Candida species may cause infection of mucosal
epithelia, skin, and nail plates, and, although not a component
of normal skin flora, favors warm, moist regions such as the diaper
region, intertriginous zones, web spaces between fingers and toes,
and the corners of the mouth. Part of normal oral and intestinal
flora, Candida albicans is the most common pathogen. Most
candidal infections are noninvasive and limited, although invasive
candidal infections are seen with increasing frequency in the settings
of immunosuppression, HIV infection, diabetes, and prematurity.
Diagnosis of cutaneous candidal infections is made on clinical grounds,
in conjunction with fungal culture and potassium hydroxide (KOH)
examination, which reveals budding yeasts and pseudohyphae.
Diaper candidiasis may occur as a primary process or,
more commonly, as a secondary infection in the setting of a primary
irritant contact dermatitis. Predisposing factors include oropharyngeal
candidiasis, diarrhea, and antibiotic therapy. Intense perianal
and flexural erythema, sometimes with maceration, followed by the
development of superficial pustules is the most common presentation. Spread
is accomplished via “satellite lesions” of erythematous
papules and papulopustules at the periphery of the erythema. The genitalia,
inferior abdomen, inner thighs, perineum, and buttocks may all eventually
be involved. In male infants, involvement of the glans penis (candidal
balanitis) (Fig. 367-10) is common,
as is involvement of the scrotum, which helps differentiate candidiasis
from tinea cruris. Involvement of the inguinal creases helps distinguish
candidiasis from irritant contact dermatitis, in which the fold
regions are often spared.
Diaper candidiasis with candidal balanitis. Beefy red
erythematous papules and plaques with peripheral satellite papulopustules.
Involvement of the glans penis (balanitis) and scrotum differentiates Candida from
Management of diaper candidiasis includes frequent diaper changes,
diaper-free periods where feasible, protective barrier pastes or
ointments, and topical antifungal agents, including nystatin or
imidazole antifungals (econazole, ketoconazole, clotrimazole, miconazole).
Low-potency topical corticosteroids, such as hydrocortisone, may
be a useful adjunct to help decrease associated inflammation, but
combination steroid-antifungal preparations should be avoided in
the diaper area. Secondary bacterial infection may need to be considered,
especially in recalcitrant cases or those with a vesiculobullous
or erosive component. Although sometimes advocated because Candida species
are known to colonize the intestine, the effectiveness of concomitant
oral antifungal therapy remains unproven.
Oropharyngeal candidiasis, or thrush,
is infection of the oral cavity with C albicans.
This is most commonly acquired during passage through an infected birth
canal or during nursing from the skin of an infected breast. Left untreated,
most cases of oropharyngeal candidiasis will resolve spontaneously,
although this may require 4 to 8 weeks. Although frequently asymptomatic
in immunocompetent children, occasional infants with thrush may
experience pain and impairment of sucking and swallowing, which
may ultimately progress to candidal esophagitis and nutritional
Oropharyngeal candidiasis presents as white to gray patches,
which may form “pseudomembranes” composed of epithelial
cells, white blood cells, food debris, and yeast forms that cover
the buccal mucosae, tongue, and gingivae. Less common sites of involvement
include the soft palate, uvula, and tonsils. Removal of the patches
by scraping with a tongue depressor reveals an erythematous, eroded
base; a KOH examination reveals ovoid yeast forms and pseudohyphae. Treatment
consists of topical nonabsorbable antifungal agents such as nystatin,
miconazole, or clotrimazole applied four times daily. Oral fluconazole
has been found effective in the treatment of oropharyngeal candidiasis
in immunocompromised children.26
Congenital candidiasis, a rare entity, is a
benign infection in the full-term infant, but life-threatening in
the premature newborn. Organisms gain entry to the amniotic fluid
from a colonized vagina. Presentation is during the first week,
and usually the first few days, of life. The placenta and/or
umbilical cord of affected infants may reveal white-yellow plaques.27,28 Invasive
candidiasis, including sepsis, pneumonitis, and renal and central
nervous system infection, is more likely in premature neonates and
is associated with a poor prognosis.
Cutaneous lesions of congenital candidiasis, which are present
in up to one half of patients, may be diffuse, intensely erythematous
macules and papules involving the trunk and extremities, often with
sparing of the diaper area; a papulopustular eruption with erosions
and possible involvement of the palms and soles that then resolves
with desquamation; or a burnlike dermatitis (mainly in extremely
low birth weight premature infants). Oral thrush and nail dystrophy
may be present, with isolated nail changes occasionally being the
sole mucocutaneous manifestation. Bullae are rarely present. Topical antifungal
therapy is usually sufficient for skin-limited disease, but intravenous
amphotericin B, sometimes in combination with 5-flucytosine, fluconazole
or caspofungin are indicated with evidence of respiratory compromise,
other signs of disseminated infection or in the premature infant
with systemic infection.27
Chronic paronychia is a long-standing infection
of the skin folds surrounding the nails that is usually caused by C
albicans, although a mixed infection with Candida species
and bacteria may often be present. Periungual erythema, cuticle
loss, and transverse ridging of the nail plate are the presenting signs.
Other nail changes may include yellow discoloration and thickening.
Pain, purulence, and discharge are usually absent. The diagnosis
may be confirmed by the finding of budding yeasts and pseudohyphae
on KOH examination or via culture. Avoidance of moisture, which
favors growth of yeast cells, and application of topical antifungal
creams are the mainstays of therapy. A combination steroid-antifungal
cream such as triamcinolone-nystatin (Mycolog II) is also effective
and oral antifungal treatment may be necessary in severe cases.
Angular cheilitis (perlèche) is characterized
by erythema, fissuring, and crusting at the mouth angles. Predisposing
conditions include any situation that results in excessive moisture
collecting in these areas, such as frequent drooling, lip licking,
and use of orthodontic appliances. Differential diagnosis includes
contact dermatitis and nutritional deficiency (riboflavin, zinc,
or biotin). C albicans is usually present, and
concomitant bacterial infection may also occur. Therapy is aimed
at correcting predisposing conditions, treating infection with topical antifungal
(and antibacterial, if necessary) agents, and applying thick barrier
ointments to decrease further exposure to moisture and subsequent
maceration. Low-strength topical corticosteroid ointments may be
helpful in patients with significant inflammation.
Tinea versicolor is a superficial skin infection caused
by the dimorphic lipophilic fungus Malassezia furfur,
also known as Pityrosporum ovale and Pityrosporum
orbiculare, depending on the form of the yeast phase. This
organism is a lipid-dependent yeast that is part of normal human
skin flora in 90% to 100% of individuals. Although most
cases occur during the postpubertal period, tinea versicolor may
occasionally occur in prepubertal children. Infection localizes to
areas of skin that are rich in lipid-producing sebaceous glands,
including the chest, back, and face.
Tinea versicolor occurs when the yeast form of the organism converts
to the mycelial form, a transition that may be prompted by various
predisposing factors, including heat, humidity, sweating, and skin
occlusion. Individual host susceptibility and immunosuppression
may also play a role. The most common clinical findings are sharply
demarcated, hypopigmented macules and patches that may have associated
fine scaling (Fig. 367-11). Other presentations include hyperpigmented
or erythematous patches, particularly in dark-skinned individuals.
Pruritus is occasionally present. The hypopigmented areas become
more noticeable after unprotected sun exposure, caused by uneven
tanning of the surrounding uninvolved skin. The hypopigmentation
seen in tinea versicolor is attributed to a product of the fungus,
azelaic acid, which inhibits dopa-tyrosinase, an enzyme involved
in the melanin synthetic pathway.
Tinea versicolor. Lipid-rich areas of skin are affected.
This condition is caused by the lipophilic yeast Malassezia
Differential diagnosis of tinea versicolor includes pityriasis
alba and vitiligo. Pityriasis alba is most common on the face, and
patients often have an associated atopic diathesis. Vitiligo results
in complete depigmentation and is most common in periorificial regions
(around the eyes, mouth, and genitalia) and over bony prominences.
Scaling is usually minimal to absent in these two disorders.29 Other
differential diagnoses include psoriasis, seborrheic dermatitis,
dermatophyte infection, and confluent and reticulate papillomatosis
of Gougerot and Carteaud. In darkly pigmented patients, hypopigmented
lesions of cutaneous T-cell lymphoma must be considered, especially
in cases with an unusual distribution or a history of recalcitrance
Potassium hydroxide (KOH) examination of scrapings from lesions
of tinea versicolor reveals numerous clusters of spores and short,
stubby hyphae, the so-called pattern of “spaghetti and
meatballs.” Culture is not useful because M furfur is
a normal skin inhabitant.
There are several treatment options, both topical and oral. Either
selenium sulfide 2.5% or ketoconazole 2% shampoo
can be applied to the affected areas and left on for 5 to 10 minutes
prior to rinsing, for 1 to 2 weeks.30 Topical antifungal
agents may be effective, but are often limited by the widespread
involvement and hence the need to apply large amounts of the medication.
The allylamine antifungal terbinafine in a 1% spray has
been approved for treatment of tinea versicolor in patients 12 years
of age and older. Oral antifungal agents are also quite effective
and may be helpful in severe or recurrent cases of tinea versicolor.
Fluconazole, itraconazole, and ketoconazole have all been demonstrated
to be effective in a variety of dosage regimens.31-34 One
oral regimen is fluconazole in an adult dose of 300 mg once weekly
for 2 weeks.31 Drug delivery to the skin may be augmented
by exercise following oral ingestion, and showering should be avoided
for 12 hours to maximize the effect.