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FIG. 6-21Contact Dermatitis. This lesion on the side of the thumb resulted from latex allergy in a nurse. The skin is
erythematous, itchy, thickened and fissured (lichenoid) due to scratching.
Autosensitization dermatitis. Sensitization to antigens from a primary, often
infectious or infected, dermatitis leads to distant lesions. The classic example
is the id reaction, a vesicular eruption on the hands or distant areas in patients
with chronic tinea pedis infection. Secondary lesions heal only after treatment
of the primary infection or inammation.
Seborrheic dermatitis. This very common disorder that produces erythema and scaling in the distribution of sebaceous glands: scalp (dandruff,
cradle cap), eyebrows, nasolabial folds, external acoustic meatus, and chest
(Fig. 6-22). The skin may be mildly pruritic. It occurs frequently with
Parkinson disease; sudden severe disease may be a sign of HIV infection.
Photodermatitis.
dermatitis triggered by sunlight.
after exposure and only on sun-exposed skin. It has a burning quality and
can blister. Polymorphic light eruption refers to a delayed sensitivity reaction
to sunlight exposure. Examples are antibiotics (tetracyclines, sulfonamides),
antidepressants, antihypertensives, diuretics (thiazides especially), NSAIDs,
sunscreens.
FIG. 6-22Seborrheic Dermatitis. Erythema and scaling in the nasolabial fold, eyebrows and glabella.
Skin sensitization to topical or systemic chemicals leads to
Erythema appears hours to a couple days
DDX: Consider polymorphic light eruption and porphyria.
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Intertrigo. Skin folds between the buttocks, under the breasts, and in skin
creases become inamed from persistent warmth, moisture, and occlusion.
Secondary infection with streptococci, Pseudomonas aeruginosa, Candida albi-
cans, and other fungi is common.
inverse psoriasis, are confused with intertrigo.
DDX: Cellulitis and psoriasis, especially
Psoriasis.
and reduced surface desquamation produce thickened skin.
in 1% to 3% of the population varying from mild to severe. Individual lesions
vary from papules to huge plaques with a characteristically adherent scale;
the surface bleeds on removing the scales. The nails are frequently pitted
and dystrophic. Lesions are bilateral, symmetrical, involve the extensor (e.g.,
elbows, knees) more than exor surfaces, and frequently the scalp and gluteal crease. Trunk and extremities are involved in any combination. Inverse
psoriasis is a pattern opposite to that expected. Skin trauma can precipitate a
new lesion (Koebner phenomena). A severe mutilating arthritis of the axial skeleton (spondyloarthropathy) and distal interphalangeal joints may accompany
or occur independently of skin and nail disease.
Guttate psoriasis.
mm pink papules appear diffusely on the trunk and extremities. The face and
scalp are relatively spared, and palm and sole involvement is rare. The lesions
resolve spontaneously over weeks. Classic plaque psoriasis may occur several
years after remission of guttate psoriasis. The lesions resemble papular eczema.
Pustular psoriasis. Sudden onset of intense painful erythema is followed
within 24 hours by deep pustular dermal lesions which rupture forming erosions. The patient has fever and leukocytosis. Patients may be severely ill.
This frequently follows withdrawal of systemic corticosteroid therapy.
Palmoplantar pustulosis. Pustules appear sporadically on the palms and
soles associated with burning pain and heal with crusting. The cause is
unknown. It may be a localized form of pustular psoriasis. It has been seen
with metal allergies and as a reaction to TNF-inhibitors.
Infectious exanthems.
bacterial or viral illness (see Erythroderma, page 132). Viral exanthems are
often accompanied by mucosal involvement, an enanthem. Individual lesions
take many forms: diffuse erythroderma (scarlatiniform), maculopapules (mor-
billiform, measles-like), or vesicles that may evolve to pustules. The diffuse
erythrodermas often heal with desquamation.
virus B19, adenoviruses, cytomegalovirus, Epstein-Barr virus, herpes simplex viruses 6 and 7 (exanthem subitum and roseola infantum, respectively),
enteroviruses, HIV, Colorado tick fever, and many others; Bacterial: Group A
streptococcus (scarlet fever), staphylococcus (toxic shock syndrome), leptospirosis, meningococcemia; Rickettsial: Rocky Mountain spotted fever, rickettsialpox, typhus.
Increased epithelial cell division with associated inammation,
Psoriasis occurs
Following an infection, often streptococcal pharyngitis, 2-10-
Exanthems are diffuse skin eruptions associated with
CLINICAL OCCURRENCE: Viral: (most common) Rubella, rubeola, parvo-
Scarlet fever. A Group-A streptococcal exotoxin causes generalized cutane-
ous erythema. Streptococcal pharyngitis (Chapter 7, page 250) is accompanied
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by a maculopapular erythematous blanching eruption initially on the neck,
axillae, and groin later becoming generalized. The skin feels slightly rough,
like ne sandpaper. The rash heals with desquamation beginning around the
nails.
Toxic shock syndrome. See Chapter 4, page 68.
Ichthyosis.
and dry, cracking hexagonally when severe. Hair follicle hyperkeratosis produces pointed follicular papules, keratosis pilaris, a common skin condition.
Granuloma annulare. Asymptomatic papules and plaques with sharply
demarcated annular or arcuate borders on the hands, feet, elbows, knees, and
distal extremities, usually bilaterally. The lesions are pink, purple, or skin colored, and typically self-limited.
Lichen planus. Purple, at-topped, sharply demarcated pruritic papules appear on the wrists, ankles, eyelids, and shins. Other forms include
hypertrophic and bullous lichen planus. Mucous membrane involvement is
common, appearing as white linear lesions in the mouth or genital mucosa
(Wickham striae). Erosions, papules, and plaques can occur in the oral mucosa.
Erosive lichen planus is associated with hepatitis C.
Genital white patches—lichen sclerosis. White atrophic lesions with sharp
borders appear most often on the vulva, perianal skin, and penis. The skin is
thin, and erosions may occur. Pruritus and dyspareunia are common.
Verrucous papules—warts.
papilloma virus leads to verrucous hyperplasia; uterine cervix infection with
specic strains causes cervical cancer.
papule with a verrucous surface, commonly on the ngers. Genital involvement is particularly troublesome. Flat conuent lesions without the verrucous
surface are at warts. Problematic areas are the sole of the foot, plantar warts,
and around the nails, periungual warts.
Pityriasis rosea. This common disorder primarily affects adolescents and
young adults in the fall. The eruption is asymptomatic to mildly pruritic
involving the trunk and proximal extremities. An inverse form occurs in the
axillae and groin. The general eruption is often preceded by a larger single
lesion, the herald patch. Lesions are oval, with the long axis in the skin folds,
classically creating a Christmas tree pattern on the back. Lesions are 0.5 to 3
cm in diameter and have a slightly raised border with a collar of ne supercial scales on an erythematous base. Resolution is spontaneous over weeks.
These are hereditary keratinocyte diseases. The skin is thickened
Skin or mucous membrane infection with human
The common wart is a well-demarcated
Actinic keratosis. Mildly erythematous macules with adherent hyperkeratotic scale appear in sun-exposed areas. They are premalignant and squamous
cell carcinoma may arise in chronic lesions.
Seborrheic keratosis.
brown macules gradually enlarging to 1–3 cm plaques with a raised adherent hyperkeratotic surface. They appear stuck-on to the skin (Fig. 6-23).
These are begin lesions that appear in midlife as
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FIG. 6-23Seborrheic Keratoses and Lipoma. Left: Multiple “stuck on” lesions on the upper back with great
variation in color. A subcutaneous lipoma is faintly visible superior and medial to the upper border of the right scapular spine.
Right: Close up of two seborrheic keratoses showing variation in coloration and degree of elevation.
DDX: Pigmented lesions are confused with malignant melanoma and macu-
lar lesions with moles or lentigines.
Dermatobroma.
The lesions are 3- to 8-mm rm, variably colored intrader-
mal papules usually on the arms and legs. When pinched the lesion retracts
rather than elevates, the dimple sign. DDX: May be confused with melanoma
and pilomatricoma.
Skin tags (acrochordons).
These insensate dermal polyps are most prevalent
on the neck, axillary folds, and perineum and are more common with obesity.
They are of no clinical signicance but can be irritated by clothing or jewelry
and are often a cosmetic concern. DDX: Nevi, and large skin tags may be
confused with neurobromas.
Vitiligo.
Autoimmune destruction of melanocytes results in complete loss of
pigmentation in affected areas. The macular lesions are symmetrical with sharp
borders. They cause signicant cosmetic discomfort in dark-skinned individuals. DDX: Vitiligo is confused with hypopigmented lesions (e.g., discoid lupus
erythematosus, leprosy), depigmentation from burns or scars, or ash leaf spots
of tuberous sclerosis. Vitiligo is more common in families with other autoimmune disorders, e.g., diabetes, Addison disease, Hashimoto thyroiditis.
Body piercing. Piercing has a long and rich cultural history. Western societies
saw a dramatic increase in piercing in the late 20th century. Piercing is done
for many reasons. Medical professionals must attend to the risks associated
with piercing, the types of piercing and their signicance, and the personality
issues that may be involved in caring for these individuals.
Skin Infections and Infestations.
Mosquito and other insect bites. Insect bites present as painful or pruritic
papules with erythema and variable cutaneous edema. Closely inspect early
lesions for the central punctum. Most bites are minor and self-limited but
extensive bites can cause systemic toxicity. Hymenoptera stings (bees, hornets, and wasps) cause severe local reactions with expansive erythema and
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edema. Sensitized individuals have systemic allergic reactions, including
anaphylaxis, to hymenoptera and some ant species. Black ies leave a 1- to
2-mm hemorrhagic mark.
Bedbugs. Bedbugs are 3 to 5 mm brown insects living in crevices of bedding
and clothing and feeding on blood, typically at night. The bite is painless
and in a sequence producing linear grouped lesions (“breakfast, lunch, and
dinner”).
Pediculosis—lice. Lice are wingless insects that feed on skin scales. Nits are
egg sacs cemented to hair shafts. Patients complain of itching and close inspection or combing the hair with a ne comb reveals the lice. The two species are Pediculosis humanus inhabiting the head (Pediculosis capitis) or body
(Pediculosis corporis) and Phthirus pubis living in pubic hair (Pediculosis pubis).
Myiasis. When being bitten by insects, eggs may be deposited on skin or
in wounds. The larvae invade and grow in subcutaneous tissue. Since they
breath air, a skin opening is always present. The patient complains of move-
ment under the skin.
Spider bites.
sive house spider attacks while a person is sleeping, so bites are usually on the
exposed face, hands, arms, or feet. Bites cause moderate skin necrosis and
scarring. The brown recluse spider is common but not aggressive. It bites in
defense when disturbed in old buildings, woodpiles, and similar habitats.
The bite is initially painless, but the site becomes intensely painful with
severe necrosis and scarring. The black widow spider bite is a minor lesion with
minimal erythema; the adverse effects are caused by a systemic neurotoxin.
Mites. Mites, arthropods related to ticks, occupy innumerable habitats bring-
ing them in contact with humans. They feed on skin and cutaneous debris.
Exposure history and lesion pattern are the best guides to diagnosis.
Scabies.
depositing feces, which incite inammation. The infestation is contagious
and passes between persons. The intensely pruritic lesions are erythematous
papules; linear burrows may be seen. The mite favors thin skin with few hair
follicles, especially intertriginous areas of hands, wrists, elbows, and genitalia. A KOH preparation reveals mites, eggs, or feces.
Chiggers. Chiggers are the <1 mm larval form of a mite living in warm grassy
or woodland environments. They feed on skin cells by injecting digestive enzymes into the skin. The lesions, commonly around the feet and ankles, are
intensely pruritic red papules, usually multiple depending on the length of
exposure.
Swimmer's eruption. Larvae of many organisms for which humans are not
the primary host (bird schistosome, jellysh or sea urchin larvae, etc.), penetrate the skin inciting a cutaneous reaction. Patients present with an intensely
pruritic rash hours after emerging from the water. Salt water bathers often
shower with freshwater in their bathing suits. Freshwater exposure triggers
Most are benign and no cause for concern. The common aggres-
Sarcoptes scabiei burrows through the epidermis laying eggs and
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stings by some free-swimming larvae. The rash may be diffuse or restricted to
an area where wet clothing held the parasites next to the skin.
Larval migrations—cutaneous larval migrans.
eggs laid in soil hatch into motile larvae that penetrate the skin then
migrate through the skin and subcutaneous tissues to their nal destinations.
time.
migratory ndings with strongyloidiasis (larva currens), fascioliasis, dracunculiasis, and others.
Bacterial infections.
Impetigo. Supercial infection with staphylococcus and streptococcus pro-
duces erythematous erosions with amber crusts. Common on children’s faces
it can occur wherever there is a skin break. Bullae form in severe cases, bullous
impetigo. Localized painful ulcerations, ecthyma, occurs with poor hygiene.
Secondarily infected skin lesions are secondary impetiginization. Impetigo commonly complicates eczema.
Folliculitis.
area, but also occurs on the scalp, trunk, legs, and buttocks. Organisms include Staphylococcus aureus, P. aeruginosa (hot tub folliculitis), herpes simplex,
and several fungi.
curled hair who shave. Papules are caused by retained hairs; pustules indicate secondary infection.
Cellulitis.
within the skin and subcutaneous structures. The lesions are warm, raised,
and tender with indistinct borders. Any break in the skin can be an entry
site.
be present. DDX: Less-common causes of cellulitis are nocardia, mycobacteria, P. aeruginosa, Haemophilus inuenzae, and vibrios (especially in
cirrhotic patients). Pasteurella multocida is common following cat and dog
bites and has a propensity to cause osteomyelitis. Erysipeloid is caused by
Erysipelothrix rhusiopathiae. Erythema chronicum migrans is caused by Lyme
borreliosis (see Chapter 4, page 50). Common causes of noninfectious inammation often confused with cellulitis are stasis dermatitis, supercial
and deep thrombophlebitis, panniculitis, erythema nodosum, and nephrogenic bro sing dermopathy.
The lesions are linear, red, serpiginous, raised and migrate over
Examples: Ancylostoma braziliense, A. caninum. There also can be
Pustular infection of hair follicles is common in men’s beard
DDX: Pseudofolliculitis barbae occurs in men with tightly
Infection with streptococci or staphylococci spreads radially
Cellulitis is most common on legs and arms. Fever may or may not
Dog and cat hookworm
Erysipelas. Streptococcal infection of the dermal lymphatics produces in-
tense dermal and epidermal edema and inammation. The lesion is intensely
erythematous with a sharp, raised border. It is common on the face, often
without an evident break in the skin.
Skin abscess—furuncle, carbuncle. Skin infections with S. aureus produce
collections of pus and necrotic debris in patterns determined by local skin
structure. Furuncles (boils) are relatively supercial single collections. Car-
buncles extend into the subcutaneous tissues involving the deep hair follicles
producing interconnected abscesses. Carbuncles arise in areas of especially
thick brotic skin such as the posterior neck.
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Hidradenitis suppurative. Inammation of areas containing apocrine glands
is associated with chronic, painful draining lesions healing with scarring.
Infection can occur secondarily. Most commonly seen in obese women in-
volving the axilla or perineum, and rarely the scalp. It can coincide in people
with cystic acne.
Erythema migrans—Lyme disease. See Chapter 4, page 50. Asymptomatic
erythema at the inoculation site expands, often with an annular conguration, reaching several centimeters in size. Vesicles are uncommon. More than
one lesion may be present. Bell palsy, heart block, and arthritis of large joints
are late manifestations.
Ulceroglandular syndromes. An often minimally symptomatic ulcer de-
velops at the inoculation site. Lymphatic dissemination produces regional
an inoculation lesion. The nature and location of exposure are key to accurate
diagnosis.
CLINICAL OCCURRENCE: Tularemia, plague, syphilis, rat-bite fever, rick-
ettsial pox, cat-scratch disease, anthrax, Mycobacterium marinum, scrub
typhus, sporotrichiosis, nocardia, lymphogranuloma venereum, herpes simples, cowpox, trypanosomiasis.
Syphilis. The primary lesion (chancre) is a painless shallow ulcer at the inocu-
lation site (penis, glans, vulva, lip, tongue, pharynx, nger, etc.). The discoid
underlying induration feels like a small coin. Painless, nonsuppurating regional lymphadenopathy follows.
On nding regional lymphadenopathy always search for
Tularemia.
tact with an infected rabbit. Following an incubation period of 1–10 days
lassitude, headache, chills, nausea and vomiting, and myalgia accompany a
benign inoculation site ulcer with surrounding erythema and little pain. Regional uctuant painful lymphadenopathy develops which may suppurate.
Splenomegaly may be present. Inoculation into the eye causes an oculoglandu-
lar syndrome with lacrimation, photophobia, lid edema, and preauricular and
cervical lymphadenopathy.
Anthrax.
mals by contact with hides or ingestion or inhalation of spores. The painless
“malignant pustule” begins as an erythematous papule which then vesiculates and ulcerates surrounded by brawny edema. A black eschar may form.
Regional lymphadenopathy is occasionally present. Inhalational exposure
leads to rapidly progressive pneumonia with hilar adenopathy and mediastinal widening.
Nodular lymphangitis. Nodular lymphangitis without an inoculation lesion
manifests as erythema, induration and nodular thickening of cutaneous and
subcutaneous lymphatics. Regional lymphadenopathy may be found. A
complete travel and exposure history is key. This is misdiagnosed as cellulits.
tularemia, coccidioidosis, histoplasmosis, blastomycosis, cryptococosis, Psue-
domonas psuedomallei, and anthrax.
Francisella tularensis is inoculated by y or tick bites or skin con-
Bacillus anthracis infection is transmitted from wild or domestic ani-
Examples: Mycobacteria marinum, Nocardia, sporotrichosis, leishmaniasis,
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Cat-scratch disease. Bartonella henselae inoculated by the scratch, lick,
or bite of a healthy cat travel to regional lymph nodes, then disseminate.
Symptoms are nonspecic with malaise and headache. Signs include fever,
an inoculation site papule, or pustule followed by painful uctuant regional
lymphadenopathy with overlying erythema. Dissemination in immunocompromised hosts leads to hepatitis (peliosis hepatitis), osteomyelitis, or
meningoencephalitis. Conjunctival infection produces preauricular lymphadenopathy (Parinaud oculoglandular syndrome) [Koehler JE, Duncan LM.
Case 30-2005: A 56-year-old man with fever and axillary lymphadenopathy.
N Engl J Med. 2005;353:1387–1394; Pael UD, Hollander H, Saint S. Index of
suspicion. N Engl J Med. 2004;350:1990–1995].
Rickettsial spotted fever syndromes. See Chapter 4, page 49. These syndromes present with an inoculation eschar, high fever, myalgias, and malaise.
A thorough travel and residential history is key to accurate diagnosis.
Necrotizing soft-tissue infections. Anaerobic or microaerophilic organisms
are inoculated deeply into a puncture wound or ascend via lymphatics. Infection spreads longitudinally along adipose tissue septa and muscle fascia and
vertically into deeper structures along neurovascular bundles penetrating
tissue planes.
injury or cutaneous erythema, which is initially minimal. The soft tissues are
edematous, indurated, and very tender. Infection progresses rapidly causing
extensive tissue necrosis, edema, hypoperfusion, compartment syndromes,
systemic hypotension, and death. Rapid diagnosis and surgical debridement
are essential to save life and limb. The most common organisms are group
A or microaerophilic streptococci. Less common are gas-forming organisms,
e.g., Clostridium perfringens (gas gangrene).
Erysipeloid. Caused by Erysipelothrix rhusiopathiae, it is acquired by han-
dling infected mammals and sh. A localized dermal infection of the ngers
or hands, rarely extending above the wrist, it presents as swollen, slightly
tender, violaceous skin with sharp borders. The inammation resolves in a
few days leaving pigmentation.
The patient complains of severe pain disproportionate to the
Mycobacterial infections. Infection with tuberculous or nontuberculous
mycobacterium present as progressive skin infections with negative cultures and unresponsive to antibiotics. A high index of suspicion and selective media for culture are required. Fungal infections are mimics, e.g.,
cryptococcus.
Digital infection—tuberculosis verrucosa cutis. Mycobacterium tuberculosis
is inoculated into the skin. A bluish-red patch appears, later becoming papil-
lomatous and warty; it may exude pus. Pathologists are infected at the autopsy; butchers and packinghouse workers handle infected meat. The lesions
are indolent with no constitutional symptoms.
Fish-tank granuloma—M. marinum. A small nodule or nodules develop
on the ngers after exposure to contaminated aquariums. The lesions may
ulcerate or form small abscesses. Lymphatic spread resembles sporotrichosis.
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Tropical ulcer—buruli ulcer. Mycobacterium ulcerans is endemic in some
tropical countries.
nonhealing ulcer.
Viral infections.
Human papilloma virus (HPV)—Warts. See page 138.
Herpes simplex virus (HSV).
person by intimate contact. Genital ulceration is more commonly caused by
type-2 (genital herpes strain) than type-1 which is more commonly associated
with oral infections. Initial type-1 infection produces severe stomatitis with
gingival involvement. Initial type-2 genital infection causes a painful vesicular eruption on the genital skin or mucosa. Regional lymphadenopathy and
aseptic meningitis can occur. Recurrences manifest grouped vesicles on an
erythematous base, commonly on the lips (herpes labialis) and buttocks but
can be elsewhere (Fig. 6-24). Recurrent lesions are preceded by 1–3 days of
discomfort at the site of subsequent lesions.
Varicella-zoster (VZV). VZV infection in childhood causes chickenpox.
Before being controlled by a humoral immune response VZV disseminates
to spinal and cranial nerve sensory ganglia establishing lifelong latency
checked by cell mediated immunity.
cell-mediated immunity due to age, immunosuppression, concurrent illness,
or immunosuppressive drugs producing herpes zoster (shingles) and, rarely,
disseminated infection.
Chickenpox.
fever beginning simultaneously. The initial skin lesions are red
trunk more than face, arms, and legs. They evolve to supercial vesicles on
erythematous bases (dew drop on a rose petal) that rapidly become pustules.
Healing is by crusting leaving little or no scar. Vesicles occur in successive
crops, so lesions are at various stages of development.
A pruritic nodule breaks down forming a chronic, shallow,
Herpes simplex viruses spread person-to-
Latent virus reactivates with waning
Initial varicella infection is a mild systemic disease with rash and
papules on the
Herpes zoster (shingles).
1–3 days by clustered vesicles on an intensely erythematous base within a
FIG. 6-24Herpes Simplex. A painful crop of vesicles and pustules has erupted on a well demarcated erythematous
base in this patient’s left groin.
Severe burning pain and dysesthesia is followed in
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spinal or cranial sensory dermatome. Unless dissemination occurs, lesions
are unilateral not crossing the midline. The vesicles burst, crust, and slowly
heal. Pain, postherpetic neuralgia, subsides in days, weeks, or months. Diagnosis is uncertain until the rash appears.
Variola—smallpox.
tular skin eruption predominately on the face and extremities. The rash is
preceded by 2–3 days of fever, myalgias, and arthralgias. Unlike varicella, the
skin lesions are synchronous, progressing from vesicles to tense deep pustules that break, crust, and heal with scarring. The mortality rate is high.
Monkeypox.
in the spring of 2003. It was transmitted to humans from infected prairie dogs.
The illness is acute with fever and malaise, followed by a macular rash with
vesicles, which may be umbilicated. The lesions may be asynchronous.
HIV and AIDS. HIV/AIDS has many cutaneous clues to diagnosis. Acute infection is associated with a morbilliform or papular exanthem and enanthem.
Herpes zoster occurs early in the chronic course of HIV infection. Severe seborrheic dermatitis is common. Candida skin and vulvovaginal infections occur
frequently. Dermatophyte infections are more common and difcult to treat.
An eosinophilic folliculitis is associated with HIV infection and its treatment.
AIDS patients often have pruritic dermatitis with dry skin. HPV-associated
cervical dysplasia and cancer are more common in HIV-infected than nonHIV-infected women. In advanced disease, Kaposi sarcoma (KS) presents
on the skin and oral and genital mucous membranes. Hairy leukoplakia is a
characteristic oral lesion. Abnormal subcutaneous fat distribution, lipodystrophy, is associated with protease inhibitor treatment of HIV/AIDS.
Human herpes virus 8—Kaposi Sarcoma.
Supercial fungal infections—dermatophytes, tinea.
the dead keratin layer of skin, nails, and hair. Though specic fungus can
be cultured, infection is clinically classied by location. Presentation usually
involves skin thickening, scaling, and mild erythema. Secondary bacterial
infection occurs in macerated chronically moist areas. DDX: Chronic noninfectious dermatitis is often confused with tinea.
Variola infection is a severe systemic illness with a pus-
This African monkey infection was imported to North America
See page 156.
Dermatophytes infect
Tinea pedis—athlete's foot. Infection is a white raised patch with ssures
that may ulcerate. It is painful or asymptomatic. Usually between lateral toes,
it may involve the entire sole being sharply demarcated at the edge of the
sole. Vesicular forms occur especially on the instep.
Tinea manuum. Infection of the palm of one or both hands often occurs in
association with tinea pedis.
Tinea unguium. Dermatophyte infection is in the nail plate. See onychomycosis.
Tinea capitis. This involves the scalp and hair. The hair is brittle. The circular
areas may become inamed and ulcerate, leading to permanent loss of hair.
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