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The genus Malassezia includes
11 species associated with significant human disease1(eTable 301.1). The organisms are dimorphic with
both yeast and mycelial growth. With the exception of M
pachydermatis, all other Malassezia species
require lipid supplementation of standard fungal growth media for
isolation. When Sabouraud media is overlaid with sterile olive oil, Malassezia species
grow within 5 to 14 days.2 Isolation on this medium causes
colonies to coalesce, making species identification difficult. Although
species identification is rarely important in clinical practice,
several commercial media avoid this problem. Dixon medium (containing
Tween 40 and glycerol monooleate) and Leeming and Notman agar (containing
Tween 60, glycerol, and full-fat cow milk) are selective media for Malassezia isolation. Rapid
identification techniques, such as identification of Malassezia DNA
by polymerase chain reaction, have been utilized in study settings.3 Malassezia species
are normal residents of human skin, usually found in sebum-rich
areas such as the trunk, face, and scalp. Extensive studies on skin
colonization have shown that the skin of healthy newborn infants
becomes colonized with Malassezia species within
the first several months of life. Over 50% of prematurely
born infants requiring prolonged hospitalization become colonized
within 2 weeks of life.4,5 Ninety to 100% of
adolescents and adults have saprophytic skin colonization with Malassezia species.6
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Clinical Manifestations
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Skin diseases are the most common manifestation of Malassezia infection.7 Confirmed dermatoses
include tinea versicolor, seborrheic dermatitis, and folliculitis.
Tinea versicolor (Fig. 367-9) is disscussed
in Chapter 367. Lesions are most commonly seen on the chest, back,
and upper arms and occur most often in adolescents and young adults.
In those who develop tinea versicolor, the yeast phase transforms
to the mycelial phase. This results in the characteristic “spaghetti
and meatballs” appearance of skin scrapings when examined
under the microscope with 10% potassium hydroxide. Heat,
moisture, and skin occlusion favor this transformation. M
globosa, M restricta, and M sympodialis are
most often associated with tinea versicolor.
++
Seborrheic dermatitis due to Malassezia occurs
in 2% to 5% of normal hosts but is prevalent in
70% to 80% of persons with untreated AIDS. This
condition varies from thick greasy scales covering the scalp of
infants in the first 3 months of life (cradle cap) to an itchy,
papular, erythematous, greasy, scaling rash most commonly found
in the nasolabial folds, postauricular scalp, eyebrows, or chest.9 Dandruff,
presenting as mildly pruritic scaling of the scalp without associated inflammation,
is felt to represent a milder variant of seborrheic dermatitis.
Diagnosis of seborrheic dermatitis and dandruff are usually made
on a clinical basis. Culture for Malassezia does
not confirm the diagnosis because the quantity of Malassezia may
not differ from that normal skin.
++
Folliculitis resulting from Malassezia may resemble
the lesion of disseminated candidiasis. This acneiform lesion presents
as follicle-limited inflammatory papules or papulopustules. It is
most commonly seen over the back and chest of patients with AIDS
or of those receiving broad-spectrum antibiotics or steroids. M
furfur is reported to cause eosinophilic pustular folliculitis
with pruritus in patients with AIDS, and in its papular form, this
lesion is pathologically a vasculitis of the dermis. This papulopustular
dermatitis responds to topical or systemic imidazole therapy. Discontinuation
of steroids or antibiotics also is helpful. Malassezia species
were described as a cause of neonatal cephalic pustulosis, characterized
by scattered erythematous papules and pustules on the face, scalp,
and neck of infants in the first few weeks of life.10 Diagnosis
can be confirmed by culture of purulent material or lesional biopsy
where budding yeast are apparent.
++
Systemic Malassezia infections have most commonly
been associated with catheter-associated fungemia due to M
furfur in patients receiving intravenous lipid feedings
or total parenteral nutrition. A characteristic syndrome is noted, most
often in premature neonates, of fever, bilateral interstitial pulmonary
infiltrates, leukocytosis, and thrombocytopenia.5,11 This
syndrome also has been reported in immunocompromised adults and
children with central venous catheters who were not receiving concurrent
intravenous lipids.12 Complications from catheter-associated infections
have included meningitis, peritonitis, endocarditis, and peripheral
thromboembolism.13,14M pachydermatis is
also associated with systemic sepsis in infants. At least 2 nursery outbreaks
have been reported; in one, colonization of health care workers
by their pet dogs was believed to be a possible source of infection.15 Diagnosis
is generally made when blood from culture-negative cases of apparent
catheter-associated sepsis is cultured on lipid-enriched media. In
one study of neonatal infections in which polymerase chain reaction was
utilized to detect M furfur from the blood, only
1 of 4 culture-positive children yielded a positive polymerase chain
reaction.
++
Malassezia species are generally susceptible
to a wide range of topical and systemic antifungal treatments. Tinea
versicolor and seborrheic dermatitis can be managed with topical
2.5% selenium sulfide, zinc pyrithione, or azole creams
(ketoconazole, itraconazole, fluconazole).7,9 Susceptibility
to terbinafine varies, but topical terbinafine is more effective
than oral terbinafine. Oral itraconazole or fluconazole have been
shown to be effective for tinea versicolor and seborrheic dermatitis.
These drugs are probably more effective than topical medications
for the treatment of Malassezia folliculitis. Topical
corticosteroids may be effective in seborrheic dermatitis, but in
children ages 2 years or older, tacrolimus or pimecrolimus may be
more effective because of antifungal as well as anti-inflammatory
activity. Recurrence within 1 to 2 years is common.
++
For sepsis, therapy includes removal of the venous catheter that
was used for alimentation and interruption of lipid feedings. A
short course of therapy with amphotericin B, fluconazole, or itraconazole
may be indicated, particularly if a new deep line is placed.5,16Malassezia species
are resistant to flucytosine.