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 bullaepustules, 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 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)

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 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. Anthonys 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
Staphylococcus or Streptococcus Subcutaneous Tissue

Erysipelas
Grp A Streptococcus 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 Woods 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. Hansens Disease 2. Cutaneous Tuberculosis

Hansens 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

Hansens 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+ 5+ 4+ 3+ >1000 bacilli/f 100-1000 10-100 1-10

2+
1+

1-10 in 10 OIF
1-10 in 100 OIF

Lepromin skin test: immunologic status

Hansens Disease
Diagnosis
Lepromin skin test: immunologic status
Fernandez reaction: 24-48 hours Mitsuda reaction: 4 weeks

Hansens 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

Hansens 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)

Hansens 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

Hansens 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

Hansens 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

Hansens 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

Hansens 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
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 Woods 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 Atheletes 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
Woods 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
Few to >100 Location: face, trunk & extremities <20 lesions Location: lower abdomen, upper thighs and penile shaft (men)

Adults
Usually STDs

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

Mucosal involvement is uncommon

Molluscum contagiosum
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 Shelleys 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

Molluscum contagiosum
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

Human Papillomavirus/Wart
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
Lesions
size: 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 infectionsrecurrences & transmission

Condyloma Acuminata
Benign Genital Warts: HPV 6 & 11 Cervical Dysplasia: HPV 16 & 18 (98%)

Human Papillomavirus/Wart
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

Human Papillomavirus/Wart
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 48 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

Varicella
Congenital
-hypoplastic limbs, cutaneous scars, ocular & CNS diseases

Neonatal

Immuno compromised
-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
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 Reyes 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
Clinical Presentation
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 -Antivirals: risk-benefit ratio Disseminated -> 20 lesions outside the affected dermatome Ophthalmic -Ophthalmic division of CNV

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

-in old & debilitated

-Hutchinsons Sign: vesicles on side & tip of the nose (external division of nasociliary nerve w/ involvement of eyeball)
- Ocular involvement: uveitis (92%) & keratitis (50%)

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

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

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 zosterassociated 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
Clinical Presentation
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 2448 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 Dariers 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: Treatment

Disease
Orolabial Herpes

Antiviral Therapy
Acyclovir 200mg 5x OD x 5 days

Others
Topical Treatment w/ drying agents: Benzoyl Peroxide, Zinc Oxide, Sunscreen

Genital Herpes Primary Acyclovir 200-400mg 5x OD x 5-7 days Famciclovir 250 mg TID x 5-7 days Valacyclovir 1gm BID x 5-7 days

Recurrence

Episodic Treatment Acyclovir 200mg 5x OD x 5 days Valacyclovir 500 mg BID x 5 days Famciclovir 125-250 mg BID x 5days

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

Herpes Simplex: Treatment

Disease
Intrauterine & Neonatal Herpes

Antiviral Therapy
IV Acyclovir 250mg/m2 q8 x 7 days

Others
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
Kopliks 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, Kopliks 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, (-) Kopliks 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 (Forscheimerss 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