Malassezia (Pityrosporum) Folliculitis 

  • Author: Siobahn M Bower, MD; Chief Editor: Dirk M Elston, MD   more...
 
Updated: Jan 23, 2012
 

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 Pityrosporum folliculitis in 1969, and, later in 1973, Potter et al[1] identified Pityrosporum folliculitis as a separate clinical and histologic diagnosis.

Yeasts, specifically Malassezia furfur, are the pathogenic agents in Pityrosporum folliculitis. M furfur has been linked to several skin diseases, including seborrheic dermatitis, folliculitis, pityriasis versicolor, and atopic dermatitis.[2] 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.[3]

Pityrosporum folliculitis is caused by Malassezia species that are part of the cutaneous microflora and not by exogenous species.[4] However, the focus of this article is M furfur, which is considered the pathologic agent of Pityrosporum folliculitis. 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 Pityrosporum folliculitis 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 Pityrosporum folliculitis.

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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 Pityrosporum folliculitis, 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.

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Epidemiology

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 Pityrosporum folliculitis. People living in warm and humid climates have a higher incidence of Pityrosporum folliculitis. One clinic in the Philippines documented that 16% of all patient visits were a result of Pityrosporum folliculitis.[5] A 2008 report from China cites that 1.5% off all dermatology patients were diagnosed with Pityrosporum folliculitis, most of them healthy, middle-aged males.[6]

Mortality/Morbidity

Pityrosporum folliculitis may be a bothersome condition (ie, severe pruritus), but the lesions are benign. Some underlying conditions that predispose the patient to Pityrosporum folliculitis include diabetes mellitus, immunodeficiency, and systemic candidiasis[7] ; these conditions may cause morbidity. Consider the presence of predisposing conditions when Pityrosporum folliculitis is diagnosed.

Race

No known racial differences in the frequency of Pityrosporum folliculitis exist.

Sex

Reports of Pityrosporum folliculitis 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

Pityrosporum folliculitis is recognized as one that affects youths and young and middle-aged adults[8] ; Pityrosporum folliculitis is most common in those aged 13-45 years. However, 3 cases of Pityrosporum folliculitis 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.[9]

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Contributor Information and Disclosures
Author

Siobahn M Bower, MD  Internal Medicine Physician, Boys Town National Research Hospital

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  Clinical Professor of Internal Medicine (Dermatology), Nova Southeastern University College of Osteopathic Medicine; 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

Stephen H Mason 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.

Specialty Editor Board

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.

Michael J Wells, MD  Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine

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.

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.

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

Dirk M Elston, MD  Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

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

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