Infectious Dermatology 1

Dermatological Infections & Infestations Mariecon O. Escuadro, MD Diplomate, Philippine Dermtological Society Diplomate, Philippine Society of Venereologists, Inc

Superficial Bacterial Skin Infections 1. 2. 3. 4. 5. 6. 7. 8.

Impetigo Contagiosa Bullous Impetigo Folliculitis Furuncle & Carbuncle Ecthyma Cellulitis Erysipelas Erythrasma

Impetigo Contagiosa • Etiology: – Staphylococcus aureus: 50-70% – Streptococcus pyogenes or mixed • Group A Strep- usual • Group B Strep- newborn • Group C, G Strep-rare

Impetigo Contagiosa • Common sources: – Adults • Barbershops, parlors, meat packing plants, swimming pools, infected children

– Children • Pets, dirty fingernails, daycare, crowded housing and other infected children

Impetigo Contagiosa • Clinical Presentation – Age group: early childhood most common – Sites: exposed areas (face, hands, neck & extremities) – Lesions: starts as 2 mm erythematous macules-thin-walled vesicles or bullaepustules, which rupture: seropurulent discharge-dries up: honey-colored/goldenyellow crusts.

Impetigo Contagiosa • Complications – Acute Glomerulonephritis (Grp A Beta-hemolytic Strep) • Incidence: 10-15% with Nephritogenic strains • Prognosis: excellent in children, not as good in adults

Bullous Impetigo • Etiology – Phage type 71 coagulase positive Staphylococcus aureus – Group 2 phage type Staphylococcus aureus

Bullous Impetigo • Clinical Presentation – Age groups: – newborn (4th&10th day) – children

– Sites: – Face & hands – Axilla & groin- adults in warm climates

– Lesions: – Large fragile bullarupture: circinate, weeping or crusted lesions with varnish-like crusts (impetigo circinata)

Bullous Impetigo • Constitutional Symptoms: • Fever & weakness develops • Diarrhea

• Complications: • Bacteremia • Pneumonia • Meningitis

Folliculitis • Etiology – Staphylococcus aureus

• Clinical Presentation – Sites: • Extremities and scalp • Axillae, thighs, pubis & eyelashes • Gluteal & genital maybe STDs

– Lesions: • Thin-walled pustule at follicle orifices

Furuncle & Carbuncle • Etiology – Break in the skin (pressure, friction, irritation, hyperhidrosis, dermatitis, dermatophytosis or shaving), provides portal of entry of Staphylococcus aureus – Autoinoculation from a carrier focus (nose or groin) – Predisposing factors: alcoholism, malnutrition, blood dycrasias, disorder of neutrophil function, iatrogenic or immunosuppression (HIV or Diabetes)

Furuncle & Carbuncle • Clinical Presentation – Sites • Nape, axilla, buttocks

– Lesions • Furuncle/boil: acute, round, tender, circumscribed perifollicular abscess • Carbuncle: 2 or more confluent furuncles with multiple opening, +/- purulent discharge

Furuncle & Carbuncle • Complications – Cavernous sinus thrombosis, meningitis & septicemia (upper lip & nose)

• Treatment – Warm compress – Systemic Antibiotics • Cloxacillin • 1st gen Cephalosporin

– Surgical: incision (acutely inflamed), incision & drainage (fluctuant)

Ecthyma • Etiology – Streptococcus – Staphylococcus aureus- IVD users & HIV

• Predisposing Factors – Malnutrition – Poor hygiene – Trauma

Ecthyma • Clinical Presentation – Sites: shins or dorsal feet – Lesions: vesicle or vesicopustules- increase in size-thickly crusted. Removal of crust: superficial, saucer shaped ulcer w/ elevated edges & raw base • (+) scarring • (+/-) lymphadenopathy

Cellulitis • Suppurative inflammation of the subcutaneous tissue

• Etiology: – Staphylococcus aureus – Steptococcus pyogenes

• Predisposing Factors: – Breaks in the skin – Tinea pedis- most common portal of entry – Others: hematologic malignancy, diabetes mellitus, IVD abuse, cardiovascular disorder

Cellulitis • Clinical Presentation: – Lesions: mild local erythema & tenderness associated with malaise & chilly sensation. +/fever & chills – Erythema spreadswarmth, swelling & tenderness, +/- pitting on pressure – Occasionally: vesicles appear, rupture & discharge purulent material – (+/-) streaks of lymphangitis

Cellulitis • Complications – Gangrene, metastaic abscess & sepsis in children & immunocompromised

• Treatment – Syatemic Antibiotics

Erysipelas • Aka St. Anthony’s Fire • Etiology: – Grp A Beta hemolytic Strep-supfl dermal lymphatics – Strep C or G-occasional – Grp B Strep- newborns, abdominal or perineal erysipelas in post partum women

Erysipelas • Predisposing Factors – Break in the skin barrier – Operative wounds – Fissures in the nares, auditory meatus, under the earlobes, on the anus, penis, between or under the toes (little toe) – Accidental scalp wounds – Chronic leg ulcers

Erysipelas • Clinical Presentation – Sites: face & legs – Prodrome: malaise, chills, high grade fever, headache, vomiting & joint pains – Lesions: intensely erythematous (scarlet), warm, swollen, brawny, well-demarcated plaque w/ characteristic raised indurated border • +/- vesicles/bullae w/ seropurulent fluid • Spread; peripheral extension

Erysipelas • Lesions, contd… • On face: ear may become swollen & distorted; +/delirium • Leukocytosis (PMNLs >/= 20,000/mm3)

• Complications: • Septicemia • Deep Cellulitis – *** in newborns or surgical operations in the elderly

Erysipelas • Treatment – Systemic: at least 10 days, rapid improvement in 24-48 hours – Penicillin V – IV Penicillin – Erythromycin

– Supportive Measures: cold compresses

Cellulitis & Erysipelas Cellulitis

Erysipelas

Staphylococcus or Streptococcus

Grp A Streptococcus

Subcutaneous Tissue

Superficial Dermal lymphatics

Poorly demarcated

Well-demarcated with characteristic raised indurated border

Erythrasma • Etiology – Corynebacterium minutissimum – Extensive: diabetes or debilitating diseases

• Clinical Presentation – Sites: intertriginous areas (axilla, genitocrural crease & the webs between the 4th & 5th toes> 3rd & 4th toes; intergluteal cleft, perianal skin, inframammary area & nails)

Erythrasma • Clinical Presentation, contd… – Lesions: • asymptomatic except for groin lesions which may present with burning & pruritus • Sharply delineated, dry, brown, slightly scaling patches • (+) Coral Red Fluorescence with Wood’s light – Due to Porphyrin

Erythrasma • Treatment – Localized • Topical erythromycin/clindamycin • Topical azoles • Topical Benzoyl Peroxide Wash or 5% gel

– Widespread • Oral Erythromycin

Mycobacterial Infections 1. Hansen’s Disease 2. Cutaneous Tuberculosis

Hansen’s Disease • Mycobacterium leprae • Classification: – 1. Indeterminate – 2. Tuberculoid (TT) – 3. Borderline Tuberculoid (BT) – 4. Borderline (BB) – 5. Borderline Lepromatous (BL) 6. Lepromatous (LL)

Indeterminate Leprosy • Solitary, ill-defined hypopigmented macule or patch • Sensory: normal or minimally altered (earliest: sense of cold & light touch) • Peripheral nerves: not enlarged • If immunity is good: resolves spontaneously

Tuberculoid Leprosy (TT) • Lesions are solitary, few & asymmetrical • Lesion: large erythematous plaque w/ sharply elevated border & atrophic center • Sensory: anesthetic or hyposthetic & anhidrotic • Nerve involvement: early, superficial peripheral nerves are enlarged, tender or both

Tuberculoid Leprosy (TT) • Contracture of fingers (claw hand), facial muscle paralysis & foot drop may occur • Interosseous muscles may be atrophied: wasting of thenar & hypothenar eminences • Slow skin lesions evolution • (+) Lepromin skin test, good cell-mediated immunity

Tuberculoid Leprosy (TT) • Histopathology – Well defined granuloma with Langhans giant cells, perineural infiltrates, AFB rare

Borderline Tuberculoid (BT) • Similar to TT but smaller & more numerous

Borderline Leprosy (BB) • Skin lesions numerous, asymmetrical & irregularly shaped • Moderate anesthesia

Borderline Lepromatous (BL) • Lesions are numerous, symmetrical & small • Nerve involvement is symmetrical & appears later

Lepromatous Leprosy (LL) • Lesions are ill-defined, infiltrated, numerous & symmetrical • Nerve involvement: symmetrical, develops slowly and at later stages • Nerve damage: massive bacillary infiltration w/ compression & fibrosis • +/- hyperesthesia • (-) changes in sweating

Lepromatous Leprosy (LL) • Hair: slow progressive hair loss w/ thinning of outer thrid of eyebrow • Progressively worsen w/o treatment • (-) lepromin skin test, poor CMI

Lepromatous Leprosy (LL) • Histopathology: – Foamy histiocytes, abundant AFB

Hansen’s Disease • Diagnosis – Sensory Test- “pin-prick” or “ballpen-point” test – Skin biopsy stained with Fite –Faraco stain – Skin slit smears: “ Zieh-Neelsen stain – Bacteriologic Index’

6+

>1000 bacilli/f

5+

100-1000

4+

10-100

3+

1-10

2+

1-10 in 10 OIF

1+

1-10 in 100 OIF

– Lepromin skin test: immunologic status

Hansen’s Disease • Diagnosis – Lepromin skin test: immunologic status • Fernandez reaction: 24-48 hours • Mitsuda reaction: 4 weeks

Hansen’s Disease • Treatment – Paucibacillary (Indeterminate & TT) – Multibacillary (BT, BB, BL, LL) – WHO Protocol: • 1. Single lesion Paucibacillary – Single dose: Rifampin 600mg, Ofloxacin 400mg & Minocycline 100mg (ROM)

• 2. Paucibacillary (Indeterminate, TT) – Rifampin 600mg once a month x 6 months – Dapsone 100mg OD x 6 months

Hansen’s Disease WHO Protocol: • 3. Multibacillary (BT, BB,BL,LL) – Rifampin 600mg and Clofazimine 300mg once a month – Dapsone 100mg and Clofazimine 50mg OD x 12 months, or until smear negative

• 4. Special Cases • For patients who cannot take dapsone & rifampin – Clofazimine 50 mg , Ofloxacin 400mg & Minocycline 100mg OD x 6mos, – Ffd by: Clofazimine 50mg plus Ofloxacin 400mg OD or Minocycline 100 mg OD x 18 months

• For patients who refuse Clofazimine – Minocycline 100mg or Ofloxacin 400mg OD x 12 mos or – Rifampin 600mg, Ofloxacin 400mg & Minocycline 100mg once a mo x 24 months (ROM)

Hansen’s Disease Treatment Dapsone effective, inexpensive & free of side effects at recommended doses side effects: Methemoglobinemia & anemia (in G6PD deficient); exfoliative dermatitis, hepatitis, neuropathy & agranulocytosis

Rifampin highly bactericidal, not used as monotherapy to avoid resistance side effects: red-orange urine, elevated liver enzymes & flu-like lesions

Clofazimine bacteriostatic & anti-inflammatory Side effects: red-brown to grayish blue skin pigmentation

Hansen’s Disease • Reactional States – Acute episodes characterized by remissions & relapses for a week to a few months in a chronic course of infection – Neuritis is the most imptortant consideration – Precipitating factors: infection, surgery, physical, physiologic & mental stress, vaccination, pregnancy, Vitamin A, iodides & bromides

Hansen’s Disease • Reactional States – 1. Type 1 reaction • Cell mediated; in BT, BB, BL • Inflammation (swollen, erythematous & tender) of existing lesions • No systemic symptoms; mj complication- nerve damage • a. Reversal- w/ antibiotic tx, shift toward tuberculoid pole • B. Downgrading- before antibiotic, shift toward lepromatous pole

Hansen’s Disease • Reactional States 2. Type 2 reaction/Erythema nodosum leprosum • Circulating immune complex-mediated dse;In BL, LL • Painful, erythematous subcutaneous & dermal nodules • With systemic symptoms: fever, myalgia, arthralgia, anorexia & iritis

Hansen’s Disease • Management of Reactions: – Type 1 Reversal Mild • Analgesics • Chloroquine (1-2weeks)

– Type 1 Reversal Severe • Prednisone 40-80mg OD x 5-7 days then taper for 2-6 months • Clofazimine 300mg OD x 6 weeks

– Type 2/ ENL • Clofazimine 300 mg OD x 6 weeks, 200mg OD x 2-6 mos & 100 mg OD x 1-2 years • Thalidomide 400mg OD, tapered to 50-100 mg OD in 1 week (teratogenic) • Prednisone 40-80mg OD

Cutaneous Tuberculosis

Cutaneous TB • M. tuberculosis, M. bovis • Classification is based on the mode of onfection & immunologic state of the host • Diagnosis is based on clinical manifestations, histopathologic analyisis, demonstration of relevant mycobacteria in tissue or in culture & host reaction

Cutaneous TB • 1. Primary Inoculation TB/Tuberculous Chancre/ Tuberculous Primary Complex • 2. Tuberculous Verrucosa Cutis/Warty TB

• 3. Lupus Vulgaris • 4. Scrofuloderma/TB Colliquativa Cutis • 5. Orificial TB/TB Ulcerosa Cutis et mucosae • 6. Others: Tuberculous Gumma, Acute Miliary TB of the skin, Sequelae of BCG inoculation

Tuberculous Chancre • Tuberculous chancre & affected regional LN • Children • Sites: face, conjunctivae & oral cavity; hands & lower extremities • Pathogenesis (MBPB): – Tubercle bacilli are introduced into the tissue at the site of minor wounds – Oral lesions caused by bovine bacilli in nonpasteurized milk & after mucosal trauma or tooth extraction

Tuberculous Chancre • Chancre (small papule, crust or erosion w/ little tendency to heal) appears 2-4 weeks after inoculation • Painless ulcer: shallow w/ a granular or hemorrhagic base studded w/ miliary abscess or covered by necrotic tissue; undermined ragged edges & reddish blue huemore indurated w/ thick adherent crusts

Tuberculous Chancre • Mucosal: painless ulcers or fungating granulomas • Slowly progressive, regional LAD x 3-8 weeks after infectionweeks or months: cold abscess that perforate to surface & form sinuses

Tuberculous Chancre • Histopathology (Fite Stain): • 3-6 weeks: tuberculoid appearance & caseation

• Diagnosis – Ulcer w/ little or no tendency to heal – Unilateral regional LAD – Bacterial culture

Tuberculous Chancre • Course – Untreated: 12 mos – Hematogenous spread: bones & joints – Calcification of regional LN

Tuberculosis Verrucosa Cutis • Paucibacillary caused by exogenous re infection (inoculation) in previously sensitized individuals w/ high immunity

• Clinical Manifestations: – Small asymptomatic papule or papulopustule w/ puple inflammatory halo – Hyperkeratotic – Slow growth & peripheral expansion verrucous plaque w/ irregular border; solitary – Spontaneous involutionatrophic scar

Tuberculosis Verrucosa Cutis • Histopathology – Pseudoepitheliomatous hyperplasia w/ marked hyperplasia w/ marked hyperkeratosis, a dense inflammatory infiltrate & abscess in the supfl dermis or within the pseudoepitheliomatous rete pegs – Epitheloid cells & giant cells in upper & middle dermis

Lupus Vulgaris • Chronic, progressive form • Moderate immunity & a high degree of tuberculin sensitivity • Females, 2-3x • Pathogenesis: post primary, PB caused by hematogenous, lymphatic or contguous spread

Lupus Vulgaris • Clinical Manifestation – Sites: nose, cheek, earlobe or scalp – Initial lesion: • brownish red, soft or friable macule or papule w/ a smooth or hyperkeratotic surface. • Apple jelly color on diascopy

– Progression: • Elevation, deeper brownish color & plaque • Nasal or auricular cartilage: extensive destruction & disfigurement

Lupus Vulgaris • Clinical Manifestation – Sites: nose, cheek, earlobe or scalp – Initial lesion: • brownish red, soft or friable macule or papule w/ a smooth or hyperkeratotic surface. • Apple jelly color on diascopy

– Progression: • Elevation, deeper brownish color & plaque • Nasal or auricular cartilage: extensive destruction & disfigurement

Lupus Vulgaris • Diagnosis – Softness of lesion, brownish red color & slow evolution – Apple jelly nodules

• Histopathology – Typical tubercles – Secondary changes: epidermal thinning, atrophy or acanthosis w/ excessive hyperkeratosis or psedoepitheliomatous hyperplasia

Lupus Vulgaris • Course – Long term disorder – Functional impairment & disfigurement – Squamous Cell CA – Pulmonary TB: 4-10x

Scrofulderma • Subcutaneous TB leading to cold abscess formation breakdown of overlying skin • MB or PB • Represents contiguous involvement of skin overlying another site of infection (TB lymphadenitis, bones & joints or epididymitis) • Children, adolescents & aged

Scrofulderma • Site: parotidal, submandibular & supraclavicular; bilateral • Lesion: firm, subcutaneous nodule, well defined, freely movable & asymptomatic softens, liquefaction w/ perforation causing ulcers & sinuses

Scrofulderma • Histopathology: • Massive necrosis & abscess formation in center

• Course – protracted

Orificial TB • Rare TB of mucous membranes • Autoinoculation • Underlying Disease: far advanced pulmonary, intestinal or genitourinary TB • Clinical Manifestation: – Small, yellowish or reddish nodules  soft ulcer w/ typical punched-out appearance, undermined edges & circular or irregular border

Orificial TB • Clinical Manifestation: – Multiple yellowish tubercles & bleeds easily – Edematous & inflamed – Extremely painful: dysphagia – Sites: • TB of Pharynx & Larynx: tongue (tip & lateral margins), soft & hard palate; lips (advanced cases) • TB of Genitourinary: vulva

Orificial TB • Histopathology – Massive, non-specific inflammatory infiltrate & necrosis, but tubercles w/ caseation maybe found

Mycobacterial Infections

Superficial Fungal Infections

Dermatophytoses • Infects non-viable keratinized cutaneous tissues including stratum corneum, nails & hair – Microsporum – Trichophyton – Epidermophyton

• Factors that promote dermatophytoses – Environmental – Immunosuppression – Genetic susceptibility

Dermatophytoses • Diagnostics – KOH smear- septated hyphae – Histopathology- with PAS & methenamine silver stains exhibiting septated hyphae within the stratum corneum – Fungal cultures – Wood’s lamp

Dermatophytoses • • • • • • •

Tinea capitis (ringworm of scalp & kerion) Tinea barbae (beard) Tinea faciei (face) Tinea corporis (body) Tinea manus (hands) Tinea pedis (feet) Onychomycosis (nail)

Tinea Capitis • Clinical Manifestations – 1. Non Inflammatory Type a. Black-dot b. Gray patch

– 2. Inflammatory Type a. Kerion b. Favus

Tinea Capitis • Non-inflammatory Type – A. Black dot- endothrix; infected hairs broken off at or below the surface of the scalp – B. Gray patch- ectothrix; scaly patches with areas of stubs of broken hair

Tinea Capitis • Endothrix: arthrospores are formed inside the hair shaft; no fluorescence • T. tonsurans • T. schoenleinii • T. violaceum

• Ectothrix: hair is surrounded w/ sheath of tiny spores; greenish fluorescence • • • •

Microsporum species T. verrucosum T. mentagrophytes T. megnini

Tinea Capitis • Inflammatory Type • Begins as erythematous, scaly, papular eruptions w/ loose & broken off hairs

– A. Kerion- localized spot w/ pronounced swelling, creating a boggy & indurated area exuding pus – B. Favus- concave, sulfur-yellow crust forming around loose wiry hairs – Hyphae & air spaces within the hairshaft – Bluish-white fluorescence

Tinea Capitis • Treatment – Griseofulvin x 2-4 mos or at least 2 weeks after negative microscopic and culture examinations – Terbinafine 250mg/ Tab x 2 weeks (Trichophyton) and 4 weeks (Microsporum) – Itraconazole 100mg/caps, 2 caps/day x 4-6 weeks – Ketoconazole 200mg/tab x 4-6 weeks – Others: short courses of systemic steroids for inflammatory type; Selenium sulfide Shampoo or Ketoconazole Shampoo left for 5 mins 3x a week

Tinea Barbae • Clinical Manifestations- usually on the neck &/or beard area

– 1. Deep Type – 2. Superficial, crusted Type

Tinea Barbae • 1. Deep Type • Develops slowly • Does not usually involve the upper lip except the mustache • Produces nodular thickenings & kerion-like swellings, which are confluent & form diffuse boggy infiltrations w/ abscesses • Overlying skin is inflamed • Hairs are loose or absent • Pus may be expressed through the remaining follicular openings

Tinea Barbae • 1. Superficial, crusted Type • Mild pustular folliculitis – With broken off hairs – Without broken off hairs

• Hairs are loose, dry, brittle & when extracted, the bulb appears intact

Tinea Barbae • Treatment – Micronized or Ultramicronized Griseofulvin 500-1000mg/ day x 4-6 weeks – Terbinafine 250mg/ Tab x 2 weeks (Trichophyton) and 4 weeks (Microsporum) – Itraconazole 100mg/caps, 2 caps/day x 4-6 weeks – Ketoconazole 200mg/tab x 4-6 weeks

Tinea Barbae • Treatment – Topical Antifungals: miconazole, clotrimazole, oxiconazole, sulconazole, econazole, ketoconazole, naftitine, terbinafine, ciclopirox olamine BID x 2-4 weeks – Affected areas washed with soap and water – Healthy areas maybe shaved or clipped

Tinea Faciei • Erythematous, slightly scaling patches or plaques with indistinct borders & with slight central regression

Tinea Faciei • Treatment – Topical Antifungals: miconazole, clotrimazole, oxiconazole, sulconazole, econazole, ketoconazole, naftitine, terbinafine, ciclopirox olamine BID x 2-4 weeks – Oral Antifungals: • Micronized or Ultramicronized Griseofulvin 500-1000mg/ day x 4-6 weeks • Terbinafine 250mg/ Tab x 2 weeks (Trichophyton) and 4 weeks (Microsporum) • Itraconazole 100mg/caps, 2 caps/day x 4-6 weeks • Ketoconazole 200mg/tab x 4-6 weeks

Tinea Corporis • Sites: neck, upper & lower extremities and trunk • Characterized by one or more circular, sharply circumscribed, slightly erythematous, dry, scaly plaques w/ central clearing • Borders are usually elevated & more inflames & scaly than the central part

Tinea Corporis • Lesions may widen to form rings, sometimes making concentric rings or rings of intricate patterns (Tinea imbricata) • Disseminated patches of both dry (macular) & moist (vesicular) types of Tinea circinata

Tinea Corporis • Treatment – For Extensive lesions • Micronized or Ultramicronized Griseofulvin 370-750mg/ day x 4-6 weeks • Terbinafine 250mg/ Tab x 2 weeks • Itraconazole 200mg/day x 1 week • Fluconazole 150mg/tab once a week x 4 weeks

– For Localized lesions • Topical Antifungals: miconazole, clotrimazole, oxiconazole, sulconazole, econazole, ketoconazole, naftitine, terbinafine, ciclopirox olamine BID x 2-4 weeks

Tinea Cruris • Aka “Jock Itch” • Sites: upper & inner surfaces of the thighs • Begins as a small erythematous and scaling or vesicular & crusted patch that spreads peripherally & partly clears in the center • Curved with well-defined border particularly on its lower edge • Border: vesicles, pustules or papules • Extends: downward- thighs & backwardsperineum or anus

Tinea Cruris • Treatment – Same as Tinea Corporis – Reduce perspiration and enhance evaporation on crural area – Area should be kept dry by wearing loose underclothing and trousers, application of plain talcum powder or antifungal powder

Tinea Pedis • Aka “Athelete’s Foot” • Most common dermatophytosis • Consists of maceration, slight scaling & occasional vesiculation & fissures between & under the toes • Most common site: third toe web • If untreated: ulcerative, exudative process affecting web spaces or entire sole

Tinea Pedis • Types: – 1. Non-inflammatory • Dull erythema & pronounced scaling (moccasin or sandal appearance)

– 2. Inflammatory • Acute vesicular or bullous eruption • Vesicles contain clear tenacious fluid w/ glycerin consistency which dries up leaving yellowish brown crusts • Symptoms: burning & itching

Tinea Pedis • Treatment – Reduce perspiration and enhance evaporation on the interdigital areas – Toe webs & soles should be dried immediately after bathing – Use antiseptic powder on the feet after bathing ( eg Tinactin powder or Zeasorb Medicated Powder) – Plain tlac, cornstarch or rice powder maybe dusted to the socks & shoes to keep feet dry

Tinea Pedis • Treatment – Severe Tinea Pedis • Micronized or Ultramicronized Griseofulvin 370750mg/ day x 4-6 weeks • Terbinafine 250mg/ Tab x 2 weeks • Itraconazole 200mg/day x 1 week • Fluconazole 150mg/tab once a week x 4 weeks • *** With severe maceration: One part Aluminum Acetate to 20 parts of water as dressing • ***Secondary Infections: Oral or Topical antibacterial

Tinea Pedis • Treatment – Localized Tinea Pedis • Topical Antifungals: miconazole, clotrimazole, oxiconazole, sulconazole, econazole, ketoconazole, naftitine, terbinafine, ciclopirox olamine BID x 2-4 weeks • Keratolytic Agents (eg Salicylic Acid, Lactic Acid Lotions) for areas protected by thick layers of underlying skin

Tinea Manum • Dry, scaling, erythematous or may be verrucous • Moist, vesicular and eczematous

Tinea Manum • Treatment – Severe Tinea Manum • Micronized or Ultramicronized Griseofulvin 370750mg/ day x 4-6 weeks • Terbinafine 250mg/ Tab x 2 weeks • Itraconazole 200mg/day x 1 week • Fluconazole 150mg/tab once a week x 4 weeks • *** With severe maceration: One part Aluminum Acetate to 20 parts of water as dressing • ***Secondary Infections: Oral or Topical antibacterial

Tinea Manum • Treatment – Localized Tinea Manum • Topical Antifungals: miconazole, clotrimazole, oxiconazole, sulconazole, econazole, ketoconazole, naftitine, terbinafine, ciclopirox olamine BID x 2-4 weeks • Keratolytic Agents (eg Salicylic Acid, Lactic Acid Lotions) for areas protected by thick layers of underlying skin

Onychomycosis • Types – 1. Distal Subungal Onychomycosis – 2. Superficial White Onychomycosis – 3. Proximal Subungal Onychomycosis – 4. Candidal Onychomycosis

Distal Subungal Onychomycosis • Involves the distal nail bed & hyponychium w/ sec involvement of the underside of nailplate • Whitish-yellowish discoloration starting at the distal corner of the nail & involves the junction of the nail & its bed and becomes brown-black in color • Later: opaque, thickened, friable & raised by underlying hyperkeratotic nail bed

Superficial White Onychomycosis • Aka Leukonychia Trichophytica • Invasion of the toenail plate on the surface producing chalky white nail plate • Maybe eroded: nail loss

Proximal Subungal Onychomycosis • Involves the proximal nail fold • White spot appears from beneath the PNF which gradually fills the lunula & moving distally • Maybe an indicator of HIV infection

Candidal Onychomycosis • • • •

Aka Total Dystrophic Onychomycosis Involves the whole nail plate Fingernails>toenails Begins under the lateral & proximal nail fold & the adjacent cuticle is pink, swollen & tender on pressure\ • Neighboring nail becomes dark, ridged & separated from the nail bed

Candidal Onychomycosis • Later: total onycholysis • Nail plate doe not become white, yellow or friable • Seen in chronic mucocutaneous candidiasis

Onychomycosis Therapy • Terbinafine 250mg/day x 6 weeks for fingernails and 12 weeks for toenails • Itraconazole Pulse Treatment: 200mg BID for 1 week of each month for 2 months for fingernails and 3 months for toenails • Fluconazole 150-300mg once a week x 6-12 months • Griseofulvin 350mg TID with meals x 4-6 months for fingernails and 10-18 months for toenails (note: not used for Candidal Onychomycosis)

Dermatophytid • “Id reaction” to the fungal antigen especially the inflammatory types • Diagnosis depends on presence of fungal infection at site different from the lesion – Pruritic vesicles on the hand & sides of fingers-most common site esp of Tinea Pedis – Acute widespread eruption usually follicular, lichenoid & scaly papules on the trunk esp of Tinea Capitis – Erysipelas-like dermatophytid on the shin esp of toe web tinea – *** resolves once infection subsides

Pityriasis/Tinea Versicolor • Etiology: – Malassezia furfur or Pityrosporum orbiculare • Short thick fungal hyphae &spores (“spaghetti & meatballs”)

• Clinical Manifestation – Yellowish or brownish macules in pale skin or hypopigmented macules in dark skin – Coalesce to form patches – Delicate scaling (“grattinage”) – Mild itching & minimal inflammation

Pityriasis/Tinea Versicolor • Clinical Manifestation, contd… – Sites of Predilection • • • • • •

Sternal region & sides of chest Abdomen Back Pubis Neck Intertriginous areas

– *** Hypopigmentation- fungus compels production of abnormally small melanosomes which are not transferred to the keratinocytes properly

Pityriasis/Tinea Versicolor • Diagnosis – Wood’s Lamp: yellowish or brownish fluorescence – Skin Scarping w/ 10% KOH: spaghetti & meatballs

Pityriasis/Tinea Versicolor • Treatment – 1. Topicals • • • • • • • •

Imidazoles- Ketoconazole Shampoo Selenium Sulfide Shampoos Ciclopirox Olamine Shampoo Zinc Pyrithione Shampoo Sulfur Preparations Propylene Glycol lotions Benzoyl Peroxide Terbinafine Cream or Sprays

Pityriasis/Tinea Versicolor • Treatment – 2. Oral • Ketoconazole 200 mg/day x 10 days • Fluconazole 400mg single dose • Itraconazole 200mg x 5-7 days • *** hypopigmentation will take time to resolve and is not a sign of treatment failure

Candidiasis • Aka candidosis, moniliasis, thrush or oidiomycosis • Etiology: Candida albicans • Features: – Normal inhabitant at various sites (skin, nails, mucous membranes & viscera), until there is some change in the state of the area then it becomes a pathogen – Areas: perianal and inguinal folds, interdigital, nail folds & axillae • *** warmth, moisture & maceration permit the organism to thrive

Candidiasis • Types: – – – – – – – – –

1. Oral 2. Perleche 3. Candidal Vulvovaginitis 4. Candidal Intertrigo 5. Pseudodiaper rash 6. Congenital Cutaneous Candidiasis 7. Perianal Candidiasis 8. Candidal Paronychia 9. Chronic Mucocutaneous Candidiasis

Oral Candidiasis • Newborn/ Infant – Grayish white membranous plaques w/ reddish base on mucous membrane of mouth – Angles of the mouth

• Adults – Buccal mucosa and tongue – Papillae of tongue atrophied w/ smooth, glazed and bright red surface – *** elderly, debilitated & malnourished – *** often 1st manifestation of HIV

Oral Candidiasis • Treatment – Clotrimazole troches – Fluconazole 100-200mg/day x 5-10 days – Itraconazole 200 mg OD x 5-10 days

Perleche/Angular Cheilitis • Maceration w/ transverse fissuring of the oral commisures • Early lesions: ill-defined, grayish white thickened areas w/ slight erythema of mucous membrane at oral commisure • More developed lesions: bluish white ot mother of pearl color, contiguous w/ a wedge shaped erythematous scaling dermatitis of skin portion of commisure fissure, maceration & crust formation

Perleche/Angular Cheilitis • Also seen in Riboflavin deficiency & in malocclusion caused by ill-fitting dentures • Can be bilateral

Candidal vulvovaginitis • Labia: erythematous, moist & macerated • Cervix: hyperemic, swollen & eroded with small vesicles on the surface • Sx: severe pruritus, irriattion, extreme burning • Vaginal Discharge: thick & tenacious

Candidal vulvovaginitis • Pregnancy, In diabetes or secondary to broad spectrum antibiotic therapy • Frequent recurrences • Male partner should be examined

Candidal vulvovaginitis • Treatment – Fluconazole 150mg single dose or 100mg/day x 5-7days – Itraconazole – Topical Antifungals – Antifungal Vaginal Tablets

Candidal Intertrigo • Arises between folds of genital, in groins or armpits, between buttocks, under large pendulous breasts, over hanging abdominal folds or umbilicus • Pinkish intertriginous moist patches surrounded by a thin, overhanging fringe of macerated epidermis (“collarette of scale”) • Characteristic “Satellite Lesions”

Pseudo Diaper Rash • Perianal region spread over entire area enhanced by maceration produced by wet diapers

• Scaly macules & vesicles w/ maceration: pruritus, burning & extreme discomfort • Erythematous desquamating “satellite” or “daughter” lesions scattered along edges

Congenital Cutaneous Candidiasis • Infection of an infant during passage through a birth canal infected with C. albicans • Erythematous macules progress to thin walled pustules, that rupture, dry & desquamate • Lesions are widespread, involving even the nailfolds. • Oral cavity & diaper area are spared

Perianal Candidiasis • • • • •

(+) pruritus ani Erythema, oozing & maceration Svere pruritus & burning Maybe precipitated by oral antibiotic tx Treatment: – Imidazoles – Topical corticosteroids – Antipruritic meds

Candidal Paronychia • Chronic inflammation of nailfold produces discharge of pus • Involves all nail plate • Cushion-like thickening of paronychial tissue • Slow erosion of lateral NF • Gradual thickening & brownish discoloration of nailplate • Transverse ridges, one nail

Candidal Paronychia • Sual: dishwashers & diabetics • Treatment – Oral Fluconazole weekly – Itraconazole in pulse doses – Anticandidal lotions – *** continued for 2-3months to prevent recurrence

Chronic Mucocutaneous Candidiasis • Chronic but superficial • Before age of 6 • Oral Lesions: diffuse perleche & lip fissures • Nail: thickened & dystrophic, (+) paronychia • Skin: hyperkeratotic, horn-like or granulomatous lesions

Chronic Mucocutaneous Candidiasis • Adult onset: heralds the occyrence of Thymoma • Inherited or sporadic

Viral Infections with Cutaneous Manifestations

Purely Cutaneous Involvement • Molluscum contagiosum • Verruca/Wart

Molluscum contagiosum • Etiologic Agent: – Molluscum contagiosum virus (poxvirus)

• Epidemiology: – MCV 1: general population – MCV 2: 60% among HIV patients – 3 groups: young children, sexually active adults & immunosuppressed patients (HIV) – Direct skin to skin contact

Molluscum contagiosum • Clinical Presentation – Lesions: • smoothed surface, firm, dome-shaped, pearly papules • 3-5mm in diameter (giant: 1.5cm) • Characteristic: central umbilication

Molluscum contagiosum Children

Adults Usually STD’s

Few to >100

6 episodes/year) Acyclovir 200mg TID or 400 mg BID

Herpes Simplex: Treatment Disease

Antiviral Therapy

Others

Intrauterine & Neonatal Herpes

IV Acyclovir 250mg/m2 q8 x 7 days

Deliver via ceasarean section within 4 hours of membrane rupture, and if during labor, there are active lesions.

Immunocompromised

Acyclovir 200-400 mg 5x daily or IV acyclovir 5 mg/kg

Suppressive Therapy: Acyclovir 400mg BID Valacyclovir 500 mg BID Famciclovir 250 mg BID

Measles • Etiology – Paramyxovirus

• Epidemiology – Worldwide distribution – Usually infects young children – Transmission: respiratory droplets – Incubation period: 9-12 days

Measles • Pathogenesis – Virus enters cells of respiratory tract replicates locally & spreads to regional lymph nodes  disseminates hematogenously to skin & mucous membranes – Viral replication also occurs in skin & mucosa

Measles • Clinical Presentation – Prodrome: fever, malaise, conjunctivitis & prominent upper respiratory symptoms (nasal congestion, sneezing, coryza & barking cough)

Measles • Clinical Presentation – Rash • • • •

1-7 days after prodrome Macular or maculopapular Anterior scalp line & post auricular Discrete erythematous papules that coalesce, spreads quickly over face extending down the trunk to extremities (cephalocaudal & centrifugal) • Clears in 6-7 days after appearnce w/ fever lysis

Measles • Clinical Presentation – Koplik’s Spots • Pathognomonic • Appears during the prodrome • Location: buccal mucosa nearest to the lower molars, spreading to involve other areas of buccal mucosa & pharynx • 1mm white papules on erythematous base

Measles • Diagnosis – High fever, Koplik’s spots, conjunctivitis, upper respiratory sx & typical exanthem – Lymphopenia is common

• Histopathology – Syncytial keratinocytic giant cells

Measles • Treatment – Vitamin A in high dose (reduces morbidity & mortality of hospitalized children w/ measles) • Retinyl palmitate 200,000 IU OD x 2 doses

– Bed rest – Analgesics – Antipyretics

Measles • Complications – Otitis media, pneumonia, encephalitis, thrombocytopenic purpura – In Malnourished & T cell deficiencies – Exanthems are less prominent in HIV-infected children

• Special Cases – Pregnant- associated w/ fetal deaths – Partially immune host( prior infection, persistent maternal antibodies or immunization) • Milder, shorter, less confluent exanthems, (-) Koplik’s spots

Rubella • Etiology – Togavirus

• Transmission – Respiratory secretions

Rubella • Clinical Presentation – Incubation Period: 12-23 days (15-21 days) – Prodrome • 1-5 days • Fever, malaise, sore throat, eye pain, headache, red eyes, runny nose, post auricular LAD • Pain on lateral & upward eye movement

Rubella • Clinical Presentation – Exanthem • Begins on the face progressing caudad, covering the entire body in 24 hours • Resolves by 3rd day (3-day measles) • Pale pink, morbilliform macules, smaller than measles

– Enanthem • Pinhead-sized red macules or petechiae on soft palate and uvula (Forscheimers’s sign)

Rubella • Complication – Arthritis or Arthralgias- adult women lasting for > 1 month

Skin Infestations 1. Scabies 2. Pediculosis

Scabies • Sarcoptes scabiei var hominis • Produces diffuse, pruritic eruption after an initial IP of 6-8 weeks • Pathognomonic Clinical Feature: burrow produced by tunneling of the mite in the stratum corneum

Scabies • Transmission – Close physical contact – Fomite

Scabies

Pediculosis • 1. Pediculosis Capitis (Head Lice) • 2. Pediculosis Corporis (Body Lice) • 3. Pediculosis Pubis

Pediculosis Capitis • Pediculosis humanus var capitis • Spread: close physical contact & sharing of head gears, combs, brushes & pillows

• Site: occipital and retroauricular • Symptom: pruritus • Diagnostic Sign: live nits on proximal hair shaft

Pediculosis Capitis

Pediculosis Corporis • Pediculosis humanus var humanus • Spread: contaminated clothing or bedding • Site: waist, buttocks & thighs • Symptom: pruritus

• Diagnostic Sign: maculae cerulea- slightly slate colred macule

Pediculosis Corporis • Treatment – Single application of Permethrin 5% cream/lotion, left on for 8-10 hours and then washed off thoroughly – All household contacts

Pediculosis Pubis • Pthirus pubis • Spread: STD or direct contact • Site:pubic hair & any other hair-bearing region • Symptom: pruritus • Diagnostic Sign:microscopic examination of plucked hair

Pediculosis Pubis