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Pathology: SKIN INFECTIONS

Viral Skin Infections 1. Verrucae 2. Herpes Simplex Virus infection 3. Varicella Zoster 4. Molluscum contagiosum 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 Common wart Associated with HPV-2,4, and 7 Occur at any site but most frequently on the dorsal aspect of the finger and hands Painless, circumscribed, firm, elevated, papules 110mm in size with papillomatous (verrucous ) hyperkeratotic surfaces 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)

Verruca plantaris and palmaris (palmoplantar wart=both) Occur on the soles (Verruca plantaris) and palms (Verruca Palmaris) Rough scaly lesions, 1-2 cm in diameter; may coalesce and be confused with calluses Morphology:

Condyloma acuminatum Venereal wart, Anogenital wart Occurs on the penis, female genitalia, urethra, perianal area and rectum Appear as soft, tan, cauliflower- like masses Low risk: HPV 6, 11 (BENIGN) High risk: HPV 16,18,31,33 associated with anogenital cancers(MALIGNANT)

Circumscribed, firm, elevated, papules 1-10mm in size with papillomatous (verrucous ) hyperkeratotic surfaces

Histopathology: Verucae Acanthosis, papillomatosis, hyperkeratosis, parakeratosis Verruca plana : same histologic features as verruca vulgaris but without papillomatosis(reason kung bakit sya flat)

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 Pathogenesis: Produce acute and latent infections Replicate in the skin and mucous membranes at the site of entrance (usually oropharynx or genitals) 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 the retropharynx; (+) cervical lymphadenopathy 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)

Koilocytic cells in the upper stratum malphigii and in the granular layer Koilocytes : small, round, deeply basophilic nuclei surrounded by a clear halo and palestaining cytoplasm

Clumped keratohyaline granules(Hypergranulosis)

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 Disseminates hematogenously widespread vesicular skin lesions 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) Vesicle: contains intranuclear inclusions Lesions in varying stages are present at one time Vesicles rupture crust over heal by regeneratiion Complications: pneumonitis, encephalitis

Re-activation of infections appear on the dermatomal lines

Histopathology:

In ganglia: (+) lymphoplasmacytic infiltrates with intranuclear inclusions within neurons

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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 Caused by group A- beta hemolytic Streptococci and Staphylococcus aureus Impetigo contagiosa (nonbullous impetigo) : Strep Impetigo bullosa : Staph Involves exposed skin, i.e. face and hands Erythematous macule pustule shallow erosions covered with drying serum (honey colored crust) Gross:

Scrapings are subjected to PAP Smear Multinucleated giant cells andinclusion bodies are found on tzanck smear

IV. Molluscum contagiosum Common, self-limited Caused by Poxvirus Transmission : direct bodily contact or indirectly via fomites Multiple lesions on the skin and mucous membranes (trunk, and anogenital areas) Gross:

Lesions are firm, often pruritic, pink to skincolored, umbilicated papules (0.2-0.4cm) Curd-like material may be expressed from umbilication

Histopathology: Accumulation of neutrophils beneath stratum corneum Subcorneal pustules Crust: serum, neutrophils and debris

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

RITTERS DISEASE -Caused by S. aureus Gross: Split in granular layer Dermal edema, no necrosis of epidermis Acantholysis may be present DDx: Toxic Epidermal Necrolysis (Lyells 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: Ritters 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

VI. Erysipelas Middle-aged, warm climates Caused by exotoxins from superficial infections with S. pyogenes Rapidly spreading, erythematous cutaneous swelling May begin on the face, or less commonly, on the body or extremity Well-demarcated, serpiginous border : butterfly on face

Diffuse, acute, edematous, neutrophilic, interstitial reaction : dermis, epidermis and subcutaneous tissue Perivascular(surround blood vessels) and periadnexal(surround eccrine glands and hair follicles of the skin) microabscess Tissue necrosis may be minor

VII. Mycobacteria LEPROSY (Hansens Disease) Slowly progressive infection of skin and peripheral nerves 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 Less severe form Dry, scaly skin lesions that lack sensation Asymmetric peripheral nerve involvement Skin anesthesia, skin and muscle atrophy Contractures, paralyses, autoamputation of 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

Gross: Skin, peripheral nerves (ulnar and peroneal), anterior chamber of the eye, upper airways (down to the larynx), testes, hands and feet are involved Hypoesthetic anesthetic Leonine facies

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 perineural macrophages

Globi : large aggregates of lipid-laden histiocytes (LEPRA 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

Area that is not affected by the disease between the dermis and epidermis(white zone)

Very well demarcated, often hairless patches of skin with mild erythema, very itchy and presence of scaling

TInea Corporis

Tuberculosis of the Skin *REFER TO GIVEN HANDOUT* Fungal skin infections 1. Dermatophytosis 2. Pityriasis versicolor 3. Chromoblastomycosis 4. Phaeohyphomycosis 5. Sporotrichosis 6. Mycetoma DERMATOPHYTES a) Epidermophyton b) Trichophyton c) Microsporum

Common superficial fungal infection of the body surface that commonly affects persons of all ages, but particular in children Predisposing factors: excessive heat and humidity, exposure to infected animals, chronic dermatophytosis of feet or nails Seen as expanding, erythematous plaque with an elevated scaling border

Histopathology: Parakeratosis, acanthosis, neutrophils in parakeratotic crust Fungal hyphae seen in parakeratotic stratum corneum

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Mild dermal inflammation Acanthosis, parakeratosis and mixed inflammatory infiltrate in superficial dermis

Tinea Pedis Athletes foot Diffuse erythema and scaling Initially localized in the interdiginous areas Tinea unguium: specific term which refers to dermatophyte infection of the nail. Discoloration, thickening and deformity of the nail plate Onychomycosis : general term which refers to nail infection due to any fungus including dermatophytes

II. Tinea Versicolor(Ptyriasis Versicolor) Malassezia furfur Common in tropical climate Multiple, irregular areas of hypo-and hyperpigmentation seen primarily on the upper trunk Circular, macular, scaling, and erythematous

Gross:

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

Gross:

Always appear as a nodule in the digits Histopathology:

Pseudoepitheliomatous hyperplasia with heavy dermal infiltrate of epithelioid histiocytes, multinucleated giant cells, small abscesses, mixed inflammatory infiltrate and a granulomatous reaction

Suppurative granulomatous inflammation single large cavity with surrounding fibrous capsule, contg PMNs and fibrin Organisms found within cavity and cavity edge, often within histiocytes

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V. Sporotrichosis Caused by Sporothrix schenkii Dimorphic fungus (filamentous=outside the body and yeast-like=inside the body) Ovoid bodies 2 cutaneous forms: Lymphocutaneous : Painless papule ulcerating nodules usually on a finger or hand Chain of asymptomatic nodules appear along the lymph vessel draining the area undergo suppuration with subsequent ulceration Fixed cutaneous: Solitary plaque or occasionally a group of lesions, most commonly on an arm or the face superficial crusting or verrucous surface No tendency toward lymphatic spread Gross:

Pseudoepitheliomatous epidermal hyperplasia with microabscess formation Central suppurative zone composed of neutrophils, surrounded by epitheloid cells, giant cells, plasma cells, lymphocytes Asteroid bodies=Splendore Hoeppli Material

VI. Mycetoma Chronically discharging infection of skin and subcutaneous tissue Caused by: Actinomycetoma: Bacteria (Nocardia, Actinomyces, Streptomyces), Eumycetoma: Fungi (Madurella mycetoma, M.guisea, P.boydii, etc.) Nodule abscess discharging fistula to skin muscles and tendons damaged eventually may affect bone osteomyelitis Madura foot Sulfur granules or grains discharged from draining sinuses Gross:

1 picture: Lymphocutaneous nd 2 picture: Fixed Cutaneous

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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 Burrows: Pathognomonic lesion 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

Histopathology:

Eggs &Scybala

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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 BACTERIAL : Impetigo Furuncle Carbuncle SSSS Erysipelas Cellulitis Leprosy FUNGAL INFECTIONS Dermatophytosis Pityriasis versicolor Chromoblastomycosis Phaeohyphomycosis Sporotrichosis Mycetoma ARTHROPOD INFESTATIONS Scabies Pediculosis

2.

3.

4.

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

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