Dermatological
Infections & Infestations
Mariecon O. Escuadro, MD
Diplomate, Philippine Dermtological Society
Superficial
Bacterial Skin Infections
1. Impetigo Contagiosa 2. Bullous Impetigo
3. Folliculitis
4. Furuncle & Carbuncle 5. Ecthyma
6. Cellulitis 7. Erysipelas 8. 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
Bullous Impetigo
• Etiology
– Phage type 71 coagulase positive
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:
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
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
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
Cellulitis
• Complications
– Gangrene, metastaic abscess & sepsis in
children & immunocompromised
• Treatment
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
Erysipelas
• Treatment
– Systemic: at least 10 days, rapid improvement
in 24-48 hours
– Penicillin V – IV Penicillin – Erythromycin
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 4
th& 5
thtoes>
3
rd& 4
thtoes; 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
Erythrasma
• Treatment
– Localized
• Topical erythromycin/clindamycin • Topical azoles
• Topical Benzoyl Peroxide Wash or 5% gel
– Widespread
Mycobacterial Infections
1.
Hansen’s Disease
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
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
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:
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 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
Hansen’s Disease
• Reactional States
– Acute episodes characterized by remissions &
relapses for a week to a few months in a
chronic course of infection
– Neuritis is the most imptortant consideration
– Precipitating factors: infection, surgery,
physical, physiologic & mental stress,
vaccination, pregnancy, Vitamin A, iodides &
bromides
Hansen’s Disease
• Reactional States
– 1. Type 1 reaction
• Cell mediated; in BT, BB, BL
• Inflammation (swollen, erythematous & tender) of existing lesions
• No systemic symptoms; mj complication- nerve damage
• a. Reversal- w/ antibiotic tx, shift toward tuberculoid pole
• B. Downgrading- before antibiotic, shift toward lepromatous pole
Hansen’s Disease
• Reactional States
2. Type 2 reaction/Erythema nodosum
leprosum
• Circulating immune complex-mediated dse;In BL, LL
• Painful, erythematous subcutaneous & dermal nodules
• With systemic symptoms: fever, myalgia, arthralgia, anorexia & iritis
Hansen’s Disease
• Management of Reactions:
– Type 1 Reversal Mild
• Analgesics
• Chloroquine (1-2weeks)
– Type 1 Reversal Severe
• Prednisone 40-80mg OD x 5-7 days then taper for 2-6 months
• Clofazimine 300mg OD x 6 weeks
– Type 2/ ENL
• Clofazimine 300 mg OD x 6 weeks, 200mg OD x 2-6 mos & 100 mg OD x 1-2 years
• Thalidomide 400mg OD, tapered to 50-100 mg OD in 1 week (teratogenic)
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
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
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
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
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
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)
Scrofulderma
• Site: parotidal, submandibular &
supraclavicular; bilateral
• Lesion: firm, subcutaneous nodule, well
defined, freely movable & asymptomatic
softens, liquefaction w/ perforation
Scrofulderma
• Histopathology:
• Massive necrosis & abscess formation in center
• Course
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
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)
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
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
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
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
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
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
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
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
Proximal Subungal Onychomycosis
• Involves the proximal nail fold
• White spot appears from beneath the PNF
which gradually fills the lunula & moving
distally
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
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
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”)
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
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
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
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
Candidal vulvovaginitis
• Pregnancy, In diabetes or secondary to
broad spectrum antibiotic therapy
• Frequent recurrences
Candidal vulvovaginitis
• Treatment
– Fluconazole 150mg single dose or 100mg/day
x 5-7days
– Itraconazole
– Topical Antifungals
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”)
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.
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
Candidal Paronychia
• Sual: dishwashers & diabetics
• Treatment
– Oral Fluconazole weekly
– Itraconazole in pulse doses
– Anticandidal lotions
– *** continued for 2-3months to prevent
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
Viral Infections with
Purely Cutaneous Involvement
• Molluscum contagiosum
• Verruca/Wart
Molluscum contagiosum
• Etiologic Agent:
– Molluscum contagiosum virus (poxvirus)
• Epidemiology:
– MCV 1: general population
– MCV 2: 60% among HIV patients
– 3 groups: young children, sexually active
adults & immunosuppressed patients (HIV)
– Direct skin to skin contact
Molluscum contagiosum
• Clinical Presentation
– Lesions:
• smoothed surface, firm, dome-shaped, pearly papules
• 3-5mm in diameter (giant: 1.5cm) • Characteristic: central umbilication
Molluscum contagiosum
Children
Adults
Usually STD’s Few to >100 <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
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
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
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
Molluscum contagiosum
• Course and Prognosis
– Spontaneous resolution in 2-4 months
Human Papillomavirus/Wart
• Etiologic Agent:
– Human Papillomavirus (HPV)
• 80 types to date
Human Papillomavirus/Wart
• Clinical Presentation:
– Verruca Vulgaris/Common Wart
– Verruca Plana/ Flat warts
– Verruca Plantaris/ Plantart 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)
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
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
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
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
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
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
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
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
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
Varicella
Congenital
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
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
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
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
Herpes Simplex
• Clinical Presentation
– Orolabial Herpes
– Herpetic Whitlow
– Genital Herpes
– Intrauterine & Neonatal Herpes***
– Eczema Herpeticum
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
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