epidermis.

Reactive epithelial change and mild superficial dermal inflammation accompany pustules.

The superficial location explains the propensity for crusting and healing without scarring.

Slide 45 · Bullous impetigo: Desmoglein 1 injury

Staphylococcal toxin

→

Desmoglein 1 cleavage

→

Loss of upper-cell cohesion

→

Superficial epidermal blister

Desmoglein 1 is an intercellular adhesion protein; Cleavage creates a high epidermal plane of separation.

Slide 46 · One target, two diseases: Dsg1

Feature

Bullous impetigo

Pemphigus foliaceus

Primary mechanism

Bacterial toxin cleaves desmoglein 1

Autoantibodies compromise desmoglein 1

Disease class

Superficial infection

Autoimmune blistering disease

Shared morphology

Superficial epidermal separation

Superficial epidermal separation

Similar blister planes do not prove identical pathogenesis.

Slide 47 · Why uncomplicated impetigo does not scar

Healing potential reflects the depth of damage.

The virtual absence of substantial dermal involvement.

Epidermal repair can proceed after microbial elimination.

Deep dermal destruction is not a typical feature of uncomplicated superficial impetigo.

Slide 48 · Recognition of impetigo: The combined clues

No single feature should be interpreted in isolation.

Look for clustered pustules, shallow erosions and adherent yellow-gold crust.

Consider exposed skin sites and interpersonal spread.

A subcorneal neutrophilic pustule strongly supports the characteristic tissue reaction.

Remember that similar-appearing superficial blisters may have noninfectious causes.

Slide 49 · Superficial fungal infections favor keratinized sites

Anatomic restriction is foundational.

The Robbins section contrasts superficial fungi with deep infections of the dermis or subcutis.

Dermatophyte infections involve cornified skin, hair or nails.

Different sites produce different tinea names and clinical appearances.

Slide 50 · Depth matters in dermatophytosis

Stratum corneum

Living epidermis

Dermis

Subcutis

Dermatophytes

Predominantly cornified surface

HPV / molluscum

Epidermal epithelial lesions

Impetigo

Superficial intraepidermal pustules

Slide 51 · Where dermatophytes come from

Transmission and local milieu affect susceptibility.

Dermatophytes can be associated with soil and animals in the source account.

Exposure to infected animals is a recognized risk for some tinea corporis lesions.

Heat, humidity, friction and maceration favor selected distributions.

Persistent infection in one keratinized site can coexist with spread to others.

Slide 52 · Dermatophytosis: The anatomic nomenclature

Name

Location

Characteristic association

Tinea capitis

Scalp / hair

Patchy scale and hair loss

Tinea barbae

Beard region

Adult male beard-area infection

Tinea corporis

Glabrous skin

Expanding scaly plaque

Tinea cruris

Inguinal / upper thigh

Warm, moist fold distribution

Tinea pedis

Feet / toe webs

Scale, erythema and maceration

Slide 53 · Tinea capitis: Hair-bearing scalp disease

The hair unit makes the presentation distinctive.

Scalp dermatophytosis is described mainly in children.

Patchy lesions may produce mild erythema, scale and crust.

Associated hair loss is a clinically informative site-specific clue.

Slide 54 · Tinea barbae: Beard-area infection

The same family of organisms presents differently by site.

Dermatophytes can involve the beard region.

The disease is comparatively uncommon in the Robbins survey.

Its recognition requires distinguishing a keratin-related infection from other follicular lesions.

Slide 55 · Tinea corporis: An expanding annular lesion

The active edge often provides the key morphological clue.

Typical disease is a round, slightly erythematous plaque.

The peripheral border is raised and scaly.

Heat, humidity, exposure to animals and another dermatophyte focus are described risk contexts.

Slide 56 · Tinea corporis: The border is diagnostic

Expanding raised scaly edge

An outwardly expanding scaly edge defines the lesion.

The center may appear less active than the advancing margin.

A ring-like lesion is a clinical pattern, not proof of an organism without context.

Original schematic; Not a clinical image or photomicrograph

Slide 57 · Tinea cruris: Macerated inguinal skin

The local environment shapes disease distribution.

The process commonly affects the upper inner thighs and groin.

Heat, friction and maceration are predispositions.

The lesions appear as moist, erythematous patches with raised scaly borders.

Slide 58 · Tinea pedis: Interdigital scaling

Toe webs are a common starting location.

Scaling and erythema frequently localize initially to interdigital spaces.

The source notes that superimposed bacterial infection can drive a substantial component of inflammation.

Not every inflamed area in tinea pedis is a direct effect of dermatophyte growth.

Slide 59 · Tinea pedis: Mixed microbial contributions

Dermatophyte in cornified skin

→

Barrier disturbance / surface change

→

Possible bacterial superinfection

→

Amplified inflammation

Primary dermatophytosis from inflammation attributable to secondary bacteria at some sites.

Slide 60 · Nail involvement: Onychomycosis

Keratinized nail tissue creates a different visible lesion.

Dermatophyte infection may involve nails directly or extend from skin infection.

The nail plate can become thickened, discolored and deformed.

The gross nail changes indicate a differential diagnosis; Species assignment requires appropriate material.

Slide 61 · Tinea versicolor is not a dermatophytosis

The causative organism belongs to a different fungal group.

Tinea versicolor to Malassezia furfur, a yeast.

The upper trunk is a typical distribution.

Patchy macules of variable coloration have fine peripheral scaling.

Do not classify every condition called “tinea” as a dermatophyte infection.

Slide 62 · Dermatophyte infection versus tinea versicolor

Feature

Dermatophyte disease

Tinea versicolor

Agent

Dermatophyte fungi

Malassezia furfur (yeast)

Distribution

Site-specific skin, hair, nails

Most often upper trunk

Lesion pattern

Scale; annular edge in tinea corporis

Varicolored macules with fine scale

Classification

Dermatophytosis

Superficial yeast-associated eruption

Slide 63 · Dermatophyte histology is not always specific

Host reaction and superinfection modify the slide.

Routine sections may show a mild spongiotic or eczematous reaction.

Intraepidermal neutrophils can accompany infection.

Morphology varies with organism, host response and bacterial coinfection.

The organism may be inconspicuous on routine H&E sections.

Slide 64 · Fungal structures are found in cornified tissue

Fungal forms within cornified layer

Look in anucleate stratum corneum or other keratinized specimens.

Hyphae can be highlighted by periodic acid–Schiff (PAS).

The conceptual diagram indicates location, not a diagnostic photomicrograph.

Original schematic; Not a clinical image or photomicrograph

Slide 65 · Confirmatory fungal examination

Scraping / affected keratin

→

Fungal visualization (PAS in tissue)

→

Culture when indicated

→

Organism identification

Culture of material scraped from affected cornified skin, hair or nails as a route to species identification.

Slide 66 · Histologic signatures: A comparative map

Infection

Architecture / level

Key feature

Verruca

Papillomatous epidermal expansion

Koilocytosis

Molluscum

Cup-like epidermal hyperplasia

Large cytoplasmic inclusions

Impetigo

Subcorneal pustule

Neutrophils; bacteria may be demonstrable

Dermatophytosis

Cornified layer involvement

Hyphae, enhanced by PAS

Slide 67 · Clinical surface patterns: Rapid recognition

Surface sign

Most relevant exemplar

Interpretation

Rough keratotic papules

Common wart

Papillomatous proliferation

Dome-like umbilicated papules

Molluscum

Poxvirus inclusion-producing lesion

Honey-colored crust

Impetigo

Ruptured superficial pustule

Raised scaly annular border

Tinea corporis

Keratin-involving fungal infection

Slide 68 · A rational approach to tissue confirmation

Sample and stain for the question being asked.

HPV-associated lesions are interpreted by papillary architecture and koilocytosis; Typing is an additional molecular question.

Molluscum bodies are visible in lesion histology or potentially in a smear of core material.

Impetigo is supported by a subcorneal neutrophilic pustule and organism demonstration when needed.

Dermatophytosis is evaluated in cornified material, with PAS or culture as applicable.

Slide 69 · Case discussion: Centrally umbilicated papules

A school-age child has several firm, skin-colored papules on the trunk. Each has a small central depression. One papule yields a curd-like central core.

Diagnostic question

Which infectious lesion best explains the surface morphology, and what cellular inclusion would you seek?

Discussion: Link the clinical clue to its tissue-level signature.

Slide 70 · Case discussion: Superficial golden crust

A child develops a red macule that evolves into small pustules. Several rupture, leaving shallow erosions with adherent yellow-gold crust on exposed facial skin.

Diagnostic question

What is the most likely process, and where should neutrophils be found histologically?

Discussion: Link the clinical clue to its tissue-level signature.

Slide 71 · Case discussion: Enlarging scaly plaque

A patient presents with a rounded erythematous plaque on the trunk. The edge is elevated and scaly, with gradual outward extension.

Diagnostic question

Which infectious group is most likely, and what tissue compartment should be evaluated?

Discussion: Link the clinical clue to its tissue-level signature.

Slide 72 · Case discussion: A rough papule on the hand

A young patient has a longstanding rough papule near a fingernail. The surface is irregular and pebble-like.

Diagnostic question

What infection is likely, and what viral cytopathic change should be sought?

Discussion: Link the clinical clue to its tissue-level signature.

Slide 73 · Integrating agent, lesion and tissue signature

Identify lesion morphology

→

Locate affected compartment

→

Recognize signature cytopathy / inflammation

→

Select focused confirmation

Reliable dermatopathologic inference combines clinical architecture, host context and the correct microscopic level.

Slide 74 · Final synthesis: Four mechanisms, four visual signatures

The clinically visible lesion arises from a specific tissue process.

HPV: Epidermal hyperplasia plus koilocytic cytopathy → verrucous papule.

Poxvirus: Abundant cytoplasmic viral inclusions → umbilicated papule.

Impetigo: Superficial neutrophilic injury, sometimes toxin-mediated splitting → pustule and crust.

Superficial fungi: Growth in cornified tissue → scale, annularity or nail/hair changes.

Slide 75 · Primary reference

Textbook material underlying this lecture

Robbins, Cotran & Kumar. Pathologic Basis of Disease. 11th edition (2026). Chapter 25: The Skin.

Relevant textbook sections: Infection; Verrucae (Warts); Molluscum Contagiosum; Impetigo; and Superficial Fungal Infections.