eMedicine Specialties > Dermatology > Fungal Infections

Pityrosporum Folliculitis

Siobahn M Bower, MD, Internal Medicine Resident, Creighton University
Daniel J Hogan, MD, Affiliate Teaching Faculty, Sun Coast Hospital; Investigator, Hill Top Research, Florida Research Center; Stephen H Mason, MD, Assistant Professor of Dermatology, Medical College of Georgia

Updated: Sep 11, 2008

Introduction

Background

Pityrosporum folliculitis (PF) is an inflammatory skin disorder that typically manifests as a pruritic, follicular papulopustular eruption distributed on the upper trunk of young to middle-aged adults. Weary et al first described PF in 1969, and, later in 1973, Potter et al¹ identified PF as a separate clinical and histologic diagnosis.

Yeasts, specifically Malassezia furfur, are the pathogenic agents in PF. M furfur has been linked to several skin diseases, including seborrheic dermatitis, folliculitis, pityriasis versicolor, and atopic dermatitis. In 1874, Malassez first described round and oval budding yeasts from scales of patients with seborrheic dermatitis. He coined the phrases "bottle bacillus of Unna" to describe the small oval cells in the scale and "spore of Malassez" to name the bud that is observed in association with the yeast. Saborouraud proposed the Pityrosporum genus in 1904 to describe the budding yeast cells without hyphal elements from normal skin. Later, in the 1900s, Pityrosporum ovale and Pityrosporum orbiculare were isolated by Castellani and Chalmers and Gordon, respectively.

These 2 yeast species, collectively with fungal forms, are classified as M furfur because of controversy and confusion of the grouping of various lipophilic yeasts and fungi of the skin. This grouping has simplified the classification to one name, which applies regardless of the morphology of the organism. With the advancement of technology, 7 species of Malassezia were recognized: M furfur, Malassezia pachydermatous, Malassezia sympodialis, Malassezia globosa, Malassezia obtusa, Malassezia restricta, and Malassezia slooffiae. However, the focus of this article is M furfur, which is considered the pathologic agent of PF. Lesions are chronic, erythematous, pruritic papules and pustules, which occur in a follicular pattern. These lesions are usually present on the back and chest and, occasionally, on the neck, shoulders, upper arms, and face.

The diagnosis of PF is based on clinical suspicion of the classic presentation of pruritic papulopustules found in a follicular pattern on the back, chest, upper arms, and, occasionally the neck. They are rarely present on the face. An improvement in the lesions with empiric antimycotic therapy supports a clinical diagnosis of PF.

A related Medscape CE course is Fungal Skin and Nail Infections: Practical Advice for Advanced Practice Clinicians. Additionally, a general folliculitis eMedicine article is Folliculitis.

Pathophysiology

M furfur (ie, P ovale and P orbiculare) is a lipophilic, saprophytic, budding, unipolar, dimorphic, gram-positive, double-walled, oval-to-round yeast. M furfur is part of the normal skin flora. It is suggested that the similar yeasts P orbiculare and P ovale are actually identical and that they are morphologic variants of M furfur.

Malassezia yeasts are classified as superficial mycoses that by definition do not invade past the cornified epithelium. In PF, however, the organism is present in the ostium and central and deep segments of the hair follicle.

Plugging of the follicle followed by an overgrowth of yeast that thrives in the sebaceous environment is believed to be the etiology. Malassezia yeasts require free fatty acids for survival. Usually, they are found in the stratum corneum and in pilar folliculi in areas with increased sebaceous gland activity such as the chest and back. The yeasts hydrolyze triglycerides into free fatty acids and create long-chain and medium-chain fatty acids from free fatty acids. The result is a cell-mediated response and activation of the alternative complement pathway, which leads to inflammation.

Frequency

United States

Malassezia organisms can be found on the skin in 75-98% of healthy people. These organisms are part of the normal skin florae of many individuals who do not have signs or symptoms of folliculitis or other disease. Colonization by M furfur begins soon after birth, and the peak presence of the yeasts occurs in late adolescence and early adult life, coinciding with increasing activity of sebaceous glands and concentration of lipids in the skin.

International

P ovale is present on 90-100% of the surface of healthy skin; higher numbers of the yeast are present on the chest and back. Certain climates influence the percentage of people with P ovale and the number of people with PF. People living in warm and humid climates have a higher incidence of PF.  One clinic in the Philippines documented that 16% of all patient visits were a result of PF.² A 2008 report from China cites that 1.5% off all dermatology patients were diagnosed with PF, most of them healthy, middle-aged males.³

Mortality/Morbidity

PF may be a bothersome condition (ie, severe pruritus), but the lesions are benign. Some underlying conditions that predispose the patient to PF include diabetes mellitus, immunodeficiency, and systemic candidiasis⁴ ; these conditions may cause morbidity. Consider the presence of predisposing conditions when PF is diagnosed.

Race

No known racial differences in the frequency of PF exist.

Sex

Reports vary from a male-to-female ratio of 1:1 to a predominance of one or the other sex. In the literature, the consensus is that the female-to-male ratio is 1.5:1.

Age

The disease is recognized as one that affects youths and young and middle-aged adults⁵ ; PF is most common in those aged 13-45 years. However, 3 cases of PF occurred in an ICU setting in older individuals who were in consecutive beds, who received care from the same nursing staff, and who all received high-dose antibiotics.⁶

Clinical

History

• The patient's history is that of a chronic, often extremely pruritic, papular and pustular eruption with perifollicular erythema most commonly on the back, upper arms, and chest.
• The main differential diagnoses of PF are acne vulgaris and staphylococcal folliculitis. Often, patients have been treated with medication appropriate for acne vulgaris, resulting in no improvement or worsening of their condition.⁷

Physical

• Multiple, discrete, 2- to 4-mm erythematous monomorphic, papules and, later, pustules are observed.
• Lesions have a definite follicular pattern.
• Material expressed from pustules is white to yellow.
• PF is present on body locations in which Malassezia organisms are most abundant: back and chest, neck, shoulders, scalp,⁸ upper arms (occasional), and face (rare).
• Under a Wood light, bright blue or white fluorescence is observed in clinically uninvolved follicles in the location of the lesions.
• PF often is mistaken for acne vulgaris; however, no comedones or cysts are associated with PF.⁹
• Many patients have coexisting seborrheic dermatitis.⁴

Causes

PF is caused by Malassezia yeasts, which are lipophilic. Several factors can lead to changes in immunity, sebum production, and the growth of skin flora. These factors help to produce favorable conditions for growth of these yeasts.

• Systemic diseases and pharmacologic agents that encourage the growth of yeast, possibly because of alterations in immunity, include the following:
  • Diabetes mellitus
  • Cushing disease
  • Hodgkin disease¹⁰
  • HIV infection
  • Corticosteroids and/or immunosuppressant therapy following organ transplantation^11,12
• An increase in sebum production, such as that in pregnancy,^13,14 and high levels of androgens may potentiate the development of PF.
• Antibiotics can alter normal skin flora, allowing the yeast to proliferate.
• PF more frequently occurs in environments of high heat and humidity.
• Occlusion of the skin and hair follicles with cosmetics, lotions, sunscreens, emollients, olive oil, or clothing creates favorable conditions for PF.
• Anticonvulsant therapy and Down syndrome¹⁵ are other conditions that are associated with PF.
• Other related and coexisting conditions may include the following:
  • Seborrheic dermatitis
  • Confluent and reticulated papillomatosis
  • Systemic candidiasis¹⁶
• Some individuals seem to have an innate propensity for PF.
  • In one experiment, Malassezia yeasts were applied to occluded forearm skin in patients with PF. Flares of PF occurred at the application site.
  • In the same experiment, PF did not develop in patients with no prior diagnosis of the condition.

Differential Diagnoses

Other Problems to Be Considered

Steroid acne¹⁷
Systemic candidiasis¹⁶
Acne aestivalis
Cryptococcosis
Torulopsis infection

Workup

Laboratory Studies

• A potassium hydroxide (KOH) preparation may be helpful for microscopic identification of the yeasts.
• Culturing and identification of the organism are rarely performed, and the tests usually are not available.
• For Malassezia yeasts to grow, olive oil must be added to the culture media. This is not a routine study for the mycology laboratory.

Histologic Findings

The basic lesion observed at histologic evaluation is that of folliculitis. The ostium of the hair follicles is dilated, with keratin plugging, cellular debris, and an inflammatory infiltrate including lymphocytes, histiocytes, and neutrophils. Monocytic, perifollicular infiltrate, and mucin deposits are observed around the infundibulum. Some follicles may be cystic and ruptured.

Malassezia yeasts are observed in the central and deep follicle, but they are most densely present in the ostium and pilary canal. Periodic acid–Schiff (PAS) and Grocott-Gomori methenamine-silver staining reveal the oval single-budding yeast; however, these organisms can be observed without stain as well. No mycelial forms are observed with staining. Also detected are 2-4 µm PAS-positive spores in the entire follicle. Most often, spores are observed as aggregates. Both methylene blue and Parker ink staining have been suggested as useful to detect Malassezia; however, Parker ink is a more specific stain for the organism.

High titers of circulating immunoglobulin G antibodies against P ovale can also be detected in persons with this disease.¹⁸

Skin biopsy is usually reserved for the diagnosis of lesions that resemble PF but are located on surfaces where PF less commonly occurs. A diagnosis of PF in these unusual locations may indicate more severe disease. Early biopsy should be considered in patients with significant immunosuppression, such as those with AIDS, because the differential is much broader in these patients.^19,20

Treatment

Medical Care

• Both topical and oral antifungals are effective agents in the treatment of PF.  Oral antifungals have the advantage of dramatic, immediate clearing of the lesions and are the most effective treatment.
• Patients have been successfully treated with oral pulse itraconazole and weekly fluconazole.
• A course of oral ketoconazole²¹ and topical ketoconazole shampoo is currently the recommended treatment.²²
  • Oral medication should be discontinued when the lesions resolve.
  • Because relapse almost always occurs when treatment is withdrawn, topical ketoconazole is indefinitely continued after successful initial treatment with oral medication.
• Other topicals that are used to treat PF are ciclopirox olamine cream, econazole cream, alcohol and salicylic acid solution (with or without benzoic acid 5%), propylene glycol 50% in water, and selenium sulfide shampoo.
• In cases associated with antibiotic use, discontinuing the antibiotic may be helpful.
• Retinoids, which are used for comedones in acne, have no effect because no comedones are present in PF.^23,24
• Tetracycline does not help in PF, and it may exacerbate the condition by further destroying the normal bacterial skin flora and allowing further spread of Malassezia yeasts.

Consultations

No consultations are necessary.

Medication

The goal of pharmacotherapy is to reduce morbidity.

Antifungals

Antifungals are used in the first-line therapy of PF. The use of topical agents has few adverse effects besides an allergic reaction to the active medicine or inactive component. The mechanism of action usually involves the inhibition of pathways (eg, enzyme, substrate, transport) that are necessary for sterol and/or cell membrane synthesis, or the permeability of the cell membrane (polyenes) of the fungal cell is altered.

Ciclopirox (Loprox)

Interferes with DNA, RNA, and protein synthesis by inhibiting the transport of essential elements in fungal cells.

Dosing

Adult

Massage into affected areas bid; re-evaluate diagnosis if no improvement occurs after 4 wk

Pediatric

<10 years: Not established
>10 years: Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

If sensitivity or irritation develops, discontinue use; for external use only; avoid contact with eyes

Ketoconazole (Nizoral tablet, Nizoral cream, Nizoral shampoo)

Ketoconazole is available as a tablet, a 2% cream, and a 1% or 2% shampoo. Imidazole broad-spectrum antifungal agent; inhibits synthesis of ergosterol, causing cellular components to leak and resulting in fungal cell death.

Dosing

Adult

Cream: Gently rub into affected and surrounding area qd/bid for 2-4 wk
Shampoo: Apply twice weekly for 4 wk with at least 3 d between each use
Tablet: 200 mg PO qd; increase to 400 mg PO qd if clinically indicated; discontinue when lesions resolve

Pediatric

Shampoo or cream: Administer as in adults
Tablet:
<2 years: Not established
>2 years: 3.3-6.6 mg/kg/d PO once

Interactions

None reported for topical formulations; isoniazid may decrease bioavailability of systemic ketoconazole; rifampin decreases effects of systemic ketoconazole; systemic ketoconazole may increase anticoagulant effects; systemic ketoconazole may increase corticosteroid and cyclosporine toxicity (cyclosporine dose can be adjusted); may decrease theophylline levels; medications metabolized via P450 system (primarily CYP 3A4)

Contraindications

Documented hypersensitivity; fungal meningitis

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Discontinue topical use if sensitivity or irritation develops (for external use only; avoid contact with eyes); hepatotoxicity may occur with systemic ketoconazole; may reversibly decrease serum corticosteroid levels (adverse effects avoided with 200-400 mg/d); administer antacid, anticholinergics, or H2 blockers at least 2 h after dose; oral ketoconazole linked to hepatic toxicity; nausea or vomiting, abdominal pain, and pruritus

Econazole (Spectazole)

Effective in cutaneous infections. Interferes with RNA and protein synthesis and metabolism. Disrupts fungal cell wall permeability, causing fungal cell death.

Dosing

Adult

Apply sparingly over affected areas bid

Pediatric

Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

If sensitivity or irritation develops, discontinue use; for external use only; avoid contact with eyes

Antiseborrheic agents

These agents are helpful in the treatment of itching and flaking associated with dermatitis.

Selenium sulfide (Exsel, Selsun Blue, Head & Shoulders)

Blocks enzymes involved in epithelial tissue growth; use 1% or 2.5% shampoo and/or lotion.

Dosing

Adult

Massage 5-10 mL into wet scalp, leave in scalp for 2-3 min, rinse thoroughly, and repeat application; use twice weekly for 2 wk and then q1-4wk

Pediatric

Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity; broken or open skin (to avoid systemic toxicity)

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Avoid use in young children

Follow-up

Further Outpatient Care

• Regular clinical follow-up may be necessary to monitor the patient's condition and refill prescriptions.

Deterrence/Prevention

• Advise the patient to avoid predisposing factors such as emollients, occlusive topicals, occlusive nylon clothing, immunosuppressants, steroids, and antibiotics.

Prognosis

• The prognosis in PF is good.
• With treatment, PF can completely resolve.
• Without treatment, PF can be pruritic.

Miscellaneous

Medicolegal Pitfalls

• PF is often misdiagnosed as acne vulgaris.
• The practitioner should keep this in mind when examining erythematous papules and pustules that are acneiform but not on the face.
• Correct diagnosis may save the patient weeks, months, or years of time seeking care; annoyance; and expense related to the use of acne medications.
• Prolonged use of oral antifungals has been associated with occasional severe cutaneous, hematologic, and hepatic toxicity.

References

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Keywords

Pityrosporum folliculitis, fungal infection, skin fungus, PF, Malassezia folliculitis, PF, Pityrosporum orbiculare, P orbiculare, Pityrosporum ovale, P ovale, Malassezia furfur, M furfur

Contributor Information and Disclosures

Author

Siobahn M Bower, MD, Internal Medicine Resident, Creighton University
Siobahn M Bower, MD is a member of the following medical societies: American College of Physicians and American Medical Association
Disclosure: Nothing to disclose.

Coauthor(s)

Daniel J Hogan, MD, Affiliate Teaching Faculty, Sun Coast Hospital; Investigator, Hill Top Research, Florida Research Center
Daniel J Hogan, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Contact Dermatitis Society, and Canadian Dermatology Association
Disclosure: Nothing to disclose.

Stephen H Mason, MD, Assistant Professor of Dermatology, Medical College of Georgia
Stephen H Mason, MD is a member of the following medical societies: American Academy of Dermatology, American College of Mohs Micrographic Surgery and Cutaneous Oncology, American Society for Dermatologic Surgery, Skin Cancer Foundation, and Women's Dermatologic Society
Disclosure: Nothing to disclose.

Medical Editor

Jean-Hilaire Saurat, MD, Chair, Professor, Department of Dermatology, University of Geneva, Switzerland
Jean-Hilaire Saurat, MD is a member of the following medical societies: American Academy of Dermatology, American Dermatological Association, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

Pharmacy Editor

Michael J Wells, MD, Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center
Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association
Disclosure: Nothing to disclose.

Managing Editor

Lester F Libow, MD, Dermatopathologist, South Texas Dermatopathology Laboratory
Lester F Libow, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, and Texas Medical Association
Disclosure: Nothing to disclose.

CME Editor

Glen H Crawford, MD, Assistant Clinical Professor, Department of Dermatology, University of Pennsylvania School of Medicine; Chief, Division of Dermatology, The Pennsylvania Hospital
Glen H Crawford, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, Phi Beta Kappa, and Society of USAF Flight Surgeons
Disclosure: Nothing to disclose.

Chief Editor

William D James, MD, Paul R Gross Professor of Dermatology, University of Pennsylvania School of Medicine; Vice-Chair, Program Director, Department of Dermatology, University of Pennsylvania Health System
William D James, MD is a member of the following medical societies: American Academy of Dermatology and Society for Investigative Dermatology
Disclosure: elsevier Royalty Other; american college of physicians Honoraria Other

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Brittany J. Oswald, MD, to the development and writing of this article.

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