infectious dermatology[1]

Dermatological Infections & Infestations

Mariecon O. Escuadro, MDDiplomate, Philippine Dermtological Society

Diplomate, Philippine Society of Venereologists, Inc

Superficial Bacterial Skin Infections

1. Impetigo Contagiosa2. Bullous Impetigo3. Folliculitis4. Furuncle & Carbuncle5. Ecthyma6. Cellulitis7. Erysipelas8. 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/golden-yellow 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 bullarupture: 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)


• 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


• 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 spreadswarmth, 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


• 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


• 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


• Hair: slow progressive hair loss w/ thinning of outer thrid of eyebrow

• Progressively worsen w/o treatment

• (-) lepromin skin test, poor CMI


• 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’

– Lepromin skin test: immunologic status

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

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 DiseaseTreatment

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 States2. 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 (MBPB): – 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 huemore indurated w/ thick adherent crusts

Tuberculous Chancre

• Mucosal: painless ulcers or fungating granulomas

• Slowly progressive, regional LAD x 3-8 weeks after infectionweeks 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 involutionatrophic 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

• 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 Typea. 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 & backwards-

perineum 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


• 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


• 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


• 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


• Diagnosis– Wood’s Lamp: yellowish or brownish

fluorescence– Skin Scarping w/ 10% KOH: spaghetti &

meatballs


• 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


• 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


• Pregnancy, In diabetes or secondary to broad spectrum antibiotic therapy

• Frequent recurrences

• Male partner should be examined


• 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


Children AdultsUsually STD’s

Few to >100 <20 lesions

Location: face, trunk & extremities Location: lower abdomen, upper thighs and penile shaft (men)

May occur in genitals as part of wide distribution; if restricted- sexual abuse maybe considered

Mucosal involvement is uncommon


• Differential Diagnoses

• Wart

• Syringoma (benign sweat gland tumor on face

around the eyes)

• Sebaceous hyperplasia (sebaceous gland

hyperplasia in seborrheic areas of face)

• Basal Cell Carcinoma (skin cancer)

Molluscum contagiosum• Complications

– Secondary bacterial infection– Eczematous reaction in 10% (molluscum dermatitis)– Conjunctivitis or keratitis– Cutaneous horn (MC cornuatum)

• Histopathology– Eosinophilic and later basophilic inclusion bodies

(Molluscum bodies or Henderson-Paterson bodies) are formed in the cytoplasm of spinous cells

Molluscum contagiosum• Diagnosis

– Clinical: centrally umbilicated dome-shaped lesion

– Diagnostics:• Cryotherapy: umbilication appears clear against a

white (frozen) background• Shelley’s method for visualization

– Expression of pasty core lesion– Squash between 2 glass slides– Methylene blue stain

Molluscum contagiosum• Treatment

– Surgical nicking with comedone extractor***– Removal by curettage– Surgical tape after bathing x 16 weeks (90% cure)– Topical Tretinoin 0.05% ODHS– Imiquimod Cream ODHS***– TCA 35%-100% application– 10% KOH– Light cryotherapy– Anthradin x 4-8 hours– Oral Cimetidine 40mkday x 2 mos (90% cure)

Molluscum contagiosum• Treatment, contd…

– Adults w/ genital molluscum• Mandatory screening for STD• Screen sexual partners• Cryotherapy• Podophyllotoxin 0.5% cream BID x 3 days per

weeks x 12 weeks• Curettage


• Course and Prognosis

– Spontaneous resolution in 2-4 months

– Average duration: 2 years

Human Papillomavirus/Wart

• Etiologic Agent:– Human Papillomavirus (HPV)

• 80 types to date• Only few are pathogenic to men


• Clinical Presentation:

– Verruca Vulgaris/Common Wart

– Verruca Plana/ Flat warts

– Verruca Plantaris/ Plantart wart

– Conduloma acuminata/Genital Wart

Verruca Vulgaris

– Most common: HPV type 2– Less frequent: HPV type 1,4,7– Age: 5-20 years old (15% occur after 35)– Children: 5%– Risk Factors:

• Frequent immersion of hands in water• Meat handlers

Verruca Vulgaris

- Spontaneous resolution- 50% by 1 year- 60-70% by 2 years

- Predilection sites- Hands (fingers & palms)- Nail biters: periungal, lips & tongue

Verruca Vulgaris

Lesionssize: pinpoint to 1 cm (ave:5mm)

increase in size: weeks to months

elevated, rounded papules with rough, grayish surface

tiny, black dots on surface w/ thrombosed capillaries

no dermatoglyphics (vs calluses)

Verruca Plana

– Most common: HPV type 3– Less frequent: HPV type 10, 27 & 41– Children & young adults– Lesions:

• 2-4mm flat topped papules, slightly erythematous or brown on pale skin & hyperpigmented on darker skin

• Generally multiple• Grouped on face (forehead, cheeks, nose, perioral), neck,

dorsa of hands, wrists or knees• Highest rate of spontaneous resolution

Verruca Plantaris

– Most common: HPV type 1– Less frequent: HPV type 2, 4– Appear at pressure points on ball of foot esp

midmetatarsal area– Soft pulpy cores are surrounded by firm, horny ring

– Mosaic wart: contiguous warts appearing as one

Verruca Plantaris

Myrmecia wart: smooth-surfaced, deep, inflamed & tender papules or plaques on palms or soles, beside or beneath nails or pulp of digits

- dome shaped

- bulkier beneath the surface

- HPV 1

- DDx: paronychia or digital mucinous cyst

Verruca Plantaris

Ridged wart:

- peculiar type, HPV 60

- dermatoglyphics persits

- slightly elevated, skin-colored, 3-5mm papules

- non weight bearing areas

Plantar verrucous cysts:

- HPV 60

-1.5-2cm epithelium lined cysts on plantar area

-weight bearing areas

Condyloma Acuminata

• Common sexually transmitted disease

among sexually active young adults

• Infection rate: 50%

• Lifetime risk: 80%

• Subclinical and latent infections-

recurrences & transmission

Condyloma Acuminata

• Benign Genital Warts: HPV 6 & 11

• Cervical Dysplasia: HPV 16 & 18 (98%)


• Differential Diagnosis:– Molluscum contagiosum-umbilicated surface– Syringoma- benign sweat gland tumor of the face– Seborrheic Keratoses-stuck-on hyperkeratotic, pigmented

papules & plaques– Acrochordon-skin tag; skin-colored, soft exophytic

papule– Callus & corn-maintained skin lines, absent thrombosed

capillaries/black dots

– Genital warts vs condyloma lata


• Treatment– Few lesions

• Light cryotherapy• Topical Salicylic Acid• Electrodessication

– More extensive• Topical Tretinoin 30-100% OD-BID• 5 Fluorouracil cream 5% BID

Human Papillomavirus/Wart• Treatment

– Refractory• Pulse dye laser before electrodessication (reduced risk of scarring)

– Genital• Podophyllin 25% in tincture of benzoin weekly, washed off 4-8

hours later.• Trichloroacetic acid 35-85% weekly or biweekly. Safe in in

pregnancy.• Cryotherapy w/ liquid nitrogen every 1-3 weeks, 1 or 2 freeze-thaw

cycles. Safe in pregnancy.• Electrofulguration or electrocauterization• Minor surgical removal• CO2 laser- more costly & highly technical

With Systemic Involvement

• Varicella/Chickenpox

• Herpes Zoster/Shingles

• Herpes Simplex

• Measles/Rubeola

• Rubella/German Measles

Varicella

• Etiology– Primary infection of VZV

• Epidemiology– 90%- children <10 years in temperate

countries; adults & adolescents in tropical– Summer months

Varicella• Pathogenesis

– Aerosol or direct contact

– Inoculation of respiratory mucosa replication in regional nodes (innate defenses) primary viremia: replication in liver & spleen & RESSecondary Viremia: mononuclear cells transport virus to skin & mucous membranes (fever & malaise) Virus released into respiratory secretions replication in epidermal cells

– Transported to Dorsal Root Ganglia: Latency

Varicella

• Clinical Characteristics– Incubation Period: 10-21 days– Transmission: direct contact & respiratory

route– Infectious: 4 days before & 5 days after

exanthem– Prodrome: low grade fever, malaise &

headache– Lifelong immunity

Varicella

• Differential Diagnosis– Drug eruption (drug intake, monomorphous)– Allergic Contact Dermatitis (symmetrical, localized)– Blistering diseases- Dermatitis Herpetiformis & Linear

IgA dermatoses

• Diagnostics– Tzank smear- multinucleated giant cells– Direct fluorescent Ab test- rapid & confirmatory

VaricellaCongenital Neonatal Immuno

compromised-hypoplastic limbs, cutaneous scars, ocular & CNS diseases

-extremely severe & even fatal-necrotic & ulceration

-maternal infections: 20 weeks AOG-in utero- zoster postnatally during 1st 2 years of life

-maternal infections: 5 days before & 2 days after delivery

Prevention: vaccination

Varicella• Treatment

– Antiviral Therapy (Aciclovir, Valaciclovir & Famciclovir)

• Within 24 hours of appearance of eruption• Acyclovir 800mg 5x a day x 7days• Valacyclovir 1 gm TID x 5days

– Immunocompromised• Mild: Aciclovir 800 mg 5x/D x 7-10 days• Severe: Aciclovir 10mkdose IV q8 x 7 days or longer• Acyclovir resistant: Foscarnet 40mkdose IV q8 until

healed

Varicella• Treatment, contd…

– Supportive: topical antipruritic lotions, oatmeal baths & cool light clothing

– Antibiotics- secondary bacterial infections

• Complications– Secondary bacterial infection w/ Staph or Strep– Cerebellar ataxia & encephalitis– Asymptomatic myocarditis & hepatitis– Reye’s syndrome- Aspirin is CI– Purpura Fulminans-low levels of protein C & S

Herpes Zoster

• Etiology:– Varicella Zoster Virus Secondary infection

• Latency in DRG replicates & travels down sensory nerve into skin

• Epidemiology:– Increases with age, sun exposure, smoking,

trauma, stress & immunocompromised states

Herpes Zoster

• Classically occurs unilaterally within the distribution of cranial or spinal sensory nerve

• Dermatomes:– Thoracic- 55%– Cranial-20% (Trigeminal)– Lumbar- 15%– Sacral- 5%

Herpes Zoster


– Eruption is preceded by pain over affected areas

– Papules & plaques of erythema in dermatome,

followed by blisters within hours

– Lesions maybe hemorrhagic, necrotic or bullous

– Duration: depends on age, severity of eruption &

underlying immunosuppression ( 2-3 weeks in

younger & up to 6 weeks in elderly)

Herpes Zoster

Pregnancy Disseminated Ophthalmic

-Antivirals: risk-benefit ratio

-> 20 lesions outside the affected dermatome

-Ophthalmic division of CNV

-Acyclovir has been commonly given during pregnancy without direct effect to the fetus

-in old & debilitated -Hutchinson’s Sign: vesicles on side & tip of the nose (external division of nasociliary nerve w/ involvement of eyeball)

-Usually localized to the skin & does not affect the fetus

-fever, protration, headache, signs of meningeal irritation or viral meningitis

- Ocular involvement: uveitis (92%) & keratitis (50%)

Herpes Zoster

• Diagnosis– Histopathology: intraepidermal vesicles, balloon cells

which are degenerated cells of spinous layer, marked intercellular & intracellular edema

• Treatment– Supportive:

• Bedrest- prevention of neuralgia in middle aged & elderly

• Warm compresses

Herpes Zoster

• Treatment, contd…– Antiviral Therapy

• Cornerstone in management, reduces zoster-associated pain

• Intitiated within 3-4 days– Acyclovir 800mg 5x/day x 7days– Valacyclovir 1 gm TID x 7 days– Famciclovir 500 mg TID x 7days

Herpes Zoster• Complications

– Ramsay-Hunt Syndrome: facial & auditory nerves• Herpetic inflammation of geniculate ganglion• Zoster of external ear or tympanic membrane• Herpes auricularis, facial paralysis & auditory symptoms

– Post herpetic Neuralgia; zoster associated pain until 1 month from resolution of lesions

• Major complication of zoster• Age or severity dependent• Treatment:

– Tricyclic Antidepressants-1st line– Anticonvulsants: phenothiazines & carbamazepine 200-400mg OD– Gabapentin in escalating doses up to 3200mg OD

Herpes Simplex

• Etiology– Orolabial: HSV Type 1– Genita; : HSV Type 2

• Epidemiology– One of the most prevalent STI worldwide– 80% are seropositive for HSV-1– HSV-2 at onset of sexual activity

Herpes Simplex


– Orolabial Herpes

– Herpetic Whitlow

– Genital Herpes

– Intrauterine & Neonatal Herpes***

– Eczema Herpeticum

– HSV in immunocompromised

Orolabial Herpes

• High fever, regional lymphadenopathy & malaise

• “Cold sore” or “fever blister”

• Grouped blisters on erythematous base

involving the lips near vermillion border

• Trigger for recurrence: UV exposure

• Sunscreens reduces recurrence

Herpetic Whitlow

• Infection of the pulp of the fingertip

• Bimodal:– Children: < 10 years old– Adults: 20-40 years old

• Tenderness & erythema, of lateral nail fold followed by formation of deep seated blisterd 24-48 hours after

Genital Herpes

• Spread by skin to skin contact usually during sexual activity

• Incubation period: 5 days• Primary Infection

– Grouped blisters & erosions in vagina, rectum or penis w/ continued devt of new lesions over 7-14 days

– Bilaterally symmetrical w/ bilaterally enlarged inguinal LN

Genital Herpes• Recurrence

– Prodrome; burning, itching or tingling

– Papules in 24 hoursvesicles in another 24 hours

erosions in 24-36 hours and heals in 2-3 days

– Milder than 1st due to antibodies

– Common site: upper buttocks

– Heals without scarring unless secondarily infected

– Chronic suppressive therapy- reduces asymtomatic

shedding by 95%

Eczema Herpeticum

• Herpes infection in:– Atopic dermatitis– Severe Seborrheic dermatitis– Scabies– Darier’s Disease– Blistering Diseases: Benign Familial

Pemphigus, Pemphigus, Pemphigoid– Wiskott-Aldrich syndrome– Burns

Eczema Herpeticum

• Hundreds of umbilicated vesicles with fever & regional adenopathy

• Self-limited

HSV in immunocompromised

• Erosions or crusts

• Hallmarks: pain, active vesicular border & scalloped periphery

• Visceral dissemination is unusual

Herpes Simplex• Diagnostics:

– Tzanck Smear• Most common procedure done• Nonspecific• HSV & VZV results in formation of multinucleate giant cells• Accurate rate: 60-90%

– Direct Fluorescent Ab test– Viral Culture– Polymerase Chain Reaction

Herpes Simplex• Diagnostics:

– Skin Biopsy• Intraepidermal blisters• Ballooning degeneration of epidermal cells to produce

acantholysis• Minute eosinophilic intranuclear bodies occur in nuclei of

epithelial cells, coalescing to occupy majority of nucleus as inclusion body

Herpes Simplex: TreatmentDisease Antiviral Therapy Others

Orolabial Herpes Acyclovir 200mg 5x OD x 5 days Topical Treatment w/ drying agents: Benzoyl Peroxide, Zinc Oxide, Sunscreen

Genital Herpes

Primary Acyclovir 200-400mg 5x OD x 5-7 daysFamciclovir 250 mg TID x 5-7 daysValacyclovir 1gm BID x 5-7 days

Recurrence Episodic TreatmentAcyclovir 200mg 5x OD x 5 daysValacyclovir 500 mg BID x 5 daysFamciclovir 125-250 mg BID x 5days

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

Herpes Simplex: TreatmentDisease 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 BIDValacyclovir 500 mg BIDFamciclovir 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


– 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


• 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


• Diagnostic Sign:microscopic examination of plucked hair

Pediculosis Pubis

infectious dermatology[1]

Documents