Upload
aaron-christian-earl-villoso
View
110
Download
3
Embed Size (px)
Citation preview
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)
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. Anthony’s Fire
• Etiology:– Grp A Beta hemolytic Strep-supfl dermal
lymphatics– Strep C or G-occasional– Grp B Strep- newborns, abdominal or perineal
erysipelas in post partum women
Erysipelas
• Predisposing Factors– Break in the skin barrier– Operative wounds– Fissures in the nares, auditory meatus, under
the earlobes, on the anus, penis, between or under the toes (little toe)
– Accidental scalp wounds– Chronic leg ulcers
Erysipelas
• Clinical Presentation– Sites: face & legs– Prodrome: malaise, chills, high grade fever,
headache, vomiting & joint pains– Lesions: intensely erythematous (scarlet),
warm, swollen, brawny, well-demarcated plaque w/ characteristic raised indurated border
• +/- vesicles/bullae w/ seropurulent fluid• Spread; peripheral extension
Erysipelas• Lesions, contd…
• On face: ear may become swollen & distorted; +/- delirium• Leukocytosis (PMNLs >/= 20,000/mm3)
• Complications:• Septicemia• Deep Cellulitis
– *** in newborns or surgical operations in the elderly
Erysipelas
• Treatment– Systemic: at least 10 days, rapid improvement
in 24-48 hours– Penicillin V – IV Penicillin– Erythromycin
– Supportive Measures: cold compresses
Cellulitis & Erysipelas
Cellulitis Erysipelas
Staphylococcus or Streptococcus
Grp A Streptococcus
Subcutaneous Tissue Superficial Dermal lymphatics
Poorly demarcated Well-demarcated with characteristic raised indurated border
Erythrasma
• Etiology– Corynebacterium minutissimum– Extensive: diabetes or debilitating diseases
• Clinical Presentation– Sites: intertriginous areas (axilla, genitocrural
crease & the webs between the 4th & 5th toes> 3rd & 4th toes; intergluteal cleft, perianal skin, inframammary area & nails)
Erythrasma
• Clinical Presentation, contd…– Lesions:
• asymptomatic except for groin lesions which may present with burning & pruritus
• Sharply delineated, dry, brown, slightly scaling patches
• (+) Coral Red Fluorescence with Wood’s light– Due to Porphyrin
Erythrasma
• Treatment– Localized
• Topical erythromycin/clindamycin• Topical azoles• Topical Benzoyl Peroxide Wash or 5% gel
– Widespread• Oral Erythromycin
Mycobacterial Infections
1. Hansen’s Disease
2. Cutaneous Tuberculosis
Hansen’s Disease
• Mycobacterium leprae
• Classification:– 1. Indeterminate– 2. Tuberculoid (TT)– 3. Borderline Tuberculoid (BT)– 4. Borderline (BB)– 5. Borderline Lepromatous (BL)
6. Lepromatous (LL)
Indeterminate Leprosy
• Solitary, ill-defined hypopigmented macule or patch
• Sensory: normal or minimally altered (earliest: sense of cold & light touch)
• Peripheral nerves: not enlarged
• If immunity is good: resolves spontaneously
Tuberculoid Leprosy (TT)
• Lesions are solitary, few & asymmetrical
• Lesion: large erythematous plaque w/ sharply elevated border & atrophic center
• Sensory: anesthetic or hyposthetic & anhidrotic
• Nerve involvement: early, superficial peripheral nerves are enlarged, tender or both
Tuberculoid Leprosy (TT)
• Contracture of fingers (claw hand), facial muscle paralysis & foot drop may occur
• Interosseous muscles may be atrophied: wasting of thenar & hypothenar eminences
• Slow skin lesions evolution
• (+) Lepromin skin test, good cell-mediated immunity
Tuberculoid Leprosy (TT)
• Histopathology– Well defined granuloma with Langhans giant
cells, perineural infiltrates, AFB rare
Borderline Tuberculoid (BT)
• Similar to TT but smaller & more numerous
Borderline Leprosy (BB)
• Skin lesions numerous, asymmetrical & irregularly shaped
• Moderate anesthesia
Borderline Lepromatous (BL)
• Lesions are numerous, symmetrical & small
• Nerve involvement is symmetrical & appears later
Lepromatous Leprosy (LL)
• Lesions are ill-defined, infiltrated, numerous & symmetrical
• Nerve involvement: symmetrical, develops slowly and at later stages
• Nerve damage: massive bacillary infiltration w/ compression & fibrosis
• +/- hyperesthesia
• (-) changes in sweating
Lepromatous Leprosy (LL)
• Hair: slow progressive hair loss w/ thinning of outer thrid of eyebrow
• Progressively worsen w/o treatment
• (-) lepromin skin test, poor CMI
Lepromatous Leprosy (LL)
• Histopathology:– Foamy histiocytes, abundant AFB
Hansen’s Disease
• Diagnosis– Sensory Test- “pin-prick” or “ballpen-point” test– Skin biopsy stained with Fite –Faraco stain– Skin slit smears: “ Zieh-Neelsen stain
– Bacteriologic Index’
– 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
• 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
• 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• *** 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 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• *** With severe maceration: One part Aluminum
Acetate to 20 parts of water as dressing• ***Secondary Infections: Oral or Topical
antibacterial
Tinea Manum
• Treatment– Localized Tinea Manum
• Topical Antifungals: miconazole, clotrimazole, oxiconazole, sulconazole, econazole, ketoconazole, naftitine, terbinafine, ciclopirox olamine BID x 2-4 weeks
• Keratolytic Agents (eg Salicylic Acid, Lactic Acid Lotions) for areas protected by thick layers of underlying skin
Onychomycosis
• Types– 1. Distal Subungal Onychomycosis– 2. Superficial White Onychomycosis– 3. Proximal Subungal Onychomycosis– 4. Candidal Onychomycosis
Distal Subungal Onychomycosis
• Involves the distal nail bed & hyponychium w/ sec involvement of the underside of nailplate
• Whitish-yellowish discoloration starting at the distal corner of the nail & involves the junction of the nail & its bed and becomes brown-black in color
• Later: opaque, thickened, friable & raised by underlying hyperkeratotic nail bed
Superficial White Onychomycosis
• Aka Leukonychia Trichophytica
• Invasion of the toenail plate on the surface producing chalky white nail plate
• Maybe eroded: nail loss
Proximal Subungal Onychomycosis
• Involves the proximal nail fold
• White spot appears from beneath the PNF which gradually fills the lunula & moving distally
• Maybe an indicator of HIV infection
Candidal Onychomycosis
• Aka Total Dystrophic Onychomycosis
• Involves the whole nail plate
• Fingernails>toenails
• Begins under the lateral & proximal nail fold & the adjacent cuticle is pink, swollen & tender on pressure\
• Neighboring nail becomes dark, ridged & separated from the nail bed
Candidal Onychomycosis
• Later: total onycholysis
• Nail plate doe not become white, yellow or friable
• Seen in chronic mucocutaneous candidiasis
Onychomycosis Therapy
• Terbinafine 250mg/day x 6 weeks for fingernails and 12 weeks for toenails
• Itraconazole Pulse Treatment: 200mg BID for 1 week of each month for 2 months for fingernails and 3 months for toenails
• Fluconazole 150-300mg once a week x 6-12 months
• Griseofulvin 350mg TID with meals x 4-6 months for fingernails and 10-18 months for toenails (note: not used for Candidal Onychomycosis)
Dermatophytid
• “Id reaction” to the fungal antigen especially the inflammatory types
• Diagnosis depends on presence of fungal infection at site different from the lesion– Pruritic vesicles on the hand & sides of fingers-most
common site esp of Tinea Pedis– Acute widespread eruption usually follicular, lichenoid
& scaly papules on the trunk esp of Tinea Capitis– Erysipelas-like dermatophytid on the shin esp of toe
web tinea– *** resolves once infection subsides
Pityriasis/Tinea Versicolor
• Etiology:– Malassezia furfur or Pityrosporum orbiculare
• Short thick fungal hyphae &spores (“spaghetti & meatballs”)
• Clinical Manifestation– Yellowish or brownish macules in pale skin or
hypopigmented macules in dark skin– Coalesce to form patches– Delicate scaling (“grattinage”)– Mild itching & minimal inflammation
Pityriasis/Tinea Versicolor
• Clinical Manifestation, contd…– Sites of Predilection
• Sternal region & sides of chest• Abdomen• Back• Pubis• Neck• Intertriginous areas
– *** Hypopigmentation- fungus compels production of abnormally small melanosomes which are not transferred to the keratinocytes properly
Pityriasis/Tinea Versicolor
• Diagnosis– Wood’s Lamp: yellowish or brownish
fluorescence– Skin Scarping w/ 10% KOH: spaghetti &
meatballs
Pityriasis/Tinea Versicolor
• Treatment– 1. Topicals
• Imidazoles- Ketoconazole Shampoo• Selenium Sulfide Shampoos• Ciclopirox Olamine Shampoo• Zinc Pyrithione Shampoo• Sulfur Preparations• Propylene Glycol lotions• Benzoyl Peroxide• Terbinafine Cream or Sprays
Pityriasis/Tinea Versicolor
• Treatment– 2. Oral
• Ketoconazole 200 mg/day x 10 days• Fluconazole 400mg single dose• Itraconazole 200mg x 5-7 days
• *** hypopigmentation will take time to resolve and is not a sign of treatment failure
Candidiasis
• Aka candidosis, moniliasis, thrush or oidiomycosis
• Etiology: Candida albicans• Features:
– Normal inhabitant at various sites (skin, nails, mucous membranes & viscera), until there is some change in the state of the area then it becomes a pathogen
– Areas: perianal and inguinal folds, interdigital, nail folds & axillae
• *** warmth, moisture & maceration permit the organism to thrive
Candidiasis
• Types:– 1. Oral– 2. Perleche– 3. Candidal Vulvovaginitis– 4. Candidal Intertrigo– 5. Pseudodiaper rash– 6. Congenital Cutaneous Candidiasis– 7. Perianal Candidiasis– 8. Candidal Paronychia– 9. Chronic Mucocutaneous Candidiasis
Oral Candidiasis
• Newborn/ Infant– Grayish white membranous plaques w/ reddish base
on mucous membrane of mouth– Angles of the mouth
• Adults– Buccal mucosa and tongue– Papillae of tongue atrophied w/ smooth, glazed and
bright red surface– *** elderly, debilitated & malnourished– *** often 1st manifestation of HIV
Oral Candidiasis
• Treatment– Clotrimazole troches– Fluconazole 100-200mg/day x 5-10 days– Itraconazole 200 mg OD x 5-10 days
Perleche/Angular Cheilitis
• Maceration w/ transverse fissuring of the oral commisures
• Early lesions: ill-defined, grayish white thickened areas w/ slight erythema of mucous membrane at oral commisure
• More developed lesions: bluish white ot mother of pearl color, contiguous w/ a wedge shaped erythematous scaling dermatitis of skin portion of commisure fissure, maceration & crust formation
Perleche/Angular Cheilitis
• Also seen in Riboflavin deficiency & in malocclusion caused by ill-fitting dentures
• Can be bilateral
Candidal vulvovaginitis
• Labia: erythematous, moist & macerated
• Cervix: hyperemic, swollen & eroded with small vesicles on the surface
• Sx: severe pruritus, irriattion, extreme burning
• Vaginal Discharge: thick & tenacious
Candidal vulvovaginitis
• Pregnancy, In diabetes or secondary to broad spectrum antibiotic therapy
• Frequent recurrences
• Male partner should be examined
Candidal vulvovaginitis
• Treatment– Fluconazole 150mg single dose or 100mg/day
x 5-7days– Itraconazole– Topical Antifungals– Antifungal Vaginal Tablets
Candidal Intertrigo
• Arises between folds of genital, in groins or armpits, between buttocks, under large pendulous breasts, over hanging abdominal folds or umbilicus
• Pinkish intertriginous moist patches surrounded by a thin, overhanging fringe of macerated epidermis (“collarette of scale”)
• Characteristic “Satellite Lesions”
Pseudo Diaper Rash
• Perianal region spread over entire area enhanced by maceration produced by wet diapers
• Scaly macules & vesicles w/ maceration: pruritus, burning & extreme discomfort
• Erythematous desquamating “satellite” or “daughter” lesions scattered along edges
Congenital Cutaneous Candidiasis
• Infection of an infant during passage through a birth canal infected with C. albicans
• Erythematous macules progress to thin walled pustules, that rupture, dry & desquamate
• Lesions are widespread, involving even the nailfolds.
• Oral cavity & diaper area are spared
Perianal Candidiasis
• (+) pruritus ani
• Erythema, oozing & maceration
• Svere pruritus & burning
• Maybe precipitated by oral antibiotic tx
• Treatment:– Imidazoles– Topical corticosteroids– Antipruritic meds
Candidal Paronychia
• Chronic inflammation of nailfold produces discharge of pus
• Involves all nail plate
• Cushion-like thickening of paronychial tissue
• Slow erosion of lateral NF
• Gradual thickening & brownish discoloration of nailplate
• Transverse ridges, one nail
Candidal Paronychia
• Sual: dishwashers & diabetics
• Treatment– Oral Fluconazole weekly– Itraconazole in pulse doses– Anticandidal lotions– *** continued for 2-3months to prevent
recurrence
Chronic Mucocutaneous Candidiasis
• Chronic but superficial
• Before age of 6
• Oral Lesions: diffuse perleche & lip fissures
• Nail: thickened & dystrophic, (+) paronychia
• Skin: hyperkeratotic, horn-like or granulomatous lesions
Chronic Mucocutaneous Candidiasis
• Adult onset: heralds the occyrence of Thymoma
• Inherited or sporadic
Viral Infections with Cutaneous Manifestations
Purely Cutaneous Involvement
• Molluscum contagiosum
• Verruca/Wart
Molluscum contagiosum• Etiologic Agent:
– Molluscum contagiosum virus (poxvirus)
• Epidemiology:– MCV 1: general population– MCV 2: 60% among HIV patients– 3 groups: young children, sexually active
adults & immunosuppressed patients (HIV)– Direct skin to skin contact
Molluscum contagiosum
• Clinical Presentation
– Lesions: • smoothed surface, firm, dome-shaped, pearly
papules• 3-5mm in diameter (giant: 1.5cm)• Characteristic: central umbilication
Molluscum contagiosum
Children 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
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• 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
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
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%)
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 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
– 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
• 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 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
• 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 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
• Clinical Presentation
– Prodrome: fever, malaise, conjunctivitis & prominent upper respiratory symptoms (nasal congestion, sneezing, coryza & barking cough)
Measles
• Clinical Presentation– Rash
• 1-7 days after prodrome• Macular or maculopapular• Anterior scalp line & post auricular• Discrete erythematous papules that coalesce,
spreads quickly over face extending down the trunk to extremities (cephalocaudal & centrifugal)
• Clears in 6-7 days after appearnce w/ fever lysis
Measles
• Clinical Presentation– Koplik’s Spots
• Pathognomonic• Appears during the prodrome• Location: buccal mucosa nearest to the lower
molars, spreading to involve other areas of buccal mucosa & pharynx
• 1mm white papules on erythematous base
Measles
• Diagnosis– High fever, Koplik’s spots, conjunctivitis,
upper respiratory sx & typical exanthem– Lymphopenia is common
• Histopathology– Syncytial keratinocytic giant cells
Measles
• Treatment– Vitamin A in high dose (reduces morbidity &
mortality of hospitalized children w/ measles)• Retinyl palmitate 200,000 IU OD x 2 doses
– Bed rest– Analgesics– Antipyretics
Measles• Complications
– Otitis media, pneumonia, encephalitis, thrombocytopenic purpura
– In Malnourished & T cell deficiencies– Exanthems are less prominent in HIV-infected
children
• Special Cases– Pregnant- associated w/ fetal deaths– Partially immune host( prior infection, persistent
maternal antibodies or immunization)• Milder, shorter, less confluent exanthems, (-) Koplik’s spots
Rubella
• Etiology– Togavirus
• Transmission– Respiratory secretions
Rubella
• Clinical Presentation– Incubation Period: 12-23 days (15-21 days)– Prodrome
• 1-5 days• Fever, malaise, sore throat, eye pain, headache,
red eyes, runny nose, post auricular LAD• Pain on lateral & upward eye movement
Rubella
• Clinical Presentation– Exanthem
• Begins on the face progressing caudad, covering the entire body in 24 hours
• Resolves by 3rd day (3-day measles)• Pale pink, morbilliform macules, smaller than
measles
– Enanthem• Pinhead-sized red macules or petechiae on soft
palate and uvula (Forscheimers’s sign)
Rubella
• Complication– Arthritis or Arthralgias- adult women lasting
for > 1 month
Skin Infestations
1. Scabies
2. Pediculosis
Scabies
• Sarcoptes scabiei var hominis
• Produces diffuse, pruritic eruption after an initial IP of 6-8 weeks
• Pathognomonic Clinical Feature: burrow produced by tunneling of the mite in the stratum corneum
Scabies
• Transmission– Close physical contact– Fomite
Scabies
Pediculosis
• 1. Pediculosis Capitis (Head Lice)
• 2. Pediculosis Corporis (Body Lice)
• 3. Pediculosis Pubis
Pediculosis Capitis
• Pediculosis humanus var capitis
• Spread: close physical contact & sharing of head gears, combs, brushes & pillows
• Site: occipital and retroauricular
• Symptom: pruritus
• Diagnostic Sign: live nits on proximal hair shaft
Pediculosis Capitis
Pediculosis Corporis
• Pediculosis humanus var humanus
• Spread: contaminated clothing or bedding
• Site: waist, buttocks & thighs
• Symptom: pruritus
• Diagnostic Sign: maculae cerulea- slightly slate colred macule
Pediculosis Corporis
• Treatment– Single application of Permethrin 5%
cream/lotion, left on for 8-10 hours and then washed off thoroughly
– All household contacts
Pediculosis Pubis
• Pthirus pubis
• Spread: STD or direct contact
• Site:pubic hair & any other hair-bearing region
• Symptom: pruritus
• Diagnostic Sign:microscopic examination of plucked hair
Pediculosis Pubis