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CLINICAL S/SX DIFFERENTIAL

DISEASE DESCRIPTION DIAGNOSIS MANAGEMENT/TREATMENT


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

Trauma assists inoculation. Trichophyton spp. (T. tonsurans in dermatophytes
Dermatophytes initially invade stratum North America; T. violaceum in usually seen in 10–14
corneum of scalp, which may be Europe, Asia, parts of Africa). days.
followed by hair shaft infection. Spread • “Black dot” tinea capitis. Variant of  Bacterial Culture.
to other hair follicles then occurs. 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,
 Dermatophytic folliculitis involving
there are scaling, circular, reddish
the androgen-sensitive beard and
patches (tinea facialis) in which
moustache areas.  S. aureus folliculitis,
hair is broken off at the surface.
 Etiology: T. verrucosum, T. furuncle, carbuncle, acne  see general  Topical agents ineffective. Systemic antifungal
Tinea Barbae Papules may coalesce to
mentagrophytes var. mentagrophytes,  vulgaris, rosacea, diagnostics therapy required
inflammatory plaques topped by
most commonly. May be acquired pustules. pseudofolliculitis
through animal exposure. T. rubrum
 Kerion: boggy purulent nodules
an uncommon cause.
and plaques as with tinea capitis
 Beard and moustache areas,
rarely, eyelashes, eyebrows.
 Regional lymphadenopathy,
especially if of long duration and
if superinfected.