Pathology: SKIN INFECTIONS Verruca plantaris and palmaris (palmoplantar wart=both)

Viral Skin Infections  Occur on the soles (Verruca plantaris) and palms
1. Verrucae (Verruca Palmaris)
2. Herpes Simplex Virus infection  Rough scaly lesions, 1-2 cm in diameter; may
3. Varicella –Zoster coalesce and be confused with calluses
4. Molluscum contagiosum
Morphology:
I. Verrucae (warts)
 Common lesions of children and adolescents but may
be encountered at any age
 Caused by human papilloma viruses
 Transmission: direct contact
 Generally self-limited, regressing spontaneously
within 6 months up to 2 years

Classification based on Location and Clinical Morphology:

 Verruca vulgaris
 Verruca plana
 Verruca plantaris / palmaris (Palmoplantar wart)
 Condyloma acuminatum

Verruca vulgaris
Condyloma acuminatum
 Common wart
 Venereal wart, Anogenital wart
 Associated with HPV-2,4, and 7
 Occurs on the penis, female genitalia, urethra,
 Occur at any site but most frequently on the dorsal
perianal area and rectum
aspect of the finger and hands
 Appear as soft, tan, cauliflower- like masses
 Painless, circumscribed, firm, elevated, papules 1-
 Low risk: HPV 6, 11 (BENIGN)
10mm in size with papillomatous (“verrucous” )
 High risk: HPV 16,18,31,33  associated with
hyperkeratotic surfaces
anogenital cancers(MALIGNANT)
 Generally self-limited but may persist for a few
months up to several years
 Koebner phenomenon : formation of new warts at
sites of trauma(pagkamot dagdag ng warts)

Histopathology: Verucae
 Acanthosis, papillomatosis, hyperkeratosis,
parakeratosis
 Verruca plana : same histologic features as verruca
 Circumscribed, firm, elevated, papules 1-10mm in size
vulgaris but “without papillomatosis”(reason kung
with papillomatous (“verrucous” ) hyperkeratotic
bakit sya flat)
surfaces

Verruca plana
 Flat wart
 Common on the face and or the dorsal surfaces of the
hand
 Slightly elevated, flat, smooth, tan papules generally
smaller than verruca vulgaris

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 II. Herpes simplex infection
 Herpes simplex virus type 1- orofacial type

Ex. Acute gingivostomatitis, Lips (herpes labialis, or

“cold sores”), any part of the skin, oral mucosa

 Herpes simplex virus type 2 – genital type

Ex. Herpes Genitalis

 Transmitted through the exchange of saliva, semen,

cervical fluid or vesicle fluid from active lesions
 Koilocytic cells in the upper stratum malphigii
and in the granular layer Pathogenesis:
 Produce acute and latent infections
 Koilocytes : small, round, deeply basophilic  Replicate in the skin and mucous membranes at the
nuclei surrounded by a clear halo and pale- site of entrance (usually oropharynx or genitals)
staining cytoplasm   produce infectious virions  vesicular lesions of the
epidermis
 Spread to sensory neurons  establish latent infection

Gross:
 Cold sores
 Blisters and vesicles around mucosal orifices (lips,
nose)
 Formed by intercellular edema and ballooning
degeneration of epidermal cells
 Gingivostomatitis
 Usually encountered in children; HSV-1
 Vesicular eruption extending from the tongue to
 Clumped keratohyaline the retropharynx; (+) cervical lymphadenopathy
granules(Hypergranulosis)  Patient will have painful swallowing
 Genital herpes
 HSV-2
 Vesicles on genital mucous membranes and
external genitalia  burst ulcerate
 Can be transmitted to neonates during passage
through the birth canal (herpes keratitis,
fulminant infection)

 Verrucus growth pattern

 Koilocytic change of the cells

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Histopathology:

 Ballooning degeneration of epidermal cells

 Acantholysis

Shingles- Herpes Zoster

Gross:
 Activation of latent infection
 Affects the elderly
 Grouped vesicles along the course of a sensory nerve
 Vesicle bases frequently hemorrhagic, some necrotic and
may ulcerate
 Some lesions indistinguishable from Varicella

 Cowdry type A inclusions:

 Large, pink to purple intranuclear inclusions
 Contain intact and disrupted virions
 Multinucleated cells(Glassy nuclei)

III. Varicella zoster

 Chicken pox and shingles
 Acute infection : chicken pox (varicella)
 Reactivation: shingles (herpes zoster)

Pathogenesis:
 Infects mucous membranes, skin, and neurons
 Self-limited primary infection in immunocompetent
individuals
 Establishes latent infection in sensory ganglia
 Transmitted in epidemic fashion by aerosols  Re-activation of infections appear on the dermatomal lines
 Disseminates hematogenously widespread
vesicular skin lesions Histopathology:
 Infects neurons and/or satellite cells around
neurons in the dorsal root ganglia
 Localized recurrence is most frequent and most
painful in dermatomes innervated by trigeminal
ganglia

Chicken pox- varicella

 90% of cases occur in children (< 14 y/o)
 Rash occurs approximately 2 weeks after
respiratory infection
 Centrifugal distribution
 Macule  vesicle (“dew drops on a rose petal”)
 In ganglia: (+) lymphoplasmacytic infiltrates with
 Vesicle: contains intranuclear inclusions
intranuclear inclusions within neurons
 Lesions in varying stages are present at one time
 Vesicles rupture  crust over heal by
regeneratiion
 Complications: pneumonitis, encephalitis
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Tzanck smear Bacterial Skin Infections
1. Impetigo
2. Furuncle
3. Carbuncle
4. SSSS
5. Erysipelas
6. Cellulitis
7. Leprosy

I. Impetigo
 Scrapings are subjected to PAP Smear  Caused by group A- beta hemolytic Streptococci and
Multinucleated giant cells andinclusion bodies Staphylococcus aureus
are found on tzanck smear  Impetigo contagiosa (nonbullous impetigo) : Strep
 Impetigo bullosa : Staph
IV. Molluscum contagiosum  Involves exposed skin, i.e. face and hands
 Common, self-limited  Erythematous macule  pustule shallow erosions 
 Caused by Poxvirus covered with drying serum (honey colored crust)
 Transmission : direct bodily contact or indirectly
via fomites Gross:
 Multiple lesions on the skin and mucous
membranes (trunk, and anogenital areas)

Gross:

Histopathology:
 Lesions are firm, often pruritic, pink to skin-  Accumulation of neutrophils beneath stratum corneum
colored, umbilicated papules (0.2-0.4cm)  Subcorneal pustules
 Curd-like material may be expressed from  Crust: serum, neutrophils and debris
umbilication

Molluscum bodies

 Nuclei are pushed toward the periphery

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II. Furuncle
 Focal suppurative inflammation of skin and
subcutaneous tissue
 Also known as “Boil” or Pigsa
 Recurrent
 Solitary or multiple
 Moist, hairy areas (face, groin, legs, axillae, and
submammary folds)
 Etiology: S.aureus
 Begins in a single hair follicle  abscess  thinning
and rupturing the overlying skin
RITTER’S DISEASE
-Caused by S. aureus
Gross:
 Split in granular layer
 Dermal edema, no necrosis of epidermis
 Acantholysis may be present
DDx:
Toxic Epidermal Necrolysis (Lyell’s disease)
-Caused by Drug interaction

III. Carbuncle
 Deeper suppuration that spreads laterally beneath
the deep subcutaneous fascia
 Eventually burrows superficially to erupt in multiple
adjacent skin sinuses
 Appear beneath the skin, upper back and posterior
neck
 May progress into osteomyelitis
 Etiology: S.aureus
V. Cellulitis
 Acute, diffuse spreading, edematous, suppurative
inflammation of deep subcutaneous tissue
 Lower extremities, periorbital area, scrotum
 Spreading infection, affecting deeper tissues
 Warm, tender, ill-defined margins
 Associated lymphangitis and lymphadenitis
 Necrotizing fasciitis : Involvement of underlying fascia and
muscle
 May ulcerate / necrose

IV. Staphylococcal Scalded Skin Syndrome: Ritter’s Disease

 Toxin-mediated, exfoliative dermatitis
 In children with Staph infection of nasopharynx and
skin
 Sunburn-like rash  bullae formation  partial or
total skin loss  sheared off
 Associated infection or source :
 URTI, conjunctivitis, umbilical sepsis or occult
infection
 Blister formation secondary to toxin that
specifically cleaves desmoglein 1 molecule
(responsible for cell to cell adhesion)
 Mortality: 2-3%

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Histopathology: Histopathology:

 Extensive Infllammation and invasion of

inflammatory cells

 Diffuse, acute, edematous, neutrophilic, interstitial

reaction : dermis, epidermis and subcutaneous tissue
VI. Erysipelas  Perivascular(surround blood vessels) and
 Middle-aged, warm climates periadnexal(surround eccrine glands and hair follicles of
 Caused by exotoxins from superficial infections the skin) microabscess
with S. pyogenes  Tissue necrosis may be minor
 Rapidly spreading, erythematous cutaneous
swelling VII. Mycobacteria
 May begin on the face, or less commonly, on the
body or extremity LEPROSY (Hansen’s Disease)
 Well-demarcated, serpiginous border :  Slowly progressive infection of skin and peripheral nerves
“butterfly” on face  Mycobacterium leprae
 Transmission: person-to-person via aerosols from lesions
in the upper respiratory tract
 Grows in cool places like skin and extremity
 Low communicability=needs large amount of pathogen
before eliciting an infection
 “Zeil-Neehlsen”-stain used for identifying acid fast
bacilli(look up nyo spelling di ko maalala tamang spelling)

Pathogenesis:
 Obligate intracellular, acid-fast organism
 Grows poorly in culture
 Grows at 32-34 C : human skin
 Cell-mediated immunity
 No toxins, virulence based on cell wall properties

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 A. TUBERCULOID LEPROSY Gross:
 Less severe form  Skin, peripheral nerves (ulnar and peroneal), anterior
 Dry, scaly skin lesions that lack sensation chamber of the eye, upper airways (down to the larynx),
 Asymmetric peripheral nerve involvement testes, hands and feet are involved
 Skin anesthesia, skin and muscle atrophy  Hypoesthetic  anesthetic
 Contractures, paralyses, autoamputation of  “Leonine facies”
fingers and toes

GROSS:
 Localized skin lesions (flat and red ) 
enlarge  irregular shapes with indurated,
elevated, hyperpigmented margins and
depressed pale centers (central healing)
 Paucibacillary (No organism)
 Prominent neuronal involvement
 (+) granulomas enclosing nerves  nerve
destruction
 T-cell immunity

Histopathology:

B. LEPROMATOUS LEPROSY
 More severe form
 Symmetric skin thickening and nodules
 Also called Anergic Leprosy
 Widespread invasioin of mycobacteria into
Schwann cells and into endoneural and  Globi : large aggregates of lipid-laden histiocytes (LEPRA
perineural macrophages cells=macrophage with organisms inside) filled with
masses of organism
 (-) granuloma formation : failure of TH1 response
 Grenz zone

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Globi (Fite Faraco) I. Dermatophytes
 Capable of colonizing keratinized tissue such as
stratum corneum of epidermis, hair and nails
 Stains used for demonstrating fungi:
 Periodic Acid Schiff (PAS) : Red Stain
 Gomori Methenamine Silver (GMS) : Black
Stain
 Dermatophytosis of the scalp
 Asymptomatic, often hairless patches of skin
associated with mild erythema, crust formation and
scale
 Arthrospores(asexual spores) coat the outside of
hairshaft and hyphae extend to the microfollicle

Tinea Capitis

Grenz zone

 Very well demarcated, often hairless patches of skin

with mild erythema, very itchy and presence of
scaling
 Area that is not affected by the disease between the
dermis and epidermis(white zone)
TInea Corporis

Tuberculosis of the Skin

*REFER TO GIVEN HANDOUT*
 Common superficial fungal infection of the body
surface that commonly affects persons of all ages, but
Fungal skin infections
particular in children
1. Dermatophytosis
2. Pityriasis versicolor  Predisposing factors: excessive heat and humidity,
3. Chromoblastomycosis exposure to infected animals, chronic
4. Phaeohyphomycosis dermatophytosis of feet or nails
5. Sporotrichosis  Seen as expanding, erythematous plaque with an
6. Mycetoma elevated scaling border

Histopathology:
DERMATOPHYTES
 Parakeratosis, acanthosis, neutrophils in
a) Epidermophyton
parakeratotic crust
b) Trichophyton
 Fungal hyphae seen in parakeratotic stratum
c) Microsporum
corneum
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  Mild dermal inflammation II. Tinea Versicolor(Ptyriasis Versicolor)
 Acanthosis, parakeratosis and mixed inflammatory  Malassezia furfur
infiltrate in superficial dermis  Common in tropical climate
 Multiple, irregular areas of hypo-and
Tinea Pedis hyperpigmentation seen primarily on the upper
 Athlete’s foot” trunk
 Diffuse erythema and scaling  Circular, macular, scaling, and erythematous
 Initially localized in the interdiginous areas
 Tinea unguium: specific term which refers to
dermatophyte infection of the nail. Gross:
 Discoloration, thickening and deformity of
the nail plate
 Onychomycosis : general term which refers
to nail infection due to any fungus including
dermatophytes

Histopathology:

Tinea cruris
 “jock itch”
 Sharply demarcated erythematous patches or thin
plaques in the inguinal area extending
crescentically down the thighs
 Common in men
 Predisposing factors:
 Heat, friction
 May spread to perineal and / or perianal regions as
well as the scrotum
 Common in men
 Erythematous plaque extending crescentically
down the thighs

 Mild acanthosis, hyperkeratosis, focal

parakeratosis, hypo-or hyperpigmentation
of basal layer
 Minimal superficial perivascular infiltrate in dermis

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“Spaghetti and meatballs”  Fungal elements: Round, dark brown, thick-walled,
ovoid sclerotic bodies, 6-12um
 “Stack of bricks” Murry-form(double check spelling)

IV. Phaeohyphomycosis
 Subcutaneous or systemic infection caused by pigmented,
fungi with both yeast-like and hyphal-like forms
 Bipolaris
 Phialophora
 Alternaria
 Exophiala
 Subcutaneous phaeohyphomycosis typically presents as a
solitary, discrete, asymptomatic, abscess or nodule on the
extremity
 History of trauma or a splinter can sometimes be elicited

III. Chromoblastomycosis Gross:

 Slowly progressive cutaneous mycosis caused by
dermatiaceous (pigmented) fungi that occur as
round, nonbudding forms in tissue sections
 Saprophytic fungi
 Phialophora
 Fonsacaea
 Exophiala
 Cladosporium
 Most common cause : Fonsacaea pedrosoi
 Primary lesion develops as a result of traumatic
implantation of the fungus into the skin
 Spread by autoinoculation of superficial lymphatic
vessels

Gross:  Always appear as a nodule in the digits

 Located in lower extremities as verrucous papules, Histopathology:
nodules and plaques(can be mistaken for verruca
because of wart-like appearance)

Histopathology:

 Suppurative granulomatous inflammation

  single large cavity with surrounding fibrous capsule,
 Pseudoepitheliomatous hyperplasia with heavy cont’g PMN’s and fibrin
dermal infiltrate of epithelioid histiocytes,  Organisms found within cavity and cavity edge, often
multinucleated giant cells, small abscesses, mixed within histiocytes
inflammatory infiltrate and a granulomatous
reaction

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V. Sporotrichosis  Pseudoepitheliomatous epidermal hyperplasia with
 Caused by Sporothrix schenkii microabscess formation
 Dimorphic fungus (filamentous=outside the body  Central suppurative zone composed of neutrophils,
and yeast-like=inside the body) surrounded by epitheloid cells, giant cells, plasma
 Ovoid bodies cells, lymphocytes
2 cutaneous forms:  Asteroid bodies=“Splendore Hoeppli Material”
 Lymphocutaneous :
 Painless papule ulcerating nodules usually VI. Mycetoma
on a finger or hand  Chronically discharging infection of skin and
 Chain of asymptomatic nodules appear along subcutaneous tissue
the lymph vessel draining the area  Caused by:
  undergo suppuration with subsequent  Actinomycetoma:
ulceration  Bacteria (Nocardia, Actinomyces,
 Fixed cutaneous: Streptomyces),
 Solitary plaque or occasionally a group of  Eumycetoma:
lesions, most commonly on an arm or the  Fungi (Madurella mycetoma,
face M.guisea, P.boydii, etc.)
  superficial crusting or verrucous surface  Nodule  abscess discharging fistula to skin 
 No tendency toward lymphatic spread muscles and tendons damaged eventually  may
affect bone  osteomyelitis
Gross:  “Madura foot”
 Sulfur granules or “grains” discharged from draining
sinuses

Gross:


st
1 picture: Lymphocutaneous

nd
2 picture: Fixed Cutaneous

Pathogenesis:
 S. schenckii commonly contacted through exposure
to vegetal matter, often a splinter or thorn

Histopathology:

 “sulfur granules” within suppuration & surrounded by

histiocytes, multinucleated giant cells and granulation
tissue
 Diagnosis can be established only by finding “sulfur
granules”
 to differentiate bacterial from fungal causes, special
stains are employed:
 Gram stain
 Lactophenol blue

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Histopathology:  Nodular variant:
 Itching nodules, commonly on the scrotum
 Acanthosis with dermal perivascular
lymphocytic and eosinophilic infiltrate
 Norwegian scabies or crusted scabies
 Innumerable mites present
 Widespread erythema, hyperkeratosis, and
crusting but no obvious burrows

 Group of mycoses  Excoriation and Burrows

 Observe the black “Sulfur Granules”

Parasitic infestations
Scabies
 Sarcoptes scabei mite
 Penetrate skin as linear burrows up to 3-cm long
 Female mite burrows under the stratum corneum
deposits eggs producing burrows on the interdigital
skin, palms, wrists, periareolar skin of women and
genital skin of men
 Larvae hatch in 3-5 days and mature in 10-14 days  Eggs &Scybala
 Burrows:
 Pathognomonic lesion Histopathology:
 Linear, poorly defined streaks
 Vesicle may be visible near the blind end of
the burrow
 Secondary excoriation and infection
 Papulovesicular variant
 burrows on the interdigital skin, palms,
wrists, periareolar skin of women and genital
skin of men
 Spongiosis in the stratum malphigii near the
mite  vesicle formation

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Pediculosis
 Caused by head louse, crab louse, and body louse
 Pruritic
 Louse or its eggs, attached to hair shafts, can usually be
seen with the unaided eye

Swabeng Recap:
Try to enumerate the causative agents, types, morphology,
histopathology and pathogenesis of each disease below
without going back. Para malaman nyo kung swabeng swabe
ang aral mo o kailangan mo ng isa pang swabeng reading.

1. VIRAL:
 Verrucae
 Herpes simplex infection
 Varicella –Zoster
 Molluscum contagiosum
2. BACTERIAL :
 Impetigo
 Furuncle
 Carbuncle
 SSSS
 Erysipelas
 Cellulitis
 Leprosy
3. FUNGAL INFECTIONS
 Dermatophytosis
 Pityriasis versicolor
 Chromoblastomycosis
 Phaeohyphomycosis
 Sporotrichosis
 Mycetoma
4. ARTHROPOD INFESTATIONS
 Scabies
 Pediculosis

END OF TRANSCRIPTION!
Oaaaaah swabeng swabe! Come join me brothaa!!!

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