“ PITYROSPORUM INFECTIONS” OF THE SKIN: PAPULOSQUAMOUS TINEA

VERSICOLOR, “PITYROSPORUM” FOLLICULITIS, AND INVERSE TINEA

VERSICOLOR

The genus Malassezia includes seven species of lipophilic basidiomycetous yeast:

Malassezia furfur, M. pachydermatis, M. sympodialis, M. globosa, M. restricta, M. slooffiae,
and M. obtusa. Previously, M. furfur, M. pachydermatis, and M. sympodialis were the only
members of the genus. In 1996, Gueho et al. proposed a new taxonomic classification based
on morphology, ultrastructure, and molecular biology that added four new species. These
yeasts cause a wide spectrum of superficial cutaneous disease, including tinea versicolor,
folliculitis, and seborrheic dermatitis.
History
Eichstedt first recognized tinea versicolor as a cutaneous fungal infection in 1846. For
several years the disease was considered to be dermatophyte in origin, but Baillon, impressed
by the yeastlike nature of the organism, coined the name Malassezia in 1889 to distinguish this
organism from the Microsporum species of dermatophytes. In 1951, Gordon isolated and
characterized the organism M. furfur and renamed it Pityrosporum orbiculare. It is now
recognized and accepted that M. furfur is the correct name and that P. orbiculare, P. ovale, and
M. ovalis are synonyms.
Etiology and Pathogenesis
M. furfur can be cultured from diseased and normal skin and is considered part of the
normal flora, particularly in sebum-rich areas of the skin. M. furfur is a dimorphic, lipophilic
organism that grows in vitro only with the addition of C 12 to C 14 fatty acids such as olive oil
and lanolin. Under appropriate conditions, it converts from the saprophytic yeast to the
predominantly parasitic mycelial morphology associated with clinical disease. Factors
responsible for mycelial transition include a warm, humid environment, heredity, Cushing's
disease, immunosuppression, and a malnourished state.
The species of Malassezia can be differentiated by their nutritional requirements,
morphology, and molecular biology. M. pachydermatis is the one member of the genus
Malassezia without an absolute requirement of exogenous lipids for growth. Although
previously recognized as a zoophilic organism, it has been identified only recently as a human
pathogen. In one study, M. pachydermatis caused a series of infections in a neonatal care
nursery, where it was presumably spread to patients from health care workers whose pet dogs
were colonized with the fungus. Other members of the genus, including M. sympodialis and M.
sloofiae, are part of the normal skin flora. A recent study also linked M. sympodialis with
neonatal cephalic pustulosis, a skin disorder also known as neonatal acne.
M. furfur has long been identified as the fungus causing tinea versicolor. However,
recent studies indicate that M. globosa may be involved in the pathogenesis of this disease.
Crespo Erchiga et al. Cultured the lesions of tinea versicolor in 96 patients, and M. globosa
was found in 97 percent.
Tinea versicolor is an opportunistic infection of the skin. Experimental inoculation of
Malassezia under occlusion can cause infection. The resulting increase in humidity,
temperature, and CO 2 tension appear to be important factors that make the skin susceptible to
infection. When the occlusion is terminated, healing occurs, although the organism is not
eradicated from the skin and can be cultured from clinically uninvolved areas. It also may
colonize follicular structures, and a high recurrence rate is expected.
Immunology
No specific deficiencies in antibodies or complement components have been found in
patients with tinea versicolor. Similar titers of specific IgG antibody are seen in healthy controls
and tinea versicolor patients. Furthermore, Sohnle and Collins-Lech have shown that M. furfur
induces IgA, IgG, and IgM antibodies and that it also activates complement through the
alternative and classical pathways. The precise role that CMI and other immunologic factors
play in the disease process is unknown.
The immune response seen in Malassezia folliculitis is likewise poorly understood.
Patients with Malassezia folliculitis have higher titers of IgG antibodies than those with tinea
versicolor or controls. Both nonspecific inflammatory responses and specific cellular immunity
are also observed. Faergemann et al. have shown that patients with seborrheic dermatitis and
Malessezia folliculitis have an increased number of NK1+ and CD16+ cells and complement
activation consistent with irritant stimulation of the immune system. In addition, biopsies of
involved skin lesions showed an increase in inflammatory cytokines.
Clinical Features
Cutaneous infections with Malassezia may take three forms: (1) papulosquamous, (2)
folliculitis, and (3) inverse tinea versicolor. The most common presentation is scaly hypo- or
hyperpigmented macules observed in characteristic areas of the body, including the chest, back,
abdomen, and proximal extremities ( Fig. 206-6). Less common areas of involvement include
the face, scalp, and genitalia. The characteristic scale is described as dustlike or furfuraceous.
This characteristic feature of the disease can be produced by lightly scraping a scalpel blade
over the involved skin. The color of the lesions varies from almost white to reddish brown or
fawn-colored. The presenting complaint is usually a cosmetic one because lesions often fail to
tan with sun exposure. Pruritus is mild or absent.

FIGURE 206-6 A. Pityriasis versicolor. These lesions are darker because of hyperemia secondary to inflammatory
response and increased melanin. B. Tinea versicolor. There are sharply marginated, uniformly hypopigmented macules
with a fine, sometimes barely perceptible scale, but they are easily scraped off with a glass slide. When the lesions are
very large, as on the left, they can be confused with vitiligo.

The yeast may filter the rays of the sun and interfere with normal tanning. Furthermore,
the metabolites of M. Furfur such as azaleic acid, a dicarboxylic acid, can cause depigmentation
by inhibiting tyrosinase and injuring melanocytes. This long-standing damage to melanocytes
may explain why most hypopigmented lesions persist for months and some persist for years.
In Malassezia ( Pityrosporum) folliculitis, lesions typically appear on the back, chest,
and sometimes the extremities ( Fig.206-7A). Pruritus is more common than with typical tinea
versicolor. The primary lesion is a perifollicular, erythematous, 2- to 3-mm papule or pustule.
Only appropriate culture and KOH examination can distinguish this infection from a bacterial
folliculitis. Frequently, biopsy with special stains for fungus is necessary (see Fig. 206-7B).
Diabetes mellitus or prior glucocorticoid or antibiotic therapy can predispose to this disorder.
FIGURE 206-7 A, B. Pityrosporum folliculitis on the anterior chest. Note the organisms in the follicular ostia on staining
with hematoxylin and eosin.

The lesions of inverse tinea versicolor are encountered predominantly in flexural areas.
Because of its location, inverse tinea versicolor can be confused with seborrheic dermatitis,
psoriasis, erythrasma, candidiasis, and dermatophyte infections.
Rarely, M. furfur can infect organs other than the skin. A premature infant on total
parenteral nutrition with intravenous lipid supplementation has been reported who showed no
skin lesions but had an extensive vasculitis of small pulmonary arteries as well as pneumonia.
M. furfur was seen microscopically in areas of lipid deposition. The organism has been cultured
from peritoneal dialysate and blood and, with increasing frequency, from patients receiving
parenteral intravenous lipid supplementation. Presumably, this provides an appropriate growth
medium for M. furfur.
Each of the cutaneous variants has an equal sex distribution and tends to flare during
the summer months, presumably due to increased heat and humidity. These infections are also
more common in tropical climates. Although the disease can occur at any age, late adolescents
and early adults are predominantly affected.
Laboratory Findings
To identify the Malassezia yeast forms, scale from involved skin should be scraped
onto a glass slide and treated with 10% KOH. Alternatively, cellophane tape can be used to
pick up skin scales from the lesion. The tape is mounted on a glass slide with methylene blue,
and the organism is selectively stained.
 Sabouraud's dextrose agar overlaid on the surface with sterile olive oil or lanolin readily
supports the growth of this lipophilic yeast. To reduce the growth of contaminating organisms,
antibiotics such as penicillin, streptomycin, and cycloheximide are incorporated into this
medium. In general, cultures are not required for diagnosis because organisms can be
demonstrated with 10% KOH.
Pathology
In tinea versicolor, the organisms inhabit the stratum corneum. There is usually no
dermal infiltrate. Yeast may be observed with hematoxylin and eosin (H&E) stain alone. PAS
staining is confirmatory. Microscopic examination reveals clusters of oval budding yeast cells
3.5 × 4.5 μm long with short, septate, and occasionally branching hyphae ( Fig.206-8). The
microscopic appearance of the yeast is classically described as “spaghetti and meatballs.” In
Malassezia folliculitis, organisms are noted in widened follicular ostia mixed with keratinous
material (see Fig. 206-7B). Rupture of the follicular wall can occur with a resulting mixed
inflammatory and foreign-body giant cell response.

FIGURE 206-8 “Spaghetti and meatballs” appearance of tinea versicolor in a KOH preparation.

Diagnosis
The clinical appearance of tinea versicolor is usually characteristic, and KOH
examination is confirmatory. A Wood's lamp examination may show yellowish fluorescence
of involved skin. The differential diagnosis includes pityriasis alba, confluent and reticulated
papillomatosis of Gougerot and Carteaud, pityriasis rosea, seborrheic dermatitis, vitiligo, or
secondary syphilis.
For the folliculitis variant, both bacterial and candidal folliculitis should be considered
in the differential diagnosis. The skin lesions of disseminated candidiasis also can be confused
with Malassezia folliculitis.
Treatment and Prognosis
There are multiple topical products that are useful in treating tinea versicolor. The most
widely used has been 2.5% selenium sulfide shampoo. This should be applied liberally over
and beyond the affected areas, left on for at least 10 min, and then washed off. The cycle is
repeated every day for 2 weeks. Subsequently, we recommend applying the drug once or twice
per month to prevent recurrence. All the topical azole antifungals have been effective in the
treatment of tinea versicolor. Ketoconazole 2% shampoo may be lathered on affected areas and
left for 5 min; this is repeated for 3 consecutive days. Recent studies have shown that topical
terbinafine, 1% solution applied twice daily to lesions for 7 days, has cure rates of greater than
80 percent.
While topical therapy is ideal for this condition, systemic treatment may be necessary
for patients with extensive disease, frequent recurrences, or failure of topical agents. 87 In
addition, patients often prefer the convenience of oral therapy. Cure rates range from 90 to 100
percent with ketoconazole (200 mg daily for 7 days) or itraconazole (200–400 mg daily for 3–
7 days). Fluconazole is also effective and can be given as a single dose of 400 mg. 86, 88Oral
terbinafine is not an effective treatment, likely because therapeutic drug levels are not achieved
in the stratum corneum. In addition, griseofulvin is not effective in the treatment of tinea
versicolor. Whether systemic or oral medications are used, clinical improvement is not seen
until 3 to 4 weeks after treatment because the involved epidermis must slough.
 Malassezia folliculitis also can be treated successfully with both topical and systemic
therapy. As with most types of folliculitis, systemic therapy is more effective. Although there
are few controlled trials, oral ketoconazole (200 mg daily for 4 weeks), fluconazole (150 mg
weekly for 2–4 weeks), and itraconazole (200 mg daily for 2 weeks) are useful systemic agents
in the treatment of this papulopustular folliculitis.
Tinea versicolor is often a chronic, recurrent condition. Prophylactic measures, as
discussed earlier, and fastidious cleanliness may lessen the risk of recurrence.