CLINICAL S/SX DIFFERENTIAL
DISEASE DESCRIPTION
 Sarcoptes scabiei var. hominis
 Transmission: skin-to-skin contact
and fomites
SCABIES  Pathogenesis: hypersensitivity
 Distribution: Scrotum, penis, axillae,
waist, buttocks, areolae
 Chronic disorder with polygenic
predisposition and triggering
environmental factors such as
bacterial infection, trauma, or drugs.
 Pathogenesis: Cell Mediated CD 8 T-
Cell immunity; hyperkeratosis
 Triggers
 Physical trauma (rubbing and
scratching)
 Acute streptococcal infection
PSORIASIS precipitates guttate psoriasis.
 Stress is a factor in flares of
psoriasis
 Drugs: Systemic glucocorticoids,
oral lithium, antimalarial drugs,
interferon, and β-adrenergic
blockers can cause flares and
cause a psoriasis form drug
eruption.
 Alcohol ingestion is a putative
trigger factor.
 Hereditary diathesis, but Malassezia
furfur may play a pathogenic role
 Synonyms: “Cradle cap” (infants),
pityriasis sicca (dandruff)
 Distribution:
 Hairy Areas of Head Scalp,
eyebrows, eyelashes (blepharitis),
beard (follicular orifices)
 cradle cap: erythema and yellow-
orange scales and crusts on the
scalp in infants
 Face. The flush (“butterfly”) areas
SEBORRHEIC
on forehead (“corona
DERMATITIS
seborrhoica”), nasolabial folds,
eyebrows, and glabella
 Ears: retroauricular, meatus,
sticky crusts, and fissures.
 Trunk. Simulating lesions of
pityriasis rosea or pityriasis
versicolor; yellowish-brown
patches over the sternum
common.
 Body Folds. Axillae, groins,
anogenital area, submammary
areas, umbilicus, and diaper area
DIAGNOSIS MANAGEMENT/TREATMENT
SKIN LESION DIAGNOSIS
 Permethrin 5% Cream applied to all areas of the body
 Nocturnal pruritus applied thinly to all areas of the body from the neck
 Burrows: Skin-colored ridges, 0.5–  Psoriasis down; wash off thoroughly after 8 h
1 cm in length, either linear or  microscopy: (Three
 Eczematous  Lindane (g-Benzene Hexachloride) 1% lotion or cream
findings) S. scabiei
serpiginous, with minute vesicle or dermatitis applied thinly to all areas of the body from the neck
mites, eggs, and fecal
papule at end of tunnel  seborrheic dermatitis down; wash off thoroughly after 8 h
pellets (scybala)
 Affects other family members  erythroderma  Systemic infection: mupirocin ointment or systemic
antimicrobial agent.
 Malathion spray
 Typical lesions are chronic,
recurring, scaly papules, and
plaques. Pustular eruptions and
erythroderma occur
 Acute Guttate Type: Salmon-pink
papules, 2.0 mm to 1.0 cm with or
without scales. Scales are lamellar,  Seborrheic dermatitis
 Biopsy
loose, and easily removed by
 Lichen simplex  Dermatopathology:  Steroid
scratching. Removal of scale
chronicus Marked overall  Clobetasol
results in the appearance of
 Psoriasiform drug thickening of the  Tar sopa
minute blood droplets (Auspitz
eruptions epidermis  Tar shampoo
sign).
 Tinea corporis (acanthosis) and
 Chronic Stable Type. Sharply
 Mycosis fungoides thinning of epidermis
marginated, dull red plaques with
loosely adherent, lamellar, silvery-
white scales. Plaques coalesce to
form polycyclic, geographic lesions
and may partially regress,
resulting in annular, serpiginous,
and arciform patterns
 psoriasis
 impetigo (rule out by
smears for bacteria)
 dermatophytosis
 Orange-red or gray-white skin,  pityriasis versicolor
often with “greasy” or white dry  intertriginous
scaling macules, papules of candidiasis (rule out
varying size (5–20 mm), or dermatophytes and  Ketoconazole shampoo
patches, rather sharply yeasts by KOH)  Biopsy  Low potent glucocorticoids
marginated.  subacute lupus
 On the scalp, there is mostly erythematosus (rule
marked scaling (“dandruff”), out by biopsy)
diffuse involvement of scalp  “seborrheic” papules
in secondary syphilis
(rule out Treponema
pallidum by dark
field)

DISEASE DESCRIPTION
in infants
 Genitalia.
 acute, subacute, or chronic relapsing
skin disorder
 Very common in infancy
 Characterized principally by dry skin
and pruritus; consequent rubbing
leads to increased inflammation and
lichenification and to further itching
and scratching: itch–scratch cycle
ATOPIC  associated with a personal or family
DERMATITIS history of AD, allergic rhinitis, and
asthma
 Associated with skin barrier
dysfunction, IgE reactivity.
 Synonyms: IgE dermatitis, “eczema,”
atopic eczema.
 Pathogenesis: type I (IgE Mediated)
Hypersensitivity
 localized disease confined to areas
exposed to irritants
IRRITANT
 caused by exposure of the skin to
CONTACT chemical or other physical agents that
DERMATITIS
are capable of irritating the skin.
 hands are the most commonly affected
area.
ALLERGIC
 Pathogenesis: classic, delayed, cell-
CONTACT
mediated hypersensitivity reaction.
DERMATITIS
CLINICAL S/SX
SKIN LESION
 Skin lesion: Poorly defined
erythematous patches, papules,
and plaques with or without scale
 Erosions: moist, crusted. Linear or
punctate, resulting from
scratching. Secondarily infected
sites: S. aureus. Oozing erosions
and/or pustules (usually
follicular)
 Chronic. Lichenification
(thickening of the skin with
accentuation of skin markings)
 Characteristic infraorbital fold
below eyelids (Dennie–Morgan
sign)
 Predilection for the flexures, front
and sides of the neck, eyelids,
forehead, face, wrists, and dorsa of
the feet and hands
 Acute:
 range from erythema to
vesiculation and caustic burn
with necrosis.
 Sharply demarcated erythema
and superficial edema,
corresponding to the
application site of the toxic
substance
 do not spread beyond the site
of contact.
 Configuration is often bizarre
or linear (“outside job” or
dripping effect
 Chronic:
 Dryness → chapping →
erythema → hyperkeratosis
and scaling → fissures and
crusting
 Sharp margination gives way
to ill-defined borders,
lichenification
 Acute
 Well-demarcated erythema
and edema with superimposed
closely spaced papules or
DIFFERENTIAL
DIAGNOSIS MANAGEMENT/TREATMENT
DIAGNOSIS
 Acute
 Wet dressings and topical glucocorticoids; topical
antibiotics (mupirocin ointment) when indicated
 Hydroxyzine, 10–100 mg four times daily for
pruritus
 Oral antibiotics (dicloxacillin, erythromycin)
 Subacute and Chronic
 Hydration (oilated baths or baths with oatmeal
powder) followed by application of unscented
emollients is basic daily treatment to counteract
 SD xerosis; 12% ammonium lactate or 10% α-
hydroxy acid lotion is very effective for xerosis
 ICD
 Topical anti-inflammatory agents such as
 ACD  Clinical findings
glucocorticoids, hydroxyquinoline preparations,
 Psoriasis  Bacterial culture
and tar are the mainstays of treatment.
 nummular eczema  Viral culture
 calcineurin inhibitors, tacrolimus and
 dermatophytosis  Blood studies
pimecrolimus, are gradually replacing
 early stages of
glucocorticoids in most patients. They potently
mycosis fungoides.
suppress itching and inflammation and do not
lead to skin atrophy.
 Oral H1-antihistamines are useful in reducing
itching
 UVA–UVB phototherapy (combination of UVA
plus UVB and increasing the radiation dose each
treatment, with a frequency of two to three
times weekly). Narrow band UV (311 nm)
phototherapy and PUVA photochemotherapy are
also effective.
 Patients should learn and use stress
management techniques.
 Acute
 remove the etiologic agent
 Wet dressings with Burow’s solution, changed
every 2–3 h.
 Clinical diagnosis  Topical class I–II glucocorticoid preparations
 Histopathology: Acute  Prednisone: 2-week course, 60 mg initially,
 epidermal cell tapering by steps of 10 mg.
 ACD
necrosis, neutrophils,  Subacute and Chronic.
 Palmoplantar
vesiculation, and  Remove etiologic/pathogenic agent
psoriasis
necrosis; Chronic ICD  Potent topical glucocorticoids (betamethasone
 Photoallergic contact
 acanthosis, dipropionate or clobetasol propionate) and
dermatitis.
hyperkeratosis, and adequate lubrication.
lymphocytic infiltrate.  In chronic ICD of hands, a “hardening effect” can be
 Patch Tests achieved in most cases with topical (soak or bath)
PUVA therapy
 Systemic Treatment. Alitretinoin 0.5 mg/kg body
weight for up to 6 months.
 Psoariasis  hx and clinical findings  Termination of Exposure. Identify and remove the
 ICD  Histopathology etiologic agent
 atopic dermatitis  Patch Test:  Topical Therapy: glucocorticoid ointments/gels
(AD) verification of (classes I–III)

DISEASE DESCRIPTION
 special localized form of
lichenification, occurring in
circumscribed plaques
 Results from repetitive rubbing and
scratching.
 Lichenification is a characteristic
LICHEN
feature of AD, whether generalized or
SIMPLEX
localized.
CHRONICUS
 LSC can last for decades unless the
rubbing and scratching are stopped by
treatment
 Occurs in individuals older than 20
years, is more frequent in women, and
possibly more frequent in Asians
 chronic, pruritic, inflammatory
dermatitis
 common on the extremities during
winter months when xerosis is
maximal; often seen in atopic
NUMMULAR
individuals.
ECZEMA
 S. aureus is often present but
pathogenic significance not proven.
 Course is chronic
 Synonyms: Discoid eczema, microbial
eczema.
 Etiology: S. Aureus, GAS
IMPETIGO  Point of Entry: Minor breaks in the
skin
 highly contagious primary infection
VARICELLA caused by VZV
 Synonym: Chicken pox.
CLINICAL S/SX DIFFERENTIAL
DIAGNOSIS MANAGEMENT/TREATMENT
SKIN LESION DIAGNOSIS
nonumbilicated vesicles  seborrheic dermatitis offending agent  Systemic Therapy (indicated if severe and in airborne
 Severe reactions, bullae, (SD) (allergen) ACD. Prednisone beginning at 70 mg (adults), tapering
confluent erosions exuding by 5–10 mg/d over a 1- to 2-week period.
serum, and crusts.
 Subacute.
 Plaques of mild erythema
showing small, dry scales,
 Chronic
 Plaques of lichenification
(thickening of the epidermis
with deepening of the skin
lines in parallel or rhomboidal
pattern), scaling with satellite,
small, firm, rounded or flat-
topped papules, excoriations,
and pigmentation.
 solid plaque of lichenification,
arising from the confluence of
small papules  Explain to the patient that rubbing and scratching must
 Skin is palpably thickened; skin be stopped.
markings (barely visible in normal  Occlusive bandages can be used at night.
skin) are accentuated and can be  Dermatopathology:
 Topical glucocorticoid preparations or tar
seen readily Hyperplasia of all preparations covered by occlusive dressings are
 Psoriasis components of
 Excoriations: Usually dull red, effective for legs and arms.
 early stages of epidermis:
later brown or black  Glucocorticoids incorporated in adhesive plastic tape
mycosis fungoides hyperkeratosis,
hyperpigmentation, especially in are also effective, if left for 24 h.
 ICD acanthosis, and
skin of color  Unna boot: A gauze roll dressing impregnated with
 ACD elongated and broad
 Round, oval, linear (following path zinc oxide paste is wrapped around a large lichenified
 epidermal rete ridges. In the
of scratching) area such as the calf. It can be left on for up to 1 week.
dermatophytosis. dermis, there is a
 Usually sharply defined.  Intralesional triamcinolone is often highly effective in
chronic inflammatory
 Isolated single lesion or several infiltrate. smaller lesions (3 mg/mL; higher concentrations may
plaques. cause atrophy).
 Nuchal area (female), scalp, ankles,  Oral hydroxyzine, 25–50 g at night, may be helpful.
lower legs, upper thighs, exterior
forearms, vulva, pubis, anal area,
scrotum, and groin.
 coin-shaped plaques composed of  Hydrate skin with hydrated moisturizer or
grouped small papules and moisturizing cream
vesicles on an erythematous base    Topical glucocorticosteroids or 2–5% crude coal tar
 Very pruritic Ointment
 lesions last from weeks to months  PUVA or UVB-311 therapy
 Prevention. Benzoyl peroxide wash. Check family
 Excoriation
 Clinical findings members for signs of impetigo. Ethanol or isopropyl
 allergic contact
confirmed by culture: gel for hands and/or involved sites
dermatitis
S. aureus, commonly;  Topical Treatment. Mupirocin and retapamulin
 Erosions with crusts  herpes simplex
failure of oral ointment is highly effective in eliminating S. aureus
 epidermal antibiotic suggests from the nares and cutaneous lesions
dermatophytosis
MRSA. GAS  Systemic Antimicrobial Treatment. According to
 scabies sensitivity of isolated organism.
 Initial lesions are papules (often  Disseminated HSV  Usually made on  Symptomatic Therapy. Antihistamines lotions; avoid
not observed) that may appear as infection clinical findings alone antipyretics due to risk of Reye syndrome
wheals and quickly evolve to  cutaneous  Seroconversion, i.e.,  Antiviral Agents. Decrease severity of course if given

DISEASE DESCRIPTION
 Characterized by successive crops of
pruritic vesicles that evolve to
pustules, crusts, and, at times, scars.
 acute dermatomal infection associated
with reactivation of VZV
 Synonym: Shingles
 Characterized by unilateral
dysesthesia. A vesicular or bullous
HERPES
eruption limited to a dermatome(s)
ZOSTER
innervated by a corresponding
sensory ganglion
 Postherpetic neuralgia is a major
morbidity
 Distribution: Unilateral, dermatomal
MOLLUSCUM  Etiology. MCV with four discrete viral
CONTAGIOSUM subtypes, I, II, III, IV
VERRUCA  Papillomaviruses - double-stranded DNA
VULGARIS viruses of the papovavirus class
 Infections are restricted squamous
epithelia of skin and mucous membranes.
 Transmission. Skin-to-skin contact.
CLINICAL S/SX DIFFERENTIAL
DIAGNOSIS MANAGEMENT/TREATMENT
SKIN LESION DIAGNOSIS
vesicles, superficial and thin- dissemination of fourfold or greater rise within 24 hours of onset
walled with surrounding zoster in VZV titers.  Neonates: Acyclovir 10 mg/kg every 8h for 10
erythema.  eczema herpeticum days
 Vesicles rapidly evolve to pustules  rickettsialpox  Children: (2 to 18 yrs) Valaciclovir 20 mg/kg every
and crusted erosions over an 8- to  enterovirus 8 h for 5 days or acyclovir 20 mg/kg every 6 h for
12-hour period infections. 5 days
 Characteristic punched-out  Adolescents: Valaciclovir 1 g PO every 8 h for 7
permanent scars may persist days
 First lesions begin on face and  Immunocompromised: Valaciclovir 1 g PO for 7 to
scalp, spreading inferiorly to trunk 10 days; or acyclovir 800 mg by mouth 5 times a
and extremities day or famciclovir 500 mg by mouth every 8 h for
7 to 10 days.
 Severely immunocompromised: acyclovir 10 mg/
kg IV every 8 h for 7 to 10 days
 Acyclovir resistant: Foscarnet 40 mg/kg IV every 8
h until resolution.
 Herpes zoster manifests in three
distinct clinical stages: (1)
prodrome, (2) active infection, and
(3) PHN  Prodromal  Antiviral Therapy. Oral famciclovir 500 mg every 8 h
 Prodrome: Pain, tenderness, Stage/Localized Pain. for 7 days or valaciclovir 1 g every 8 h for 7 days or
paresthesia in the involved Can mimic migraine,
acyclovir 800 mg 5 times a day for 7 days
dermatome precedes the eruption cardiac or pleural
 Mildly immunocompromised: As above but for up to
 Dermatomal Lesions: Papules(24 disease, an acute
10 days
hours) → vesicles-bullae (48 abdomen, or  Clinical
vertebral disease  Severely immunocompromised: acyclovir 10 mg/kg IV
hours) → pustules (96 hours) →  Tzanck test
every 8 h for 7–10 days
crusts (7–10 days). New lesions  Dermatomal  DFA, or viral culture to
 Acyclovir resistant: IV foscarnet 40 mg/kg IV every 8h
continue to appear for up to 1 Eruption. HSV rule out HSV infection.
until resolution
week. Erythematous, edematous infection,
base with superimposed clear photoallergic (poison  Supportive Therapy. Bed rest, sedation, pain
management with narcotic analgesics; moist dressings
vesicles, sometimes hemorrhagic. ivy, poison oak)
Vesicles erode forming crusted contact dermatitis,  Postherpetic Neuralgia. Gabapentin, pregabalin,
erosions. Dermatomal crusting erysipelas, and tricyclic antidepressants, i.e. doxepin, capaicin cream
usually resolves in 2–4 weeks. necrotizing fasciitis. topically. Nerve block
 Condylomata
acuminate
 Syringoma
 Papules, nodules, tumors with
 sebaceous
central umbilication or depression
hyperplasia
 Skin-colored. Round, oval,  Keratoacanthoma
hemispherical.  Clinical
 Multiple Facial  Curettage
 Isolated single lesion; multiple,  Biopsy lesion in HIV
Mollusca in HIV  Cryosurgery
scattered discrete lesions; or disease if
Disease  Electrodessication
confluent mosaic plaques. disseminated invasive
 Disseminated fungal infection  Imiquimod 5% cream may be effective.
 Larger mollusca may have a
invasive fungal
central keratotic plug, which gives
infection
the lesion a central dimple or
 Cryptococcosis
umbilication.
 Histoplasmosis
 Coccidioidomycosis
 penicilliosis
 Common Wart or Verruca  molluscum  Dermatopathology:  the natural history of cutaneous HPV infections is for
Vulgaris: Firm papules, 1–10 mm contagiosum Acanthosis, spontaneous resolution in months or a few years.
or larger hyperkeratotic, clefted  seborrheic keratosis papillomatosis,  Plantar warts that are painful because of their location
surface, with vegetations. Isolated  actinic keratosis hyperkeratosis. warrant more aggressive therapies.
lesion, scattered discrete lesions.  keratoacanthoma,  Characteristic feature  For Small Lesions. 10–20% salicylic acid and lactic acid

DISEASE DESCRIPTION
Minor trauma with breaks in stratum
corneum facilitates epidermal
infection.
 Demography. Host defense defects
are associated with an increased
incidence of and more widespread
cutaneous warts: HIV disease,
iatrogenic immunosuppression with
solid organ transplantation.
 HPV 6 and 11- acquired
during vaginal delivery and
cause warts of the oropharynx
and upper airways.
VERRUCA
VULGARIS
 Epidermodysplasia Verruciformis.
Autosomal recessive hereditary
disorder. Acquired EDV like lesions
seen in HIV disease.
CLINICAL S/SX
SKIN LESION
Occur at sites of trauma: hands,
fingers, and knees. Palmar lesions
disrupt the normal line of
fingerprints. Return of fingerprints
is a sign of resolution of the wart.
CHARACTERISTIC: “red or brown
dots,” best visualized with
dermatoscope, are pathognomonic,
representing thrombosed dermal
papilla capillary loops.
 Linear arrangement:
inoculation by scratching.
 Annular warts: at sites of
prior therapy
 Butcher’s warts: large
cauliflower-like lesions on
hands of meat handlers
 Filiform warts have
relatively small bases,
extending out with
elongated cap
 Plantar Warts (Verruca
Plantaris): Early small, shiny,
sharply marginated papule →
plaque with rough hyperkeratotic
surface
 Mosaic warts: Confluence
of many small warts.
“Kissing” warts
 Flat Warts (Verruca Plana):
Sharply defined, flat papules (1–5
mm); “flat” surface; the thickness
of the lesion is 1–2 mm. Skin-
colored or light brown. Round,
oval, polygonal, linear lesions
(inoculation of virus by
scratching). Occur on face, beard
area, dorsa of hands, and shins.
 Epidermodysplasia
Verruciformis: Autosomal-
recessive condition. Flat-topped
papules. Tinea versicolor-like
lesions, particularly on the trunk.
Color: skin-colored, light brown,
pink, hypopigmented. Lesions may
be numerous, large, and confluent.
Seborrheic keratosis-like and
actinic keratosis-like lesions.
Linear arrangement after
traumatic inoculation.
Distribution: face, dorsa of hands,
arms, legs, anterior trunk.
Premalignant and malignant
lesions arise most commonly on
face. SCC: in situ and invasive.
DIFFERENTIAL
DIAGNOSIS MANAGEMENT/TREATMENT
DIAGNOSIS
 SCCIS is foci of vacuolated in collodion.
 invasive SCC. cells (koilocytosis),  For Large Lesions. 40% salicylic acid plaster for 1 week,
vertical tiers of then application of salicylic acid–lactic acid in
parakeratotic cells, collodion.
and foci of clumped  Imiquimod Cream. At sites that are not thickly
keratohyaline keratinized, apply half-strength three times per week.
granules. Persistent warts may require occlusion.
 Diagnosis. Usually Hyperkeratotic lesions on palms/soles should be
made on clinical debrided frequently; Imiquimod used alter alternately
findings. with a topical retinoid such as tazarotene topical gel
 With host defense may be effective.
defects, HPV-induced  Hyperthermia for Verruca Plantaris. Hyperthermia with
SCC at periungual sites hot water [45°C (113°F)] immersion for 20 minutes or
or anogenital region three times weekly for up to 16 treatments is effective
should be ruled out by in some patients.
lesional biopsy.  Cryosurgery - light cryosurgery using a cotton-tipped
applicator or cryospray, freezing the wart and 1–2 mm
of surrounding normal tissue for approximately 30
seconds, is quite effective. Freezing kills the infected
tissue but not HPV. Cryosurgery is usually repeated
about every 4 weeks until the warts have disappeared.
 callus Painful.
 corn  Electrosurgery. More effective than cryosurgery, but
 keratosis also associated with a greater chance of scarring.
 exostosis EMLA cream can be used for anesthesia for flat warts.
Lidocaine injection is usually required for thicker
warts, especially palmar/plantar lesions.
 CO2 Laser Surgery. May be effective for recalcitrant
warts, but no better than cryosurgery or
 syringoma (facial) electrosurgery in the hands of an experienced clinician.
 molluscum  Surgery. Single, nonplantar verruca vulgaris: curettage
contagiosum after freon freezing; surgical excision of cutaneous HPV
infections is not indicated in that these lesions are
epidermal infections.
 pityriasis versicolor
 actinic keratosis
 seborrheic keratosis
 SCCIS
 basal cell carcinoma.
 CLINICAL S/SX DIFFERENTIAL
DISEASE DESCRIPTION DIAGNOSIS MANAGEMENT/TREATMENT
SKIN LESION DIAGNOSIS
 Direct Microscopic
Examination of
Scales Prepared with
KOH. Filamentous
 Etiology. Associated with the hyphae and globose
 Chronic
superficial overgrowth of the mycelial yeast forms, termed
 Well-demarcated scaling patches.
form of Malassezia furfur. Lipophilic spaghetti and
 Variable pigmentation: hypo and
yeast that normally resides in the meatballs are seen.
hyperpigmented; pink. Most
keratin of skin and hair follicles of  Wood’s Lamp. Blue-
commonly on the trunk.
individuals at puberty and beyond. An green fluorescence of
 Macules, sharply marginated
opportunistic organism, causing tinea scales; may be
or pityriasis versicolor (TV) round or oval in shape, varying negative in individuals
 Hypopigmented
insize. Fine scaling is best
and Malassezia folliculitis; it is Macules. Vitiligo, who have showered
TINEA implicated in the pathogenesis of appreciated by gently abrading pityriasis alba, recently because the  Topitcal agents. Selenium sulfide (2.5%) lotion or
lesions. shampoo. Ketoconazole shampoo. Azole creams
VERSICOLOR seborrheic dermatitis. postinflammatory fluorescent chemical is
(Tinea that is not Malassezia infections are not  Demography. Young adults. Less hypopigmentation. water soluble. Vitiligo (ketoconazole, econazole, micronazole, clotrimazole).
a contagious; overgrowth of resident common when sebum production appears as  Terbinafine 1% solution.
dermatophytosis cutaneous flora (cutaneous is reduced or absent; tapers off
 Scaling Lesions. depigmented, white,  Systemic therapy: Ketoconazole 400 mg stat, 1 hour
but a yeast microbiome) occurs under certain during fifth and sixth decades. Tinea corporis, and has no scale. before exercise. Fluconazole 400 mg stat. Itraconazole
infection) favorable conditions.  Predisposing Factors. Sweating. seborrheic 400 mg stat
 Dermatopathology.
Warm season or climates; tropical dermatitis, cutaneous
 Pathogenesis. Malassezia changes Budding yeast and
from blastospore form to mycelial climate. Hyperhidrosis; aerobic T cell lymphoma. hyphal forms in the
form under the influence of exercise. Oily skin. Temperate
most superficial layers
predisposing factors. Dicarboxylic acid zones: more common in of the stratum
formed by enzymatic oxidation of fatty summertime; 2% prevalence in
corneum, seen best
acids in skin surface lipids inhibits temperate climates; 20% in with periodic acid–
tyrosinase in epidermal melanocytes tropics. Application of lipids such
Schiff (PAS) stain.
and lead to hypomelanosis; the as cocoa butter predisposes youn Variable
enzyme is present in M. furfur. children.
hyperkeratosis,
psoriasiform
hyperplasia, chronic
inflammation with
blood vessel dilatation.
ERYSIPELLAS  READ    
CELLULITIS  READ    
DERMATOPHYSOSIS
 unique group of fungi capable of infecting nonviable keratinized cutaneous structures
including stratum corneum, nails, and hair
 Arthrospores can survive in human scales for 12 months
 infection caused by dermatophytes.
Etiology
Three genera of dermatophytes (“skin
plants”):
1) Trichophyton
 Trichophyton rubrum- most common cause of epidermal dermatophytosis and
onychomycosis in industrialized nations. Currently, 70% of the U.S. population
experience at least one episode of T. rubrum infection (usually tinea pedis).
Soldiers wearing occlusive boots in tropical climates developed “jungle rot”—
extensive tinea pedis with secondary bacterial infection. In U.S. adults, T. rubrum is
the most common cause of dermatophytic folliculitis.
 Tinea capitis. Etiology in children varies geographically. Trichophyton tonsurans:
Most common cause in North America and Europe. Previously, M. audouinii, T.
violaceum: Europe, Asia, and Africa
2) Microsporum
3) Epidermophyton.
. able to establish chronic infection. Organisms such as Microsporum canis cause an acute infection associated with a
Age of Onset. Children have scalp infections (Trichophyton, Microsporum). Young and older adults have
intertriginous infections. The incidence of onychomycosis is correlated directly with age; in the United
States, up to 50% of individuals aged 75 years have onychomycosis.
Demography. Adult blacks may have a lower incidence of dermatophytosis. Tinea capitis is more
common in black children.
Geography. Some species have a worldwide distribution; others are restricted to particular continents
or regions. However, T. concentricum, the cause of tinea imbricata, is endemic to the South Pacific and
parts of South America. T. rubrum was endemic to Southeast Asia, Western Africa, and Australia but
now occurs commonly in North America and Europe. Transmission. Dermatophyte infections can be
acquired from three sources:
• Most commonly from another person [usually by fomites, less so by direct skin-to-skin contact (tinea
gladiatorum)]
• From animals such as puppies or kittens.
• Least commonly from soil.
Classification of Dermatophytes. Based on their ecology, dermatophytes classified:
• Anthropophilic: Person-to-person transmission by fomites and by direct contact.
• Zoophilic: Animal-to-human by direct contact or by fomites.
• Geophilic: Environmental.
Predisposing Factors.
Atopic diathesis: Cell-mediated immune deficiency for T. rubrum.
Topical immunosuppression by application of glucocorticoids: tinea incognito.
Systemic immunocompromised: Patients have a higher incidence and more intractable
dermatophytoses; follicular abscesses and granulomas may occur (Majocchi granuloma).
Classification
In vivo, dermatophytes grow only on or within keratinized structures and, as such, involve the
following:
• Epidermal dermatophytosis. Tinea facialis, tinea corporis, tinea cruris, tinea manus,
tinea pedis.
• Dermatophytoses of nail apparatus. Tinea unguium (toenails, fingernails). Onychomycosis (more inclusive term,
including nail infections caused by dermatophytes, yeasts, and molds).
• Dermatophytoses of hair and hair follicle. Dermatophytic folliculitis, Majocchi granuloma,
tinea capitis, tinea barbae.
Pathogenesis
Dermatophytes synthesize keratinases that digest keratin and sustain existence of fungi in keratinized structures.
Cell-mediated immunity and antimicrobial activity of polymorphonuclear leukocytes restrict dermatophyte
pathogenicity.
Host factors that facilitate dermatophyte infections: atopy, topical and systemic glucocorticoids, ichthyosis, collagen
vascular disease.
Local factors favoring dermatophyte infection: sweating, occlusion, occupational exposure, geographic location, high
humidity (tropical or semitropical climates)
The clinical presentation of dermatophytoses depends on several factors: site of infection, immunologic response of
the host, and species of fungus. Dermatophytes (e.g., T. rubrum) that initiate little inflammatory response are better
brisk inflammatory response and spontaneous resolution. In some individuals, infection can involve the dermis, as
in kerion and Majocchi granuloma.
Diagnosis.
Direct Microscopy
Dermatophytes are recognized as septated, tubelike structures (hyphae or
mycelia;
Wood’s lamp examination: Hairs infected with Microsporum spp. fluoresce greenish. Coral red fluorescence of
intertriginous site confirms diagnosis of erythrasma.
Fungal Culture - Sabouraud’s glucose medium.
Treatment
Topical agents for epidermal dermatophytoses: Imidazoles (clotrimazole, miconazole, ketoconazole, econazole,
oxiconazole, sulconazole, sertaconazole); allylamines (naftifine, terbinafine); naphthionates (tolnaftate); substituted
pyridine (ciclopirox olamine).
Systemic Antifungal Agents
• Terbinafine 250-mg tablet. Allylamine. Most effective oral antidermatophyte antifungal; low efficacy against other
fungi. Approved for onychomycosis in the United States.
• Itraconazole 100-mg capsules; oral solution (10 mg/mL): Intravenous. Triazole. Needs acid gastric pH for
dissolution of capsule. Raises levels of digoxin and cyclosporine. Approved for onychomycosis in the United
States.
• Fluconazole 100-, 150-, 200-mg tablets; oral suspension (10 or 40 mg/mL); 400 mg IV.
• Ketoconazole 200-mg tablets. Needs acid gastric pH for dissolution of tablet. Take with food or cola beverage;
antacids and H2 blockers reduce absorption. The most hepatotoxic of azole drugs; hepatotoxicity occurs in an
estimated one of every 10,000–15,000 exposed persons. Not approved for treatment of dermatophyte infections in
the United States.

DISEASE DESCRIPTION
 Dermatophytic infection of the feet.
 Interdigital Type. Two patterns: dry
scaling; maceration, scaling, fissuring
of toe webs + Hyperhidrosis common.
Most common site: between fourth
and fifth toes. Infection may spread to
adjacent areas of feet.
 Moccasin Type. Well-demarcated
scaling with erythema with minute
papules on margin, fine white scaling,
and hyperkeratosis (confined to heels,
soles, lateral borders of feet).
Distribution: Sole, involving area
covered by a ballet slipper. One or
both feet may be involved with any
Tinea Pedis
pattern; bilateral involvement more
common.
 Inflammatory/Bullous Type.
Vesicles or bullae filled with clear
fluid Pus usually indicates secondary
infection with S. aureus infection or
GAS. After rupturing, erosions with
ragged ringlike border. May be
associated with “id” reaction
(autosensitization or dermatophytid).
Distribution: Sole, instep, webspaces.
 Ulcerative Type. Extension of
interdigital tinea pedis onto plantar
and lateral foot. May be secondarily
by S. aureus.
 Chronic dermatophytosis of the
hand(s).
Tinea Mannum
CLINICAL S/SX
SKIN LESION
 Erythema, scaling, maceration,
and/or bulla formation.
 Usually asymptomatic. Pruritus.
 Pain with sec bacterial infection
due to breaks in the integrity of
the epidermis
 Frequently symptomatic.
Pruritus.
 Dyshidrotic type: Episodic
symptoms of pruritus. Well-
demarcated scaling patches,
hyperkeratosis, fissures on
palmar hand Borders well
demarcated; central clearing.
 May extend onto dorsum of hand
with follicular papules, nodules,
and pustules with dermatophytic
folliculitis
 Dyshidrotic type: Papules, vesicles,
bullae (uncommon on the margin
of lesion) on palms and lateral
fingers, similar to lesions of
bullous tinea pedis.
 Secondary changes: Lichen
simplex chronicus, prurigo
nodules, secondary S. aureus
infection.
 Distribution: Diffuse
hyperkeratosis of the palms with
pronounced involvement of
palmar creases or patchy scaling
on the dorsa and sides of fingers;
50% of patients have unilateral
involvement. Usually associated
DIFFERENTIAL
DIAGNOSIS MANAGEMENT/TREATMENT
DIAGNOSIS
Direct Microscopy (+)
hyphae
Wood’s Lamp. Negative
fluorescence usually
rules out erythrasma in
interdigital infection.
Erythrasma and
 Interdigital Type.
interdigital tinea pedis
Erythrasma, pitted
may coexist.
keratolysis
Culture. Dermatophytes
 Moccasin Type. can be isolated in
Psoriasis, eczematous
11% of normal-
dermatitis (dyshidrotic,
appearing interspaces
atopic, allergic contact),  See above management
and 31%
pitted keratolysis.
of macerated toe webs.
 Inflammatory/bullous Candida spp. may be
type. Bullous impetigo, copathogens in
allergic contact
webspaces. In
dermatitis, dyshidrotic individuals with
eczema, bullous disease.
macerated interdigital
space, S. aureus, P.
aeruginosa,
and diphtheroids are
commonly isolated.
S. aureus causes
secondary infection.
 Atopic dermatitis
 Must eradicate tinea unguium of fingernails as well as
 lichen simplex toenails; also tinea pedis and tinea cruris, otherwise,
chronicus tinea manuum will recur.
 allergic contact  Oral agents eradicate dermatophytoses of hands, feet,
 See above diagnosis
dermatitis and nails: Terbinafine: 250 mg daily for 14 days.
 irritant contact Itraconazole: 200 mg daily for 7 days. Fluconazole:
dermatitis 150–200 mg daily for 2–4 weeks. Note: Eradication of
fingernail onychomycosis requires longer use.
 psoriasis vulgaris.

DISEASE DESCRIPTION
 Subacute or chronic dermatophytosis
of the upper thigh and adjacent
inguinal and pubic regions. A better
Tinea Cruris name is tinea inguinalis (groin); cruris
refers to the lower leg. “Always”
associated with tinea pedis, the
source of the infection.
 infections of the trunk, legs, arms,
and/or neck, excluding the feet, hands,
and groin.
 Etiology. Most commonly caused by
Tinea Corporis T. rubrum. M. canis lesions are often
inflammatory or bullous.
 T. tonsurans caused tinea corporis in
parents of black children with tinea
capitis.
 Dermatophytosis of the glabrous
facial skin. Well circumscribed
erythematous patch. More commonly
misdiagnosed than any other
dermatophytosis.
Tinea Facialis  Synonym: Tinea faciei
 Etiology. T. tonsurans associated with
tinea capitis in black children and
their parents. T. mentagrophytes, T.
rubrum most commonly; also M.
audouinii, M. canis.
 Epidermal dermatophytosis, often
associated with dermatophytic
folliculitis.
Tinea Incognito  Occurs after the topical application of
a glucocorticoid preparation to a site
colonized or infected by
dermatophyte.
CLINICAL S/SX DIFFERENTIAL
DIAGNOSIS MANAGEMENT/TREATMENT
SKIN LESION DIAGNOSIS
with tinea pedis and cruris
 Large, scaling, well-demarcated
dull red/tan/ brown plaques.
 Central clearing.
 Papules, pustules may be present
at margins: dermatophytic
folliculitis. Treated lesions: lack
 Erythrasma, Candida  Prevention. After eradication minimize reinfection
scale; postinflammatory
intertrigo, intertriginous
hyperpigmentation in darker-  same with shower shoes and antifungal powders;
psoriasis, tinea, or
skinned persons. In atopics,  Antifungal Agents
pityriasis versicolor.
chronic scratching may produce
secondary changes of lichen
simplex chronicus.
 Distribution. Groins and thighs;
may extend to buttocks. Scrotum
and penis are rarely involved.
 Scaling, sharply marginated
plaques.  Allergic contact
 Peripheral enlargement and dermatitis,
central clearing produce annular  atopic dermatitis,
configuration with concentric  annular erythemas
rings or arcuate lesions; fusion of
 psoriasis
lesions produces gyrate patterns.
 seborrheic dermatitis,
 Single and occasionally scattered
 pityriasis rosea  Direct Microscopy and
multiple lesions.  Same as above mgt
 pityriasis alba culture
 Psoriasiform plaques. Lesions of
 tinea versicolor,
zoophilic infection (contracted
from animals) are more  erythema migrans,
inflammatory, with marked  subacute lupus
vesicles, pustules, crusting at  erythematosus,
margins.  cutaneous T cell
 Papules, nodules, pustules: lymphoma.
dermatophytic folliculitis
 Seborrheic dermatitis,
 Well-circumscribed macule to
 contact dermatitis,
plaque of variable size; elevated
 erythema migrans
border and central regression
 lupus erythematosus
 Scaling is often minimal.  Direct Microscopy and
 polymorphous light  Same as above mgt
 Pink to red; in black patients, culture
hyperpigmentation. eruption
 phototoxic drug
 Any area of face but usually not
eruption
symmetric.
 lymphocytic infiltrate.
 Variably inflamed patches. Occurs
when an inflammatory
dermatophytosis is mistaken for
psoriasis or an eczematous
dermatitis
 Involved sites often have
exaggerated features of epidermal  Systemic antifungal therapy may be indicated due to
 
dermatophytoses, being a deep deep involvement of the hair apparatus.
red or violaceous. Scaling often
not apparent. Papules or pustule
within involved sites is
dermatophytic folliculitis.
 Epidermal atrophy caused by
chronic glucocorticoid application

DISEASE DESCRIPTION
 Dermatophytic trichomycosis of the
scalp, predominantly in preadolescent
children.
Clinical presentations vary widely:
 Noninflammatory scaling
 Scaling and broken-off hairs
Toddlers and school-age children (6–10
year of age) most commonly affected
Transmission. Person-to-person,
Tinea Capitis animal-to-person, via fomites. Spores
are present on asymptomatic carriers,
animals, or inanimate objects.
Pathogenesis. Scalp hair traps fungi
from the environment or fomites.
Asymptomatic colonization is common.
Trauma assists inoculation.
Dermatophytes initially invade stratum
corneum of scalp, which may be
followed by hair shaft infection. Spread
to other hair follicles then occurs.
 Dermatophytic folliculitis involving
the androgen-sensitive beard and
moustache areas.
 Etiology: T. verrucosum, T.
Tinea Barbae
mentagrophytes var. mentagrophytes,
most commonly. May be acquired
through animal exposure. T. rubrum
an uncommon cause.
CLINICAL S/SX DIFFERENTIAL
DIAGNOSIS MANAGEMENT/TREATMENT
SKIN LESION DIAGNOSIS
may be present.
 Severe, painful inflammation with  Wood’s Lamp. T.
painful, boggy nodules that drain tonsurans does not
pus (kerion) and result in fluoresce.
scarring alopecia  Direct Microscopy.
 Synonyms: Ringworm of the scalp, Skin scales contain
tinea tonsurans hyphae and
arthrospores.
Classification Ectothrix:
• Ectothrix infection. Occurs outside arthrospores can
hair shaft. Hyphae fragment into be seen surrounding
arthroconidia, leading to cuticle the hair shaft in
 Chronic untreated kerion and favus, especially if
destruction. Caused by Microsporum cuticle.
secondarily infected with S. aureus, result in scarring
spp. (M. audouinii and M. canis) Endothrix: spores
alopecia. Regrowth of hair is the rule if treated with
Scaling. Diffuse or circumscribed within hair shaft.
systemic antifungal agents
alopecia. Occipital or posterior Favus: loose
 Seborrheic dermatitis,  Children are treated with systemic antifungal
auricular adenopathy. chains of arthrospores
psoriasis, atopic specifically terbinafine
• Endothrix infection. Occurs within and airspaces in hair
dermatitis, lichen
hair shaft without cuticle shaft
simplex chronicus, and
destruction Arthroconidia found alopecia areata.  Fungal Culture.
within hair shaft. Caused by Growth of

Trichophyton spp. (T. tonsurans in dermatophytes
North America; T. violaceum in usually seen in 10–14
Europe, Asia, parts of Africa). days.
• “Black dot” tinea capitis. Variant of  Bacterial Culture.
endothrix resembling seborrheic Rule out bacterial
dermatitis. Broken-off hairs near infection, usually S.
the scalp give appearance of “dots” aureus or GAS.
 Pustular folliculitis: hair follicles
surrounded by red inflammatory
papules, pustules, nodules, or
plaques. Involved hairs are loose
and easily removed.
 With less follicular involvement,
there are scaling, circular, reddish
patches (tinea facialis) in which
 S. aureus folliculitis,
hair is broken off at the surface.
furuncle, carbuncle, acne  see general  Topical agents ineffective. Systemic antifungal
Papules may coalesce to
 vulgaris, rosacea, diagnostics therapy required
inflammatory plaques topped by
pustules. pseudofolliculitis
 Kerion: boggy purulent nodules
and plaques as with tinea capitis
 Beard and moustache areas,
rarely, eyelashes, eyebrows.
 Regional lymphadenopathy,
especially if of long duration and
if superinfected.